Internal Medicine

MEDICINE
By Dr.Mohammad Z. abu sheikha@
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GASTROENTEROLOGY
+Leukoplakia refer to a white patch
+Causes Of Mouth Ulceration :
.herpes simplex type II
.syphilis
.crohn's disease
.behcet's disease
+Causes Of Macroglossia :
.hypothyroidism
.down's syndrome
.acromegaly
.amyloidosis
+Features Of Herpetic Stomatitis :
.vesicles and ulcers on the buccal mucosa as well as tongue and palate
.inflamed gums
.pain
.cervical lymph glands enlargement
**Dyspepsia
-Is term used to describe symptoms such as bloating and nausea which are thought to originate from the upper GI
-Dyspepsia is a common problem and is frequently caused by gastroesophageal reflux disease (GERD) or gastritis. It may be the
first symptom of peptic ulcer disease (an ulcer of the stomach or duodenum)
-Signs & Symptoms :
.upper abdominal pain
.upper abdominal fullness (feeling full earlier than expected when eating)
.heartburn
.nausea
.belching
-Causes :
.psychological, anxiety, depression
.post infectious dyspepsia (is the term given when dyspepsia occurs after an acute gastroenteritis infection)
.systemic disease (renal failure, hypercalcemia)
.diseases of the gastrointestinal tract (GERD, peptic ulcer disease, gastritis, gastric cancer, esophageal cancer, coeliac disease,
food allergy, IBD, IBS, chronic intestinal ischemia, esophageal spasm, colonic carcinoma and gastroparesis)
.liver and pancreas diseases (cholelithiasis, gallstones, chronic pancreatitis, hepatitis and pancreatic cancer-metastasis)
.food or drug intolerance (overeating, eating too quickly, eating high-fat foods, eating during stressful situations, or drinking too
much alcohol or coffee)
.many medications cause dyspepsia (aspirin, nonsteroidal anti-inflammatory drugs NSAIDs, antibiotics (metronidazole,
macrolides), diabetes drugs (metformin, Alpha-glucosidase inhibitor, amylin analogs, GLP-1 receptor antagonists),
antihypertensive medications (angiotensin converting enzyme [ACE] inhibitors, Angiotensin II receptor antagonist), cholesterol-
lowering agents (niacin, fibrates), neuropsychiatric medications (cholinesterase inhibitors [donepezil, rivastigmine]), SSRIs
(fluoxetine, sertraline), serotonin-norepinephrine-reuptake inhibitors (venlafaxine, duloxetine), Parkinson drugs (Dopamine
agonist, monoamine oxidase [MAO]-B inhibitors), corticosteroids, estrogens, digoxin, iron, and opioids)
-Diagnosis :
.people under 55yrs without alarm symptoms can be treated without investigation, but are considered for investigation for
peptic ulcer disease caused by Helicobacter pylori infection
.people over 55yrs with recent onset dyspepsia or those with alarm symptoms should be urgently investigated by upper
gastrointestinal endoscopy. This will rule out peptic ulcer disease, medication-related ulceration, malignancy and other rarer
causes
+Medication-related dyspepsia is usually related to NSAIDs and can be complicated by bleeding or ulceration with perforation
of stomach wall
-Treatment :
proton pump inhibitors (PPIs) - omeprazole (which are effective for the treatment of heartburn) (this drugs used to reduction of
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gastric acid production)

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By Dr.Mohammad abu sheikha@

+These Drugs (PPIs) Are Used In The Treatment Of :
.Dyspepsia
.Peptic ulcer disease including after endoscopic treatment for bleeding
.As part of Helicobacter pylori eradication therapy
.Gastroesophageal reflux disease (GERD or GORD) including symptomatic endoscopy-negative reflux disease and associated
laryngopharyngeal reflux causing laryngitis and chronic cough
.Barrett's esophagus
.Eosinophilic esophagitis
.Stress gastritis and ulcer prevention in critical care
.Gastrinomas and other conditions that cause hypersecretion of acid including Zollinger–Ellison syndrome
+Alarm Features In Dyspepsia :
.weight loss
.anemia
.vomiting
.hematemesis and melena
.dysphagia
.palpable abdominal mass
**Dysphagia
-Is difficulty in swallowing
+Odynophagia (is painful swallowing, in the mouth or esophagus. It can occur with or without dysphagia)
-Signs & Symptoms :
.swallowing difficulty
.difficulty controlling food in the mouth
.inability to control food or saliva in the mouth
.coughing
.choking
.frequent pneumonia
.unexplained weight loss
.gurgle or wet voice after swallowing
.nasal regurgitation
+The M.C symptom of esophageal dysphagia is the inability to swallow solid food, which the patient will describe as 'becoming
stuck' or 'held up' before it either passes into the stomach or is regurgitated
+Pain on swallowing or odynophagia is a distinctive symptom that can be highly indicative of carcinoma, although it also has
numerous other causes that are not related to cancer
-Dysphagia Is Classified Into Three Major Types :
1.Oropharyngeal dysphagia (Swallowing disorders can occur in all age groups, resulting from congenital abnormalities,
structural damage, and/or medical conditions - in patients who have had strokes, and in patients who are admitted to acute
care hospitals or chronic care facilities, head and neck cancer and progressive neurologic diseases like parkinson's disease,
dementia, multiple sclerosis, multiple system atrophy, or amyotrophic lateral sclerosis)
2.Esophageal dysphagia (arises from the body of the esophagus, lower esophageal sphincter, or cardia of the stomach, usually
due to mechanical causes or motility problems)
3.Functional dysphagia (is defined in some patients as having no organic cause for dysphagia that can be found)
-Causes (all causes of dysphagia are considered as differential diagnosis) :
.esophageal atresia
.paterson-Kelly syndrome
.zenker's diverticulum
.benign strictures
.achalasia
.esophageal diverticula
.scleroderma (systemic sclerosis)
.diffuse esophageal spasm
.webs and rings
.esophageal cancer
.eosinophilic esophagitis
.hiatus hernia (especially paraesophageal type)
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.dysphagia lusoria
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.gastroesophageal reflux
.infections (candida esophagitis, HSV)

.aortic aneurysm
.chagas` disease
.autonomic nervous system pathologies (stroke and Amyotrophic lateral sclerosis ALS)
-Complications :
.pulmonary aspiration
.pneumonia (secondary to food or liquids going the wrong way into the lungs)
.dehydration
.weight loss (malnutrition)
.renal failure
+Some people present with "silent aspiration" and do not cough or show outward signs of aspiration
-Investigation :
.endoscopy (investigation of choice)
.barium swallow (of abnormality is found in endoscopy)
-Treatment (treating dysphagia depends on the type and severity of a patient's swallowing difficulty) :
.for difficulties in the mouth and throat areas, treatments are generally focused on swallowing therapy, including exercises, and
dietary changes
.for problems in the esophagus, treatment options may include surgery or medicine
.feeding tubes are also options for treating dysphagia (nasogastric or endoscopic tubes)
+The incidence of dysphagia is higher in the elderly, in patients who have had strokes, and in patients who are admitted to
acute care hospitals or chronic care facilities
**Achalasia
-Failure of relaxation of the lower oesophageal sphincter LES / Is a failure of smooth muscle fibers to relax, which can cause a
sphincter to remain closed and fail to open when needed
+Achalasia can happen at various points along the gastrointestinal tract; achalasia of the rectum, for instance, in Hirschsprung's
disease
-Characterized By :
.F > M / 40yrs of age
.regurgitation and aspiration pneumonia are common (food and liquid, including saliva, are retained in the esophagus and may
be inhaled into the lungs - aspiration)
.difficulty in swallowing (dysphagia - tends to become progressively worse over time and to involve both fluids and solids)
.regurgitation (of undigested food)
.sometimes chest pain (behind the sternum) (cardiospasm and non-cardiac chest pain can often be mistaken for a heart attack)
.weight loss
.coughing when lying in a horizontal position
+The M.C form is primary achalasia (which has NO known underlying cause, it is due to the failure of distal esophageal
inhibitory neurons)
+Secondary achalasia (occurs to other conditions, such as esophageal cancer or Chagas disease)
-Causes :
.lymphoma
.carcinoma
.chaga`s disease
.neurotropic viruses
.ischemia
.irradiation
.drugs and toxins
.postvagotomy
+The cause of most cases of achalasia is unknown
-Diagnosis :
.esophageal manometry
.barium swallow radiographic studies
.esophagogastroduodenoscopy EGD
-Treatment :
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.pneumatic balloon dilation

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.pneumatic dilation or surgery (surgical myotomy)

.botulinum toxin
**Diffuse Esophageal Spasm (DES)

-Is a condition characterized by uncoordinated contractions of the esophagus, which may cause difficulty swallowing
(dysphagia) or regurgitation
-Signs & Symptoms :
.dysphagia (for solid foods and liquids hot or cold)
.intermittent chest pain (the pain similar to heart disease)
.on x-ray imaging are commonly observed in DES, such as a "corkscrew" or "rosary bead esophagus"
-Causes :
.caused by uncontrolled brain signals running to nerve endings
.suppression medication, such as (antidepressants and antiepileptic medication)
.very cold or hot beverages can trigger an esophageal spasm
+The cause of DES remains unknown
-Diagnosis :
.barium swallow x-ray “corkscrew”
-Treatment :
.nitroglycerin, calcium channel blockers (nifedipine, nitrates), hydralazine
.proton pump inhibitors PPIs
.botulinum toxin
**Esophagitis
-Is inflammation of the esophagus. It may be acute or chronic
+Acute esophagitis can be catarrhal or phlegmonous (Catarrh is a disorder of inflammation of the mucous membranes in one of
the airways or cavities of the body. It can result in a thick exudate of mucus and white blood cells caused by the swelling of the
mucous membranes in the head in response to an infection / Phlegmon is a spreading diffuse inflammatory process with
formation of suppurative/purulent exudate or pus)
+Chronic esophagitis may be hypertrophic or atrophic
-Signs & Symptoms :
.heartburn (pain in chest/abdomen, which may radiate to neck/jaw)
.nausea, vomiting
.abdominal pain
+Symptoms may be relieved by antacids. Esophagitis causes symptoms of abdominal pain and vomiting. If not treated, it causes
discomfort and scarring of the esophagus. This makes swallowing food more difficult
-Causes :
.infectious (are typically seen in immunocompromised people)  Types :
.Esophageal candidiasis M.C / Viral - Herpes simplex (Herpes esophagitis), Cytomegalovirus albicans
+M.C infection is from Candida
+Endoscopy can be used to distinguish among these conditions
.GERD (M.C.C)
.chemical injury by alkaline or acid solutions
.physical injury resulting from radiation therapy or by nasogastric tubes
.pill esophagitis
.hyperacidity
.alcohol abuse
.eosinophilic esophagitis
.esophageal carcinoma
.esophageal obstruction
.Crohn's disease – a type of IBD which is also an autoimmune disease where the immune system in flames the gastrointestinal
tract
.certain medications (doxycycline)
**Gastroesophageal Reflux Disease GERD

-Is a chronic condition of mucosal damage caused by stomach acid coming up from the stomach into the esophagus (chronic
reflux) / GERD is caused by a failure of the lower esophageal sphincter
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-Signs & Symptoms :

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.heartburn and regurgitation (M.C symptoms of GERD)

.dyspepsia, odynophagia
.sore throat, hoarseness
.nausea, vomiting (repeated vomiting in infants)
.epigastric pain, chest pain (pain in the substernal area)
.coughing
.respiratory problems (wheezing, bad breath)
.increased salivation (also known as water brash)
.weight loss
.gastritis
-Risk factors :
.hiatal hernia
.obesity (delayed gastric emptying, increase-gastric volume as after large meal, gastric pressure as obesity)
.smoking, alcohol
.pregnancy
.surgery in achalasia
.Zollinger-Ellison syndrome
.high blood calcium level (hypercalemia)
.scleroderma and systemic sclerosis
.the use of medicines (prednisolone, tricyclic)
.visceroptosis or Glénard syndrome
+Factors that have been linked with GERD (but not conclusively) :
.obstructive sleep apnea
.gallstones
-Differential Diagnosis :
.chest pain such as heart disease
.respiratory and laryngeal signs and symptoms, is called laryngopharyngeal reflux (LPR) or "extraesophageal reflux disease"
(EERD). Unlike GERD, LPR rarely produces heartburn, and is sometimes called silent reflux
-Diagnosis :
.pH monitor (gold standard) (may be useful in those who do not improve after PPIs and is not needed in those in whom
Barrett's esophagus is seen)
+Investigation for H. pylori is NOT usually needed
-Treatment :
.PPIs (proton-pump inhibitors - omeprazole, esomeprazole, lansoprazole (will all reliably increase the PH of gastric contents)
.H2 blockers (should only be used in Pt. has very mild, intermittent symptoms)
-Complications :
.anemia (iron deficiency)
.recurrent chest infections
.esophagitis (M.C.C of esophagitis is GERD)
.pulmonary (aspiration pneumonia, cough and asthma)
.barrett's esophagus
.motility disturbances
.benign esophageal stricture
.esophageal Carcinoma
.gastric volvulus
**Benign Esophageal Stricture

-Is a narrowing or tightening of the esophagus that causes swallowing difficulties
-Occurs most often in elderly Pts. who have poor esophageal clearance
-Signs & Symptoms :
.heartburn
.bitter or acid taste in the mouth
.choking, coughing, shortness of breath
.frequent burping or hiccups
.pain or trouble swallowing, throwing up blood
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.weight loss
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-Causes :
.GERD
.webs and rings

.carcinoma of the esophagus
.dysfunctional lower esophageal sphincter (following long-term nasogastric intubation)
.esophagitis
.disordered motility
.lye ingestion
.hiatal hernia
.after esophageal surgery and other treatments such as laser therapy or photodynamic therapy / post-radiotherapy
-Diagnosis :
.X-ray while the patient swallows barium (called a barium study of the esophagus)
-Treatment :
.Esophageal dilatation
.If it is caused by esophagitis, in turn caused by an underlying infection, it is commonly treated by treating the infection
(typically with antibiotics)
.H2 antagonist (e.g. ranitidine) or a proton-pump inhibitor (e.g. omeprazole) can treat underlying acid reflux disease
**Tumors Of The Esophagus (Esophageal Cancer)

-Is cancer arising from the esophagus—the food pipe that runs between the throat and the stomach
+Squamous cancer can arise in any part of the esophagus, and almost all tumors in the upper oesophagus are squamous
cancers
+Adenocarcinomas typically arise in the lower third of the oesophagus from barrett's esophagus or from the cardia of the
stomach
-Types :
.squamous-cell carcinoma
.adenocarcinoma
+Squamous-cell carcinoma (is linked to lifestyle factors such as smoking and alcohol)
+Adenocarcinoma (is linked to effects of long-term acid reflux - history of GERD and Barrett's esophagus)
+Long standing GERD can induce a change of cell type in the lower portion of the esophagus in response to erosion of its
squamous lining
+Tobacco is a risk factor for both types
+Both types are more common in men and in the over-60s (M > F)
-Signs & Symptoms :
.narrowing of the tube
.difficulty in swallowing (M.C symptom) (with solid foods and later with softer foods and liquids)
.weight loss (is often an initial symptom in cases of squamous-cell carcinoma, though not usually in cases of adenocarcinoma)
.pain behind the breastbone or in the region around the stomach
.heartburn
.husky, raspy, or hoarse-sounding cough
.nausea and vomiting, regurgitation
-Complications :
.increased risk of aspiration pneumonia
.fistulas (that may develop between the esophagus and the trachea)
.coughing on drinking or eating
.vomiting of blood
.upper airway obstruction
.superior vena cava syndrome
.hypercalcemia
.result of the tumor affecting the recurrent laryngeal nerve
-Diagnosis :
.endoscopy (BEST)
.barium swallow
-Treatment :
.esophagectomy is the removal of a segment of the esophagus
.chemotherapy depends on the tumor type (chemotherapy may be given after surgery or if surgery is not possible; in this case,
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cisplatin and 5-FU are used)

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.radiotherapy is given before, during, or after chemotherapy or surgery, and sometimes on its own to control symptoms
+In patients with localised disease but contraindications to surgery, "radical radiotherapy" may be used with curative intent
**Barrett's Esophagus
-The epithelium of the lower esophagus undergoes histologic change from a normal squamous epithelium to a columnar
epithelium (GERD for long time) / Refers to an abnormal change (metaplasia) in the cells of the lower portion of the esophagus
-Is a complication of long standing reflux disease. After several years of GERD
+The risk of developing Barrett's esophagus is increased by central obesity
-Signs & Symptoms :
.frequent and long standing heartburn
.trouble swallowing (dysphagia)
.vomiting blood (hematemesis)
.pain under the sternum (where the esophagus meets the stomach)
.weight loss (because eating is painful)
-Diagnosis :
.endoscopy (Pt. with Barrett's Esophagus should have a repeat endoscopy every 2-3yrs to see whether dysplasia or esophageal
cancer)
.esophagectomy is warranted if high grade dysplasia is found
-Treatment :
.PPIs
.operative therapy prevents further progression of the disease
**Hiatus Hernia
1.Oesophago-gastric hernia (Sliding)
.M.C type / Herniations of the cardia and very small part of the stomach through the diaphragm
.it is common in old age obese female (increase the intra-abdominal pressure)
2.Para-oesophageal hernia (Rolling)
.part of stomach (fundus) herniated through the diaphragm without herniations of the cardia
.usually there are no symptoms
3.Mixed hernia
**Plummer–Vinson Syndrome (PVS)

-Is a rare disease characterized by difficulty in swallowing + iron deficiency anemia + glossitis, cheilosis and esophageal webs
+Generally occurs in postmenopausal women. Its identification and follow-up is considered relevant due to increased risk of
squamous cell carcinomas of the esophagus and pharynx
+It is M.C in women (in middle age - peak age is over 50)
-The Condition Is Associated With :
.genetic factors and nutritional deficiencies
.koilonychia
.glossitis
.inflammation of the lips (cheilitis)
.splenomegaly
+Esophageal web in Plummer-Vinson syndrome is found at upper end of esophagus (post cricoid region) and Schatzki ring may
be found at the lower end of esophagus
-Signs & Symptoms :
.dysphagia (difficulty in swallowing)
.pain
.weakness
.odynophagia (painful swallowing)
.atrophic glossitis
.angular stomatitis
.post-cricoid web
.iron deficiency
-Complications :
.developing squamous cell carcinoma of the oral cavity, esophagus, and hypopharynx
-Treatment :
.with iron supplementation, IF NOT;
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.the web can be dilated during upper endoscopy to allow normal swallowing and passage of food
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**Mallory-Weiss Syndrome
-Refers to bleeding from a laceration in the mucosa at the junction of the stomach and esophagus
+This is usually caused by severe vomiting because of alcoholism or bulimia, but can be caused by any conditions which causes
violent vomiting and retching such as food poisoning
+The syndrome presents with painful hematemesis. The laceration is sometimes referred to as a Mallory-Weiss tear
+Is a non transmural tear of the lower esophagus that is related to repeated episodes of retching and vomiting
+The tear involves mucosa and submucosa but not the muscular layer (contrast to Boerhaave syndrome which involves all the
layers)
-Signs & Symptoms :
.painless swallowing (NOT difficulty)
.painless upper GI bleeding
.black stool from melena (if the volume of bleeding is >100mL or with hematemesis)
-Causes :
.alcoholism
.eating disorders
.hiatal hernia
.forceful vomiting
.NSAID abuse
+The mean age is more than 60yrs (M > F)
-Diagnosis :
.upper endoscopy
-Treatment :
.epinephrine
.cauterization
**Abdominal Pain
-Causes Of Chronic Or Recurrent Abdominal Pain :
.aortic aneurysm
.malignancy
.lymphadenopathy
.abscess
.depression
.anxiety
.hypochondriasis
.somatization
.DM
.addison's disease
.hypercalcemia
.drugs/toxins (corticosteroids, lead, alcohol, azathioprine)
.haematological (sickel-cell disease, haemolytic disorders)
.spinal cord lesions
.esophageal causes (spasm, GERD, oesophagitis)
.gastro-duodenal casues (overfeeding, gastritis, peptic ulcer)
.intestinal causes (UC-CD, diverticulitis, appendicitis, intestinal parasites, tuberculosis, obstruction-irritable colon)
.biliary causes (gallstones, cholecystitis)
.pancreatic causes
.hepatic causes
.urinary causes
.genital causes
.vascular casuses
**Vomiting
-Causes :
.CNS disorders (vestibular neuronitis, migraine, raised intracranial pressure, meningitis)
.gastroduodenal (PUD, gastric cancer, gastroparesis)
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.uraemia
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.the acute abdomen (appendicitis, cholecystitis, pancreatitis, intestinal obstruction)

.alcoholism
.drugs (NSAIDs, opiates, digoxin, antibiotics, cytotoxins)
.infections (hepatitis, gastroenteritis, UTI)
.metabolic (diabetic ketoacidosis, addison`s disease, cyclical vomiting syndrome, hyperglycaemia, hypoglycaemia ,acidosis,
alkalosis, hyperparathyroidism)
**Gastritis
-Inflammation, erosion or damage of the gastric lining that has not developed into an ulcer / Is inflammation of the lining of the
stomach. It may occur as a short episode or may be of a long duration
+Gastrin is produced primarily in the Pylorus
-Types :
+type A (autoimmune)
.gastritis from atrophy of the gastric mucosa and is associated with autoimmune processes, such as Vit B12 deficiency
.also linked to diminished gastric acid production and achlorhydria, and it is lead to gastric cancer
+Achlorhydria (production of hydrochloric acid in gastric secretions of the stomach and other digestive organs is absent or low)
+Hypochlorhydria Is Caused By :
.carcinoma of stomach
.pregnancy
.pernicious anemia
.atrophic gastritis
+Type B (increased gastric acid production)
.M.C type of gastritis. It is also associated with increased gastric acid production
-Signs & Symptoms :
.abdominal pain (M.C symptom)
.nausea, vomiting (if present, may be clear, green or yellow, blood-streaked, or completely bloody, depending on the severity of
the stomach inflammation)
.belching (if present, usually does not relieve the pain much)
.bloating
.loss of appetite, early satiety, weight loss
.heartburn
-Causes Of Gastritis :
.H.pylori (M.C.C of chronic gastritis)
.alcohol, smoking, cocaine abuse
.NSAIDs (aspirin)
.drugs as (iron preparation)
.radiation therapy
.autoimmune problems or disease (Crohns disease)
.sever stress as (burn, trauma, infection, surgery and organ failure)
-Complications :
.bleeding
.stomach ulcers
.stomach tumors
.low red blood cells due to not enough (vitamin B12) - a condition known as pernicious anemia
-Diagnosis :
.endoscopy (BEST)
.Presence of H. pylori
.blood cell count
.stool sample (to look for blood in stool)
-Treatment :
.PPIs
.H2 blockers
.antibiotics
**Zollinger-Ellison Syndrome (ZES)

-Is caused by a non–beta islet cell (islet of Langerhans), gastrin-secreting tumor of the pancreas that stimulates the acid-
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secreting cells of the stomach (parietal cells) to maximal activity, with consequent gastrointestinal mucosal ulceration
+Is hypergastrinemia caused by cancer of gastrin-producing cells (gastrinoma) – excessive production and release of gastrin G
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cells
+The primary tumor associated with ZES is usually located in the pancreas (M.C site), duodenum, stomach or abdominal lymph
nodes, but ectopic locations have also been described (e.g., heart, ovary, gallbladder, liver, kidney)
+ZES may occur sporadically or as part of an autosomal dominant familial syndrome called multiple endocrine neoplasia type
1 (MEN 1)
+A small percentage are associated with parathyroid, pituitary and pancreatic tumors, anemia, chronic gastritis, renal failure,
hyperthyroidism
+Malignant tumors that most commonly spread to the liver and lymph nodes near the pancreas and small bowel
+Patients with gastrinomas have multiple tumors as part of a condition called multiple endocrine neoplasia type I (MEN I) -
MEN I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas
-Signs & Symptoms :
.abdominal pain and diarrhea
.chronic diarrhea, including steatorrhea (fatty stools)
.pain in the esophagus (especially between and after meals at night)
.nausea
.wheezing
.vomiting blood (digested blood)
.malnourishment
.loss of weight due to loss of appetite
-Diagnosis :
.endoscopy
+Laboratory Tests :
.secretin stimulation test, which measures evoked gastrin levels
.fasting gastrin levels, on at least three separate occasions
.gastric acid secretion and pH
.increased level of chromogranin A (is a common marker of neuroendocrine tumors)
+Normal basal gastric acid secretion is less than 10 mEq/hour, while in Zollinger–Ellison syndrome it is usually more than 15
mEq/hour
+The source of the increased gastrin production must be discovered. This is either done using MRI or somatostatin receptor
scintigraphy, the investigation of choice
-Treatment :
.PPIs (omeprazole, lansoprazole)
.H2 blockers (famotidine, ranitidine)
+Octreotide is the best drug for pharmacologic management. Cure is only possible if the tumors are surgically removed, or
treated with chemotherapy
**Peptic Ulcer Disease PUD

-Is a break in the lining of the stomach, first part of the small intestine, or occasionally the lower esophagus
+An ulcer in the stomach is known as a gastric ulcer
+In the first part of the intestines is known as a duodenal ulcer
-Signs & Symptoms :
.at night with upper abdominal pain or upper abdominal pain that improves with eating (pain as burning or dull ache)
.belching
.nausea, vomiting (copious vomiting)
.hematemesis (vomiting of blood) (this can occur due to bleeding directly from a gastric ulcer, or from damage to the
esophagus from severe/continuing vomiting)
.weight loss, or poor appetite
.bloating and abdominal fullness
.water-brash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated
with gastroesophageal reflux disease)
.melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin)
.rarely, an ulcer can lead to a gastric or duodenal perforation, which leads to acute peritonitis, extreme, stabbing pain
+The pain caused by peptic ulcers can be felt anywhere from the navel up to the sternum, it may last from few minutes to
several hours and it may be worse when the stomach is empty
-Causes :
.history of heartburn
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.gastroesophageal reflux disease (GERD)

.medicines associated with peptic ulcer include (NSAIDs that inhibit cyclooxygenase) (glucocorticoids - dexamethasone,
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prednisolone)
.H.pylori (60% of gastric and up to 50-75% of duodenal ulcers) (M.C.C)
.stress (it does not seem to independently increase risk. Even when coupled with H. pylori infection)
.dietary factors, such as (spice consumption, caffeine and coffee, alcohol, smoking) (it does not seem to independently increase
risk. Even when coupled with H. pylori infection)
.gastrinoma (Zollinger–Ellison syndrome), rare gastrin-secreting tumors, also cause multiple and difficult-to-heal ulcers
-Complications :
.gastrointestinal bleeding (M.C complication) (it occurs when the ulcer erodes one of the blood vessels, such as the
gastroduodenal artery)
.perforation (sign is Valentino's syndrome)
.penetration (is a form of perforation in which the hole leads to and the ulcer continues into adjacent organs such as the liver
and pancreas)
.gastric outlet obstruction (is the narrowing of pyloric canal by scarring and swelling of gastric antrum and duodenum due to
peptic ulcers / Patient often presents with severe vomiting without bile)
.cancer
.gastritis
.stomach cancer
.gastroesophageal reflux disease GERD
.pancreatitis
.hepatic congestion
.cholecystitis
.biliary colic
.inferior myocardial infarction
.referred pain (pleurisy, pericarditis)
.superior mesenteric artery syndrome
+The Diagnosis Of Helicobacter Pylori Can Be Made By :
.urea breath test (radioactive carbon to detect H. pylori - carbon dioxide)
.direct culture from an EGD biopsy specimen
.direct detection of urease activity in a biopsy specimen by rapid urease test
.measurement of antibody levels in blood (does not require EGD)
.stool antigen test
.histological examination and staining of an EGD biopsy
+Malignancy (gastric cancer) (this is especially true in ulcers of the greater (large) curvature of the stomach; most are also a
consequence of chronic H. pylori infection)
+The M.C presentation of ulcer disease is midepigastric pain / There is no definite way to distinguish between duodenal and
gastric ulcers simply by symptoms
-Treatment :
.younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before endoscopy
.people who are taking non steroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue
(misoprostol) in order to help prevent peptic ulcers
.acid reducing medication (ranitidine and famotidine, which are both H2 receptor antagonists, provide relief of peptic ulcers,
heartburn, indigestion. They decrease the amount of acid in the stomach helping with healing of ulcers)
+In the absence of H. pylori, 4 weeks of a PPIs are also often used
.When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. clarithromycin,
amoxicillin, tetracycline, metronidazole) and a proton-pump inhibitor (PPI)
.In complicated, treatment-resistant cases, 3 antibiotics (e.g. amoxicillin + clarithromycin + metronidazole) may be used
together with a PPI and sometimes with bismuth compound
+Surgery (stop bleeding with cautery, injection, or clipping - endoclip)
*Duodenal Ulcers (DU)

-Commoner than GU / M > F / The M.C pathophysiologic mechanism of DU is primarily related to (Gastric acid hypersecretion)
+Increased gastric acid secretion / increased gastric emptying / decreased duodenal pH
+Chronic duodenal ulcer usually occurs in the first part of the duodenum (bulb of duodenum) just distal to the junction of lyloric
and duodenal mucosa; 50% are on the anterior wall
-Signs & Symptoms :
12
.mid-epigastric pain, tenderness typically before meals at night, relieved by eating or drinking milk
.abdominal pain (in case of duodenal ulcers the pain appears about 3hrs after taking a meal, when the stomach begins to
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release digested food and acid into the duodenum)

.nausea, vomiting
+Symptoms of duodenal ulcers would initially be relieved by a meal, as the pyloric sphincter closes to concentrate the stomach
contents, therefore acid is not reaching the duodenum
+Perforation (anterior duodenal ulcer) / Bleeding (posterior peptic ulcer)
-Risk Factors :
.H.pylori
.drugs (aspirin, NSAIDs, steroids)
.blood group O
.smoking
.cancer of stomach
.zollinger-ellison syndrome (syndrome must you always think of with a duodenal ulcer)
.crohns disease
.head truma
.hyperparathyroidism
.chronic pulmonary insufficiency
-Diagnosis :
.upper GI endoscopy
*Gastric Ulcer (GU)

-Occur mainly on the elderly / Affects the Pts. of >40yrs of age / GU may become malignant (DU are not)
+Commonly occurs at the lesser curvature of the stomach
-Signs & Symptoms :
.asymptomatic or epigastric pain
+Pain during the meal, as gastric acid production is increased as food enters the stomach
.weight loss
-Risk Factors :
.H.pylori
.smoking
.NSAIDs
.reflux of deudenal-contents
.delayed gastric emptying
.stress
.alcohol
.neurosurgery (cushing`s ulcers)
-Diagnosis :
.upper GI endoscopy
.biopsies from the ulcer`s rim and base
-Drugs (used in the treatment of duodenal ulcer) :
.sucralfate
.sismuth
.sirazepine
.H2-receptors antagonists
+H. pylori Can Lead To :

.MALT lymphoma
.gastric ulcers
.duodenal ulcers
.gastric cancer
+Drugs Are Used In The Management Of Peptic Ulcer Disease : (FSOARC)
.Famotidine
.Sucralfate
.Omeprazole
.Anticholinergic drugs
.Ranitidine
.Cimetidine
13
+Drugs Are Used For H. Pylori Eradication :

.Tetracycline
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.Metronidazole
.Clarithromycin
.Amoxicillin
+Cimetidine is a selective H2 receptor blocker which inhibits gastric secretion
**Cancer Stomach (Gastric Cancer)

-Most commonly in the antrum or the lesser curvature
-Histopathology :
.adenocarcinoma (90%) (is a malignant epithelial tumor)
.lymphomas (5%) (MALTomas, or MALT lymphoma)
.carcinoid and stromal tumors
-Signs & Symptoms :
.metastases
.paramalignant syndrome as dermatomyositis and thrombophlebitis (Trousseau's`s sign)
.asymptomatic (producing no noticeable symptoms)
.heartburn
.upper abdominal pain
.abdominal discomfort
.nausea, vomiting
.diarrhea or constipation
.loss of appetite, weight loss (M.C symptom)
.yellow skin and whites of the eyes
.difficulty swallowing
.blood in the stool, vomiting blood
.melena (leading to anemia)
.dysphagia (suggests a tumour in the cardia or extension of the gastric tumour into the esophagus)
+Can be symptoms of other problems such as a stomach virus, gastric ulcer, or tropical sprue
+The cancer may spread from the stomach to other parts of the body, particularly the liver, lungs, bones, lining of the abdomen
and lymph nodes
-Risk Factors :
.old age (M > F) (Estrogen may protect women against the development of this cancer form)
.blood group A
.H.pylori (M.C.C)
.autoimmune gastritis
.adenomatous gastric polyp
.GERD
.obesity
.smoking, alcohol
.iodine deficiency
.genetic risk factor for gastric cancer is a genetic defect of the CDH1 gene (E-cadherin, lies on the 16th chromosome) known as
hereditary diffuse gastric cancer (HDGC) (autosomal dominant)
.AIDS
.DM
.pernicious anemia
.chronic atrophic gastritis
.Menetrier's disease (hyperplastic, hypersecretory gastropathy)
.intestinal metaplasia
+A Mediterranean diet is also associated with lower rates of stomach cancer, as is regular aspirin use
+Sister mary joseph's sign is (periumbilical lymph node gastric cancer metastasis; present as periumbilical mass)
+Krukenberg's tumor is (gastric cancer or other adenocarcinoma, that has metastasized to the ovary)
+Irish`s node is (left axillary adenopathy from gastric cancer metastasis)
+Surveillance laboratory findings is (CEA elevated in 30% of cases)
+Histology (adenocarcinoma) / anus – esophagus (squamous cell carcinoma)
-Histologic Types :
.intestinal (glands)
14
.diffuse (no glands)

-Morphology Types :
.ulcerative (M.C morphologic type of gastric cancer)
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.polypoid
.scirrhous
.superficial
.linitis plastica (leather bottle)
+Gastric cancer more common on the lesser curvatures / proximal gastric cancer is more common
-Gastric Adenocarcinoma Metastasize (spread to other sites in the body by metastasize) :
.hematogenously
.lymphatically
.90% are adenocarcinoma
.5% of gastric malignancies are lymphomas (M.C GI lymphoma)
.M.C site for GI lymphoma is stomach
.metastasis occurs in 80-90% of individuals with stomach cancer
.M.C site for metastasis is liver
-Diagnosis :
.upper endoscopy + biopsy
-Treatment :
.surgery
+Endoscopic mucosal resection (EMR) is a treatment for early gastric cancer (tumor only involves the mucosa)
+Endoscopic submucosal dissection (ESD), used to resect a large area of mucosa in one piece
.chemotherapy and/or radiation therapy
+5-FU (fluorouracil) or its analog capecitabine, BCNU (carmustine), methyl-CCNU (semustine) and doxorubicin (Adriamycin), as
well as mitomycin C, and more recently cisplatin and taxotere
**Inflammatory Bowel Disease (IBD)

-Is a group of inflammatory conditions of the colon and small intestine. Crohn's disease and ulcerative colitis are the principal
types of inflammatory bowel disease
-Inflammatory bowel diseases fall into the (Class Of Autoimmune Diseases), in which the body's own immune system attacks
elements of the digestive system
+Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin
manifestations and eye problems) in different proportions
+Diagnosis is generally by assessment of inflammatory markers in stool followed by colonoscopy with biopsy of pathological
lesions
+Both treated with anti-inflammatory medications such as (mesalamine, azathioprine, 6-mercaptopurine ‘6MP’)
+The way doctors can tell the difference between Crohn's disease and UC is the location and nature of the inflammatory
changes (Crohn's can affect any part of the gastrointestinal tract, from mouth to anus (skip lesions), although a majority of the
cases start in the terminal ileum) (Ulcerative colitis, in contrast, is restricted to the colon and the rectum)
-Signs & Symptoms :
.abdominal pain
.vomiting
.diarrhea
.rectal bleeding
.severe internal cramps/muscle spasms in the region of the pelvis
.weight loss
.anemia
.arthritis
.pyoderma gangrenosum
.primary sclerosing cholangitis
.non-thyroidal illness syndrome (NTIS)
+Associations with deep vein thrombosis (DVT) and bronchiolitis obliterans organizing pneumonia (BOOP)
-The Extraintestinal Manifestations Of IBD Are :
.episcleritis
.scleritis
.iritis
.sclerosing cholangitis
.joint pain
.skin manifestations (pyoderma gangrenosum and erythema nodosum)
15
-Causes :
.IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors
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enteral bacteria can contribute to inflammatory gut diseases (can be altered by environmental factors, such as concentrated
milk fats - a common ingredient of processed foods and confectionery)
.oral medications such as (antibiotics and oral iron preparations)
.high protein intake, specifically animal protein via meat and fish consumption has been significantly associated with
inflammatory bowel disease as well as ulcerative colitis
+Other Forms Of IBD (which are NOT always classified as typical IBD) :
.Collagenous colitis
.Lymphocytic colitis
.Diversion colitis
.Behçet's disease
.Indeterminate colitis
*Crohn`s Disease CD
-Crohn's can affect any part of the GI tract, from mouth to anus (skip lesions), although a majority of the cases start in the
terminal ileum
-Crohn's disease affects the full thickness of the bowel wall (transmural lesions) / It is a chronic transmural granulomatous
inflammation
+Genetic factor (CARD 15/NOD-2) mutations predispose / More common in smokers / Colon cancer (Slight) (UC > CD)
+ASCA (anti-saccharomyces cerevisiae antibodies) are associated with CD / Cytokine response - Associated with Th17
+CD is more likely to be associated with a palpable abdominal mass because CD has granulomas in the bowel wall
+Caused by a combination of environmental, immune and bacterial factors in genetically susceptible individuals
+CD can result in (vitamin B12 ,calcium ,vitamin K and iron deficiencies because of malabsorption)
+Prothrombin time PT may be prolonged in CD because of Vit K malabsorption
+Kidney stones form more often in CD because the fat malabsorption results (in a low calcium level and an increased
absorption of oxalate, wich forms kidney stones)
-Signs & Symptoms :
.skip lesions
.small bowel obstruction
.stones (only with CD)
.clubbing
.stenosis
.Weight loss, loss appetite
.rheumatologic disease (ankylosing spondylitis, sacroiliac joint, joints-arthritis, erythema nodosum)
.conjunctivitis
.pulmonary embolism PE
.diarrhea (bloody diarrhea)
.hematologic disorders (autoimmune hemolytic anemia, vitamin B12, folate, iron deficiency)
.CNS disorders (seizures, stroke, myopathy, peripheral neuropathy, headache and depression)
.diarrhea, abdominal pain, weight loss
.liver disorders (fatty liver, liver cirrhosis, chronic hepatitis)
.dysphagia
.inability to maintain growth in children
-Systemic Complications :
.Ankylosing spondylitis
.Sclerosing cholangitis (1ry)
.uveitis/iritis
.Episcleritis
.Pericarditis
-Complications :
.perforation, fistula
.intestinal obstruction
-Investigations :
16
.colonoscopy and biopsy

.barium (show string sign)
.in children fecal calprotectin is useful
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*Ulcerative Colitis UC
-That causes inflammation and ulcers in the colon. It may affect just in the rectum (Colon and rectum only) – large bowel, it is
exclusively a mucosal disease / Ulcerative colitis is restricted to the mucosa (epithelial lining of the gut)
-Genetic factor (HLA-DR103) associated with severe disease / More common in non-smokers / M > F / Colon cancer (common-
Considerable) (UC > CD)
-ANCA (anti-neutrophil cytoplasmic antibody) is associated with UC / Cytokine response - Vaguely associated with Th2
-Signs & Symptoms :
.no skip lesions, no fistula formation and no oral or perianal involvement
.rectum is involved in most cases
.diarrhea, blood & mucus (bloody diarrhea)
.crampy abdominal discomfort
.fever, malaysia, anorexia
.anemia (Vit B12 deficiency - are NOT because at duodenum / only in CD)
.weight loss (rare in UC) (CD > UC)
.clubbing
.rheumatologic disease (ankylosing spondylitis, sacroiliac joint, joints-arthritis, erythema nodosum, arthropathy)
.conjunctivitis
.sacroilitis, osteomalacia
.fatty liver
.renal stones (more in CD)
.amyloidosis
.bile duct involvement (cholangitis)
+UC don't cause heartburn
-Systemic Complications :
.uveitis/iritis
.Episcleritis
.Pericarditis
-Complications :
.perforation, fistula (rare)
.toxic megacolon
.intestinal obstruction
-Investigations :
.colonoscopy and biopsy
.barium (show lead pipe sign)
.stool studies
.abdominal X-ray
.serologic studies (ANCA)
.in children fecal calprotectin is useful
+TREATMENT :
.Mesalazine Less useful (CD) More useful (UC)
.Antibiotics Effective in long-term (CD) Generally not useful (UC)
.Surgery Often returns following removal of affected part (CD)
Usually cured by removal of colon (UC)
+IBD may require immunosuppression to control the symptom, such as prednisone, TNF inhibition, azathioprine (Imuran),
methotrexate, or 6-mercaptopurine
+Severe cases may require surgery, such as bowel resection, strictureplasty or a temporary or permanent colostomy or
ileostomy
+Ulcerative colitis can in most cases be cured by proctocolectomy
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+Upper endoscopy (Are NOT)

+Both are most accurately DIAGNOSED with endoscopy
+Both are TREATED with anti-inflammatory medications (mesalamine, azathioprine, 6-mercaptopurine 6MP, steroids)
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+Both forms of IBD can lead to colon cancer after 8-10 years of involvement of the colon (UC > CD)
+Definite diagnosis of inflammatory bowel diseases by colonoscopic findings
+Diagnostic Findings CD UC
.Terminal ileum involvement Commonly Rarely
.Colon involvement Usually Always
.Rectum involvement Rarely Usually
.Involvement around the anus Common Rarely
.Bile duct involvement No increase in rate of primary Higher rate
sclerosing cholangitis
.Distribution of disease Patchy areas of inflammation Continuous area of inflammation
(skip lesions)
.Endoscopy Deep geographic and serpiginous Continuous ulcer
(snake-like) ulcers
.Depth of inflammation May be transmural, deep into tissues Shallow, mucosal
.Stenosis Common Rarely
.Granulomas on biopsy May have non-necrotizing non-peri-intestinal Non-peri-intestinal crypt granulomas not seen
crypt granulomas
+Signs And Symptoms CD UC

.Defecation Often porridge-like, sometimes steatorrhea Often mucus-like and with blood
.Tenesmus Less common More common
.Fever Common Indicates severe disease
.Fistulae Common Rarely
.Weight loss Often Rarely
**Diarrhea
-Having three or more loose or liquid stools per day, or as having more stools than is normal for that person / Increased stool
water (>200mL/daily)
+Exudative diarrhea, occurs with the presence of blood and pus in the stool. This occurs with inflammatory bowel diseases,
such as Crohn's disease or ulcerative colitis, and other severe infections such as E. coli or other forms of food poisoning
+Inflammatory diarrhea, occurs when there is damage to the mucosal lining or brush border, which leads to a passive loss of
protein-rich fluids and a decreased ability to absorb these lost fluids. It can be caused by bacterial infections, viral infections,
parasitic infections, or autoimmune problems such as inflammatory bowel diseases. It can also be caused by tuberculosis, colon
cancer, and enteritis
+Dysentery diarrhea, if there is blood visible in the stools, it is also known as dysentery. The blood is trace of an invasion of
bowel tissue. Dysentery is a symptom of, among others, Shigella, Entamoeba histolytica, and Salmonella
+Pts. who present with a history of diarrhea lasting more than 10 days rarely have an infective cause
+If the Pt. is hypotensive, febrile and having abdominal pain, (Pt.) should be admitted to the hospital and given intravenous
fluids and antibiotics / The presence of blood in the stool is especially serious ans is probably the single strongest indication for
the use of antibiotics, such as ciprofloxacin
+Acute Diarrhea
.viral gastroenteritis with rotavirus
.travelers however bacterial infections predominate
.various toxins such as mushroom poisoning
.drugs (antibiotics, cytotoxic drugs, PPIs and NSAIDs)
+Chronic Diarrhea
.IBS (M.C.C of chronic or relapsing diarrhea)
.IBD (CD, UC)
.microscopic colitis
.celiac disease
.amoebic colitis
.cancer colon (carcinoma) - colonic neoplasia
.diverticulosis
.malabsorption
18
.hyperthyroidism-thyrotoxicosis
.lactose-intolerance
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.DM
.carcinoid syndrome
.Zollinger-Ellison syndrome
.food poisoning
.Zinc deficiency
.Vit A deficiency
.lincomycin intake
+Ulcerative colitis is marked by chronic bloody diarrhea and inflammation mostly affects the distal colon near the rectum
+Crohn's disease typically affects fairly well demarcated segments of bowel in the colon and often affects the end of the small
bowel
*Infectious Diarrhea
-The M.C.C of infectious diarrhea are campylobacter and salmonella, especially in Pts. with sickle cell and achlorhydria
-Causative Agent :
.campylobacter (reactive arthritis, Guillain-Barre` Syndrome – M.C.C)
.cryptosporidium, isospora (found in HIV-positive Pts.)
.E.coli (associated with the ingestion of contaminated hamburger meat – the organism can releases a shiga toxin, hemolytic
uremic syndrome)
.giardia (the ingestion of unfiltered water – is best diagnosed with ELISA stool antigen test and treated with metronidazole -
never gives blood in the stool, there is abdominal fullness, bloating and gas – can also stimulate celiac disease)
.salmonella (ingestion of chicken and eggs)
.scombroid (Pts. who ingest contaminated fish experience vomiting, diarrhea, flushing)
.shigella, yersinia (yersinia can mimic appendicitis, also common in people with iron overload, hemochromatosis)
.vibrio parahaemolyticus
.vibrio vulnificus
.viral
.staphylococcus aureus (ingestion of dairy products, eggs, salads, short incubation period 1-6hrs, upper GI symptoms –nausea,
vomiting, rarely diarrhea)
.ciguatera-toxin (2-6hrs after ingestion of large reef fish, also neurological symptoms)
+Giardiasis-Cholera (watery diarrhea)
-Causes Of Bloody Diarrhea :
.campylobacter
.shigella
.salmonella
.E.coli
.IBD (CD, UC)
.colonic polyps
.colorectal cancer
.ischaemic colitis
.amoeba
.schistosomiasis
-Causes Of Infectious Diarrhea :
+Bacterial
.campylobacter Species (M.C.C of bacterial diarrhea)
.shigella species
.salmonella species
.E.coli (Escherichia coli)
.giardia lamblia
.yersinia enterocolitica
.cholera
.clostridium
+Viral
.rotavirus (M.C.C of viral diarrhea in children under five years old)
.norovirus (M.C.C of viral diarrhea in adults)
.adenovirus (types 40, 41)
.astroviruses
.norwalk virus
19
.enterovirus
+Parasites
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.balantidium coli
.helminth (ascaris lumbricoides, ancylostoma duodenale, strongyloides)
.protozoa (Cryptosporidium spp., Giardia spp., Entamoeba histolytica, Blastocystis spp., Cyclospora cayetanensis)
+Are frequently the cause of diarrhea that involves chronic infection
+The broad-spectrum antiparasitic agent nitazoxanide has shown efficacy against many diarrhea-causing parasites
+Nitazoxanide is a broad-spectrum antiparasitic and broad-spectrum antiviral drug that is used in medicine for the treatment of
various helminthic, protozoal, and viral infections. It is indicated for the treatment of infection by Cryptosporidium parvum and
Giardia lamblia in immunocompetent individuals and has been repurposed for the treatment of influenza
+H.pylori (are NOT)
*Antibiotic-Associated Diarrhea
-M.C.C of diarrhea secondary to antibiotic use is Clostridium Difficile (any antibiotic can lead to diarrhea with C.difficile,
although clindamycin may have one of the highest frequencies of association)
-Treatment :
.metronidazole (is drug of choice)
.oral vancomycin (is only to be used in the very occasional case that does not resolve with metronidazole)
*Irritable Bowel Syndrome

-Is a symptom-based diagnosis. It is characterized by chronic abdominal pain, discomfort, bloating, and alteration of bowel
habits. Diarrhea or constipation may predominate, or they may alternate / F > M
-Signs & Symptoms :
.abdominal pain or discomfort in association with frequent diarrhea or constipation and a change in bowel habits
.feeling of incomplete evacuation – defecation (tenesmus)
.bloating, or abdominal distension
.GERD
.backache
.rectal mucus
.symptoms are chronic (>6 months)
-Causes :
.after acute gastrointestinal infection (Post Infection)
.prolonged fever, anxiety and depression
.antibiotic use also appears to increase the risk of developing IBS
-Diagnostic Criteria - ROME CRITERIA (must occur for At Least 3 Months) :
.pain relieved by a bowel movement or by a change in bowel habit
.fewer symptoms at night
.diarrhea alternating with constipation
+Abdominal discomfort relieved by defecation and unusual stool (diarrhea or constipation) for at least 3 days a week over the
previous 3 months
-Treatment :
.high-fiber diet
.anti-diarrheal (loperamide or codeine)
.anti-spasmodic
+About 30% of patients with diarrhea-predominant IBS have bile acid malabsorption diagnosed with an abnormal SeHCAT test
(taurocholic acid - is a drug used in a clinical test to diagnose bile acid malabsorption)
*Carcinoid Syndrome
-Describes tumors of the neuroendocrine syndrome. They are most often located in the appendix and the ileum
-Signs & Symptoms :
.diarrhea
.flushing
.tachycardia
.hypotension
.rash (from niacin deficiency-serotonin and niacin are both produced from tryptophan. If there is an overproduction of
serotonin, it produces a tryptophan deficiency, which lead to a deficiency of niacin)
.endocardial fibrosis (because of a constant exposure of the right side of the heart to the serotonin)
20
.can lead to tricuspid insufficiency and pulmonic stenosis

-Diagnosis :
.urinary 5-hydroxyindoleacetic acid level (5-HIAA)
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*Malabsorption
-Causes :
.enzyme deficiencies or mucosal abnormality, as in food allergy and food intolerance, e.g. celiac disease (gluten intolerance),
lactose intolerance (intolerance to milk sugar) and fructose malabsorption
.pernicious anemia, or impaired bowel function due to the inability to absorb vitamin B12
.loss of pancreatic secretions, which may be due to cystic fibrosis or pancreatitis
.structural defects, like short bowel syndrome (surgically removed bowel) and radiation fibrosis, such as usually follows cancer
treatment and other drugs, including agents used in chemotherapy
.certain drugs, like orlistat, which inhibits the absorption of fat
-Causes :
.Giardia lamblia
.Celiac disease
.Pancreatic insufficiency
.Intestinal lymphoma
.Crohn's disease
.Gluten enteropathy
.Systemic sclerosis
.Bacterial overgrowth
.Lymphoma
.Tropical sprue
.Systemic sclerosis
.Pancreatic carcinoma
.Diverticula
.radiation enteritis
.HIV
.Parasites (giardia lamblia, fish tape worm, roundworm)
.gastroenteritis
.Short bowel syndrome
.Gastrectomy, vagotomy
.Lactose intolerance
.Cystic fibrosis
.Chronic pancreatitis (NOT acute)
+Vitamins (AKED) dependent on bile salts for its absorption

+Vitamins Deficiency (D – Rrickets / A – nigh blindness-xerophthalmia and can cause keratinization of mucosa membrane and
skin - Overdose may cause pseudotumor cerebri / K – hemorrhage / B12 – megaloblastic anemia / C – scurvy / B1-thiamine –
beriberi) (fluride – dental caries / iodine – congenital thyroid goiter / zink – acrodermatitis enteropathica / iron – spoon nail)
+Absorpation (calcium, iron, folates (jejunum) – duodenum and jejunum-upper small intestine / B12 – ileum / bile salts –
terminal ileum)
+1.25-dihydrocholecalciferol (has the greatest effect on enhancing calcium absorption from the GI tract)
+Pellagra (characterized by the diarrhea, dementia, dermatitis)
**GI Bleeding
*Upper Gastrointestinal Bleeding (UGIB)
-Bleeding arising from the esophagus, stomach, or duodenum
-Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena)
-Signs & symptoms :
.hematemesis
.coffee ground vomiting
.melena, or hematochezia (maroon coloured stool) if the hemorrhage is severe
+Laboratory findings include anemia, coagulopathy, and an elevated BUN-to-creatinine ratio
.complications of anemia, including (shock, chest pain, syncope, fatigue and shortness of breath)
-Causes :
.Esophageal causes (gastrorrhagia) (esophageal varices (due to liver cirrhosis), esophagitis (hiatus hernia), esophageal cancer,
21
esophageal ulcers, Mallory-Weiss tear)

.Gastric causes (gastric ulcer, gastric cancer, gastritis, gastric varices, gastric antral vascular ectasia, gastric erosions (alcohol,
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NSAIDs), dieulafoy's lesions)

.Duodenal causes (duodenal ulcer - M.C.C of UGIB), vascular malformation, including aorto-enteric fistula, hemobilia, or
bleeding from the biliary tree, hemosuccus pancreaticus, or bleeding from the pancreatic duct, severe superior mesenteric
artery syndrome)
.medications increase the risk of bleeding including (NSAIDs and SSRIs)
+Selective serotonin reuptake inhibitor SSRIs (used as antidepressants in the treatment of major depressive disorder and
anxiety disorders)
-Management :
.endoscopy
.surgery (if endoscopy fails to stop active bleeding - endoscopic clipping)
+In people with a confirmed peptic ulcer, there is conflicting evidence if proton pump inhibitors reduce death rates, but PPIs do
reduce the risk of re-bleeding and the need for surgery among this group
+Somatostatin and octreotide while recommended for variceal bleeding have not been found to be of general use for non
variceal bleeds (for initial fluid replacement colloids or albumin is preferred in people with cirrhosis) (vasopressin and
nitroglycerin to reduce portal pressures) ( beta blockers and nitrates may be used for the prevention of re-bleeding. If bleeding
continues then balloon tamponade with a Sengstaken-Blakemore tube or Minnesota tube may be used in an attempt to
mechanically compress then varices. This may then be followed by a transjugular intrahepatic portosystemic shunt)
+Procedures :
.the benefits versus risks of placing a nasogastric tube in those with upper GI bleeding are not determined
.endoscopy within 24 hours is recommended (prokinetic agents such as erythromycin before endocopy can decrease the
amount of blood in the stomach and thus improve the operators view)
.Proton pump inhibitors, if they have not been started earlier, are recommended in those in whom high risk signs for bleeding
are found. It is also recommended that people with high risk signs are kept in hospital for at least 72 hours
.blood is not recommended to correct anemia, unless the patient is cardiovascularly unstable as this can worsen outcomes
.oral iron can be used, but this can lead to problems with compliance, tolerance, darkening stools which may mask evidence of
rebleeds and tends to be slow, especially if used in conjunction with PPIs
+The Physical Examination performed by the physician concentrates on the following things :
.Vital signs, in order to determine the severity of bleeding and the timing of intervention
.Abdominal and rectal examination, in order to determine possible causes of hemorrhage
.Assessment for portal hypertension and stigmata of chronic liver disease in order to determine if the bleeding is from a variceal
source
+Vital signs - are a group of the 4 to 6 most important signs that indicate the status of the body’s vital (life-sustaining)
functions. These measurements are taken to help assess the general physical health of a person, give clues to possible diseases,
and show progress toward recovery
1.body temperature
2.blood pressure (normal blood pressure would be 120 being the systolic over 80, the diastolic)
3.pulse (heart rate)
4.breathing rate (respiratory rate) (normal reference range for an adult is 16–20 breaths/min)
+Normal Blood Pressure :
.Infants (1-12 months) (85sys./60dia.)
.Toddlers (1-4 yrs) (95/65)
.Preschoolers (305 yrs) (95/65)
.School age (6-13 yrs) (100/65)
.Adolescents (13-18 yrs) (115/75)
+Normal Heart Rate/pulse (beats per minute) :
.Newborn (100-160) (130)
.0-5 months (90-150) (120)
.6-12 months (80-140) (110)
.1-3 yrs (80-130) (105)
.3-5 yrs (80-120) (100)
.6-10 yrs (70-110) (90)
.11-14 yrs (60-105) (80)
.15-20 yrs (60-100) (80)
+Normal Respiratory Rate (breaths per minute) :
.Newborn (30-50) (40)
22
.0-5 months (25-40) (30)

.6-12 months (20-30) (25)
.1-3 yrs (20-30) (25)
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.3-5 yrs (20-30) (25)

.6-10 yrs (15-30) (20)
.11-14 yrs (12-20) (16)
.15-20 yrs (12-30) (20)
+Glasgow-Blatchford score (the Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a
patient with an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood transfusion
or endoscopic intervention)
-Score (score is equal to "0" if the following are all present) :
.Hemoglobin level >12.9 g/dL (men) or >11.9 g/dL (women) (for men; 12.0-12.9 1 / 10.0-11.9 3 / <10.0 6)
(for women; 10.0-11.9 1 / <10.0 6)
.Systolic blood pressure >109 mm Hg (100–109 1 / 90–99 2 / <90 3)
.Pulse <100/minute
.Blood urea nitrogen level <18.2 mg/dL (6.5-8.0 2 / 8.0-10.0 3 / 10.0-25 4 / >25 6)
.No melena or syncope
.No past or present liver disease or heart failure
Other markers
.Pulse ≥100 (per min) 1
.Presentation with melaena 1
.Presentation with syncope 2
.Hepatic disease 2
.Cardiac failure 2
*Lower Gastrointestinal Bleeding (LGIB)

-Is referred as any bleed that occurs distal to the ligament of Treitz and superior to the anus. This includes the last 1/4 of the
duodenum and the entire area of the jejunum, ileum, colon, rectum, and anus
-LGIB is a common ailment seen at emergency departments. It presents less commonly than upper gastrointestinal bleeding
-Bleeding it usually stops spontaneously but commonly recurs
+The stool of a person with a lower gastrointestinal bleed is a good (but not infallible) indication of where the bleeding is
occurring
+A person with a LGIB will not present with any signs of internal bleeding, especially if there is a chronic bleed with ongoing low
levels of blood loss. In these cases, a diagnostic assessment or pre-assessment should watch for other signs and symptoms that
the patient may present with. These include, but are not limited to, hypotension, tachycardia, angina, syncope, weakness,
confusion, stroke, myocardial infarction/heart attack, and shock
-Causes :
.coagulopathy — specifically a bleeding diathesis
.colitis (ischaemic colitis, ulcerative colitis, infectious colitis; E. coli O157:H7-Shigella-Salmonella-Campylobacter jejuni)
.hemorrhoids
.angiodysplasia
.neoplasm — cancer
.diverticular disease (diverticulosis - M.C.C, diverticulitis)
.anal fissures
.rectal foreign bodies
.crohn's disease
.pseudomembranous colitis
.infectious diarrhea
.radiation colitis
.mesenteric ischemia
.colonic polyps
.colon cancer
-Diagnosis :
.andoscopy, flexible sigmoidoscopy, colonoscopy, rarely barium enema
23
+Blood coating the stool suggests hemorrhoidal bleeding while blood mixed in the stool implies a more proximal source
+Bloody diarrhea and tenesmus is associated with inflammatory bowel disease
+Bloody diarrhea with fever and abdominal pain especially with recent travel history suggests infectious colitis
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+Pain with defecation occurs with hemorrhoids and anal fissure

+Change in stool caliber and weight loss is concerning for colon cancer
+Abdominal pain can be associated with inflammatory bowel disease, infectious colitis, or ischemic colitis
+Painless bleeding is characteristic of diverticular bleeding, arteriovenous malformation (AVM), and radiation proctitis
+NSAID use is a risk factor for diverticular bleeding and NSAID-induced colonic ulcer
+In some Pts. who present with major gastrointestinal bleeding, upper endoscopy and colonoscopy fail to reveal a diagnosis.
Urgent mesenteric angiography in indicated
+Occult bleeding may reach 200mL per day, cause iron deficiency anemia
+Colorectal cancer, particularly carcinoma of the caecum which may have NO gastrointestinal symptoms
+A Pt. presents with unxplained iron deficiency anemia. Testing the stool for the presence of blood is Unnecessary and should
not influence because bleeding from tumors is often intermittent and a nigative faecal occult blood FOB test (many colorectal
cancer Pts. are FOB-negative at presentation)
+An upper GI bleed is more common than lower GI bleed
+Risk of bleeding is more common in males and increases with age
+Drugs May Produce GI Bleeding :

.Salicylates
.Steroids
.Anticoagulants
.Phenothiazines
+In acute bleeding from esophageal varices after resuscitation, the treatment of choice is Balloon tamponade
+Melena is four-times more likely to come from an upper gastrointestinal bleed than from the lower GI tract; however, it can
also occur in either the duodenum and jejunum, and occasionally the portions of the small intestine and proximal colon
-Causes :
.peptic ulcer disease (M.C.C)
.sign of drug overdose if a patient is taking anticoagulants, such as warfarin
.tumors, especially malignant tumors affecting the esophagus, more commonly the stomach & less commonly the small
intestine
.hemorrhagic blood diseases (e.g. purpura & hemophilia)
.gastritis
.esophageal varices
.aorto-duodenal fistula
.Meckel's diverticulum
.Mallory-Weiss syndrome
.iron supplements, Pepto-Bismol, Maalox, and lead
.blood swallowed as a result of a nose bleed (epistaxis)
+Hematochezia - Bright red stool, is the sign of a fast moving active GI bleed. The bright red or Maroon color is due to the
short time taken from the site of the bleed and the exiting at the anus. The presence of hematochezia is six-times greater in a
LGIB than with a UGIB
-Causes :
.hemorrhoids and diverticulosis (M.C.C)
.colorectal cancer, which is potentially fatal
.in a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an
initial symptom of necrotizing enterocolitis
.in babies, haematochezia in conjunction with abdominal pain is associated with intussusception
.in adolescents and young adults, inflammatory bowel disease, particularly ulcerative colitis, is a serious cause of
haematochezia that must be considered and excluded
.crohns disease
.other types of inflammatory bowel disease, inflammatory bowel syndrome, or ulceration
.rectal or anal hemorrhoids or anal fissures
.shigella or shiga toxin producing E. coli food poisoning
.necrotizing enterocolitis
.salmonellosis
+Haematochezia can be due to upper gastrointestinal bleeding
.upper gastrointestinal bleeding
.peptic ulcer disease
24
.esophageal varices
.gastric cancer
Page
**Portal Hypertension
-Is hypertension (high blood pressure) in the hepatic portal system, which is composed of the portal vein and its branches and
tributaries. Portal hypertension is defined as elevation of hepatic venous pressure gradient
-Portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins)
-Normal portal pressure is generally defined between (5-10mm Hg) / Complications do not usually develop until the portal
venous pressure exceeds 12mmHg
-Signs & Symptoms :
.splenomegaly - hypersplenism (M.C signs of portal HTN) (with consequent accumulation of RBCs, WBCs, platelets, together
leading to mild pancytopenia)
.ascites (free fluid in the peritoneal cavity)
.hepatic encephalopathy
.increased risk of spontaneous bacterial peritonitis
.increased risk of hepatorenal syndrome
.dilated veins in the anterior abdominal wall
-Causes :
.intrahepatic (schistosomiasis - M.C.C, hepatic cirrhosis, acute alcoholic hepatitis, primary biliary cirrhosis, idiopathic portal
hypertension, acute and fulminant hepatitis, congenital hepatic fibrosis)
.prehepatic (portal and splenic vein thrombosis, extrinsic compression (tumors), congenital atresia or stenosis of portal vein)
.posthepatic (Rt. heart failure, Budd-Chiari Syndrome/hepatic vein thrombosis, constrictive pericarditis, tricuspid regurgitation)
-Complications :
.portacaval anastomoses (esophageal variceal bleeding, gastric varices, anorectal varices, caput medusae)
.abdominal tenderness (spontaneous bacterial peritonitis; causes-liver cirrhosis, ascites, E.coli-due to spontaneous
bacter/treated by antibiotic-ceftriaxone)
.carcinoma
.congestive gastropathy
.iron deficiency anemia
.renal failure
.jaundice (Hepatorenal syndrome)
+Portal hypertension does NOT increase the risk of hemorrhoids
-Diagnosis :
.HVPG (hepatic venous pressure gradient)
-Treatment :
+Prophylaxis of variceal bleeding (B-blocker like propranolol and isosorbide mononitrate) (endoscopic – banding ligation)
+TIPS (transjugular intrahepatic portosystemic shunting) to reducing rate of rebleeding (Disadvantages of TIPS include, high
cost, increased risk of hepatic encephalopathy)
+Management Of Active Variceal Bleeding :
.vasoactive drugs (somatostatin, octreotide, terlipressin)
.endoscopic banding ligation
.balloon tamponade
.TIPS
+Management Of Ascites :
.salt restriction
.diuretics (spironolactone)
.paracentesis
.TIPS
.peritoneovenous shunt (LeVeen Shunt - is a shunt which drains peritoneal fluid from the peritoneum into veins)
+For control of hepatic encephalopathy (dietary protein, followed by lactulose, use of oral antibiotics like neomycin)
**Viral Hepatitis
+All hepatitis virus types are (RNA), except HBV is (DNA) / A-B (only have vaccine)
*Hepatitis A
-Infectious jaundice is caused by hepatitis A virus / Antibodies (HAV IgM) / Incubation 2-4wks (15-45days) / Severity (mild-
acute)
25
-Markers (IgM anti HAV in acute infection / IgG anti HAV in old infection)
+Its acute form and does not have a chronic stage (A-E)
Page
-Transmission :
.fecal-oral route
.associated with ingestion of contaminated food
+A vaccine is avaliable that will prevent HAV infection for up to 10yrs (Vaccine is protection for 10yrs)
+Infected people excrete HAV with their feces 2wks before and 1wks after the appearance of jaundice
+Symptoms less in children than adults
*Hepatitis B
-Incubation 6wks-6months (45-160days) / Antibodies HBsAg, HBeAg (highly infectious-chronic active) / Severity (chronic-severe)
-HBV-DNA by PCR technique (is the most sensitive test) / Vaccine is protection for 15yrs or lifelong immunity – 3 doses
-Transmission :
.blood (blood transfusion)
.tattoos
.sexually (sexual intercourse or through contact with blood or bodily fluids)
.via mother to child by breast feeding
-Comlications :
.chronic hepatitis (develops in 15% of adults)
.cirrhosis
.hepatocellular carcinoma (after 30yrs)
-Treatment :
.alpha-interferon
*Hepatitis C
-No vaccine / Incubation 2-26wks (15-150days) / Antibodies (Core antigen) / Severity (chronic) / NO vaccine
-Markers HCV AB-appear after 3-6 months of infection
-HCV-RNA by PCR technique is the most sensitive test
-Transmission :
.blood
.saliva
-Complications :
.chronic hepatitis
.cirrhosis (after 15-20yrs)
+It usually remains asymptomatic
-Treatment :
.interferon
.antiviral drug ribavirin
*Hepatitis D
-It can only propagate in the presence of the hepatitis B virus / Antibodies (Delta antigen) / Incubation 6-9wks (30-60days) /
Severity (exacerbated symptoms of HBV; chronic HBV) / NO vaccine
-Markers (IgM in acute infection / IgG in chronic infection / hepatitis B marker in positive)
-Transmission :
.blood (blood transfusion)
.tattoos
.sexually (sexual intercourse or through contact with blood or bodily fluids)
.via mother to child by breast feeding
*Hepatitis E
-The hepatitis E virus (HEV) produces symptoms similar to hepatitis A / Incubation 3-8wks (15-60days) / Severity (normal Pt. –
acute, mild) (Pregnant women – severe) / NO vaccine
-It can take a fulminant course in some Pts. (pregnant women)
-Markers (IgM in acute infection / IgG in old infection)
-Transmission :
.oral
26
**Chronic Hepatitis
-Chronic inflammatory reaction in liver more than 6 months
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-Causes :
.viral hepatitis B-C-D
.drugs
.autoimmune hepatitis
.wilson`s disease
.hemochromatosis
.alpha-1 antitrypsin
+Medications That Can Cause Chronic Hepatitis :
.isoniazid
.propylthiouracil
.nitrofurantoin
.minocycline
.fibrates
.statins
.hydralazine
.methyldopa
+These medications can also cause acute hepatitis or an autoimmune hepatitis like syndrome
-Clinical :
.asymptomatic (it may be discover accidental aselevation of liver enzymes)
.mild non-specific symptoms as (easy fatigue, malaise, anorexia and weight loss)
.jaundice (yellowish coloration of skin and mucous membrane, pale stool and dark urine)
.other liver cell failure manifestations as oedema, ascites, bleeding tendency and encephalopathy
.in late case liver cirrhosis with (liver cell failure, portal hypertension, hepatocellular carcinoma)
.extrahepatic symptoms (rash, urticaria, arthritis, glomerulonephritis, lymphocytic sialadenitis, poly arteritis nodosa PAN,
polyneuropathy, porphyria)
-Treatment :
.interferon – indications (no cirrhosis, young age, elevated enzymes, biopsy evidence of chronic hepatitis, in case of hepatitis B-
C)
+Dose (HBV-5 million units daily at least 4 months) (HCV-3 million units 3 times/week for 12-18 months)
+Side effects (bone marrow depression, autoimmune disease, CNS syndrome, anorexia, sleep disturbance)
.antiviral drugs (HBV-lamivudine or famciclovir, alone without interferon for 12months) (HCV-ribavirin with interferon)
+Chronic hepatitis interferes with hormonal functions of the liver which can result in acne, hirsutism (abnormal hair growth),
and amenorrhea (lack of menstrual period) in women
+Cirrhosis can lead to other life-threatening complications such as hepatic encephalopathy, esophageal varices, and
hepatorenal synrome
*Autoimmune Hepatits
-Is a disease of the liver that occurs when the body`s immune system attacks cells of the liver
-Types :
.associated with anti smooth muscle AB and anti nuclear AB
.associated with anti liver-kidney microsomal AB
-Signs & Symptoms :
.F > M (young-middle age)
.fatigue, amenorrhea
.cirrhosis, low albumin, spider nivae, elevated serum aminotransferase levels (ALT-AST) (signs of chronic liver disease)
.progressive jaundice, fever, painful hepatomegaly (signs of acute hepatitis)
.hereditary hemochromatosis
.skin hyperpigmentation
.extrahepatic manifestations (rash, arthritis, thyroiditis, haemolytic anemia and glomerulonephritis)
.DM
.pseudogout
.cardiomyopathy (all signs due to iron overload)
-Diagnosis :
.elevated serum aminotransferase levels (elevated ALT, AST)
.liver function tests (in 50% of Pts., abnormal results – decreased albumin levels, PPT)
.liver biopsy
27
.antibodies found in blood (antinuclear antibody ANA, anti-smooth muscle antibody SMA, liver/kidney microsomal antibody
LKM-1, LKM-2, LKM-3, anti soluble liver antigen SLA/LP and antimitochondrial antibody AMA)
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-Treatment :
.immunosuppressive glucocorticoids with or without prednisolone / azathioprine
*Wilson`s Disease (Hepatolenticular Degeneration)

-Is an autosomal recessive genetic disorder in which copper accumulates in tissues; this manifests as neurological or psychiatric
symptoms and liver disease (cirrhosis) / The main sites of copper accumulation are the liver, brain and cornea
+It is treated with medication that reduces copper absorption or removes the excess copper from the body, but occasionally a
liver transplant is required
+The absorbed copper is transported to the liver to binf with apoceruloplasmin forming ceruloplasmin
+Wilson disease is a disorder of plasma protein of Copper
+The wilson`s disease gene (ATP78) has been mapped to chromosome 13
+The combination of neurological symptoms, Kayser-Fleischer rings and a low ceruloplasmin level is considered sufficient for
the diagnosis of Wilson's disease / Serum copper is low / Urine copper is elevated in Wilson's disease
-Signs & Symptoms :
.liver disease (cirrhosis)
.neuropsychiatric symptoms (about the half the people with Wilson's disease have neurologic or psychiatric symptoms)
.extrapyramidal syndrome (parkinsonism, ataxia, dystonia, tremor, demontia). Other neurological manifestations as seizures
and migraine and pschiatric manifestations as behavioral change, depression, anxiety, psychosis, altered mental status
.eyes (Kayser-Fleischer rings – KF rings), a pathognomonic sign, may be visible in the cornea of the eyes
+KF signs - greenish brown pigmentation at the the corneoscleral junction
.kidneys (renal tubular acidosis, aminoaciduria - presence of amino acids in the urine)
.heart (cardiomyopathy)
.hormones (hypoparathyroidism - failure of the parathyroid glands leading to low calcium levels, infertility, abortion)
.haemolytic anemia
-Characterized by :
.liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis
.symptoms usually appear between the ages of 6 and 20 years
.failure of both binding of copper with apo ceruloplasmin and copper excretion in the bile, wich leading to deposition of copper
in liver and other tissue
.low serum ceruloplasmin level
+Ceruloplasmin - is a ferroxidase enzyme that in humans is encoded by the CP gene / is the major copper-carrying protein in
the blood, and in addition plays a role in iron metabolism
.increase hepatic copper content on liver biopsy
-Investigations :
.liver biopsy is the best
.ceruloplasmin is usually low
.total serum copper is usually low
.free serum copper is usually increased (>25 ug/dl)
.urinary copper is usually elevated (>100ug/dl)
.MRI (to show basal ganglia affection-giant panda sign)
.urine analysis and renal function test
.genetic testing
-Treatment :
.diet low in copper-containing foods is recommended with the avoidance of (mushrooms, nuts, chocolate, dried fruit, liver,
shellfish)
.penicillamine (1st treatment used – copper chelating), zinc acetate
.liver transplantation (effective cure for Wilson's disease)
**Alpha 1-antitrypsin Deficiency (A1AD)

-Is a genetic disorder that causes defective production of alpha 1-antitrypsin (A1AT), leading to decreased A1AT activity in the
blood and lungs, and deposition of excessive abnormal A1AT protein in liver cells
+A1AD is M.C.C indication for liver transplantation in newborns
+A1AT (produced in liver and one of its functions is to protect the lungs from neutrophil elastase)
-Signs & Symptoms :
28
.shortness of breath
.wheezing
Page
.rhonchi
.rales
+The patient's symptoms may resemble recurrent respiratory infections or asthma that does not respond to treatment
.emphysema (during their thirties or forties even without a history of significant smoking)
.cirrhosis
.liver failure
+A1AD (also causes impaired for liver function in some Pts. and may lead to cirrhosis and liver failure)
+In newborns, alpha-1 antitrypsin deficiency has indicators that include early onset jaundice followed by prolonged jaundice
+It is a leading indication for liver transplantation in newborns (M.C.C)
-Associated Conditions (α1-antitrypsin deficiency has been associated with a number of diseases) :
.cirrhosis
.COPD
.asthma
.pneumothorax
.gallstones
.pancreatitis
.glomerulonephritis
.pelvic organ prolapse
.bronchiectasis
.emphysema
.cancers (lymphoma, hepatocellular carcinoma-liver, lung cancer, gallbladder cancer, bladder carcinoma)
+Severe A1AT deficiency causes panacinar emphysema - Panlobular emphysema or COPD in adult life in many people with the
condition (especially if they are exposed to cigarette smoke)
-Diagnosis :
.level of AAT in your blood (low AAT levels)
.genetic test is the most certain way to check for AAT deficiency
.lung-related tests (lung function tests / CT scan)
+AAT Genetic testing is also recommended if you have a relative who has been diagnosed with A1AD or a family history of early
emphysema or liver disease
-Treatment :
.intravenous infusion of alpha 1-antitrypsin
.transplantation of the liver
**Hepatic Encephalopathy HE
-Is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure
+In the advanced stages it is called hepatic coma or coma hepaticum. It may ultimately lead to death
-Types :
.type A (acute) describes hepatic encephalopathy associated with acute liver failure, typically associated with cerebral edema
.type B (bypass) is caused by portal-systemic shunting without associated intrinsic liver disease
.type C (cirrhosis) occurs in patients with cirrhosis - this type is subdivided in episodic, persistent and minimal encephalopathy
-Signs & Symptoms :
.mild confusion, and irritability
.inverted sleep-wake pattern (sleeping by day, being awake at night) (the first stage of hepatic encephalopathy)
.lethargy and personality changes (the second stage)
.worsened confusion (the third stage)
.progression to coma (the fourth stage)
.asterixis
.neurological examination (clonus and positive Babinski sign)
.coma and seizures represent the most advanced stage
.cerebral edema (swelling of the brain tissue) leads to death
.jaundice
.ascites
.peripheral edema (swelling of the legs due to fluid build-up in the skin)
.tendon reflexes
-Causes :
.barbiturate
29
.morphine
.diuretic therapy
Page
.high protein diet

.gastrointestinal hemorrhage
.infection
.hypokalemia
.sedation
.constipation
.narcotics
.paracentesis
.narcosis
.shunt operations
.abdominal surgery
**Hemochromatosis (Bronzed diabetes)

-It is autosomal recessive disorder, characterized by increase Fe absorption and subsequent deposition in liver and other tissue
+It is rarely acquired due to repeated Fe injection or blood transfusion
-Signs & Symptoms :
.usually presenting in middle aged men
.skin pigmentation
.DM (in most of cases)
.hypogonadism manifestations (secondary to pituitary dysfunctions as testicular atrophy and loss of libido)
.peripheral neuropathy
.cirrhosis
.jaundice
.edema
.ascites
.bleeding tendency
.encephalopathy
.dyspepsia
.splenomegaly
.esophageal varices and piles
-Investigations :
.serum Fe is increased
.serum ferritin is increased
.blood glucose for DM
.genetic testing for other family members
**Iron Overload (Hemochromatosis)

-Indicates accumulation of iron in the body from any cause. The most important causes are hereditary haemochromatosis
(HHC), a genetic disorder, and transfusional iron overload
+Result from repeated blood transfusions
-Signs & Symptoms :
.organs commonly affected by haemochromatosis are (liver, heart, and endocrine glands)
.cirrhosis of the liver
.diabetes due to selective iron deposition in pancreatic islet beta cells leading to functional failure and cell death
.cardiomyopathy
.arthritis (calcium pyrophosphate deposition in joints)
.testicular failure
.slate gray discoloration of the skin (tanning of the skin) (Bronze-Skin)
.joint pain and bone pain
-Causes :
+The causes can be distinguished between primary cases (hereditary or genetically determined) and less frequent secondary
cases (acquired during life)
.primary hemochromatosis (most types of hereditary haemochromatosis have autosomal recessive inheritance, while type 4
has autosomal dominant inheritance)
.secondary hemochromatosis (thalasemia/severe chronic haemolysis (haemolysis within the bone marrow), multiple blood
30
transfusions, excess parenteral iron supplements (what can acutely happen in iron poisoning), excess dietary iron)
+Some disorders do not normally cause haemochromatosis on their own, but may do so in the presence of other predisposing
factors. These include cirrhosis (especially related to alcohol abuse), steatohepatitis of any cause, porphyria cutanea tarda,
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prolonged haemodialysis, and post-portacaval shunting

-Diagnosis :
.serum ferritin elevated
.liver biopsy (BEST)
+Untreated develop due to hepatocullular carcinoma (Tumor marker is alpha fetoprotein AFP)
-Treatment :
.deferoxamine (iron-chelating)
+Human hemochromatosis protein HFE gene associated with HLA-A3
**Celiac Disease (Gluten enteropathy)

-Is an autoimmune disorder of the small intestine that occur in genetically predisposed people pf all ages from middle infancy
onward / F > M
-Coeliac disease is associated with other human leukocyte antigen (HLA-DO2)-linked autoimmune disorders
+It can present at any age with positive family history in 25% of cases
-Signs & Symptoms :
.diarrhea
.weight loss
.anemia (iron deficiency anemia, folat anemia, Vit B12, megaloblastic anemia)
.malabsorption
.oral ulceration
.osteoporosis
.dermatitis herpetiformis
.growth failure
.hypocalcemia
.hyposplenism (disease can cause it - celiac disease, UC, sickle cell anemia-autosplenectomy)
.Vit D malabsorption
.IgA deficiency
.adenocarcinoma (small intestine cancer and lymphoma of the small bowel)
-Complications :
.increased incidence of T cell lymphoma
.increased incidence of carcinoma of small intestine and oesophagus
-Diagnosis :
.intestine biopsy (duodenal biopsy – BEST)
.response to gluten-free diet
.antiendomysial antibodies on the immunoglobulin A (IgA) + antimicrosomal
-Treatment :
.life-long gluten-free diet
**Diseases Of The Pancreas

**Pancreatitis
-Inflammation of the pancreas (can be acute or chronic)
-Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment
-Signs & Symptoms :
.usually begins with gradual or sudden pain in the upper abdomen that sometimes extends through the back (epigastric
tenderness)
.swollen and tender abdomen
.fever
.rapid pulse (tachycardia)
.nausea, vomiting
.decreased bowel sounds (adynamic ileus) (M.C.C of ileus is hypokalemia)
.dehydration, shock (hypovolemic)
.cyanosis
.dyspnea
.hypotension
31
.jaundice
.abnormal lung sounds - Crackles
.discoloration of abdominal wall – Turner’s or Cullen’s sign / fox sign
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+Epigastric pain that radiates to back and relieved by leaning forward – aggravated by lying supine
-Causes :
.gallstones (M.C of acute pancreatitis)
.scorpion bite (the least common cause)
.idiopathic
.ethanol (alcohol abuse)
.trauma
.mumps virus (coxsackievirus)
.autoimmune
.steroids
.hyperlipidemia/hypercalcemia
.ERCP
.diuretics (thiazide)
.azathioprine (immunosuppressive drug) - used in organ transplantation and autoimmune diseases
-Diagnostic (Lap Tests) :
.CBC (high WBC)
.LFT
.elevated amylase and lipase
.CT-scan / abdomen ultrasound
.ABG
.calcium
.chemistry
.coags
.serum lipids
.RBS
.KFT
.LDH
-Complications :
.pseudocyst – resolve spontaneously by 6wks (M.C complication) (M.C indication for surgery in acute pancreatitis)
.infection and sepsis (M.C.C if death in acute pancreatitis)
.pancreatic necrosis, abscess
.pancreatic hemorrhage
.splenic / mesenteric / portal vessel rupture or thrombosis
.pancreatic ascites
.pancreatic pleural effusion (left)
.DM (type 1)
.ARDS / sepsis / MOF (multiple organ failure)
.coagulopathy
.encephalopathy (NH3) (treated by lactulose)
.severe hypocalcemia
.acidosis
.shock
+Prognosis (Based On Ranson`s Criteria)
-Ranson`s Criteria :
+At admission
.age >55
.WBC >16000 cells/mm3
.blood glucose Glc >200 mg/dL
.AST >250 IU/L
.LDH >350 IU/L
+During The Initial 48hrs
.base deficit >4 mEq/L (bycarbonate)
.BUN increase >5 mg/dL / I.V fluid hydration
.sequestration of fluids >6L
.serum calcium Ca <8.0 mg/dL
32
.Hematocrit (fall) decrease >10%

.Oxygen (PO2 (ABG) <60 mm Hg) - (type 1 respiratory failure)
Page
+Amylase + lipase - protein (enzyme) value is NOT one of Ranson`s criteria

+Mortality per positive criteria = (0-2) <5% / (3-4) 15% / (5-6) 40% / (7-8) 100%
-Treatment :
.NPO (non per oral)
.I.V fluids
.antibiotics
.analgesia
.if the cause is gallstone (cholycystectomy should be done once patient stabilized)
+Indication For Surgery :
.>6cm
.>6wks
.obstruction (stomach)
.pain
*Chronic Pancreatitis
-Is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as
episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption
-Signs & Symptoms :
.epigastric pain
.malabsorption, diarrhea (steatorrhea)
.DM
.skin pigmentation (over the abdomen and back-flank)
.jaundice (obstructive)
+Chronic pancreatitis (Risk for pancreatic cancer)
+Pain may be relieved by leaning forwards or by drinking alcohol
-Causes :
.alcohol abuse (M.C.C)
.idiopathic
+Possible Complications Of Chronic Pancreatitis :
.insulin dependent diabetes mellitus
.steatorrhea (cystic fibrosis/celiac disease)
.biliary obstruction
.malnutrition
.splenic vein thrombosis
.splenic artery aneurysm
.gastric varices
.pancreatic pseudocyst (M.C) / abscess (pseudocyst and pancreatic ascites – in both types of pancreatitis)
.cancer
.narcotic addiction
.duodenal stenosis
.peptic ulcer
.pancreatic ascites/pleural effusion
+Complications is associated with splenic vein thrombosis is (Gastric varices - treatment with splenectomy)
-Diagnosis :
.CT-scan (Best)
-Treatment :
.analgesia
.pancreatic enzyme (lipase, protease)
.insulin
+M.C indication for surgery is pain
+In chronic cases (may be normal amylase + lipase)
+Cullen`s Sign (Bluish discoloration of the periumbilical area from retroperitoneal hemorrhage)
+Grey Turner`s Sign (Ecchymosis or discoloration of the flank in Pts. with retroperitoneal hemorrhage from dissecting blood
from the retroperitoneum)
+Fox's Sign (Ecchymosis of the inguinal ligament from blood tracking from the retroperitoneum and collecting at the inguinal
ligament)
33
**Pancreatic Pseudocyst
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-Encapsulated collection of pancreatic fluid

-Wall is formed by inflammatory fibrosis, Not epithelial lining
-Associated Risk Factors :
.chronic pancreatitis > acute pancreatitis
.pancreatitis from alcohol
+Chronic pancreatitis (alcohol) / Acute pancreatitis (gallstone)
+M.C.C of pancreatic pseudocyst is (Chronic alcoholic pancreatitis)
-Treatment :
.drainage of the cyst or observation
+M.C.C of death due to pancreatic pseudocyst is (Massive hemorrhage into the pseudocyst)
**Pncreatic Carcinoma
-Adenocarcinoma of the pancreas arising from duct cells
+Percentage arise in the pancreatic head is (66% in the head / 33% arise in the body and tail)
-Signs & Symptoms :
.painless jaundice
.pruritus
.courvoisier`s sign (Palpable, nontender, distended gallbladder)
.back pain
-Metastatic lymph nodes described classically for gastric cancer can be found with metastatic pancreatic cancer :
.virchow`s node (Lt. side)
.sister mary joseph`s nodule (per umbilicus)
+Tumor markers (pancreatic cancer) is (CA-19-9)
-Treatment Based On Location :
.head of the pancreas (Whipple procedure / pancreaticoduodenectomy)
.body or tail (Distal resection)
+WADHA syndrome (Pancreatic VIPoma-Vasoactive Intestinal Polypeptide tumor or Verner-Morrison Syndrome)
+Tumor Secretes VIP :
.watery
.diarrhea
.hypokalemia
.achlorhydria (inhibit gastric acid secretion)
+M.C islet cell tumor is (Insulinoma)
+Regarding anular pancreas usually present with duodenal obstruction
**Juvenile Polyposis JPS

-Is a syndrome characterized by the appearance of multiple juvenile polyps in the gastrointestinal tract
-1/3 of cases are inherited in an autosomal dominant manner and up to 20% of Pts. develop colorectal cancer before the age of
40yrs
-Criteria For Diagnosis Are :
.10 or more colonic juvenile polyps, or
.juvenile polyps elsewhere in the gut, or
.any number of polyps in those with a family history
+Colonoscopy with Polypectomy should be performed every 1-3 yrs
**Colorectal Carcinoma
-Adenocarcinoma of the colon or rectum
-Incidence :
.M.C GI cancer
(Female : lung cancer / breast cancer / colon cancer)
(Male : prostate cancer / lung cancer / colon cancer)
(M-F : lung cancer / colon cancer)
.second M.C.C of cancer deaths
.second M.C internal malignancy
.incidence increase with age starting at 49yrs and peaks at 70-80yrs
34
-Signs & Symptoms :

.weight loss (late sign)
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.blood in the stool

.constipation
.change in bowel habit (if associated with bleeding)
.rectal bleeding
.anemia (iron-deficiency anemia)
+Right-Sided Lesions (Bleeding)
.right side of bowel has a large luminal diameter (large size tumor)
.microcytic anemia
.occult / melena more than hematochezia (fresh blood)
.postprandial discomfort
.fatigue
+Left-Sided Lesions (Obstruction)
.smaller lumen and semi-solid contents
.change in bowel habits (small-caliber stools)
.colicky pain
.sign of obstruction
.abdominal pain
.heme (+) or gross red blood
.nausea, vomiting, constipation
+Lt. > Rt.
+Melena more common from (Rt. sided colon cancer)
+Hematochezia more common from (Lt. side colon cancer)
+Rt. Colon cancer (bleeding) / Lt. Colon cancer (obstruction)
+Cancer on the Rt. Side (ascending colon and cecum) / Lt. Side tend to be circumferential, and can obstruct the bowel
-Signs & Symptoms :
.hematochezia (M.C symptom)
.tenesmus
.feeling of incomplete evacuation of stool (because of the mass)
.rectal mass
-Risk Factors :
.dietary (low-fiber, high-fat diets, alcohol, red meat intake, obesity, smoking)
.genetic (family history is important when taking history, FAP, gardner syndrome, HNPCC or lynch syndrome)
.IBD (UC > CD) (previous colon cancer)
.type 2 DM
.use of aspirin or NSAIDs (COX-2 inhibition)
+Lynch`s Syndrome (Hereditary nonPolyposis Colorectal Cancer / autosomal-dominant / inheritance of high risk for
development of colon cancer / 100% malignant)
-Diagnostic Test Is (colonoscopy / CBC / heme occult)
.via tumor biopsy, typically done during sigmoidoscopy or colonoscopy
+Microcytic anemia signify until proven otherwise in a man or postmenopausal women in colon cancer
+Preoperative workup for colorectal cancer is (CEA)
-TNM stages :
.stage 1 (invades submucosa or muscularis propria)
.stage 2 (invades through muscularis propria or surrounding structures but with negative nodes)
.stage 3 (positive nodes, no distant metastasis)
.stage 4 (positive distant metastasis)
-Treatment :
.resection (surgical margins are needed for colon cancer is- >5cm (you should take as minimum 5cm); the minimum safety
margins in colectomy must be at least 2cm)
.chemotherapy (for advanced disease)
.NO radiotherapy in colon cancer
+Types Of Colon Cancer Surgery :
.low anterior resection (LAR)
.abdomino-perineal resection (APR) (if colon cancer is >7cm – from anal canal)
-Follow-up :
.carcinoembryonic antigen (CEA) blood level measurments (if CEA increased after surgery – recurrence / recurrence is more in
first 2-3yrs) (CEA is for FOLLOW-UP NOT for DIAGNOSIS)
35
+M.C site of distant (hematogenous) metastasis from colorectal cancer is liver

+M.C.C of colonic obstruction in the adult population (colon cancer, diverticular disease, colonic volvulus)
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+Colon cancer is M.C.C of Large bowel obstruction

+M.C colon cancer is adenocarcinoma
-Prevention :
.increasing the consumption of whole grains, fruits and vegetables
.reducing the intake of red meat
.aspirin and celecoxib (decrease the risk of colorectal cancer in those at high risk)
.Vit D intake
-Screening (three main screening tests) :
.fecal occult blood testing
.flexible sigmoidoscopy
.colonoscopy
+Carcinoma Of The Rectum usually causes early bleeding, mucus discharge or a feeling of incomplete emptying. Some of Pts
present with iron deficiency anemia or weight loss, on examination there may be a palpable mass ,hepatomegaly from
metastases
*Colonic And Rectal Polyps (Colorectal Polyps)

-Tissue growth into bowel lumen, usually consisting of mucosa, submucosa, or both
-Signs & Symptoms :
.bleeding per rectum
.mucus
.diarrhea
.hypokalemia
-Anatomically Classified :
.sessile (flat)
.pedunculated (on a stalk)
-Histologically Classified (Types) :
.inflammatory (benign) (pseudopolyp - no malignant) - as an CD or UC (UC > CD)
.hamartomatous (benign) (normal tissue in abnormal configuration - no malignant)
.hyperplastic (benign-normal cells - no malignant)
.neoplastic (adenomatous-adenomas or malignant) (proliferation of undifferential cells - premalignant or malignant cells)
+Subtypes Of Neoplastic Polyps :
.tubular adenomas (M.C type) – 5% risk of cancer
.tubulovillous adenomas – 20% risk of cancer
.villous adenomas – 40% risk of cancer
+Histology and cancer potential of an adenomatous polyp (villous > tubulovillous > tubular)
+Most polyps are found in (rectosigmoid)
+Size Of Polyp :
.<1cm (<1% risk of cancer)
.1cm (10% risk of cancer)
.2cm (15% risk of cancer)
-Diagnosis :
.Colonoscopy
-Treatment :
.removal of polyp during colonoscopy
.prophylactic (colectomy)
**Polyposis Syndromes
*Familial Adenomatous Polyposis (FAP)
-Familial adenomatous polyposis FAP - Autosomal dominant
+Mutation on chromosome 5 – APC gene - Genetic defect (tumor marker) is (APC-adenomatous polyposis coli) gene
-Characteristics :
.100% malignant
.hundreds (>100) of adenomatous polyps within the rectum and colon
.developing at puberty (start at young age) / all undiagnosed; untreated Pts. develop cancer by ages 40-50 yrs
-Treatment :
36
.total proctocolectomy and ileostomy

.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis
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+With FAP, other tumor must be looked for is (duodenal tumors)

*Gardner`s Syndrome
-Autosomal dominant
-Characteristics :
.100% malignant
.neoplastic (adenomatous) polyps of the small bowel and colon
.cancer by age 40yrs in 100% of undiagnosed Pts., as in FAP
-Other Associated Findings :
.osteomas of skull (seen on x-ray)
.sebaceous cyst
.adrenal and thyroid tumors (Desmoid tumor)
-Treatment :
.total proctocolectomy and ileostomy
.total colectomy and rectal mucosal removal (mucosal proctectomy) and ileoanal anastomosis
*Peutz-Jeghers` Syndrome
-Autosomal dominant / Hemartoma polyp + Hyperpigmentation
-Characteristics :
.hamartomas (not malignant) (jejunum-ileum > colon > stomach)
+Associated cancer risk for women with peutz-jeghers is (Ovarian cancer)
-Other Signs :
.melanotic pigmentation (Hyperpigmentation) (black/brown) of buccal mucosa (mouth), lips, digits, palms, feet (soles), nippels
-Treatment :
.removal pf polyps
+Juvenile Polyps is (benign hamartomas in the small bowel and colon; not premalignant)
+Turcot Syndrome (Colonic polyp + CNS tumor) +Juvenile Polyp (Hemartoma / Benign)
+Colonic Volvulus (Twisting of colon on itself about its mesentery, resulting in obstruction and if complete, vascular
compromise with potential necrosis, perforation, or both / Most type of colonic volvulus is - Sigmoid volvulus)
**Diverticular Disease Of The Colon

*Diverticulosis
-Condition in which diverticula can be found within the colon, especially the sigmoid; diverticula are actually false diverticula /
diverticula involve all layers of the bowel wall and RARE in the colon (False Diverticulum)
+Most common site is (Sigmoid)
+M.C.C of massive painless lower GI bleeding
-Symptoms :
.constipation
.lower GI bleeding
-Risk Factors :
.low-fiber diet
.old age
.constipation
-Complications :
.bleeding (may be massive)
.diverticulitis
.asymptomatic (80% of all cases)
-Diagnosis :
.colonoscopy or barium enema
*Diverticulitis
-Infection or perforation of a diverticulum
-Pathophysiology is (obstruction of diverticulum by a fecalith)
-Symptoms :
37
.LLQ pain
.fever
-Diagnosis :
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.Best test is (abdominal CT-scan) (colonoscopy + barium enema is contraindicated) / Best test for diverticulosis is (Colonscopy)
-Treatment :
.I.V antibiotics
.surgery (after 2 attacks / abscess or perforation)
-How common is massive lower GI bleeding with diverticulitis ?
.very RARE ! Massive lower GI bleeding is seen with diverticulosis, NOT with diverticulitis
+M.C.C of massive lower GI bleedign in adults is (Diverticulosis / 2nd cause is vascular ectasia or angiodysplasia)
+M.C.C of massive bleeding lower GI bleeding in children is (meckel's diverticulum)
+M.C.C of bleeding lower GI bleeding in children is (anal fissure)
*Hemorrhoids
-Engorgement of the venous plexuses of the rectum, anus, or both; with protrusion of the mucosa, anal margin, or both
+Internal hemorrhoid is (M.C) (hemorrhoid above the ‘proximal’ dentate line / not painful / may bleed)
+M.C.C of LGIB in young adults
+External hemorrhoid is (hemorrhoid below the dentate or pectinate line / painful / prone to thrombosis)
-Signs & Symptoms :
.anal mass / prolapse
.bleeding-per rectum (M.C symptom of internal hemorrhoids is bright red blood)
.itching
.pain (external hemorrhoids are painful)
-Causes Of Hemorrhoids :
.constipation / straining
.portal hypertension
.pregnancy
-Hemorrhoid Quadrants :
.left lateral (3 o'clock)
.right posterior (7 o'clock)
.right anterior (11 o'clock)
.circum firential (3-7-11 o'clock)
-Classification By Degree (for internal hemorrhoids) :
.1st degree hemorrhoid (NO prolapse)
.2nd degree hemorrhoid (prolapses with defecation, but spontaneously reduce)
.3rd degree hemorrhoid (prolapses with defecation and must be manually reduced)
.4th degree hemorrhoid (prolapsed hemorrhoid that cannot be reduced + pain)
-Treatment :
.conservative treatment typically consists of increasing dietary fiber, sitz baths, laxatives
.grade 3-4 needs surgery (Hemorrhoidectomy)
+Contraindication for hemorrhoidectomy (crohn`s disease)
+Hemorrhoidectomy is the M.C.C of anal stricture (anal stenosis)
+You must be ruled out with lower GI bleeding believed to be caused by hemorrhoid (Colon cancer-colonoscopy) if Pt. >50yrs
**Jaundice
-Is usually detectable clinically when the plasma bilirubin exceeds 50mol/L (3mg/dL)
-Causes Of Elevated Serum Transaminases (ALT-AST):
+ (<100 U/L)
.chronic hepatitis (C-B)
.haemochromatosis
.fatty liver disease
+(100-300 U/L)
.alcoholic hepatitis
.wilson`s disease
+(<300U/L)
.drugs (paracetamol)
.acute viral hepatitis
38
.autoimmune liver disease

.ischaemic liver
Page
.toxins
.flare of chronic hepatitis B
-Cholestatic Jaundice :
.is a condition where bile cannot flow from the liver to the duodenum
.causes of cholestatic jaundice (primary biliary cirrhosis, pregnancy, chronic right heart failure, alcohol, drugs ,cystic fibrosis,
severe bacterial infections, carcinoma, choledocholithiasis, parasitic infection, chronic pancreatitis)
.complications (jaundice, pale stools, dark urine, pruritus-malabsorption Vit ADEK, weight loss, steatorrhea ,osteomalacia,
bleeding tendency, xanthelasma and xanthomas)
**Ascites
-Is present when there is accumulation of free fluid in the peritoneal cavity. Small amount of ascites are asymptomatic, but with
large accumulations of fluid (>1L)
-Signs & Symptoms :
.abdominal distension
.”flank bulging” (bulging of the flanks in the reclining patient)
."shifting dullness" (difference in percussion note in the flanks that shifts when the patient is turned on the side)
."fluid wave" (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite
side of the abdomen)
.portal hypertension (perhaps due to cirrhosis or fibrosis of the liver)
.leg swelling
.bruising
.gynecomastia
.hematemesis
.mental changes due to encephalopathy
.weight loss
.heart failure
.shortness of breath as well as wheezing and exercise intolerance
.distortion or eversion of the umbilicus
.hernia
.abdominal striae
.divarication of the recti and scrotal oedema
.dilated superficial abdominal veins may be seen if the ascites is due to portal hypertension
-Causes :
+"Transudate" (high SAAG)
.cirrhosis - 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
.heart failure - 3%
.hepatic venous occlusion (Budd-Chiari syndrome or veno-occlusive disease)
.constrictive pericarditis
.kwashiorkor (childhood protein-energy malnutrition)
+"Exudate" (low SAAG)
.cancer (metastasis and primary peritoneal carcinomatosis)
.infection (tuberculosis or spontaneous bacterial peritonitis)
.pancreatitis
.serositis
.nephrotic syndrome
.hereditary angioedema
+Other Rare Causes
.meigs syndrome
.vasculitis
.hypothyroidism
.renal dialysis
.peritoneum mesothelioma
.abdominal tuberculosis
+Serum-ascites albumin gradient SAAG
.A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of
non-portal hypertensive etiology
39
-Complications :
.spontaneous bacterial peritonitis
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.hepatorenal syndrome
.thrombosis
+Ascites exists in three grades :
.Grade 1 : mild, only visible on ultrasound and CT
.Grade 2 : detectable with flank bulging and shifting dullness
.Grade 3 : directly visible, confirmed with the fluid wave/thrill test
**Cirrhosis
-Replacement of liver tissue by fibrosis as result of chronic liver disease
+Hepatic cirrhosis is a common disease characterised by diffuse hepatic fibrosis and nodule formation. It can occur at any age
+The M.C.C of cirrhosis are chronic viral hepatitis (B-C-D) and prolonged excessive alcohol consumption
+Cirrhosis is the M.C.C of portal hypertension and its associated complications
+The liver tissue shows fibrosis, cell necrosis, degeneration and regeneration nodules with loss of lobular and vascular
architecture
-Signs & Symptoms :
.hepatomegaly, splenomegaly-hypersplenism (pancytopenia)
.jaundice, parotid enlargement
.ascites
.circulatory changes (spider telangiectasia-spider angioma vs spider nevi, palmar erythema, cyanosis)
.endocrine changes (loss of libido, hair loss, gynecomastia (elevated estrogen, low testosterone), testicular atrophy, impotence-
breast atrophy, irregular menses, amenorrhea)
.portal hypertension (splenomegaly, collateral vessels, variceal bleeding)
.hepatic encephalopathy
.pigmentation, clubbing, itching (pruritus)
.hepatocellular carcinoma (hepatoma-tumor marker ‘AFP’)
.esophageal varices
.fetor hepaticus
.hypogonadism
.caput medusa
-Causes :
.alcohol (alcoholic liver disease – alcoholic cirrhosis has a worse prognosis than any cause)
.chronic hepatitis (B or C) (HBV – is M.C.C) / autoimmune hepatitis (F > M)
.non-alcoholic fatty liver disease
.immune (primary sclerosing, cholangitis, autoimmune liver disease)
.biliary (primary biliary cirrhosis (gold standard diagnosis is antimitochondrial antibodies with liver biopsy), secondary biliary,
cirrhosis, cystic fibrosis)
.genetic (hemochromatosis, wilson's disease, alpha-1 antitrypsin deficiency, DM, skin hyperpigmentation, pseudogout,
cardiomyopathy, iron overload)
.cryptogenic
.chronic venous outflow obstruction
.Budd-Chiari syndrome
+The Budd-Chiari syndrome is due to occlusion of the Hepatic veins
-Diagnosis :
.liver biopsy (Gold standard)
-Lab Findings :
.AST-ALT elevated (AST>ALT)
.alkaline phosphatase elevated
.albumin (levels fall)
.prolonged PT
.hyponatremia
.thrombocytopenia (low platelet)
.coagulation factor
.leukopenia and neutropenia
-Complications :
.ascites
.esophageal variceal bleeding
40
.hepatic encephalopathy (due to ammonium)

.spontaneous bacterial peritonitis (liver cirrhosis, ascites, E.coli due to spontaneous bacteria/treated by antibiotic ‘ceftriaxone’)
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.carcinoma
.hypersplenism
+Causes Hemorrhagic Ascites :
.Malignancy
.Ruptured ectopic pregnancy
.Abdominal trauma
.Acute pancreatitis
.Liver cirrhosis (NOT)
*Cardiac Cirrhosis
-Due to chronic Rt. sided heart failure, which leads to liver congestion
-Causes :
.hepatotoxic drugs or toxins
.cystic fibrosis
.veno occlusive diseases
.budd-chiari syndrome
.IVC obstruction
.pericardial effusion
*Primary Biliary Cirrhosis

-Autoimmune disease of the liver, marked by the slow progressive destruction of the small bile ducts within the liver (this can
lead to scarring fibrosis & cirrhosis) / Affecting middle age female (40-60yrs)
-Causes :
.idiopathic
.autoimmune progressive
.destructive intrahepatic cholangitis
-Diagnosis :
.GGT (elevated gamma-glutamyl transferase) and alkaline phosphatase
.U/S & CT
.antibodies (antimitochondrial antibody)
*Budd-Chiarri Syndrome
-Is a condition caused by occlusion of the hepatic veins that drain the liver
-Causes :
+Primary Budd–Chiari syndrome (75%): thrombosis of the hepatic vein
+Hepatic vein thrombosis is associated with the following in decreasing order of frequency :
.Polycythemia vera
.Pregnancy
.Postpartum state
.Use of oral contraceptives
.Paroxysmal nocturnal hemoglobinuria
.Hepatocellular carcinoma
.Lupus anticoagulants
+Secondary Budd–Chiari syndrome (25%): compression of the hepatic vein by an outside structure (e.g. a tumor)
.infection such as tuberculosis
.genetic tendencies include (protein C deficiency, protein S deficiency, the Factor V Leiden mutation)
.hormonal contraception
.other risk factors include the antiphospholipid syndrome, aspergillosis, Behçet's disease, dacarbazine, pregnancy and trauma
**Tumors Of The Liver

+M.C liver cancer is (Metastatic disease – primary site is usually the GI tract)
+M.C primary malignant liver tumor is (hepatocellular carcinoma – hepatoma) (Hepatoblastoma is M.C in infants and children)
+M.C primary benign liver tumor is (hemangioma)
+Lobectomy is (removal Rt. or Lt. lobe of the liver)
41
*Hepatocellular Carcinoma (Hepatoma)

-Signs & Symptoms :
Page
.RUQ pain (painful hepatomegaly)

.weight loss
.ascites
.fever
.anemia
.splenomegaly
.polycythemia
-Associated Risk Factors (Hepatoma - a cancer of the cells of the liver) :
.hepatitis B virus (HBV)
.cirrhosis
.aflatoxin (from aspergillus)
.alpha-3-antitrypsin deficiency
.hemochromatosis
.steroids
.clonorchis sinensis
.polyvinyl chloride (PVC)
-Diagnosis :
.needle biopsy
-Treatment :
.surgical resection / liver transplant
.if not fit for surgery (intra-arterial chemotherapy / ethanol injection)
+Fibrolamellar hepatoma is the best prognosis / usually affect after young adult
+M.C site of metastasis is lung
+Tumor marker (hepatoma) is (elevated alpha-fetoprotein) (AFP, α-fetoprotein, alpha-1-fetoprotein, alpha-feto globulin)
+M.C location of abscess in the liver is (Rt. lobe > Lt. lobe)
+M.C type world wide is (amebic)
*Hepatocellular Adenoma
-Benign liver tumor / F > M (9:1) / Age 30-35yrs
-Histology (hepatocyte without bile duct)
+Associated with use of OCP
-M.C complications (rupture, bleeding)
-Treatment (small – stop OCP / large >5cm – surgical resection)
*Focal Nodular Hyperplasia FNH

-Benign liver tumor / F > M
-Histology (hepatocyte with bile duct)
-Treatment (observation)
*Hepatic Hemangioma
-M.C benign liver tumor
-Complications :
.pain
.heart failure
.obstructive jaundice
.kasabach-merritt syndrome (thrombocytopenia-coagulopathy)
-Diagnosis :
.CT-scan with contrast
+Biopsy is contraindicated (risk of bleeding)
*Amebic Liver Abscess

-Entamoeba histolytica (typically reaches liver via portal vein from intestinal amebiasis)
-Bacterial - M.C is Gram(-), E.coli / Treated by (aspiration + I.V antibiotics) / Most commonly involved is (Rt. lobe of the liver)
-Viral – Treated by (metronidazole)
-Spread (fecal – oral transmission)
42
*Hydatid Liver Cysts

-Hydatid disease is a parasitic infestation by a tapeworm of the genus. Usually a Rt. lobe cyst filled with (Echinococcus
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granulosus)
+Echinococcosis can involve any organ. The liver is the M.C organ involved, followed by the lungs
-Signs & Symptoms :
.most symptomatic cysts are larger than 5cm in diameter
.RUQ pain
.obstructive jaundice
.abdominal pain
.involvement of the lungs produces chronic cough, dyspnea, pleuritic chest pain and hemoptysis
-Risk Factors :
.travel
.sheep, pigs, camels, cattle, goats, horses, dogs and other animals are the host
-Diagnosis :
.serology (Echinococcus titer – antibody)
.CT-scan (cyst with calcification)
.Casoni test
.Indirect hemagglutination antibody test (don`t stool test with E.g)
+Findings on AxR is (Possible calcified outline of cyst)
+Risk of surgical removal of echinococcal (hydatid) cyst is (Rupture or leakage of cyst contents into the abdomen may cause a
fatal anaphylactic shock)
-Treatment :
.mebendazole-albendazole, followed by surgical resection
+Toxic irrigations are used (Hypertonic saline, ethanol or cetrimide)
*Hepatomegaly
-Is the condition of having an enlarged liver
-Sings & Symptoms :
.weight loss
.poor appetite
.lethargy
.jaundice
.bruising
-Causes :
1.Liver inflammation
+Viral (hepatitis, mononucleosis, cytomegalovirus CMV, herpes simplex HSV, yellow fever)
+Bacterial (pyaemic abscesses, brucellosis, typhoid, syphilis, leptospirosis)
+Protozoa (amoebic liver abscess, malaria, kala-azar)
+Helminth (schistosomiasis, hydatid cyst, fasciola)
2.Liver congestion
.inferior vena cava obstruction
.budd-chiari syndrome
.veno-occlusive disease
3.Obstructive jaundice
4.Liver cirrhosis
5.Neoplastic
.metastatic tumors
.hepatocellular carcinoma (liver)
.myeloma
.leukemia
.lymphoma
6.Blood diseases
.hemolytic anemia
.megaloblastic anemia
.sickle cell disease
.polycythaemia vera
.leukemia
.hodgin`s lymphoma
.non-hodgin`s lymphoma
43
7.Metabolic
.fatty liver
Page
.wilson`s disease
.amyloidosis
.gaucher`s disease (lipoid storage disease)
.von gierke's disease (glycogen storage disease)
8.Drugs and alcohol
9.Biliary
.primary biliary cirrhosis
10.Others
.hunter syndrome (spleen effected)
.zellweger`s syndrome
.sarcoidosis
-Treatment :
+In the case of cirrhosis, prednisone and azathioprine for autoimmune hepatitis is used in treatment
+In the case of lymphoma the treatment options include single-agent (or multi-agent) chemotherapy and regional radiotherapy,
also surgery may be an option in specific situations
+Meningococcal group C conjugate vaccine
+In primary biliary cirrhosis ursodeoxycholic acid
*Liver Transplantation
-In case of irreversible progressive liver disease with no alternative therapy as liver cirrhosis, fulminant liver failure and inborn
errors of metabolism
-Contraindications :
.extra hepatobiliary sepsis
.metastatic malignancy
.sever cardio-pulmonary disease
.AIDS
.age above 70yrs
.previous abdominal surgery
.portal and superior mesenteric vein thrombosis
+Selection Of The Donor :
.matched for ABO blood group compatibility
.matched for liver size
.negative HIV-HBV-HCV
+Immunosuppression :
.cyclosporine
.prednisone
.azathioprine
-Complications :
.graft rejection
.graft dysfunction (hepatic artery thrombosis, biliary leak or obstruction, recurrence of hepatitis)
.infections
.renal dysfunction
.neuropsychiatric disorders
**Gallstone
-Presence of stones in the gallbladder is referred to as cholelithiasis
-Characteristics And Composition :
.mixed stones (M.C type)
.cholesterol stones (2nd M.C)
.pigment stones (Ca+2 bilirubinate) (is seen in hemolytic disease)
-Signs & Symptoms :
.may be asymptomatic (do not require treatment)
.pain in the upper Rt. Side of the abdomen (RUQ pain) radiate to Rt. shoulder or scapula
.nausea, vomiting
44
.a Pt. may also experience referred pain between the shoulder blades or below th Rt. Shoulder
.positive Murphys sign (on physical findings) (seen too in cholecystitis)
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-Causes :
.female, faty, fertile (multiparity), fair, forty (40yrs of age)
.low-fiber and high-cholesterol diets
.rapid weight loss
.hemolytic anemias (such as sickle-cell disease and hereditary spherocytosis)
.cirrhosis and biliary tract infections
-Diagnosis :
.ultrasound
-Treatment :
.surgical (cholecystectomy – gallbladder removal) (surgery is only indicated in symptomatic Pts.)
+M.C artery injured during cholecystectomy is Rt. Hepatic artery
-Complications Of Gallbladder Stones :
.choledocholithiasis
.ascending cholangitis (fever, jaundice, obstructive intestinal)
.pancreatitis (M.C.C of acute pancreatitis is Gallstone)
.gallstone ileus
.gallbladder cancer
++Pigmented stones (Brown – infected / Black – non-infected)
+Brown stones (associated with biliary tract infection)
+Black stones (contain calcium bilirubinate) (causes-hemolysis, cirrhosis
*Acute Cholecystitis
-Obstruction of cystic duct leads to inflammation of the gallbladder
-Risk factor is (Gallstones)
-Signs & Symptoms :
.unrelenting RUQ pain or tenderness
.fever
.nausea, vomiting
.painful palpable gallbladder
.positive Murphy`s sign (acute pain and inspiratory arrest elicited by palpation of the RUQ during inspiration) (negative – stones
and cholangitis)
.right subscapular pain (referred)
.epigastric discomfort (referred)
-Complications :
.abscess
.perforation
.choledocholithiasis
.cholecystoenteric fistula formation
.gallstones ileus
-Lab Results :
.increased WBS
.elevation in alkaline phosphatase
.LFTs
.elevation in amylase
-Signs Of Acute Cholecystitis On U/S :
.thickened gallbladder (>3mm)
.distended gallbladder
.pericholecystic fluid
.gallstones present / cystic duct stones
.sonographic Murphy`s sign
-Treatment :
.IV fluid
.antibiotics
.cholecystectomy
45
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NEPHROLOGY
**Chronic Renal Disease CRD-CKD
-Is a progressive loss in renal function over a period of months or years
-Glomerular filtration rate (GFR) is the best overall index of kidney function
+The M.C.C of death in people with CRD is therefore cardiovascular disease rather than renal failure
+Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis, shows that is allowing
the loss of protein
-Signs & Symptoms :
.HTN (Bp is increased due to fluid overload and production of vasoactive hormones created by the kidney via the RAS ‘renin-
angiotensin system’)
.urea accumulates (leading to azotemia and ultimately uremia - symptoms ranging from lethargy to pericarditis and
encephalopathy)
."uremic frost" (is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates)
.sweating
.hyperkalemia (potassium accumulates in the blood - hyperkalemia with a range of symptoms including malaise and potentially
fatal cardiac arrhythmias)
+Hyperkalemia usually does not develop until the glomerular filtration rate falls to less than 20-25 ml/min/1.73 m2
+Hyperkalemia in CKD can be exacerbated by acidemia (which leads to extracellular shift of potassium) and from lack of insulin
.erythropoietin synthesis is decreased causing anemia
.fluid volume overload (symptoms may range from mild edema to life-threatening pulmonary edema)
.hyperphosphatemia (due to reduced phosphate excretion) follows the decrease in glomerular filtration
+Hyperphosphatemia is associated with increased cardiovascular risk
.hypocalcemia, due to 1,25 dihydroxyvitamin D3 deficiency (caused by stimulation of FGF-23 and reduction of renal mass)
+Later, this progresses to secondary hyperparathyroidism, renal osteodystrophy (brown tumor of bone), and vascular
calcification that further impaired cardiac function
.metabolic acidosis
.sexual dysfunction is very common in both men and women with CKD
+A majority of women have trouble with sexual arousal, and painful menstruation
-Causes :
.DM (M.C.C)
.HTN
.glomerulonephritis
.polycystic kidney disease
.drug and toxin induced chronic tubulointerstitial nephritis
.obstructive nephropathy (kidney stones, diseases of prostate)
.recurrent pyelonephritis (M.C bacteria is E.coli)
.SLE
.vascular diseases (bilateral renal artery stenosis)
.amyloidosis
+Alkalosis are not complication
-Stages :
.stage 1 (slightly diminished function; kidney damage with normal or relatively high GFR >90mL/min/173m2)
.stage 2 (mild reduction in GFR 60-90mL/min/173m2)
.stage 3 (moderate reduction in GFR 30-59 mL/min/173m2)
.stage 4 (15-30mL/min/173m2)
.stage 5 (end stage renal disease ESRD <15) (treated by dialysis, renal transplant BEST)
-Treatment :
.control of Bp and treatment of the original disease ‘DM’
.replacement of erythropoietin and calcitriol-‘Vit D3’
.phosphate binder (used to control the serum phosphate levels)
.when one reaches stage 5 CRD, renal replacement therapy, dialysis, transplant (BEST)
46
+Drugs are contraindicated in chronic renal failure :

.Tetracycline
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.Nalidixic acid
.Nitrofurantoin
.Aspirin
+In chronic renal failure the serum concentration of the following substances is increased :
.Uric acid
.Urea
.Creatinine
.Phosphorus
+Glomerular filtration rate GFR = creatinine clearance’ (normal is 100-140ml/min)
(140-age) * Mass (in Kg) * 0.85 (if female)
72 * creatinin
+GFR (age, mass, creatinine, sex) / Low GFR (renal failure) / High GFR (pregnancy, early DM)
++Urine Retention
+Acute (painful / prostatic hyperplasia is M.C.C / bladder capacity is normal 700-1000cc / rapid foley's)
+Chronic (painless / prostatic hyperplasia is M.C.C / bladder capacity up to 4L / NOT rapid)
**Acute Renal Failure ARF

-Is a rapid loss of kidney function / Reversible condition but chronic irreversible
-Elevated blood urea nitrogen (BUN) and creatinine (rapid rise in blood urea nitrogen BUN or creatinine)
-Signs & Symptoms :
.may be asymptomatic
.fatigue
.decreased mental acuity
.seizures
.anorexia
.nausea
.decreased taste and smell
.coma
.proteinuria may be present
.creatinine is usually increased
.urine is usually hyperosmotic
-Causes :
+Pre-renal M.C (those that decrease blood flow to the kidney) (hypotension dehydration) (urea creatinine >20:1 / urine >500 /
FENa <1%)
.low blood volume
.low blood pressure
.heart failure
.liver cirrhosis
.renal artery stenosis
.renal vein thrombosis
.renal ischaemia (can result in depression of GFR)
.hypovolemia or vascular diseases (causing reduced perfusion of both kidneys)
+Intrinsic (renal) (M.C.C is glomerulonephritis, acute tubular necrosis ATN, acute interstitial nephritis AIN,cytotoxic drugs)
.glomeruli
.renal tubules
.interstitium
.rhabdomyolysis
.tumor lysis syndrome
+Post-renal (urinary tract obstruction, benign prostatic hyperplasia, kidney stones) (urea creatinine <20:1 / urine <350 / FENa
>1%)
.urinary tract obstruction
.benign prostatic hyperplasia
.kidney stones
.obstructed urinary catheter
.bladder stone
.bladder, ureteral or renal malignancy
47
+Other causes :
.Goodpasture’s syndrome
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.Hemolytic uremic syndrome

.Scleroderma crisis
.Post infectious glomerulonephritis
.Severe dehydration
.Severe burn
.Severe hemorrhage
.Hemolytic uremic syndrome
-Complications :
.metabolic acidosis
.hyperkalemia
.hypocalcemia
.hypoalbuminemia
.hyperphosphatemia
.pulmonary edema
.bleeding (inhibit platelet)
.pericarditis
+Retrosternal chest pain – cough (increased in lying supine) (decreased in leaning forward) (Diffuse ST-elevation)
-Diagnostic test :
.the blood urea nitrogen BUN
+A diagnosis is made when there is rapid reduction in kidney function, as measured by serum creatinine, or based on a rapid
reduction in urine output, termed oliguria (less than 400 mls of urine per 24 hours)
-Treatment :
.in pre renal ARF, administration of IV fluid (is 1st step)
.NSAIDs (ibuprofen, iodinated contrast)
.antibiotics (gentamicin)
+Indications of dialysis in ARF :
.refractory HTN or pulmonary edema
.uncontrollable hyperkalemia >7
.uremic encephalitis
.pericarditis
.bleeding diathesis (epistaxis, GI bleeding)
.severe metabolic acidosis Ph<7
.blood urea nitrogen BUN >70-100 mg/dl
+Pre-renal (urea >20:1 / urine >500 / FENA <1%)
+Renal or Post-renal (urea <20:1 / urine <350 / FENA >1%)
**Azotemia
-Is a medical condition characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine,
various body waste compounds, and other nitrogen-rich compounds) in the blood. It is largely related to insufficient or
dysfunctional filtering of blood by the kidneys. It can lead to anemia if not controlled
+Is a form of renal insufficiency caused by diminished perfusion of the kidney on`any basis. The kidney itself is normal - is an
abnormally high level of nitrogen waste products in the blood
-Signs & Symptoms :
.oliguria or anuria (decreased or absent urine output)
.fatigue
.asterixis (flapping tremor)
.decreased alertness
.confusion
.pale skin
.tachycardia (rapid pulse)
.xerostomia (dry mouth)
.thirst
.edema, anasarca (swelling)
.orthostatic blood pressure (fluctuates depending on body position)
.uremic frost
48
+A urinalysis will typically show (None of these is particularly useful in diagnosis) :

.decreased urine sodium level
.high urine creatinine-to-serum creatinine ratio
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.high urine urea-to-serum urea ratio

.concentrated urine (determined by osmolality and specific gravity)
+In pre-renal and postrenal azotemia, elevation of the BUN exceeds that of the creatinine (i.e., BUN>12*creatinine). This is
because BUN is readily absorbed while creatinine is not
+In congestive heart failure (a cause of pre-renal azotemia) or any other condition that causes poor perfusion of kidneys, the
sluggish flow of glomerular filtrate results in excessive absorption of BUN and elevation of its value in blood. Creatinine,
however, is not absorbable and therefore does not rise significantly
-Causes :
.hypovolemia on any basis (dehydration, burn, poor oral intake, diuretic, vomiting, diarrhea, sweating, hemorrhage)
.hypotension on any basis (septic shock, cardiogenic shock, anaphylactic shock)
.third spacing of fluids such as (peritonitis, osmotic diuresis or low aldosterone states such as addison disease)
+Low albumin states also lead to decreased renal perfusion. Nephrotic syndrome and other malabsorptive states lead to a low
albumin level. This leads to renal failure
-Types :
.prerenal azotemia
.primary renal azotemia
.postrenal azotemia
+All Forms Of Azotemia Are Characterized By :
.decrease in the glomerular filtration rate (GFR) of the kidneys
.increases in blood urea nitrogen (BUN)
.serum creatinine concentrations
+The BUN-to-creatinine ratio (BUN:Cr) is a useful measure in determining the type of azotemia. A normal BUN:Cr is equal to 1
-Treatment :
.hemodialysis or peritoneal dialysis
.medications to increase cardiac output and increase blood pressure
.treatment of the condition that caused the azotemia
*Prerenal Azotemia
-Prerenal azotemia is caused by a decrease in blood flow (hypoperfusion) to the kidneys. However, there is no inherent kidney
disease
-It Can Occur Following :
.hemorrhage
.shock
.volume depletion
.congestive heart failure
.adrenal insufficiency
.narrowing of the renal artery among other things
+The BUN : Cr in prerenal azotemia is greater than 20
*Primary Renal Azotemia

-Renal azotemia (acute renal failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of
renal parenchymal damage. Causes include renal failure, glomerulonephritis, acute tubular necrosis, or any other kind of renal
disease
+The BUN : Cr in renal azotemia is less than 15
*Postrenal Azotemia
-Blockage of urine flow in an area below the kidneys results in postrenal azotemia / From bilateral obstruction to the flow of
urine out of the kidney. Like in prerenal azotemia, there is no inherent renal disease / The increased resistance to urine flow can
cause back up into the kidneys, leading to hydronephrosis
+You cannot get renal failure by the obstruction of only a single kidney if a Pt. has both kidneys in place (only one kidney does
not cause renal failure – creatinine will only begin to rise when you have lost at least 70-80% of renal function)
+Acute tubular necrosis ATN is the most common cause of ARF (intrinsic) in hospitalized Pts.
-Causes :
.congenital abnormalities (vesicoureteral reflux)
.blockage of the ureters by kidney stones
49
.pregnancy
.compression of the ureters (by cancer, prostatic hyperplasia, or blockage of the urethra by kidney)
.bladder stones
Page
.bilateral ureteral disease (retroperitoneal fibrosis)

.neurogenic bladder (or any other cause of bilateral obstructive disease)
+large stone in one ureter cannot cause renal failure because the creatinine does not rise if there is a loss of only one kidney. A
small tone or clot in the bladder can obstruct both kidneys and this can cause post renal azotemia
+The BUN:Cr in postrenal azotemia is initially >1
**Renal Artery Stenosis

-Is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This
narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary
type of high blood pressure
-Renal artery stenosis results in high BUN (blood urea nitrogen) and creatinine
-Signs & Symptoms :
.M.C of renal artery stenosis are asymptomatic
.high Bp that cannot be controlled with medication
.decreased kidney function may develop if both kidneys do not receive adequate blood flow
.pulmonary edema
-Causes :
.atherosclerosis (arteriosclerotic vascular disease or ASVD)
.fibromuscular dysplasia FMD (non-atherosclerotic, non-inflammatory disease of the blood vessels) ( in young patients, usually
females under 40 years of age)
-Complications :
.Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease
.if the restenosis is long standing and severe the glomerular filtration rate in the affected kidneys never recovers and (prerenal)
kidney failure is the result
.the pathophysiology of renal artery stenosis, leads to changes in the structure of the kidney that are most noticeable in the
tubular tissue
+Changes include :
.fibrosis
.tubular cell size (decrease)
.thickening of Bowman capsule
.tubular sclerosis
.glomerular capillary tuft(atrophy)
-Treatment :
.atherosclerotic renal artery stenosis (diuretics, and medications for blood pressure control / nephrectomy)
.fibromuscular dysplasia (angioplasty with or without stenting is the best option for the treatment of renal artery stenosis due
to fibromuscular dysplasia)
**Hepatorenal Syndrome HRS

-Is a life-threatening medical condition that consists of rapid deterioration in kidney function in individuals with cirrhosis or
fulminant liver failure and elevated pressures in the portal vein system (termed portal hypertension)
-Signs & Symptoms :
.altered liver function
.abnormalities in circulation
.kidney failure
.jaundice
.altered mental status (evidence of decreased nutrition)
.ascites
.oliguria
+Most people who develop HRS have cirrhosis
+The definitive treatment for hepatorenal syndrome is liver transplantation
-Causes :
.cirrhosis alcoholic (cirrhosis, acute onset of liver failure, termed fulminant liver failure)
.elevated pressures in the portal vein system (termed portal hypertension)
.iatrogenic precipitants of HRS, include (the aggressive use of diuretic medications or the removal of large volumes of ascitic
fluid by paracentesis from the abdominal cavity without compensating for fluid losses by intravenous replacement)
-Types :
50
1.Type 1HRS
-Characterized by :
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.rapidly progressive kidney failure

.doubling of serum creatinine to a level greater than 221 μmol/L (2.5 mg/dL)
.halving of the creatinine clearance to less than 20 mL/min over a period of less than two weeks
.Pts.with type 1 HRS are usually ill, may have low blood pressure
.Pts. with type 1 HRS may require therapy with drugs to improve the strength of heart muscle contraction (inotropes) or other
drugs to maintain blood pressure (vasopressors)
2.Type 2HRS
-Characterized by :
.slower in onset and progression
.it is defined by an increase in serum creatinine level to >133 μmol/L (1.5 mg/dL) or a creatinine clearance of less than 40
mL/min, and a urine sodium < 10 μmol/L
.it also carries a poor outlook, with a median survival of approximately six months unless the affected individual undergoes liver
transplantation
.thought to be part of a spectrum of illness associated with increased pressures in the portal vein circulation, which begins with
the development of fluid in the abdomen (ascites)
**ACE Inhibitor Effect On The Kidney

*Hepatopulmonary Syndrome
-Is a syndrome of shortness of breath and hypoxemia (low oxygen levels in the blood of the arteries) caused by vasodilation
(broadening of the blood vessels) in the lungs of patients with liver disease
+This syndrome is similar to hepatorenal syndrome in that kidneys themselves are intrinsically normal
+Dyspnea and hypoxemia are worse in the upright position (associated with a marked change in saturation levels with changes
in bodily position, this change in saturation with a change in position is characteristic of hepatopulmonary syndrome - which is
called platypnea and orthodeoxia)
-Treatment :
.liver transplantation (definitive treatment)
.supplemental oxygen or somatostatin to inhibit vasodilation
*Tubulointerstitial Disease
1.Acute Tubular Necrosis ATN
-Is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys
-The presence of "muddy brown casts - a type of granular cast” of epithelial cells found in urinalysis is pathognomonic for ATN /
high urine sodium >40 and low urine osmolality <350
-ATN presents with acute kidney failure-injury (AKI) and is one of the M.C.C of AKI. Common causes of ATN include low blood
pressure and use of nephrotoxic drugs
-ATN may be classified as either toxic or ischemic :
.Toxic ATN occurs when the tubular cells are exposed to a toxic substance (nephrotoxic ATN)
.Ischemic ATN occurs when the tubular cells do not get enough oxygen, a condition that they are highly sensitive and
susceptible to, due to their very high metabolism
-Phases :
.Prodromal - this is time between the acute injury and the onset of renal failure
.Oliguric - <400mL per 24hrs or Anuric-<100mL per 24hrs
.Postoliguric - this is a diuretic phase when all the water not previously excreted will now leave the body in a vigorous polyuria
2.Allergic Interstitial Nephritis AIN / Tubulo-Interstitial Nephritis TIN

-Is a form of nephritis affecting the interstitium of the kidneys surrounding the tubules. This disease can be either acute,
meaning it occurs suddenly, or chronic, meaning it is ongoing and eventually ends in kidney failure
-Presence of fever, rash, joint pain and eosinophils in both blood and urine
-Causes :
.infection
.reaction to medication such as an analgesic or antibiotics such as methicillin (methicillin)
+Reaction to medications causes 71% to 92% of cases (M.C.C)
.other diseases and toxins that damage the kidney (bacterial infection in the kidneys known as pyelonephritis)
+The drugs that are known to cause this sort of reaction :
.antibiotics (penicillin and cephalexin, and nonsteroidal anti-inflammatory drugs - aspirin less frequently than others)
51
.proton-pump inhibitors
.rifampicin
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.sulfa drugs
.fluoroquinolones
.diuretics
.allopurinol
.phenytoin
+The time between exposure to the drug and the development of acute tubulointerstitial nephritis can be anywhere from 5
days to 5 months (fenoprofen 'NSAIDs' induced)
+The difference between tha basis of allergic interstitial nephritis and direct toxins is that allergic nephritis occurs with the first
dose and is associated with fever, rash, joint pain and eosinophils in both blood and urine
+Nonsteroidal anti-inflammatory drugs (NSAIDs) are a frequent cause of renal failure, by several mechanisms :
.interstitial nephritis
.direct toxic effect on the tubules
.papillary necrosis
.inhibition of vasodilatory prostaglandins in the afferent arteriole
.membranous glomerulonephritis
**Glomerulonephritis GN
-Several kidney diseases (usually affecting both kidneys). Many of the diseases are characterised by inflammation either of the
glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory
component / Autoimmune event, circulating antibodies or vasculitis
+RBCs cast urinary findings is most characteristic of glomerulonephritis / Erythrocyte casts is most characteristic of acute
glomerulonephritis
-As it is NOT strictly a single disease, its presentation depends on the specific disease entity: it may present with :
.hematuria and/or proteinuria (blood or protein in the urine)
.or as a nephrotic syndrome, a nephritic syndrome, acute kidney injury, or chronic kidney disease
-DM and HTN cause glomerular disease and are certainly the most common causes of nephrotic syndrome and end-stage renal
disease
-All Forms Of GN Can Be Characterized By :
.edema (can found anywhere)
.hematuria
.red cells casts
.HTN
.low urine sodium with a fractional excretion of sodium of <1%
-Causes Of GN :
1.Vascular Disease
.wegener granulomatosis
.churg-strauss syndrome
.henoch-schonlein purpura
.polyarteritis nodosa
.TTP
.hemolytic uremic syndrome HUS
.cryoglobulinemia
2.Glomerular Disease
.goodpasture syndrome
.post infectious glomerulonephritis
.IgA nephropathy (berger disease)
.SLE
.idiopathic rapidly progressive glomerulonephritis
.alport syndrome
.DM and HTN
.amyloid
+To diagnose GN is the renal biopsy
+The most important distinction between GN and nephrotic syndrome is the degree of proteinuria
+Glomerulonephritis refers to an inflammation of the glomerulus, which is the unit involved in filtration in the kidney. This
inflammation typically results in one or both of the nephrotic or nephritic syndromes
52
**Nephritic Syndrome
-Is a collection of signs (known as a syndrome) associated with disorders affecting the kidneys, more specifically glomerular
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disorders
-Signs & Symptoms :
.hematuria (blood in the urine) - with RBC casts present in the urine
.proteinuria (protein in the urine) – small amounts of protein (<3.5g/day or <40mg/day)
.hypertension (high Bp – mild)
.blurred vision
.azotemia (elevated blood nitrogen)
.oliguria (low urine output <400ml/day)
-Causes :
+Nephritic syndrome is caused by inflammation of glomerulus and has urine waste, furthermore the cause can be infectious,
autoimmune or thrombotic
+Children/Adolescents
.IgA nephropathy (berger`s disease - M.C.C of GN in adult)
.Post-streptococcal glomerulonephritis (common in children)
.Hemolytic uremic syndrome HUS (M.C.C od acute renal failure in children)
.Henoch-Schonlein purpura
+Adults
.Goodpasture syndrome (hemoptysis + hematuria)
.hepatitis B-C
.Infective endocarditis
.membranoproliferative GN1
.membranoproliferative GN2
.Rapidly progressive glomerulonephritis (RPGNs)
.PTT
.SLE or lupus nephritis (worse type)
.vasculitis
+Myeloma is most prominently a cause of nephritic syndrome
-Diagnosis :
+The classic diagnosis of nephritic syndrome is post-streptococcal glomerulonephritis, which is a common complication of
Streptococcus bacterial infections, typically of the skin.
+Tests done to diagnose if an individual has nephritic syndrome are :
.blood electrolytes
.blood urea nitrogen
.potassium test
.protein in the urine
.urinalysis
.kidney biopsy
+The difference between the basis of allergic interstitial nephritis and direct toxins is that allergic nephritis occurs with the first
dose and is associated with fever, rash, joint pain and eosinophils in both blood and urine
*IgA Nephropathy (Berger`s Disease)

+M.C type of glomerulonephritis in adults worldwide / M.C.C of glomerulonephritis in world
-Signs & Symptoms :
.macroscopic haematuria (visibly bloody in urine)
.IgA deposits
.a urinalysis will show RBCs
.affects young males within (24-48hrs) after an upper respiratory tract or GI infections (M > F)
.can cause (HTN, renal failure)
.proteinuria usually less than 2gm/day
+Worse prognosis (HTN, male, proteinuria, renal failure) / >20% of adults develop end-stage renal disease (ESRD)
-Treatment :
.cortisone
.cyclophosphamide
.ACE inhibitor for HTN
*Post-Streptococcal Glomerulonephritis PSGN

53
-Is a disorder of the glomeruli (glomerulonephritis), or small blood vessels in the kidneys. It is a common complication of
bacterial infections, typically skin infection by Streptococcus bacteria types 12,4 and 1 (impetigo) but also after streptococcal
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pharyngitis
+Streptococcus bacteria.This disorder can occur 3 weeks after a skin infection, (M.C in children)
+It can be a risk factor for future albuminuria. In adults, the signs and symptoms of infection may still be present at the time
when the kidney problems develop
-Signs & Symptoms :
.hematuria
.oliguria
.edema
.HTN
.fever, headache, malaise, anorexia, nausea
-Diagnosis :
.elevated ASO titer in blood
.low complement (C3, C4) in blood
-Treatment :
.antibiotic treatment (this decision is immediate with skin infections due to the fact that the differential diagnosis is between
staphylococcal and streptococcal impetigo)
+The streptozyme test measures different streptococcal antibodies (Serological Markers a diagnosis can be done) :
.Antistreptolysin
.Antihyaluronidase
.Antistreptokinase
.Antinicotinamide-adenine dinucleotide
.Anti-DNAse B antibodies
+Complications Of Post-Streptococcal Acute Glomerulonephritis May Include :
.Hyperkalemia
.Encephalopathy
.Pulmonary edema
.Anuria
+Causes Of Generalized Edema :
.malnutrition
.malabsorption
.renal affection
.liver cell failure
.right side heart failure
.angioedema
*Goodpasture Disease
-Is a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding
from the lungs and kidney failure (Goodpasture syndrome may quickly result in permanent lung and kidney damage, often
leading to death). It is thought to attack the alpha-3 subunit of type IV collagen, which has therefore been referred to as
Goodpasture's antigen
+The anti glomerular basement membrane (GBM) antibodies primarily attack the kidneys and lungs / Hemoptysis + Hematuria
-Signs & Symptoms :
.malaise
.weight loss
.fatigue
.fever
.chills
.joint aches and pains
.lung symptoms usually antedate kidney symptoms
+Lung symptoms, include (coughing up blood, chest pain (in less than 50% of cases overall), cough, and shortness of breath)
+Kidney symptoms, include (blood in the urine, protein in the urine, unexplained swelling of limbs or face, high amounts of urea
in the blood, and high blood pressure)
-Causes :
.exposure to organic solvents (e.g. chloroform) or hydrocarbons
.exposure to tobacco smoke
.certain gene mutations (HLA-DR15)
54
.infection, such as influenza A

.cocaine inhalation
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.metal dust inhalation

.bacteraemia
.sepsis
.high-oxygen environments
.treatment with antilymphocytic treatment (especially monoclonal antibodies)
*Hemolytic Uremic Syndrome HUS

-Is a disease characterized by hemolytic anemia (anemia caused by destruction of red blood cells), acute kidney failure (uremia),
and a low platelet count (thrombocytopenia)
+M.C.C of acute renal failure in children
+HUS is more common in children and it is associated with E.coli (food poisoning)
-Signs & Symptoms :
.HUS occurs after ingestion of a strain of bacteria expressing shiga toxin(s), usually types of E. coli, that expresses verotoxin
(also called Shiga-like toxin)
.once the bacteria colonized, diarrhea followed by bloody diarrhea, hemorrhagic colitis
.HUS develops about 5–10 days after onset of diarrhea (bloody diarrhea)
.oliguria (decreased urine output)
.hematuria (blood in the urine)
.thrombocytopenia (low levels of platelets)
.destruction of red blood cells (microangiopathic hemolytic anemia)
.thrombotic microangiopathy (TMA), include (abdominal pain, low platelet count, elevated lactate dehydrogenase LDH, a
chemical released from damaged cells, and which is therefore a marker of cellular damage)
.decreased haptoglobin (indicative of the breakdown of red blood cells)
.anemia (low red blood cell count)/schistocytes (damaged red blood cells)
.elevated creatinine (a protein waste product generated by muscle metabolism and eliminated renally)
.proteinuria (indicative of kidney injury)
.confusion
.fatigue
.edema (swelling)
.nausea/vomiting
.signs and symptoms of acute kidney failure
.hypertension (high blood pressure)
.myocardial infarction (heart attack)
.stroke
.lung complications
.pancreatitis (inflammation of the pancreas)
.liver necrosis (death of liver cells or tissue)
.encephalopathy (brain dysfunction)
.seizure
.coma
.failure of cardiac, renal, and gastrointestinal (GI) organs
.death, can occur unpredictably at any time, either very quickly or following prolonged symptomatic or asymptomatic disease
progression
+HUS
.hemolytic anemia
.thrombocytopenia
.fever
.renal failure
.don't cause neurological symptoms
+Usually occur post-infection by E.coli 157:H7 (and causes bloody diarrhea)
+Don't give antibiotic for bloody diarrhea (increased risk of HUS) and don't transfuse platelets
*Thrombotic Thrombocytopenic Purpura TTP / Moschcowitz syndrome

-Is a rare disorder of the blood-coagulation system, causing extensive microscopic clots to form in the small blood vessels
throughout the body. These small blood clots, called thrombi, can damage many organs including the kidneys, heart and brain
55
-More in adult
-Most Cases Of TTP Arise From :
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.inhibition of the enzyme ADAMTS13

.metalloprotease responsible for cleaving large multimers of von Willebrand factor (vWF) into smaller units, by autoantibodies
+A hereditary form of TTP is called the Upshaw Schulman syndrome; this is generally due to inherited deficiency of ADAMTS13
+Is caused by spontaneous aggregation of platelets and activation of coagulation in the small blood vessels
-Signs & Symptoms :
.hemolytic anemia (anemia, jaundice and a blood film featuring evidence of mechanical fragmentation of red blood cells)
.thrombocytopenia (low platelet count), leading to bruising or purpura
.fever
.renal failure
.neurologic symptoms (fluctuating), such as hallucinations, bizarre behavior, delirium, stroke, or headaches
.malaise
.fever
.headache
.HTN
.diarrhea
.bruising
.rarely bleeding - spontaneous (from the nose or gums)
.larger bruises (ecchymoses)
+Neurological Symptoms are present in up to 65% of patients, and may include headache, difficulty speaking, transient
paralysis, numbness, fits, or coma, the last of which is a poor prognostic indicator
-Treatment :
.cortisone + plasma exchange
+TTP
.hemolytic anemia
.thrombocytopenia
.fever
.renal failure
.can cause neurological symptoms
+Secondary TTP is diagnosed when the Pts. history mentions one of the known features associated with TTP (Risk factors)
.cancer
.bone marrow transplantation
.pregnancy
.HIV-1 infection
.medication use (Antiviral drugs (acyclovir), Quinine, Oxymorphone, Platelet aggregation inhibitors (ticlopidine, clopidogrel, and
prasugrel), Immunosuppressants (cyclosporine, mitomycin, tacrolimus/FK506, interferon-α), Hormone altering drugs
(estrogens, contraceptives, hormone replacement therapy)
**Nephrotic Syndrome
-Is a nonspecific kidney disorder characterized by three signs of disease (large proteinuria, hypoalbuminemia, and edema)
+Essentially, loss of protein through the kidneys (proteinuria) leads to low protein levels in the blood (hypoalbuminemia), which
causes water to be drawn into soft tissues (edema)
+Very low hypoalbuminemia can also cause a variety of secondary problems, such as water in the abdominal cavity (ascites),
around the heart or lung (pericardial effusion, pleural effusion), high cholesterol (hence hyperlipidemia), loss of molecules
regulating coagulation (hence increased risk of thrombosis)
-Signs & Symptoms :
.proteinuria (>3.5g/day or 40mg/hr)
.hypoalbuminemia (<2.5 g/dL)
.hyperlipidaemia
.edema
.lipiduria (lipids in urine) (not essential for the diagnosis of nephrotic syndrome)
.hyponatremia (occurs with a low fractional sodium excretion)
.hyperlipidemia
+Hyperlipidaemia is caused by two factors :
1.hypoproteinemia stimulates protein synthesis in the liver, resulting in the overproduction of lipoproteins
2.lipid catabolism is decreased due to lower levels of lipoprotein lipase
.it is common among (2-6yrs) old boys
56
.edema begins in the face (1st sign of nephrotic in children is usually swelling of the face)
.HTN (rarely)
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.anemia
.dyspnea (may be present due to pleural effusion or due to diaphragmatic compression with ascites)
.erythrocyte sedimentation rate (ESR) is increased due to increased fibrinogen and other plasma contents
.actual urinary complaints (haematuria or oliguria are uncommon, though these are seen commonly in nephritic syndrome)
.rash associated with systemic lupus erythematosus, or the neuropathy associated with diabetes
.examination should also exclude other causes of gross edema—especially the cardiovascular and hepatic system
.muehrcke's nails; white lines (leukonychia)
.excess fluid in the body due to the serum hypoalbuminemia (M.C sign). This may take several forms (puffiness around the eyes,
characteristically in the morning / pitting edema over the legs / fluid in the pleural cavity causing pleural effusion. More
commonly associated with excess fluid is pulmonary edema / fluid in the peritoneal cavity causing ascites / generalized edema
throughout the body known as anasarca)
+The Main Signs Of Nephrotic Syndrome Are :
.proteinuria (3.5 g/day is considered to be proteinuria in the nephrotic range or greater than 40 mg/hr in children)
.hypoalbuminemia (<2.5 g/dL) (that exceeds the hepatic clearance level, that is, protein synthesis in the liver is insufficient to
increase the low blood protein levels)
.edema
+Nephrotic syndrome edema initially appears in parts of the lower body (such as the legs) and in the eyelids. In the advanced
stages it also extends to the pleural cavity and peritoneum (ascites) and can even develop into a generalized anasarca
.hyperlipidaemia (is caused by an increase in the synthesis of low and very low-density lipoproteins in the liver that are
responsible for the transport of cholesterol and triglycerides. There is also an increase in the hepatic synthesis of cholesterol)
.thrombophilia, or hypercoagulability (is a greater predisposition for the formation of blood clots that is caused by a decrease in
the levels of antithrombin III in the blood due to its loss in urine)
.lipiduria or loss of lipids in the urine
-Causes :
1.Primary Nephrotic Syndrome (primary glomerulonephritis)
.Membranous nephropathy
.Hereditary nephropathies (Alport Syndrome)
.Minimal change disease (MCD) (M.C.C of primary nephrotic syndrome in children) (good prognosis ‘steroid-sensitive’)
.Focal segmental glomerulosclerosis (FSGS) (M.C.C of primary nephrotic syndrome in adults) / It is characterized by the
appearance of tissue scarring in the glomeruli (bad prognosis – most Pts. with FSGS end with ESRD and associated with HIV)
.Membranous glomerulonephritis (MGN) / The inflammation of the glomerular membrane causes increased leaking in the
kidney, although an auto-immune mechanism is suspected
.Membranoproliferative glomerulonephritis (MPGN) / Is the inflammation of the glomeruli along with the deposit of antibodies
in their membranes / can cause hepatitis C
.Rapidly progressive glomerulonephritis (RPGN) / Usually presents as a nephritic syndrome
2.Secondary Nephrotic Syndrome
.DM (M.C.C of nephrotic syndrome) (Diabetic nephropathy - is a complication that occurs in some diabetics. This leads to the
leakage of proteins into the urine)
.Systemic lupus erythematosus SLE (or Lupus erythematosus - this autoimmune disease can affect a number of organs, among
them the kidney, due to the deposit of immune complexes that are typical to this disease. The disease can also cause lupus
nephritis)
.amyloidosis and paraproteinemias
.Hepatitis B – C
.preeclampsia
.Sarcoidosis
.Syphilis (kidney damage can occur during the secondary stage of this disease - between 2 and 8 weeks from onset)
.Sjögren's syndrome (this autoimmune disease causes the deposit of immune complexes in the glomeruli, causing them to
become inflamed, this is the same mechanism as occurs in systemic lupus erythematosus)
.HIV
.Multiple myeloma
.Vasculitis
.Cancer
.Genetic disorders (congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin)
.Drugs ( e.g. gold salts, penicillin, captopril)
-Diagnosis :
.24hrs urine protein measurment (Best test)
.hypoalbuminemia (<2.5g/dL)
57
.high levels of cholesterol (hypercholesterolemia, elevated LDH)

-Complications :
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.venous thrombosis
.infection
.hypothyroidism
.hypocalcemia
.Vit D deficiency
.microcytic hypochromic anemia
-Treatment :
.immunossuppresion for the glomerulonephritides (corticosteroids, ciclosporin)
+Nephritic syndrome
(proteinuria <3.5 gm/day - <40mg/day) (hematuria, HTN, renal failure, mild edem)
+Nephrotic syndrome
(proteinuria >3.5gm/day - >40gm/day) (sever edema – mainly face and more in morning, NO hematuria, NO HTN)
*Minimal Change Disease (Nil Disease, or Lipoid Nephrosis)

-Is a disease of the kidney that causes nephrotic syndrome and usually affects children (peak incidence at 2–3 yrs of age)
+M.C.C of nephrotic syndrome (NS) in children between the ages of 1-7
+People with one or more autoimmune disorders are at increased risk of developing minimal change disease. Having minimal
change disease also increases the chances of developing other autoimmune disorders
-Signs & Symptoms :
.proteinuria
.edema (start on face and around eyes, more in morning, and lower extramities)
.hypoalbuminemia
.ascites
+Creatinin is normal
-Causes :
.drugs, especially NSAIDs in the elderly
.malignancy, especially Hodgkin's lymphoma
.allergy
.bee sting
*Focal Segmental Glomerulosclerosis FSGS

-Is a cause of nephrotic syndrome in children and adolescents, as well as a leading cause of kidney failure in adults
-Causes :
.hypertensive nephrosclerosis
.HIV
.obesity
.kidney loss
*Membranous Nephropathy (MN)

-Causes :
.Sjögren's syndrome
.Systemic lupus erythematosus (SLE)
.Diabetes mellitus
.Sarcoidosis
.Drugs (such as corticosteroids, gold, intravenous heroin)
.Malignancy (cancer)
.Bacterial infections, e.g. leprosy & syphilis
.Protozoal infections, e.g. malaria
*Amyloidosis
-Is a rare disease that results from the buildup of misfolded proteins known as amyloids. They become insoluble and deposit in
organs or tissues, disrupting normal function
+Amyloid deposition in the kidneys can cause nephrotic syndrome, which results from a reduction in the kidney's ability to filter
and hold on to proteins. The nephrotic syndrome occurs with or without elevations in creatinine and blood urea concentration
-Signs & Symptoms :
58
.deposition of amyloids in the liver can lead to elevations in serum aminotransferases and alkaline phosphatase
.liver enlargement is common. Spleen enlargement is rare
.presence of Howell-Jolly bodies on blood smear
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.malabsorption
.enlarged tongue
.difficulty swallowing
.thyroid and adrenal gland can be infiltrated
.hypothyroidism
.orthostatic hypotension (low blood sodium concentration may be attributed to autonomic neuropathy and heart failure)
+Amyloid deposits occur in the pancreas of Pts. with diabetes mellitus
-Types :
1.AL (plasma cell dyscrasia causing deposition of protein derived from immunoglobulin light chains. This may be associated with
multiple myeloma)
2.AA (amyloid is produced as a proteinaceous material in association with multiple chronic infectoius or inflammatory
conditions, such as rheumatoid arthritis, inflammatory bowel disease or myeloma)
-The amyloid protein builds up in the (associated with) :
.kidney (causing glomerulonephritis)
.GI tract (malabsorption)
.nerves
.muscles
.heart (amyloid associated with restrictive cardiomyopathy, rhythm disorders and heart block)
.macroglossia
.neural involvement produces carpal tunnel syndrome
-Diagnosis :
.congo red testing shows green birrefringence
-Treatment :
.melphalan and prednisone can control protein production
*Alport Syndrome
-Is a genetic disorder affecting children, characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. Alport
syndrome can also affect the eyes, though the changes do not usually affect sight, except when changes to the lens occur in
later life
+Hereditary nephritis (X-linked dominant); renal biopsy shows foam cells (Genetic family history)
-Signs & symptoms :
.hematuria
.proteinuria
.hearing loss (hearing is normal at birth. Hearing loss develops progressively, usually at the stage when kidney function is
normal)
.eye changes (abnormalities are often be seen including lenticonus, keratoconus, cataracts as well as retinal flecks in the macula
and mid-periphery. Severe cases may require a corneal transplant)
.aortic dissection
.leiomyomas (tumours of smooth muscle affecting the oesophagus and female genital tract, may occur in a rare overlap
syndrome involving the adjacent COL4A5 and COL4A6 genes)
**Metabolic Acidosis
-Anion Gap = (Na+ + K+) – (CL- + Hco-3) or Na+ – (CL + Hco-3) (normally, this concentration is about 8-16 mmoL)
-Causes :
1.increased anion gap, causes including :
.lactic acidosis
.DKA
.CRF
.intoxication (ethanol, salicylates, methanol, formaldehyde, INH, paraldehyde, sulfates, metformin-glucophage)
.massive rhabdomyolysis
2.normal angion gap, causes including :
.long standing diarrhea (bicarbonate loss)
.pancreatic fistula
.ureterosigmoidostomy
59
.renal tubular acidosis RTA
+Causes Of Metabolic Acidosis With Anion Gap :

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.Renal failure
.Diabetic ketoacidosis
.Lactic acidosis
.Aspirin overdose
.Alcohol poisoning
.Uremia
.Salicylate poisoning
.Metformin
.Insulin deficiency
.Diarrhea
.Shock states and cardiac arrest
.Small intestinal fistula
.Ulcerative colitis
.Ureteroenterostomy
.Renal insufficiency
.Carbon monoxide poisoning
.Biliary fistula
.Hemorrhagic shock
.Starvation
.Renal failure
.Small bowel fistula
.Diabetes mellitus
.Severe dehydration
.Renal insufficiency
.Renal Fanconi syndrome
**Metabolic Alkalosis
-Causes :
.vomiting (alkalosis) / +Diarrhea (acidosis)
.diuretics therapy (thiazides – loop diuretics)
.hyperaldosteronism (conn's syndrome)
**Respiratory Acidosis
-Hypoventilation (increased Co2)
-Causes :
.increased blood carbon dioxide concentration
.decreased pH (a condition generally called acidosis)
**Respiratory Alkalosis
-Hyperventilation (decreased Co2)
+Medical condition in which increased respiratory elevated the bloob pH
+In metabolic acidosis, physiological response is hyperventilation (Kussmaul Breathing)
+NORMAL
.pH (7.35-7.45)
.Hco3-Bicarbonate (16-24) (kidney-alkalosis)
.Co2 (35-40) (respiratory-acidosis)
**Hypertension
-Bp (120/80)
-Pre HTN (systolic 120-139 / diastolic 80-89)
-Hypertension (stage 1 – systolic 140-159 / diastolic 90-99) (stage 2 – systolic >160 / diastolic >100)
-Laboratory Investigation :
.urinalysis for protein, glucose and red blood cells
.hematocrit
60
.serum potassium to exclude hyperaldosteronism

.serum creatinine and BUN
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.electrocardiogram to evaluate for left ventricular hypertrophy

.glucose and plasma lipid analysis as an indicator of atherosclerotic risk
-Indications for specific hypertensive groups :
.diabetics (should be treated with ACE inhibitors or ARBs, which prevent the development of nephropathy / The blood pressure
goal in a diabetic is lower, at <130/80 mmHg, this is also true in those with renal insufficiency, CHF, retinopathy or stroke and
Pts. with macroalbuminuria should receive an ACE inhibitor)
.post myocardial infarction (ischemic heart disease) (should be treated with beta blockers), diminished left-ventricular systolic
function (such as congestive heart failure and postMI, should receive ACE inhibitors and/or ACE inhibitors)
.pregnant Pts. are best treated with alpha-methyldopa, labetalol, hydralazine or calcium-channel blockers (ACE inhibitors and
angiotensin-receptor blockers are absolutely contraindication in pregnant Pts. Diuretics are relatively contraindicated)
-Causes of secondary hypertension :
.renal artery stenosis (M.C.C)
.cushing syndrome
.renal disease
.vascular disease
.pheochromocytoma
.conn's syndrome (primary hyperaldosteronism)
-Who should be screened for secondary hypertension ?
.those who become hypertensive either very young or very old (<25->55)
.those with a key feature of history
.Pts. who remain hypertensive despite increasing doses and numbers of anti-hypertensive medications
*Diuretics
-Specific Indications :
.CHF
.edematous states
.african-american Pts.
-Side Effects :
.decreases in potassium and magnesium
.increases in calcium
.uric acid
.glucose
.LDL-cholesterol
.gynecomastia
-Relative contraindications :
.diabetes
.gout
.hyperlipidemia
*Beta-Blockers
+Metoprolol and atenolol are the most commonly used
.MI
.ischemic heart failure
.supraventricular arrhythmias
.migraine headaches glaucoma
.anxiety
.tachycardia
.congestive failure diastolic dysfunction
-Side Effects :
.bronchospasm
.heart block
.bradycardia
.raynaud's phenomenon
.depression
.impotence
.fatigue
61
.decreased HDL
.increased triglycerides
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.hyperglycemia
-Relative Contraindications :
.asthma or COPD
.atrioventricular conduction defects
.congestive heart failure from systolic dysfunction
.diabetes because of masking signs of hypoglycemia
*Angiotensin Converting Enzyme ACE Inhibitors

+Enalapril (only IV form), captopril, enalapril
.diabetics with hypertension to prevent neuropathy
.CHF
.post-MI with left ventricular impairment
-Side Effects :
.cough
.angioneurotic edema
.neutropenia
.hyperkalemia
.taste disturbances
.anaphylactoid reactions
-Relative Contraindications :
.less effective in african-american Pts.
-Absolute Contraindications :
.bilateral renal artery stenosis
.pregnancy
**Polyuria
-Polyuria is a condition usually defined as excessive or abnormally large production or passage of urine (greater than 2.5 or 3 L
over 24 hours in adults)
-Causes :
.General (polydipsia, psychogenic polydipsia, diuretic drugs, osmotic diuresis)
.Urinary system (interstitial cystitis, urinary tract infection, renal tubular acidosis, fanconi syndrome, nephronophthisis-genetic)
.Hormonal (hypokalemia, DM, use of a corticosteroid, pheochromocytoma, hyperparathyroidism, Diabetes insipidus,
hypercalcaemia, hyperthyroidism, hypopituitarism, Conn's disease, hyperglycemia)
.Circulation (congestive heart failure, Cardiorespiratory disease, postural orthostatic tachycardia syndrome POTS)
.Neurologic (cerebral salt-wasting syndrome, neurologic damage, migraine)
.Other (high doses of riboflavin (vitamin B2), high doses of vitamin D, altitude diuresis, side effect of lithium, Hemochromatosis)
+Polyuria and polydipsia can be due to :
.Deficiency of arginine and vasopressin
.Deficiency of insulin
.Hypercalcemia
.Psychogenic causes
**Hematuria
-Is the presence of red blood cells (erythrocytes) in the urine. It may be idiopathic and/or benign, or it can be a sign that there is
a kidney stone or a tumor in the urinary tract (kidneys, ureters, urinary bladder, prostate, and urethra), ranging from trivial to
lethal. If white blood cells are found in addition to red blood cells, then it is a signal of urinary tract infection
+Painless hematuria is the leading presentation of Renal cell carcinoma
-Types :
1.Red blood cells
.Microscopic hematuria (small amounts of blood, can be seen only on urinalysis or light microscopy)
.Macroscopic hematuria (or "frank" or "gross" hematuria)
2.Hemoglobin (only the red pigment, not the red blood cells)
3.Other pigments
.Myoglobin in myoglobinuria
62
.Porphyrins in porphyria
.Betanin, after eating beets
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.Drugs (rifampicin, phenazopyridine and sulphonamides)

-Causes :
.UTI (Escherichia coli)
.nephrolithiasis (stones in the kidney, bladder or ureter)
.polycystic kidney disease
.trauma
.cancer of the kidney, prostate or bladder
.benign prostatic hyperplasia, in older men, especially those over 50
.vigorous exercise
.glomerular bleeding (IgA nephropathy ("Berger's disease"), Alport syndrome, thin basement membrane disease)
.sickle cell disease
.schistosomiasis (caused by Schistosoma haematobium)
.recent instrumentation of the urinary tract
.prostatitis
.urethritis
.kidney diseases
.arteriovenous malformation of the kidney
.renal tuberculosis
.malignant hypertension (fibrinoid necrosis)
.cystitis
.prostate carcinoma
.tuberculosis
.papillary necrosis, renal cysts, renal calculus
.allergy (rarely cause episodic gross hematuria in children)
.left renal vein hypertension, also called "nutcracker phenomenon" or "nutcracker syndrome"
.march hematuria (secondary to repetitive impacts on the body, usually the feet)
.athletic nephritis (secondary to strenuous exercise)
.alport syndrome
.medications can cause red discoloration of the urine, but not hematuria. Some examples include (sulfonamides, quinine,
rifampin, phenytoin, use of anticoagulants)
.consumption of beets ("beeturia")
.menstruation
**Proteinuria
-The presence of an excess of serum proteins in the urine. The excess protein in the urine often causes the urine to become
foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria), retrograde ejaculation, pneumaturia
(air bubbles in the urine) due to a fistula, or drugs such as pyridium
-Causes :
.people with diabetes (M.C.C) (may have damaged nephrons and develop proteinuria) - Diabetic nephropathy (M.C.C)
.due to disease in the glomerulus (membranous glomerulonephritis)
.because of increased quantity of proteins in serum (overflow proteinuria)
.due to low reabsorption at proximal tubule (Fanconi syndrome)
.caused by certain biological agents, such as bevacizumab (Avastin) used in cancer treatment
.excessive fluid intake (drinking in excess of 4 litres of water per day)
.sign of renal (kidney) damage - Renal amyloidosis
.insufficiency of absorption or impaired filtration
.malignant hypertension
+With severe proteinuria, general hypoproteinemia can develop which results in diminished oncotic pressure. Symptoms of
diminished oncotic pressure may include ascites, edema and hydrothorax
+Proteinuria may be a feature of the following conditions :
.Nephrotic syndromes (i.e. intrinsic renal failure)
.Pre-eclampsia
.Eclampsia
.Toxic lesions of kidneys
.Amyloidosis
63
.Collagen vascular diseases (e.g. systemic lupus erythematosus)

.Dehydration
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.Glomerular diseases, such as membranous glomerulonephritis, focal segmental glomerulonephritis, minimal change disease
(lipoid nephrosis)
.Strenuous exercise
.Stress
.Benign orthostatic (postural) proteinuria
.Focal segmental glomerulosclerosis (FSGS)
.IgA nephropathy (i.e. Berger's disease)
.IgM nephropathy
.Membranoproliferative glomerulonephritis
.Membranous nephropathy
.Minimal change disease
.Sarcoidosis
.Alport's syndrome
.Diabetes mellitus (diabetic nephropathy)
.Drugs (e.g. NSAIDs, nicotine, penicillamine, lithium carbonate, gold and other heavy metals, ACE inhibitors, antibiotics, or
opiates (especially heroin)
.Fabry's disease
.Infections (e.g. HIV, syphilis, hepatitis, poststreptococcal infection, urinary schistosomiasis)
.Aminoaciduria
.Fanconi syndrome
.Hypertensive nephrosclerosis
.Interstitial nephritis
.Sickle cell disease
.Hemoglobinuria
.Multiple myeloma
.Myoglobinuria
.Organ rejection
.Ebola virus disease
.Nail patella syndrome
.Familial Mediterranean fever
.HELLP Syndrome
.Systemic lupus erythematosus
.Granulomatosis with polyangiitis
.Rheumatoid arthritis
.Glycogen storage disease type 1
.Goodpasture's syndrome
.Henoch–Schönlein purpura
.A urinary tract infection which has spread to the kidney(s)
.Sjögren's syndrome
.Post-infectious glomerulonephritis
+Proteinuria is diagnosed by a simple dipstick test
+Conditions with proteinuria consisting mainly of Bence-Jones proteins as a sign :
.Waldenstrom's macroglobulinemia
.Chronic lymphocytic leukemia
.Amyloidosis
.Malignancies (e.g., lymphoma, other cancers)
.Multiple myeloma
.Monoclonal Gammopathy of Renal Significance
+Bence Jones protein is a monoclonal globulin protein or immunoglobulin light chain found in the urine
+Proteinuria secondary to autoimmune disease should be treated with steroids or steroid-sparing agent plus the use of ACE
inhibitors
**Diabetic Nephropathy (Diabetic Kidney Disease)

-Is a progressive kidney disease caused by damage to the capillaries in the kidneys' glomeruli
-It is characterized by nephrotic syndrome and diffuse scarring of the glomeruli
64
-It is due to long standing diabetes mellitus, and is a prime reason for dialysis in many developed countries. It is classified as a
small blood vessel complication of diabetes
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-Signs & symptoms :
.severe tiredness
.headaches
.general feeling of illness
.nausea, vomiting
.frequent voiding
.lack of appetite
.itchy skin
.leg swelling
+During its early course, diabetic nephropathy often has no symptoms. Symptoms can take 5-10 years to appear after the
kidney damage begins
-Causes :
.high blood sugar
.advanced glycation end product formation, and cytokines
.poor control of blood glucose
.high blood pressure
.type 1 diabetes mellitus (before age 20)
.history of cigarette smoking
.family history of kidney problems
-Diagnosis :
+Diagnosis is usually based on the measurement of high levels of albumin in the urine or evidence of reduced kidney function
-Albumin measurements are defined as follows :
.normal albuminuria (urinary albumin excretion <30 mg/24h)
.microalbuminuria (urinary albumin excretion in the range of 30–299 mg/24h)
.clinical (overt) albuminuria (urinary albumin excretion ≥300 mg/24h)
+People with diabetes are recommended to have their albumin levels checked annually, beginning immediately after diagnosis
for type 2 diabetics, and five years after diagnosis for type 1 diabetics
-Treatment :
.ACE inhibitor medications (which usually reduce proteinuria levels and slow the progression of diabetic nephropathy)
.control of high blood pressure and blood sugar levels
.reduction of dietary salt intake
**Polycystic Kidney Disease PKD-PCKD

-Is a genetic disorder (hereditary diseases) in which abnormal cysts develop and grow in the kidneys. Cystic disorders can
express themselves at any point, infancy, childhood, or adulthood
-Is characterized by the presence of multiple cysts (hence, "polycystic") typically in both kidneys; however, 17% of cases initially
present with observable disease in one kidney, with most cases progressing to bilateral disease in adulthood
-Signs & Symptoms :
.headaches
.abdominal pain
.blood in the urine
.excessive urination
.pain in the back
-Types :
.autosomal dominant polycystic kidney disease (ADPKD)
.autosomal recessive polycystic kidney disease (ARPKD)
*Autosomal Dominant Polycystic Kidney Disease (ADPKD) (Adult type of PCKD)

-Is the M.C of all the inherited cystic kidney diseases and is typically identified in adults
-There are three genetic mutations in the PKD-1, PKD-2, and PKD3 gene with similar phenotypical presentations
+Gene PKD-1 is located on chromosome 16 and codes for a protein involved in regulation of cell cycle and intracellular calcium
transport in epithelial cells, and is responsible for 85% of the cases of ADPKD
+Gene PKD-2 is located on chromosome 4 and codes for a group of voltage-linked calcium channels
65
+PKD-3 recently appeared in research papers as a postulated 3rd gene

+Fewer than 10% of cases of ADPKD appear in non-ADPKD families
-Signs & Symptoms :
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.bilateral renal cyst

.hematuria
.HTN
.renal failure
-Associated with :
.cysts of the liver and pancreas
.intracranial aneurysm (Berry aneurysm BA) (BA – if ruptured can cause subarachnoid hemorrhage ‘severe causing headache’)
.aneurysm of the circle of wills
.commonly cause microscopic hematuria
.mitral valve prolapse
.can cause hypertensive heart disease
+Mutation on gene 16/4 (autosomal dominant) / Present in adult
*Autosomal Recessive Polycystic Kidney Disease (ARPKD) (Infant type of PCKD)

-Is the lesser common of the two types of PKD and is typically identified in the first few weeks after birth (in infant)
-Symptoms :
.bilateral renal cyst
.liver fibrosis
.bad prognosis
**Renal Tubular Acidosis RTA

-Is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify
the urine / The metabolic acidosis caused by RTA is a normal anion gap acidosis
+When blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts,
acid equivalents, and other solutes before it drains into the bladder as urine
+The word acidosis refers to the tendency for RTA to lower the blood's pH. When the blood pH is below normal (7.35), this is
called acidemia. The metabolic acidosis caused by RTA is a normal anion gap acidosis
*Type-1 (Distal) (dRTA)

-Can Cause :
.normal anion gap metabolic acidosis/acidemia
.renal stones (Ca+2 phosphate)
.hypokalemia, Hypocalcemia, Hyperchloremia
.urinary stone formation (related to alkaline urine, hypercalciuria, and low urinary citrate)
.nephrocalcinosis (deposition of calcium in the substance of the kidney)
.bone demineralisation (causing rickets in children and osteomalacia in adults)
.sjogren's syndrome
-Laps :
.hypocitraturia (low citrate in urine)
.urine (pH >5.5)
-Treatment :
.Na+ Hco3
*Type-2 (Proximal) (pRTA)

-Associated with :
.generalized dysfunction of the proximal tubular cells called Fanconi syndrome, in which there is also (phosphaturia, glycosuria,
aminoaciduria, uricosuria, and tubular proteinuria)
+The principal feature of Fanconi syndrome is bone demineralization (osteomalacia or rickets) due to phosphate wasting
-Can Cause :
.hypokalemia
*Type-3 RTA (Combined proximal and distal RTA)

-Combined dRTA and pRTA is also observed as the result of inherited carbonic anhydrase II deficiency
-Mutations in the gene encoding this enzyme give rise to an autosomal recessive syndrome of osteopetrosis, renal tubular
acidosis, cerebral calcification, and mental retardation
66
+Type 3 is rarely discussed. Most comparisons of RTA are limited to a comparison of types 1, 2, and 4
Page
*Type-4 RTA
-Can Causes :
.hyperkalemia
.aldosterone deficiency (hypoaldosteronism) (Primary vs. hyporeninemic)
.aldosterone resistance (Drugs - NSAIDs, ACE inhibitors and ARBs, Eplerenone, Spironolactone, Trimethoprim, Pentamidine)
.pseudohypoaldosteronism
+Type Type 1 Type 2 Type 4

+Location Collecting Tubules Proximal tubules Adrenal
+Acidemia Yes (severe) Yes Mild when present
+Potassium Hypokalemia Hypokalemia Hyperkalemia
+Pathophysiology Failure of α intercalated cells Failure of proximal tubular Deficiency of aldosterone,
to secrete H+ and reclaim K+ cells to reabsorb HCO3- or a resistance to its effects,
(hypoaldosteronism, pseudohypoaldosteronism)
**Dialysis
-Types :
Hemodialysis
Peritoneal dialysis (easier to perform - simple, done at home)
-Substances :
.Ethylene glycol .Procainamide .Methanol .Isopropyl alcohol .Barbiturates .Lithium
.Bromide .Sotalol .Chloral hydrate .Ethanol .Acetone, Atenolol .Theophylline .Salicylates
-Complications :
.cardiovascular disease (M.C.C of death)
.anemia (low erythropoietin)
.protein loss
.bleeding (heparin)
.renal osteodystrophy and osteitis fibrosa cystica (secondary hyperparathyroidism) (low Ca+2 and lead to elevated PTH)
+Renal osteodystrophy is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and
phosphorus in the blood. It's common in people with kidney disease and affects most dialysis patients
.infection (HBV, HCV)
.amyloidosis
.renal cyst (acquired renal cyst)
.renal cancer (increased risk of renal cancer)
**Urinary Tract Infection UTI

-Is an infection that affects part of the urinary tract. When it affects the lower urinary tract it is known as a bladder infection
(cystitis) and when it affects the upper urinary tract it is known as kidney infection (pyelonephritis)
-Signs & Symptoms :
.burning with urination (M.C symptom)
.urinate frequently (or an urge to urinate) in the absence of vaginal discharge and significant pain
.foul smelling urine are presenting complaints
.pain above the pubic bone
.in the lower back
.flank - abdominal pain
.fever
.nausea and vomiting
.the urine may appear bloody
.visible pus in the urine (pyuria)
-Causes :
.E. coli (M.C.C) with Staphylococcus saprophyticus, Staphylococcus aureus (rarely they may be due to viral or fungal infections)
+UTI (mostly related to urinary catheterization) involve :
.E. coli (27%)
.Klebsiella (11%)
67
.Pseudomonas (11%)
.the fungal pathogen Candida albicans (9%)
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.Enterococcus (7%)
.Chlamydia trachomatis and Mycoplasma genitalium (can infect the urethra but not the bladder)
+These infections are usually classified as a urethritis rather than urinary tract infection
."honeymoon cystitis"
.in post-menopausal women
+Sexual activity does not affect the risk of developing a UTI
.spermicide use
+Condom use without spermicide or use of birth control pills does not increase the risk of uncomplicated urinary tract infection
+Women are more prone to UTIs than men because, in females, the urethra is much shorter and closer to the anus
+As a woman's estrogen levels decrease with menopause, her risk of urinary tract infections increases due to the loss of
protective vaginal flora. Vaginal atrophy that can sometimes occur after menopause is associated with recurrent urinary tract
infections
.chronic prostatitis (may cause recurrent urinary tract infections in males)
.urinary catheterization
.diabetes
.being uncircumcised
.having a large prostate
+In children UTIs are associated with vesicoureteral reflux (an abnormal movement of urine from the bladder into ureters or
kidneys) and constipation
+Persons with spinal cord injury are at increased risk for urinary tract infection
+UTI is a common cause of chronic renal failure
+The most definitive diagnosis for UTIs Presence of 100.000 bacteria per/ml in a properly collected urine by culture
+The M.C toxins to be associated with renal insufficiency and ATN are :
.NSAIDs
.aminoglycosides
.cephalosporins
.contrast agents
.amphotericin
.chemotherapy (cisplatin, radiation effect)
.heavy metal (lead, mercury, gold, cyclosporine)
68
Page
Fluid And Electrolyte Disorders
**Hyponatremia (Na+)
-Is low sodium concentration in the blood. Normal serum sodium levels are between approximately 135 and 145 mEq/L (135 -
145 mmol/L)
-Signs & Symptoms :
.nausea, vomiting
.headache
.short-term memory loss
.confusion
.lethargy
.fatigue
.loss of appetite
.irritability
.muscle weakness
.spasms or cramps
.seizures
.decreased consciousness or coma
.restlessness
.leads to intracellular dehydration
.neurological manifestations may be present
.the skin is doughy
.best management is by rapid rehydration
-Causes :
.cirrhosis (liver)
.CHF
.severe pain or nausea
.primary polydipsia
.trauma or other damage to the brain
.SIADH
.nephrotic syndrome
.edema
.hypothyroidism
.glucocorticoid (steroid) deficiency
.Addison's disease
.congenital adrenal hyperplasia (which the adrenal glands do not produce enough steroid hormones)
.adrenal insufficiency
+Pseudo hyponatremia (hyperlipidemia, hyperglycemia)
+Hypovolemic hyponatremia (diuretics – thiazide, furosemide)
+Euvolemic hyponatremia (SIADH)
+Hypervolemic hyponatremia (HF, nephrotic syndrome, iatrogenic)
+Correction of hypo-hypernatremia should be slowly (NOT more than 12 meq/day)
**Hypernatremia
-Is an elevated sodium level in the blood
-Signs & Symptoms :
.coma
.signs of dehydration (dry skin, confusion, oliguria, dry mucous membranes, tachycardia, orthostatic hypotension, seizures)
.increased (albumin, urea)
.lethargy
.edema
.delirium
.come
69
-Causes :
.fluid loss (diarrhea, vomiting, burns)
Page
.incorrect IV fluid replacement (excessive saline)

.diabetes insipidus
.head injury
.CNS surgery
.osmotic diuresis (diabetic coma)
.primary aldosteronism
.Conn's syndrome
+Hypovolemic hypernatremia (dehydration, diarrhea, vomiting)
+Euvolemic hypernatremia (diabetes insipidus)
+Hypervolemic hypernatremia (Conn's syndrome-primary aldosteronism)
**Hypokalemia
-Hypopotassemia (ICD-9), refers to the condition in which the concentration of potassium (K+) in the blood is low (if K+
<2.5mmol/L) (K+ major intracellular) (Na+ major extracellular)
-Signs & Symptoms :
.elevation of blood pressure (hypotonia)
.abnormal heart rhythm
.muscle weakness
.myalgia, tremor
.muscle cramps
.constipation
.hyporeflexia
.rhabdomyolysis
.respiratory depression
.sluggish or absent intestinal movements
.ECG (inverted T waves, U wave, ST depression, and a wide PR interval)
-Causes :
.diuretics (thiazide, furosemide)
.vomiting
.diarrhea
.hypomagnesemia
.alkalosis
.pyloric stenosis
.villous adenoma rectum
.intestinal fistula
.cushing`s syndrome
.steroids-lasix / ACTH
.conn`s syndrome (primary hyperaldosteronism)
.cushing syndrome
.renal tubular failure
.renal tubular acidosis
.periodic paralysis
.Bartter's syndrome
.Ileostomy
.high dose insulin
+Mild hypokalemia (>3.0mEq/L) may be treated with oral potassium chloride supplements)
+Severe hypokalemia (<3.5mEq/L) may require I.V supplementation
+amiloride, triamterene or spironolactone magnesium
**Hyperkalemia
-Signs & Symptoms :
.plasma potassium >6.5mmol/L
.malaise
.palpitations
.muscle weakness
.metabolic acidosis
70
.cardiac arrhythmia
.sudden cardiac death
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.ECG (Peak T wave, Wide QRS, Prolonged PR, Ventricular Fibrillation)

-Causes :
.oliguric renal failure (acute and chronic)
.glomerulonephritis
.hemolysis
.K+ sparing diuretics
.rhabdomyolysis
.burn
.matabolic acidosis
.excess K+ therapy
.addison`s disease
.massive blood transfusion
.drugs (ACE-suxamethonium-captopril) (corticosterois are not cause of hyperkalemia)
-Treatment :
.Calcium resonium
.Salbutamol
.IV calcium gluconate
.IV glucose and insulin
.IV furosemide
.IV sodium bicarbonate
+Medications that can increase blood potassium levels :

.ACE inhibitors (captopil, enalapril)
.nonsteroidal anti-infalmmatory drugs NSAIDs
.angioterisin 2 receptor blockers ARBs
.potassium-sparing diuretics
+Causes coma :
.Hyperglycemia
.Hypoglycemia
.Hypernatremia
.Hyponatremia
.Hypekalemia (NOT)
**Hypocalcemia
-Normal blood calcium level is between 8.5 to 10.5 mg/dL (2.12 to 2.62 mmol/L)
-Signs & Symptoms :
.Petechiae which appear as on-off spots
.purpura
.depression
.oral, perioral and acral paresthesias
.tetany
.chvostek's sign
.trousseau's sign
.laryngo-spasm
.cardiac arrhythmias
.ventricular tachycardia
.ECG (QT prolongation - prolonged S-T interval)
.numbness and circumoral tingling
.carpopedal spasm
.abdominal cramps
-Causes :
.thyroid or parathyroid surgery (thyroidectomy)
.parathyroid hormone PTH deficiency
.Vit D deficiency (decreased sun exposure)
.hypoparathyroidism
71
.pancreatitis
.over-hydration
Page
.respiratory alkalosis
.celiac disease
.intestinal malabsorption
.medullary thyroid cancer (increased calcitation – Ca+2)
.blood transfusion
.magnesium deficiency
.exogenous inorganic phosphate excess
.DiGeorge syndrome
.renal failure (acute or chronic)
+Side effects of furosemide :
.Hypokalemia
.Hyperuricemia
.Hyperglycemia
.Ototoxicity
**Hypercalcemia
-Signs & Symptoms :
.stones (renal or biliary)
.bones (bone pain)
.groans (abdominal pain, nausea and vomiting)
.thrones (polyuria - also looks like osborn wave on ECG)
.psychiatric overtones (depression, anxiety, cognitive dysfunction, insomnia, coma)
.ECG (short QT interval)
.peptic ulcers
.cardiac arrest
.constipation
.abdominal pain
.vomiting
.weigh loss
.polydipsia
.polyuria
.HTN
.weakness and confusion
-Causes :
.malignancy (myeloma, bone metastases, lung cancer)
.Vit D intoxication (hypervitaminosis D)
.sarcoidosis
.milk-alkali syndrome
.addison's disease
.thyrotoxicosis
.thiazide use
-Treatment :
.diuretics (furosemide)
.steroids
.bisphosphonates
.salmon calcitonium
.chemotherapy (for malignancy)
+Tetany may occur in :
.Hyperventilation syndrome
.Metabolic alkalosis
.Hypocalcemia
.Hypomagnesaemia
+The serum alkaline phosphatase level is characteristically normal in Hemolytic Jaundice
+Causes of hyperuricemia :
.High dose aspirin
72
.Chronic renal disease

.Alcohol
.Leukemia
Page
.Carcinoma
.Severe psoriasis
+Causes of osteoporosis :
.Acromegaly
.Corticosteroids
.Lack of exercise
.Smoking
+Recommended treatment for osteoporosis includes :
.Estrogen
.Exercise
.Calcium
.Vit D
+Renin is secreted by Juxtaglomerular apparatus
**Hyperglycemia
-Causes :
.steroid (cortisone)
.anti-HiV medication / anti-TB drugs
.thiazide
.pancreatic problems (pancreatitis, pancreatic surgery, pancreatic cancer)
.cushing disease
.acromegaly
.pheochromocytoma
.hyperthyroidism
.pregnancy
.metabolic syndrome (Syndrome X)
.obesity
.HTN
.hyperlipidemia
.asian
.renal failure
.PCOs
.cystic fibrosis
**Hypoglycemia
-Causes :
.exogenous insulin (DM Pt. who take overdose of insulin or missed meal) (munchausen syndrome)
.panhypopituitarism
.liver failure or severe hepatitis
.addison disease (adrenal insufficiency)
.insulinoma or nesidioblastosis (diffuse B-cell hyperplasia)
.alcoholism
.dumping syndrome (post-prandial hypoglycemia)
+Treatment (25-50mL glucose I.V) (IM glucagon – short action and repeat after 20mins)
**Syndrome Of Inappropriate Antidiuretic Hormone Secretion SIADH

-Is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source
-The presentations of SIADH is similar to all forms of hyponatremia in terms of neurologic symptoms
-The increase in blood volume (hypervolemia) often results in dilutional hyponatremia in which the plasma sodium levels are
lowered and total body fluid is increased. Although the sodium level is low, SIADH is brought about by an excess of water rather
than a deficit of sodium
-Signs & Symptoms :
+Gastro-intestinal
.Anorexia
.Nausea
73
+Musculoskeletal
.Muscle aches
Page
.Generalized muscle weakness

+Neuro-muscular
.Myoclonus
.Hyporeflexia
.Ataxia
.Pathological reflexes
.Tremor
.Asterixis
+Respiratory
.Cheyne-Stokes respiration
+Neurological
.Dysarthria
.Lethargy
.Confusion
.Delirium
.Seizures
.Coma (from cerebral edema)
-Causes :
.infections (Meningitis, Encephalitis, brain abscess, rocky mountain spotted fever, AIDS)
.trauma, Subarachnoid hemorrhage, subdural hematoma, cavernous sinus thrombosis
.hydrocephalus
.Guillain-Barré syndrome
.multiple sclerosis
.cancers (carcinomas, lung cancers ‘small-cell lung cancer, mesothelioma’, GI cancers ‘stomach, duodenum, pancreas’,
genitourinary cancers, bladder, urethral, prostate, endometrial’)
.lymphoma
.sarcomas (Ewing's sarcoma)
.pulmonary causes (pneumonia, lung abscess)
.asthma
.cystic fibrosis
.transient causes (endurance exercise, general anesthesia)
.hereditary causes
.sarcoidosis
+Drugs can cause SIADH :
.Chlorpropamide
.Ciprofloxacin
.Clofibrate
.Moxifloxacin
.Phenothiazine
.Ifosfamide
.Cyclophosphamide
.Carbamazepine
.Oxcarbazepine
.Valproic Acid
.Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
.3,4-Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy). SIADH due to taking ecstasy was cited as a factor in
the death of Leah Betts)
.Oxytocin
.Vincristine
.Morphine
.Amitriptyline
+Can present with :
.Decreased serum osmolality
.Decreased serum sodium
.Increased urine sodium
.Increased urine osmolality
74
+Laboratory findings in diagnosis of SIADH :

.Euvolemic hyponatremia <134 mEq/L, POsm <275 mOsm/kg OR
Page
.Urine osmolality >100mOsm/kg of water during hypotonicity

.Urine sodium concentration >40 mEq/L
.Low blood urea nitrogen (BUN)
.Normal serum creatinine
.Low uric acid
.Normal Acid-Base, K+ balance
.Normal Adrenal, Thyroid function
-Treatment :
.demeclocycline
.conivaptan
.tolvaptan
+Clinical Findings :
.water retention and extracellular fluid volume expansion without edema or hypertension (the water retension and sodium loss
both cause hyponatremia, which is a key feature in SIADH)
.hyponatremia and concentrated urine >300mOsm (when hyponatremia is severe ‘sodium <120mOsm’
.cerebral edema (irritability, confusion, seizures and coma)
+Thiazide Side Effect :

.low K+
.high Ca+2
.low Na+2
.high glucose
.high uric acid
75
Page
ENDOCRINOLOGY
**Pituitary Gland
-The pituitary is divided into tow lobes :
1.the adenohypophysis or anterior lobe - major lobe (which constitutes 80% of the pituitary)
+Anterior pituitary (adenohypophysis) – synthesizes and secretes the following endocrine hormones :
.growth hormone (thyroid-stimulating hormone TSH - adrenocorticotropic hormone ACTH)
.prolactin hormone PRL (milk production)
.gonadotropins (luteinizing hormone LH – follicle-stimulating hormone FSH)
.MCTH
2.the neurohypophysis or posterior lobe (which is the storage site for hormones produced by the neurosecretory neurons)
+Posterior pituitary (neurohypophysis) :
.oxytocin
.antidiuretic hormone (ADH) also known as vasopressin
-The relationship between the hypothalamus and the pituitary is :
.the hypothalamus regulates the release of hormones from the anterior pituitary by different hypothalamic releasing and
inhibiting hormones ‘hypothalamic-pituitary axis’
+Hormones Are Increased With Stress :
.ACTH
.TSH
.Insulin
.Glucagon
**Disease Of The Anterior Pituitary

*Prolactinoma
-M.C type of pituitary tumor-benign / Is a benign tumor (adenoma) of the pituitary gland that produces a hormone called
prolactin
-A prolactinoma can be classified as a microprolactinoma (<10mm diameter) or macroprolactinoma (>10mm diameter)
-Signs & Symptoms :
.amenorrhea
.galactorrhea (in men)
.headache (frontal)
.loss of axillary and pubic hair
.hypogonadism, gynecomastia, erectile dysfunction (in males)
.decreased libido
+Bitemporal hemianopsia (due to pressure on optic chiasma)
-Diagnosis :
.prolactin level (very high)
.MRI
-Treatment :
.dopamine (inhibit prolactin)
.dopamine agonist (bromocriptine, cabergoline)
.surgery (if medical therapy cannot be tolerated or if it fails to reduce prolactin levels)
*Hyperprolactinemia
-Is the presence of abnormally high levels of prolactin in the blood
+Normal levels are less than 500 mIU/L for women, and less than 450 mIU/L for men / basal, fasting, morning PRL level (normal
<20mg/L) - >100-200mg/L in a nonpregnant woman indicates a need for MRI of the pituitary
-Is a common clinical problem in women and causes the syndrome of galactorrhea-amenorrhea, although hyperprolactinemia is
also seen in men, gynecomastia and especially galactorrhea are very rare
-Autonomous production of prolactin occurs with pituitary adenomas (prolactinomas) are the most common functioning
pituitary adenomas, accounting for 60% of all pituitary tumors (they are usually microadenomas when they occur in women
76
and macroadenomas in men), usually presenting with visual field deficits

-Signs & Symptoms :
Page
+In women
.presents with galactorrhea
.menstrual abnormalities (amenorrhea, oligomenorrhea)
.osteoporosis in long-standing cases
.infertility
.gynecomastia
.women are detected earlier because of menstrual symptoms. Hence microadenomas are more common in women
+In men
.present with hypogonadism
.erectile dysfunction
.decreased libido
.infertility
.gynecomastia
+Usually presenting with visual field deficits
-Causes :
.pregnancy, breast-feeding or lactation, early nursing
.drugs M.C.C (with decreased inhibitory action of dopamine and overcome the normal dopamine inhibition can lead to
hyperprolactinemia) – with the use of drugs that block dopamine synthesis (phenothiazines, metoclopramide) and dopamine-
depleting agents (alpha-methyldopa, reserpine) (antidepressants, narcotics, cocaine, SSRIs and risperidone)
.micro-macroadenoma
.prolactinoma
.polycystic ovary syndrome
.nipple stimulation
.oral contraception
.pituitary adenomas (pituitary tumor)
.seizure, exercise, sleep, stress, surgery, trauma
.cirrhosis
.chronic renal failure CRF
.hypothalamic disease - hypothyroidism
+Intrauterine contraceptive device is NOT (Just Oral Contraceptive)
+Check the TSH in Pts. with elevated prolactin
*Acromegaly
-Is a syndrome that results when the anterior pituitary gland produces excess growth hormone GH (this disease is due to
hypersecretion of GH from a pituitary tumor)
+It presents between 30-50 yrs old / is an insidious, chronic debilitating disease associated with bony and soft tissue over-
growth
+In children this is called gigantism
-Signs & Symptoms :
.features of a pituitary tumor (hypopituitarism + local mass effect)
.skeletal soft tissue changes
.enlargement of the hands, feet, nose, lips and ears, and a general thickening of the skin
.soft tissue swelling of internal organs
.generalized expansion of the skull at the fontanelle
.pronounced lower jaw protrusion (prognathism) with attendant macroglossia (enlargement of the tongue) and teeth spacing
.hypertrichosis, hyperpigmentation and hyperhidrosis may occur
.acrochordon (skin tags)
.carpal tunnel syndrome (compression of median nerve)
.sleep apnea
-Complications :
.severe headache
.arthritis and carpal tunnel syndrome
.enlarged heart (cardiomegaly and lead to heart failure)
.hypertension
.DM (excess of GH leads to insulin resistance)
.heart failure (cardiac failure is M.C.C of death in acromegaly)
.kidney failure
77
.colorectal cancer
.compression of the optic chiasm leading to loss of vision in the outer visual fields (typically bitemporal hemianopia)
Page
.increased palmar sweating and sebum production over the face (seborrhea)
.muscular weakness
.metabolic changes (glucose tolerance and diabetes)
.visual field defects and compression
-Causes :
.pituitary-adenomas
.macroadenoma
.malignant
.tumors
-Diagnosis :
.Pts. with acromegaly have symptoms for an average of 9yrs before the diagnosis is made
.the best initial test is for IGF-1 levels (a significantly elevated IGF level means acromegaly)
.confirmatory testing involves the measurement of GH after 100g of glucose is given orally, this test is positive if GH remains
high >5ng/mL
.MRI is superior to CT scan (MRI will show a tumor in 90% of people with acromegaly)
-Treatment :
.somatostatin analogues (octreotide – inhibit GH secretion)
.surgery
TSH GH Prolactin ACTH LH/FSH

+Organ thyroid all body breast gland adrenal ovary/testis
+Action T3, T4 growth milk production synthesis of FSH (ovulation‘F’, spermatogenesis’M’)
glucocorticoids (cortisol) LH (estrogen’F’, testosteron’M’)
.Oxytocin (labor, contraction of uterus / milk ejection)

.ADH (vasopressin) (collecting duct of kidney reabsorption of H2O)
*Hypopituitarism
-Is the decreased (hypo) secretion of one or more of the eight hormones normally produced by the pituitary gland at the base
of the brain. If there is decreased secretion of most pituitary hormones, the term panhypopituitarism (pan meaning "all") is
used
+Sheehan's Syndrome
-also known as Simmonds syndrome, postpartum hypopituitarism or postpartum pituitary gland necrosis, is hypopituitarism
(decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and
after childbirth
-Signs & Symptoms :
.galactorrhea (absence of lactation) and/or difficulties with lactation
.amenorrhea or oligomenorrhea after delivery
.loss of secondary sexual characteristics
.infertility
+Woman with Sheehan syndrome might be relatively asymptomatic
.secondary hypothyroidism
.tiredness
.intolerance to cold
.hypotension
.constipation
.weight gain
.hair loss
.slowed heart rate
.low blood pressure
.secondary adrenal insufficiency
.in the rather chronic case is similar to Addison's disease with symptoms including fatigue, weight loss, hypoglycemia (low blood
sugar levels)
.anemia
.hyponatremia (low sodium levels)
78
.syndrome of inappropriate antidiuretic hormone (ADH) hypersecretion

.decreased free-water clearance by glucocorticoid deficiency (independent of ADH)
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-Causes :
.after excessive blood loss (complication of pregnancy) (postpartum hemorrhage. it is 1st symptom and lead to failure of
lactation)
.disseminated intravascular coagulation (i.e., in amniotic fluid embolism or HELLP syndrome)
*Empty Sella Syndrome ESS

-ESS is in the differential diagnosis of enlarged sella caused by pituitary tumors
-Syndrome can be primary (idiopathic) and is also associated with head trauma and radiation therapy / Most Pts. with these
syndromes are obese, multiparous women with headaches; 30% will have hypertension; endocrine symptoms are less common
**Disease Of The Posterior Pituitary Lobe

*Diabetic Nephropathy (Diabetic Kidney Disease)
-Is a progressive kidney disease caused by damage to the capillaries in the kidneys' - glomeruli
-It is characterized by nephrotic syndrome and diffuse scarring of the glomeruli
-It is due to long standing diabetes mellitus, and is a prime reason for dialysis in many developed countries. It is classified as a
small blood vessel complication of diabetes
-Signs & symptoms :
.severe tiredness
.headaches
.general feeling of illness
.nausea, vomiting
.frequent voiding
.lack of appetite
.itchy skin
.leg swelling
+During its early course, diabetic nephropathy often has no symptoms. Symptoms can take 5-10 years to appear after the
kidney damage begins
-Causes :
.high blood sugar
.advanced glycation end product formation, and cytokines
.poor control of blood glucose
.type 1 diabetes mellitus (before age 20)
.history of cigarette smoking
.family history of kidney problems
-Diagnosis :
+Diagnosis is usually based on the measurement of high levels of albumin in the urine or evidence of reduced kidney function
(urinary albumin excretion <30 mg/24h)
+Albumin Measurements Are Defined As Follows :
.normal albuminuria (urinary albumin excretion <30 mg/24h)
.microalbuminuria (urinary albumin excretion in the range of 30–299 mg/24h)
.clinical (over) albuminuria (urinary albumin excretion ≥300 mg/24h)
+People with diabetes are recommended to have their albumin levels checked annually, beginning immediately after diagnosis
for type 2 diabetics, and five years after diagnosis for type 1 diabetics
-Treatment :
.ACE inhibitor medications (which usually reduce proteinuria levels and slow the progression of diabetic nephropathy)
.control of high blood pressure and blood sugar levels
.reduction of dietary salt intake
*Diabetes Insipidus DI
-Is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine (>3L/day)
-Types :
.central DI (M.C type in humans) (caused by a deficiency of vasopressin, also known as antidiuretic hormone ADH)
79
.nephrogenic diabetes insipidus - genetic (2nd M.C type) (caused by an insensitivity of the kidneys to ADH)
-Signs & Symptoms :
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.polyuria – excessive urination (production of abnormally large volumes of dilute urine)

.polydipsia – extreme thirst (especially for cold water and sometimes ice or ice water. Are typical for DI)
.dehydration
.hypernatremia
.fever
.vomiting or diarrhea
.in children (DI can interfere with decreased appetite, weight loss, dec. growth)
-Causes :
.idiopathic
.congenital
.tumors (craniopharyngioma, metastasis, pituitary tumor)
.trauma (head injury)
.sarcoidosis
.vascular (sheehan`s syndrome, haemorrhage)
.infection (meningoencephalitis)
.drugs (lithium, demeclocycline, chronic renal disease, post-obstructive uropathy)
.occurs in histiocytosis
.can be familial disease
.can cause failure to thrive
.can cause developmental delay
-Diagnosis :
.fluid deprivation test (BEST)
.urinalysis (urine osmolarity and electrolyte levels are typically low)
-Classification :
.neurogenic (known as central DI, is due to a lack of vasopressin production in the brain)
.nephrogenic (is due to the inability of the kidney to respond normally to vasopressin)
.lithium toxicity and hypercalcemia
-Treatment :
.central DI respond to desmopressin (will be ineffective in nephrogenic DI, and you can use thiazide)
*Syndrome Of Inappropriate Antidiuretic Hormone Secretion SIADH

-Is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source
-The presentations of SIADH is similar to all forms of hyponatremia in terms of neurologic symptoms
-The increase in blood volume (hypervolemia) often results in dilutional hyponatremia in which the plasma sodium levels are
lowered and total body fluid is increased. Although the sodium level is low, SIADH is brought about by an excess of water rather
than a deficit of sodium
-Signs & Symptoms :
+Gastro-intestinal
.Anorexia
.Nausea
+Musculoskeletal
.Muscle aches
.Generalized muscle weakness
+Neuro-muscular
.Myoclonus
.Hyporeflexia
.Ataxia
.Pathological reflexes
.Tremor
.Asterixis
+Respiratory
.Cheyne-Stokes respiration
+Neurological
.Dysarthria
.Lethargy
.Confusion
.Delirium
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.Seizures
.Coma (from cerebral edema)
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-Causes :
.infections (Meningitis, Encephalitis, brain abscess, rocky mountain spotted fever, AIDS)
.trauma, Subarachnoid hemorrhage, subdural hematoma, cavernous sinus thrombosis
.hydrocephalus
.Guillain-Barré syndrome
.multiple sclerosis
.cancers (carcinomas, lung cancer ‘small-cell lung cancer, mesothelioma’, GI cancers ‘stomach, duodenum, pancreas’,
genitourinary cancers, bladder, urethral, prostate, endometrial’)
.lymphoma
.sarcomas (Ewing's sarcoma)
.pulmonary causes (pneumonia, lung abscess)
.asthma
.cystic fibrosis
.transient causes (endurance exercise, general anesthesia)
.hereditary causes
.sarcoidosis
+Drugs Can Cause SIADH :
.Chlorpropamide
.Ciprofloxacin
.Clofibrate
.Moxifloxacin
.Phenothiazine
.Ifosfamide
.Cyclophosphamide
.Carbamazepine
.Oxcarbazepine
.Valproic Acid
.Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants)
.3,4-Methylenedioxymethamphetamine (MDMA, commonly called Ecstasy). SIADH due to taking ecstasy was cited as a factor in
the death of Leah Betts)
.Oxytocin
.Vincristine
.Morphine
.Amitriptyline
+Can Present With :
.Decreased serum osmolality
.Decreased serum sodium
.Increased urine sodium
.Increased urine osmolality
+Laboratory Findings In Diagnosis Of SIADH :
.Euvolemic hyponatremia <134 mEq/L, POsm <275 mOsm/kg OR
.Urine osmolality >100mOsm/kg of water during hypotonicity
.Urine sodium concentration >40 mEq/L
.Low blood urea nitrogen (BUN)
.Low uric acid
.Normal serum creatinine
.Normal Acid-Base, K+ balance
.Normal Adrenal, Thyroid function
-Treatment :
.demeclocycline
.conivaptan
.tolvaptan
+Clinical Findings :
.water retention and extracellular fluid volume expansion without edema or hypertension (the water retension and sodium loss
both cause hyponatremia, which is a key feature in SIADH)
81
.hyponatremia and concentrated urine >300mOsm (when hyponatremia is severe ‘sodium <120mOsm’)
.cerebral edema (irritability, confusion, seizures and coma)
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*VIPoma (Verner–Morrison syndrome)
-Endocrine tumor, usually (about 90%) originating from non-β islet cell of the pancreas, that produce vasoactive intestinal
peptide (VIP). It may be associated with multiple endocrine neoplasia type 1 (MEN-1)
+The Massive Amounts Of VIP In Turn Cause :
.chronic watery diarrhea
.dehydration
.hypokalemia
.achlorhydria (hence WDHA-syndrome, or pancreatic cholera syndrome)
.acidosis
.vasodilation (flushing and hypotension)
.hypercalcemia
.hyperglycemia
+WADHA-syndrome (watery diarrhea, hypokalemia, achlorhydria syndrome)
.excess vasoactive intestinal polypeptide (VIP)
-Signs & Symptoms :
.watery diarrhea (fasting stool volume > 750 to 1000 mL/day)
.hypokalemia
.dehydration
.lethargy
.muscle weakness
.nausea, vomiting
.crampy abdominal pain
.achlorhydria
.carcinoid syndrome (occur rarely)
-Diagnosis :
.blood chemistry tests (basic or comprehensive metabolic panel)
.CT scan of the abdomen
.MRI of the abdomen
.stool examination for cause of diarrhea and electrolyte levels
.vasoactive intestinal peptide (VIP) level in the blood
-Treatment :
.octreotide
*Gastrinoma
-Is a tumor in the pancreas or duodenum that secretes excess of gastrin leading to ulceration in the duodenum, stomach and
the small intestine. There is hypersecretion of the HCl acid into the duodenum, which causes the ulcers. Excessive HCl acid
production also causes hyperperistalsis, and inhibits the activity of lipase, causing severe diarrhea
+It is frequently the source of the gastrin in Zollinger-Ellison syndrome / G cell (gastrin)
+It is usually found in the duodenum, although it may arise in the stomach or pancreas. Those occurring in the pancreas have a
greater potential for malignancy
+Most gastrinomas are found in the gastrinoma triangle; this is bound by the junction of cystic and common bile ducts, junction
of the second and third parts of the duodenum, and the junction of the neck and body of the pancreas
+Gastrinomas are rare endocrine tumors and commonly present with severe recurrent peptic ulcer disease
+More than 60% of gastrinomas are malignant and multifocal (multiple) / M.C site is pancreas, 2nd M.C is duodenum
-Signs & Symptoms :
.hypergastrinemia
.ulcers of the duodenum, stomach, and small intestine
.severe diarrhea
.generalized cancer symptoms
-Diagnosis :
.fasting serum gastrin
.in case of moderate hypergastrinemia, a secretin stimulation test can help in the diagnosis
.localization by somatostatin scintigraphy
-Treatment :
82
.proton pump inhibitors

.surgery
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*Diabetic Foot
-Is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or "chronic") complication of
diabetes mellitus
+Local trauma and often in association with lack of sensation because of neuropathy in addition to microvascular disease, may
lead to a diabetic foot infection
+Presence of several characteristic diabetic foot pathologies such as (infection, diabetic foot ulcer and neuropathic
osteoarthropathy is called diabetic foot syndrome)
+Blood sugar control is the best way to prevent diabetic foot infection
-Treatment :
.antibiotics
.surgical debridement
.insulin
.limb elevation
**Thyroid Gland
*Hyperthyroidism (Thyrotoxicosis)
-Excess synthesis and secretion of thyroid hormone by the thyroid / Excess production of TSH “rare” or abnormal thyroid
stimulators. Amiodarone can induce thyrotoxicosis
-Types :
.diffuse toxic goiter (Graves disease) (M.C.C)
.toxic multinodular goiter (Plummer disease) (occurs in 15-20% of Pts. with thyrotoxicosis. Occurs more commonly in elderly
individuals)
.toxic adenoma (is caused by a single hyperfunctioning follicular thyroid adenoma)
+The hypermetabolic effect of thyrotoxicosis affects every organ system
+All thyroid disease occur more frequently in women than in men (F > M)
-Signs & Symptoms :
.nervousness
.anxiety
.increased perspiration (sweating)
.tremor
.hyperactivity, hyperreflexia
.palpitations
.weight loss, increased appetite
.reduction in menstrual flow or oligomenorrhea (infertility)
.tachycardia or atrial arrhythmia
.systolic hypertension
.warm, moist, smooth skin
.lid lag
.exophthalmos (stare)
.muscle weakness
.heat intolerance
.diarrhea
.irritability
.emotional lability
.itchy
+Other Causes Of Thyrotoxicosis :
.struma ovarii is ectopic thyroid tissue associated with (dermoid tumors or ovarian teratomas)
.Pts. with a molar hydatidiform pregnancy or choriocarcinoma have extremely high levels of beta human chorionic
gonadotropin (beta-hCG), which can weakly activate the TSH receptor
+Graves` Disease
-M.C.C of hyperthyroidism in Pt. under age 50yrs F > M / Decreased TSH – Increased T4-T3 / Diffusely enlarged thyroid
-Graves` disease or toxic diffuse goiter = hyperthyroidism + diffuse goiter + exophthalmos + dermopathy
+This is autoimmune disorder (antibody against TSH receptor) caused by stimulatory TSH-receptor antibodies
83
+It is associated with other autoimmune disease (pernicious anemia, myasthenia gravis, vitiligo, type 1 DM, addison`s disease,
adrenal insufficiency)
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-About Grave's Disease (Thyrotoxicosis) :
.eye disease (may be the 1st sign of G.d - exophthalmos)
.increased pulse
.tremor
.palmar erythema
.hair thinning
.lid lag
.lid retraction
.goitre
.pretibial myxoedema
.oedematous swelling
.above lateral malleolus
.thyroid acropachy (clubbing, painful finger and toe swelling)
.mild normocytic anaemia
.leucopenia, Ca+2 increased, LFT increased
.myopathy
.atrial fibrillation
-Treatment of thyrotoxicosis :
.Neomercazole
.Radioactive iodine
.Surgery
.Propranolol inderal
.Carbimazole
.Potassium perchlorate
.Propranolol
.acromegaly
.neurosis, anxiety
.pheochromocytoma
.cardiac disease
.ophthalmoplegia and exophthalmos
-Complications :
.unilateral (hoarseness of voice)
.bilateral (respiratory obstruction)
.heart failure (thyrotoxic cardiomyopathy)
.angina
.osteoporosis
.ophthalmopathy
.gynaecomastia
.thyroid storm
-Diagnosis :
.TSH level
.it can be confirmed by iodine-123 uptake
-Treatment :
.antithyroid medications (methimazole, propylthiouracil) – have been used for hyperthyroidism
+Methimazole (the drug of choice for hyperthyroidism in the nonpregnant women) (not safe in pregnancy)
.therapy with radioactive iodine
.thyroidectomy
+Radioactive Iodine Therapy :
.is contraindication in children / pregnancy
+Thyroidectomy (is reserved for special circumstances) :
.severe hyperthyroidism in children
.pregnant women (who are non compliant or intolerant of antithyroid medication)
.Pts. with very large goiters or severe ophthalmopathy
84
.Pts. who refuse radioactive iodine therapy

+Adverse surgical effects (recurrent laryngeal nerve damage-branch from vagus, hypoparathyroidism-hypocalcemia 2-5 days
after surgery)
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*Thyroid Storm
-Is a rare but severe and potentially life-threatening complication of hyperthyroidism (overactivity of the thyroid gland)
+It is precipitated by stress, surgery or trauma
-It is characterized by :
.high fever (often above 40°C/104°F)
.fast and often irregular heart beat (tachycardia)
.vomiting, diarrhea and agitation
.heart failure may occur and myocardial infarction is encountered
.jaundice, dehydration, hypotension
.death may occur despite treatment
.high T3-T4 / low TSH
.coma
*Hypothyroidism (Myxoedema)
-Primary hypothyroidism can occur secondary to chronic thyroiditis (Hashimoto's disease); this is the M.C.C of goitrous
hypothyroidism
-Signs & Symptoms :
.cold intolerance (increased sensitivity to cold)
.constipation
.weight gain (loss appetite and weight increased)
.fatigue, tiredness
.water retention
.bradycardia
.decreased sweating
.muscle cramps and joint pain
.dry hair – dry skin (especially on the face), itchy skin
.thin, brittle fingernails
.depression
.poor muscle tone (muscle hypotonia)
.menorrhagia (or abnormal menstrual cycle - any problems with menstrual cycles) – female infertility
.elevated serum cholesterol
.hoarse voice, slow speech
.thinning of the outer third of the eyebrows (sign of hertoghe)
.sluggish reflexes (hyporeflexia)
.deafness
.poor cognition, dementia
.myalgia
.hyponatremia
.anemia
.cerebral ataxia
.non-pitting edema
.carpal tunnel syndrome
.lethargy
.cretinism (in the newborn)
.pleural effusion
.periorbital puffiness
.Pericardial effusion
-Causes :
.iodine deficiency (M.C.C of hypothyroidism worldwide)
.Hashimoto's thyroiditis (M.C.C in developed countries – JORDAN)
.primary hypothyroidism (lymphocytic infiltration of the thyroid)
.secondary hypothyroidism (from hypopituitarism ) is very rare
-Diagnosis :
.in primary (increased TSH – decreased T4)
85
.in secondary (decreased or normal TSH – decreased T4)

+Associations :
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.turner's syndrome
.down's syndrome
.cystic fibrosis
.primary biliary cirrhosis
++Thyroid Function Test (TFTs)

+Hypothyroidism (increased TSH – decreased T4-T3)
+Hyperthyroidism (decreased TSH –increased T4-T3)
+Subclinical hypothyroidism (increased TSH –normal T4-T3)
+Subclinical hyperthyroidism (decreased TSH –normal T4-T3)
+The most sensitive indicator of primary hypothyroidism is TSH (thyroid-stimulating hormone)
+(Thyroiditis) Hashimoto's Thyroiditis

-Is the M.C form of thyroid gland inflammation (thyroiditis) and the most frequent cause of decreased thyroid hormone
production (hypothyroidism)
+It results from an autoimmune disorder, an attack on the thyroid gland by a person's own immune system / Most common in
women in middle age
-Signs & Symptoms :
.fatigue
.weight gain
.pale or puffy face
.feeling cold
.joint and muscle pain
.constipation
.dry and thinning hair
.heavy menstrual flow or irregular periods
.depression
.panic disorder
.slowed heart rate
.problems getting pregnant and maintaining pregnancy
-Risk factors :
.family history of thyroid disorders is common
.HLA-DR5 gene
.CTLA-4 (Cytotoxic T-lymphocyte Antigen-4) gene polymorphisms
.associated with autoimmune pathology seen in development of type 1 diabetes
.the incidence is increased in pts. with chromosomal disorders, including (Turner, Down's, and Klinefelter syndromes)
-Complications :
.thyroid lymphoma (generally the B-cell type)
.non-Hodgkin lymphoma
*Types Of Thyroid Carcinomas

.papillary carcinoma (M.C thyroid cancer – it is associated with history of radiation exposure / F > M)
.follicular carcinoma (more common in the elderly / F > M)
.anaplastic carcinoma (in elderly Pts. / F > M / is highly malignant with rapid and painful enlargement)
.medullary carcinoma
**Parathyroid Glands
*Hyperparathyroidism
-Is overactivity of the parathyroid glands resulting in excess production of parathyroid hormone (PTH). The parathyroid
hormone regulates calcium and phosphate levels and helps to maintain these levels
+Primary (M.C)
-Primary hyperparathyroidism results from a hyperfunction of the parathyroid glands themselves
-Over secretion of PTH due to :
.parathyroid adenoma
.parathyroid hyperplasia
86
.rarely, a parathyroid glands carcinoma

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+Secondary
-Secondary hyperparathyroidism is due to physiological secretion of parathyroid hormone (PTH) by the parathyroid glands in
response to hypocalcemia (low or normal blood calcium levels). The M.C.C are Vit D deficiency and chronic kidney failure
+Vit D deficiency lead to absorption of Ca+2 from GI
+PTH (parathyroid hormones) lead to increased Ca+2 / Calcitonin (thyrocalcitonin – parafollicular cells) lead to decreased Ca+2
-Signs & Symptoms :
.weakness, fatigue
.depression
.bone pain
.muscle soreness (myalgias)
.decreased appetite
.vomiting, nausea
.constipation
.polyuria
.polydipsia
.cognitive impairment
.kidney stones, renal osteodystrophy
.osteoporosis, pathologic fractures, osteomalacia, rickets
.racquet nails (trachyonychia)
.Parathyroid adenomas (very rarely detectable on clinical examination)
+In Hyperparathyroidism
.In primary hyperparathyroidism, parathyroid hormone (PTH) levels will be either elevated or "inappropriately normal" in the
presence of elevated calcium
.In cases of primary hyperparathyroidism or tertiary hyperparathyroidism heightened PTH leads to increased serum calcium
(hypercalcemia)
.In primary hyperparathyroidism, serum phosphate levels are abnormally low as a result of decreased renal tubular phosphate
reabsorption
.Alkaline phosphatase levels are usually elevated in hyperparathyroidism
*Hypoparathyroidism
-Is decreased function of the parathyroid glands with underproduction of parathyroid hormone. This can lead to low levels of
calcium in the blood. Often causing cramping and twitching of muscles or tetany (involuntary muscle contraction)
-Signs & Symptoms :
.low blood calcium level
.normal muscle contraction
.nerve conduction
.paresthesia
.fatigue
.headaches
.bone pain
.insomnia
.crampy abdominal pain
.phenomenon known as Trousseau's sign of latent tetany
.seizures
.severe irregularities in the normal heart beat
.spasm of the upper part of the airways or the smaller airways known as the bronchi (both potentially causing respiratory
failure)
-Causes :
.after thyroid or parathyroid gland surgery (thyroidectomy)
.autoimmune invasion and destruction is the most common non-surgical cause. It can occur as part of autoimmune
polyendocrine syndromes
.hemochromatosis (can lead to iron accumulation-iron overload and dysfunction of a number of endocrine organs)
.absence or dysfunction of the parathyroid glands is one of the components of chromosome 22q11 microdeletion syndrome
(other names: DiGeorge syndrome, Shprintzen syndrome, velocardiofacial syndrome)
87
.magnesium deficiency
.DiGeorge syndrome, a disease in which hypoparathyroidism can occur due to a total absence of the parathyroid glands at birth.
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Familial hypoparathyroidism occurs with other endocrine diseases, such as adrenal insufficiency, in a syndrome called
autoimmune polyglandular failure syndrome type 1 (APS-I)
.idiopathic (of unknown cause), occasionally familial (e.g. Barakat syndrome (HDR syndrome) a genetic development disorder
resulting in hypoparathyroidism, sensorineural deafness and renal disease)
-Diagnosis :
.by measurement of calcium, serum albumin (for correction) and PTH in blood
.ECG for abnormal heart rhythms, and measurement of blood magnesium levels
*Hypercalcemia
-Calcium is absorbed from the proximal portion of the small intestine (duodenum)
-Signs & Symptoms :
.neurologic – result in decreased mental activity such as (lethargy and confusion)
.gastrointestinal – result in decreased bowel activity such as (constipation, anorexia, nausea, vomiting, severe pancreatitis ,UD)
.renal – result in (polyuria and polydipsia)
.cardiovascular – (hypertension and will show in ECG ‘short QT’)
-Causes :
.hyperparathyroidism (M.C.C)
.sarcoidosis
.TB
.malignancy
.Vit D intoxication
.thiazide
.lithium
.paget's disease
*Hypocalcemia
-Signs & Symptoms :
.seizures
.tetany
.numbness and tingling of the extremities
.arrhythmias (because of a prolonged QT)
-Causes :
.hypoparathyroidism (M.C.C)
.massive blood transfusion
.renal failure
.hypomagnesemia
.hyperphosphatemia
.alkalosis
.drugs such as (loop diuretics, phenytoin, alendronate and doscarnet)
**Disorders Of Carbohydrate Metabolism

*Diabetes Mellitus
-Is a group of metabolic diseases in which there are high blood sugar levels over a prolonged period, diabetes is due to either
the pancreas not producing enough insulin or the cells of the body not responding properly to the insulin produced
-Characterized by chronic hyperglycemia due to relative or absolute deficiency of insulin secretion, insulin action, or both
+Insulin Deficiency Lead To 
.disturbance of carbohydrate, fat and protein metabolism
.significant disturbance of water and electrolyte homeostasis
+There Is Also 
.microvascular complication (diabetic nephropathy, retinopathy)
.macrovascular complication (increased prevalence of coronary artery disease, peripheral vascular disease and strokes)
.autonomic neuropathy
-Classification :
A) Primary
.type 1 (or insulin dependent diabetes mellitus IDDM)
.type 2 (or non insulin dependent diabetes mellitus NIDDM)
88
B) Secondary
.genetic defects (defect in beta cell function / abnormal insulin action)
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.pancreatic disease (pancreatitis, pancrectomy, hemochromatosis, cystic fibrosis, neopalstic disease)

.endocrinal disease (excess endogenous production of hormone antagonist to insulin – Counter-regulatory hormones) 
(GH – acromegaly / Glucocorticoids – Cushing`s syndrome / Thyroid hormone – Thyrotoxicosis / Catecholamines –
Pheochromocytoma / Glucagon – Glucagonoma / Human placental lactogen HPL – Pregnancy)
*NB. : Counter-regulatory hormones increase in severe burn and trauma
.viral infections (congenital rubella, mumps, coxasackie virus B)
.drugs (corticosteroids, thiazide diuretics, phenytoin)
.associated with genetic syndromes (Wolfram`s syndrome ‘DIDMOAD’ – Diabetes insipidus, DM, Optic atrophy, Deafness /
Down`s syndrome / Klinefelter`s syndrome / Turner`s syndrome / Friedreich`s ataxia / Muscular dystrophy / Lipoatrophy)
C) Gestational Diabetes Mellitus
.any degree of glucose intolerance with the onset or first recognition during pregnancy
.diagnosis (screening at 24-28wks of gestation / FBG>126 or casual glucose >200 / plasma glucose 1hr after 5mg oral glucose
 if glucose >140 mg/dl perform oral glucose tolerance test OGTT  fasting >95, 1hr >180, 2hr >155, 3hr >140)
*NB. : tow or more must be met for diagnosis
-Types :
*Type 1 DM (IDDM-insulin dependent)
-”Type 1 diabetes” has replaced several former terms, including (childhood-onset diabetes, juvenile diabetes, and insulin-
dependent diabetes mellitus). May occur at any age
-Causes :
.genetic susceptibility (account for 1/3 susceptibility to type 1 DM, 90% of type 1 DM Pts. carry HLA-DR3 or DR4 compared with
40% of the general population)
.environmental factor (viruses – mumps, coxsackie`s virus, retroviruses, rubella, CMV, EBV) (Diet – bovine serum albumin BSA
from cow`s milk, nitrosamines “found in smoked and cured meat” and coffee are potentially diabetogenic factor, dietary
proteins) (stress) (immunological factors – IDDM is slow T cell-mediated autoimmune disease in which insulin-secreting cells)
*NB. : Children who are given cow`s milk early in infancy are more likely to develop IDDM than those who are beast fed
-Characterized by :
.loss of the insulin-producing beta cells of the islets of langerhans in the pancreas, leading to insulin deficiency
.the majority of type 1 diabetes is of the immune-mediated nature
.there is no known preventive measure against type 1 diabetes
.Pt. always need insulin and prone to ketoacidosis and wight loss
.it is associated with other autoimmune diseases (HLA-B8 / HLA-B15 / HLA-DR3 / HLA-DR4)
+Cause of IDDM (loss of the insulin-producing beta cells of the islets of langerhans in the pancreas)
+(Younger Pt. / HLA-D3 & D4 linked / Autoimmune beta cell destruction / Polydipsia, polyuria, weight loss, ketoacidosis)
*Type 2 DM (NIDDM-non-insulin dependent)

-“Type 2 diabetes” has replaced several former terms, including (adult-onset diabetes, obesity-related diabetes, and non
insulin-dependent diabetes mellitus)
-Causes :
.genetic factors (it is more important than in type 1 DM as studies show that in monozygotic twins  concordance rate for type
2 DM
.environmental factor (life style - obesity and underactivity) (malnutrition in utero – it may damage B-cell development and
metabolic functions so predisposing to type 2 DM) (Age – is a disease of middle aged and elderly, affecting 10% of the
population over age of 65) (pregnancy – insulin sensitivity is reduced through action of placental hormones and his affect
glucose tolerance)
-Characterized by :
.insulin resistance
.reduced insulin sensitivity
.usually maturity onset (M > F), most Pts. are over 40yrs
.strong family history of diabetes
.it is associated with obesity and lack of exercise and calorie excess
+Causes of NIDDM (decreased insulin secretion, increased insulin resistance)
+(Older Pt. / No HLA association / Insulin resistance / Often asymptomatic, present with micro- or macrovascular complications)
89
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Type 1 DM Type 2 DM
Age of onset <40yrs >40yrs
Duration of symptoms Weeks Weeks to months
Body weight Normal or wasted Obese
Plasma insulin Low to absent Normal to high
Acute complications DKA Hyper-osmolar coma
Insulin therapy Responsive Responsive to resistant
Oral therapy Non-responsive Responsive
Auto-antibodies (islet cell Ab) Yes (common) No (rare)
Associated with other autoimmune Yes No
disease
Ketouria Yes No
Rapid death without trt with insulin No Yes
Family history of DM No Yes
Diabetic complications at diagnosis No Yes
Onset Sudden Gradual
Ketoacidosis Common Rare
Prevalence 10% 90%
-Signs & Symptoms :

.polyuria and nocturia
.polydipsia
.unexplained weight loss
.visual blurring
.genital thrush
.lethargy
.random glucose of >200mg/dl
.acute metabolic decompensation, resulting in coma (ketoacidosis for IDDM, hyperosmolar coma for NIDDM)
+Many of Pts. with type 2 DM are asymptomatic or have nonspecific symptoms as malaise and chronic fatigue may be
discovered during routine investigations
+Infection (uncontrolled DM is associated with increase susceptibility to infection and the Pts. may be presentd by  skin
sepsis, genital candidiasis
-Complications Of DM :
+Macrovascular disease
.related to atherosclerosis of larger arteries
.CVA - stroke
.cardiovascular disease (ischemic heart disease - angina, MI)
.peripheral vascular disease (chronic lower limb, ischemia, gangrene)
+Microvascular disease
.diabetic retinopathy (deterioration of vision)
.diabetic nephropathy (nephrotic syndrome and UTI)
.diabetic neuropathy-diabetic foot
+Others
.sexual dysfunction
.cataracts
.gastroparesis (vomiting, decreased gastric emptying)
.mononeuritis multiplex
.6th cranial nerve palsy
.albuminuria
.hypoglycemia
.lactic acidosis
90
.non-ketotic hyperosmolar diabetic coma

.diabetic foot (due to ischemia, neuropathy and infection)
.infection (UTI, pyelonephritis, pneumonia, TB)
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.DKA (salt and wated depletion, loss of skin turgor, furred tongue, cracked lips, leg cramps, blurred vision)
-Other Causes Of DM :
.drug induced (steroids, thiazides)
.pancreatic (pancreatitis, surgery where pancreas is removed, trauma, cystic fibrosis, pancreatic cancer)
.endocrine (cushing`s disease, acromegaly, pheochromocytoma, hyperthyroidism)
.others (acanthosis nigricans, glycogen storage diseases)
-Other Categories Of DM :
.impaired glucose tolerance IGT (fasting plasma glucose <7 mmol/L & OGTT 2h glucose >7.8mmol/L)
.impaired fasting glucose IFG (fasting plazma glucose >6.1mmol/L)
+Causes Of Insulin Resistance IR :
.obesity
.werner's syndrome
.pregnancy
.polycystic ovarian sundrome
.acromegaly
.metabolic syndrome
.cystic fibrosis
.TB drugs
.cushing`s
-Diagnostic Criteria Of DM :
.classic symptoms of DM + casual palsma glucose >200 mg/dl (any time of day without regard to meal)
.fasting plasma glucose FPG >126 mg/dl (no calory intake for at least 8hrs)
.2hr postprandial glucose >200 during oral glucose tolerance test OGTT  glucose load = 75 mg
-Treatment :
.diet, exercise and use of appropriate medications (insulin in the case of type 1 diabetes, oral medications, as well as possibly
insulin, in type 2 diabetes)
+Medications (metformin is generally recommended as a 1st line treatment for type 2 DM / Insulin)
+Sensitizers (increased sensitivity) (‫)مساعد‬
.thiazolidinediones (rosiglitazone, pioglitazone, troglitazone) (toxic on liver – increased ALT, AST)
.metformin
+Secretagogues (increased insulin secretion – increased C-peptide) (‫)منظم‬
.glipizide
.glyburide
.glibenclamide
.glimepiride
.gliclazide
+Alpha-glucosidase inhibitors (these agents slow the digestion of starch in the small intestine)
.acarbose (Acarbose is an anti-diabetic drug used to treat type 2 diabetes mellitus)
*Hypoglycemia
-This is the commonest endocrine emergency / brain damage and death can occur in severe prolonged cases
-Signs & Symptoms :
.sweating
.drowsiness
.seizures
.coma
.decreased level of consciousness
.tachycardia
.tremor
.palpitation
.visual changes
.brain death
-Causes :
.improper insulin use
.insulinoma
.hypoadrenalism
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.paracetamol overdose
.alcohol
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.postprandial
.hepatic failure
.glibenclamide therapy
.addison's disease
-Treatment :
.glucose water
*Fasting Hypoglycemia
-Causes :
.exogenous drugs
.pituitary insufficiency
.liver failure (enzyme defects)
.Addison's disease
.islet cel tumours (insulinoma, hodgkin's disease)
.non-pancreatic neoplasms
.hyperinsulinism (can occur secondary to insulinoma)
*Post-Prandial Hypoglycaemia
-May occur after gastric surgery and in type 2 diabetes
**Multiple Endocrine Neoplasia (MEN Syndrome)

-Inherited condition of propensity to develop multiple endocrine tumors (Autosomal dominant)
*MEN Type 1
-The gene defect in MEN type 1 (Chromosome 11)
-The M.C tumors (PPPs) :
.parathyroid hyperplasia (M.C)
.pancreatic islet cell tumors (gastrinoma ‘ZES’, insulinoma) (M.C gastrinoma)
.pituitary tumors (M.C prolactinoma)
.adrenal and thyroid adenomas
*MEN Type 2A
-The gene defect in MEN Type 2 (RET)
-The M.C tumors :
.medullary thyroid carcinoma
.pheochromocytoma
.hyperparathyroidism (hypercalcemia)
*MEN Type 2B
-The M.C abnormalities :
.mucosal neuromas (in the nasopharynx, oropharynx, larynx and conjunctiva)
.medullary thyroid carcinoma
.marfanoid body habitus
.pheochromocytoma
+The M.C GI complaint of Pts. with MEN-2B (Constipation)
-The major difference between MEN-2A and MENT-2B :
.MEN-2A (parathyroid hyperplasia)
.MEN-2B (NO parathyroid hyperplasia)
**Thyroid Cancer
-Most often the first symptom of thyroid cancer is a nodule in the thyroid region of the neck (Typically under 5% of these
nodules are found to be malignant) (Thyroid cancer usually found in a euthyroid Pt.)
-To achieve a definitive diagnosis before deciding on treatment (Fine needle aspiration FNA)
-Types Of Thyroid Carcinoma :
.papillary carcinoma (M.C)
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.follicular carcinoma
.medullary carcinoma
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.hurthle cell carcinoma

.anaplastic/undifferentiated carcinoma
+Oncogenes are associated with thyroid cancers (Ras gene family and RET proto-oncogene)
*Thyroid Nodules
-The Differential Diagnosis Of A Thyroid Nodule :
.multinodular goiter
.adenoma
.hyperfunctioning adenoma
.cyst
.thyroiditis
.carcinoma/lymphoma
.parathyroid carcinoma
+The diagnostic test of choice for thyroid nodule (FNA)
+The M.C.C of thyroid enlargement (Multinodular goiter)
*Papillary Carcinoma
-M.C type / F > M, usually affect young females / Excellent prognosis
-Risk factors is radiation
-Metastasis (M.C site is lymph node)
*Follicular Adenocarcinoma
-The route of spread (Hematogenous, more aggressive than papillary adenocarcinoma) (M > F)
-Metastasis (M.C site is bone)
*Hurthle Cell Thyroid Cnacer

-Metastasis (Lymphatic > Hematogenous)
*Medullary Carcinoma
-Associated (MEN type 2; autosomal-dominant genetic transmission)
*Anaplastic Carcinoma (Undifferentiated Carcinoma)

-F > M / Worst type / Associated histologic findings (giant cells, spindle cells)
-The major differential diagnosis (thyroid lymphoma)
+Diagnosis (1st step is FNA – fine needle aspiration)

+Laboratory value must be followed postoperatively after a thyroidectomy (Calcium)
+The differential diagnosis of postoperative dyspnea after a thyroidectomy :
.neck hematoma
.bilateral recurrent laryngeal nerve damage
*Thyroiditis
-The features of acute thyroiditis :
.painful
.swollen thyroid
.fever
.overlying skin erythema
.dysphagia
+The cause of acute thyroiditis (Bacteria ‘Streptococcus of Staphylococcus’)
-The features of subacute thyroiditis (De Quervain`s thyroiditis) :
.glandular swelling
.tenderness
.often follows URI
.elevated ESR
+The cause of subacute thyroiditis (Viral infection)
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-Types of chronic thyroiditis :

.hashimoto`s thyroiditis (M.C.C of hypothyroidism)
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.riedel`s thyroiditis
-The features of Hashimoto`s (chronic) thyroiditis :
.firm and rubbery gland
.F > M
.lymphocyte invasion
+The etiology of Hashimoto`s disease (Autoimmune)
-Tests you should be performed to diagnose Hashimoto`s disease :
.antithyroglobulin
.microsomal antibodies
**Disease Of The Adrenal Gland

-Endocrine glands, that sit atop the kidneys
+Cortex
.(G) zona glomerulosa (outer) is the main site for production aldosterone
.(F) zona fasciculata responsible for producing glucocorticoids (cortisone)
.(R) zona reticularis inner most cortical layer, produces androgens (sex hormones)
+Disorders Associated With Hyperfunctioning Of The Gland

*Cushing`s Syndrome
-Is a collection of signs and symptoms due to prolonged exposure to cortisol (group of clinical abnormalities caused by
prolonged exposure to increased amounts of cortisol or related corticosteroids)
-Signs & Symptoms :
.abdominal obesity but with thin arms and legs reddish stretch marks, a round red face, a fat lump between the shoulders
.weak muscles, weak bones (proximal myopathy)
.acne, and fragile skin that heals poorly
.changes in mood
.headaches
.chronic feeling of tiredness
.moon face
.excess sweating (dilation of capillaries)
.hirsutism
.insomnia
.impotence (in men)
.amenorrhoea, oligomenorrhea and infertility
.hypercortisolism (which feeds back into the hypothalamus resulting in decreased levels of GnRH release)
.hypokalemia
.hypertension
.hypocalcemia
.hypercholesterolemia
.osteoporosis
.psychiatric symptoms
.ecchymosis
.immune suppression
.rapid weight gain
.irritability, or depression
.muscle and bone weakness
.memory and attention dysfunction
-Causes :
.exogenous administration of glucocorticoids (M.C.C)
.pituitary adenoma secrets ACTH (also known as Cushing's disease)
.adrenal Cushing's, excess cortisol is produced by (adrenal gland tumors, hyperplastic adrenal glands, or adrenal glands cancer)
.small cell lung cancer (increased ACTH)
-Diagnosis :
.the 1-mg overnight dexamethasone suppression test (is the best initial diagnostic test to establish a diagnosis of cushing
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syndrome or glucocorticoid excess)

.CT scan and MRI
+High plasma ACTH levels = pituitary or ectopic source
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+Low plasma ACTH levels = adrenal tumors or hyperplasia

-Treatment :
.surgical or medical (unresectable tumors are treated with ketoconazole, metyrapone, mitomycin)
*Hyperaldosteronism (aldosteronism, also known as Conn's syndrome)

-Is a medical condition wherein too much aldosterone is produced by the adrenal glands, which can lead to lowered levels of
potassium in the blood (hypokalemia)
+The normal function of aldosterone is to reabsorbed sodium and excrete potassium and acid (H+)
+The M.C.C of primary hyperaldosteronism is a unilateral adrenal adenoma
-Signs & Symptoms :
.hypernatremia (elevated sodium level)
.hypokalemia (low potassium levels)
.hypertension
.muscle weakness
.polyuria
.polydipsia (from hypokalemia)
.metabolic alkalosis (occurs because aldosterone increases hydrogen ion (H+) excretion)
.edema is uncommon with primary hyperaldosteronism because of sodium release into the urine (don`t cause edema)
-Diagnosis :
.high urine aldosterone and low plasma renin levels confirm a diagnosis of primary hyperaldosteronism
.confirm the diagnosis with a CT-scan of the adrenals
-Treatment :
.adrenal adenomas or with single benign tumor (are removed surgically - adrenalectomy)
.bilateral hyperplasia (is treated with spironolactone)
*Syndromes Of Adrenal Androgen Excess

-Syndromes of adrenal androgen excess resul from excess production of dehydroepiandrosterone DHEA and androstenedione
-Signs & Symptoms :
.hirsutism
.oligomenorrhea
.acne
.virilization
-Causes :
.congenital adrenal hyperplasia
.adrenal adenomas
.adrenal carcinomas
*Congenital Adrenal Hyperplasia CAH

-Is a syndrome associated with increased adrenal androgen production because of enzymatic defects
-CAH is the M.C adrenal disorder of infancy and childhood / CAH arises from autosomal recessive mutations
+Common Enzymatic Defects Associated With CAH :
.C-21 (hydroxylase deficiency) – is associated with reduction in aldosterone secretion in one third of Pts (CAH is associated with
virilization) (Pts. may be male at birth with macrogenitosomia)
.C-11 (hydroxylase deficiency) – this can lead to hypertension and hyperkalemia
.C-17 (hydroxylase deficiency) – is characterized by hypogonadism, hypokalemia and hypertension
**Adrenal Insufficiency
*Primary Adrenocortical Insufficiency (Addison's Disease)
-Is a rare, chronic endocrine system disorder in which the adrenal glands do not produce sufficient steroid hormones
(glucocorticoids ”cortisol” and mineralocorticoids “aldosterone”)
+Resulting from adrenocortical hypofunction (adrenal insufficiency post-bilateral adrenalectomy)
-Addison's disease is associated with the development of other autoimmune diseases, such as type 1 diabetes, thyroid disease
(Hashimoto's thyroiditis) and vitiligo
-Signs & Symptoms :
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.sudden penetrating pain in the legs, lower back or abdomen

.severe vomiting and diarrhea, resulting in dehydration
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.low blood pressure

.syncope
.confusion, psychosis, slurred speech
.severe lethargy
.hypoglycemia
.hyponatremia
.hyperkalemia
.hypercalcemia
.convulsions
.fever
.weight loss
.nausea, vomiting
.axillary hair loss
.hyperpigmentation of the skin
.ACTH is high
.causes small heart
.may be secondary to tuberculosis
.fatigue, weakness, anorexia, weight loss, dizziness
-Treatment :
.IV fluids
.IV steroids
*Pheochromocytoma PCC
-Is a rare tumor of adrenal gland tissue (neuroendocrine tumor of the medulla of the adrenal glands)
+It results in the release of too much (secretes excessive amounts of) catecholamines, usually epinephrine-adrenaline and
norepinephrine-noradrenaline, hormones that control heart rate, metabolism, and blood pressure
+It usually develops in the center (medulla) of one or both adrenal glands and associated with paroxysmal hypertension
-Signs & Symptoms :
.abdominal-chest pain
.irritability, anxiety
.nervousness
.pallor
.palpitations
.rapid heart rate (tachycardia)
.severe headache
.sweating (diaphoresis)
.weight loss
.hand tremor
.high blood pressure (HTN)
.sleeping difficulty
.seizures
.visual disturbances
.nausea
.constipation
-Diagnosis :
.urinary metanephrine
.VMA (vanillylmandelic acid)
**Diabetic Ketoacidosis DKA

-It happens predominantly in those with type 1 diabetes, but it can occur in those with type 2
-Is a result of severe insulin insufficiency. It is associated with hyperkalemia. It occur in type 1 diabetics may be the presenting
manifestation (may occur in type II diabetes - insulin independent) but very rare
+DKA results from a shortage of insulin; in response the body switches to burning fatty acids and producing acidic ketone
bodies that cause most of the symptoms and complications
+May be precipitated by infection, surgery, MI, wrong insulin dose
-Signs & Symptoms :
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.polyuria (excessive urine production)

.hypervetilation (kussmaul breathing – air hunger)
.polydispia
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.ketotic breath (smell of acetones)

.lethargy
.dehydration
.tachycardia
.hypotension
.hypothermia
.anorexia
.nausea, vomiting
.abdominal pain (severe)
.com, confusion, drowsiness
.thirst
.weight loss, weakness
.leg cramps
.blurred vision
-Causes :
.neglected treatment or severe DM
.stress which need high energy as (infection and sever exertion, trauma and operations, pregnancy and labor, starvation or
excess intake of fat “ketone bodies)
.interruption of insulin therapy
-The diagnosis can be made by (finding) :
.ketosis and acidosis (pH<7.3)
.ketones in the blood or on urinalysis
.hyperglycemia (high blood sugar)
.elevated blood glucose
.increased serum levels of acetoacetate
.acetone and hydroxybutyrate
.metabolic acidosis (increased anion gap)
-Investigations :
.lab glucose (blood glucose)
.blood cultures
.blood urea
.urine analysis (ketone bodies and glucose)
.electrolytes changes
.serum HCO3
.arterial blood gases and pH (acidosis)
.ECG (arrhythmia)
-Complications :
.cerebral edema
.acute RDS
.DIC
.acute circulatory failure
.aspiration pneumonia
.hypokalaemia
.hypomagnesaemia
.hypophosphatemia
.hypoglycaemia
.hyponatremia
.thrombo-embolism
.hyperosmolar non-ketotic coma
.Increased anion gap
.Pseudohyponatremia
.Paco2 decreased
.PH decreased
.leukocytosis
-Treatment :
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.give K
.monitor intake – output
.correct acidosis when pH is less than 7.1
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.monitoring ketones in the blood is more important than in urine

.heparin may be used prophylactically
**Nonketotic Hyperosmolar Diabetic Coma HONK

-Is a type of diabetic coma associated with a high mortality seen in DM type 2 (NO ketones / NO acidosis)
-Serum glucose that is usually higher than (600mg/dL), and a resulting serum osmolarity that is greater than 320 mOsm
+Characterized by 
.severe hyperglycemia (>900 mg/fl without significant ketonemia or acidosis)
.severe dehydration and pre-renal uremia
*NB. : affect elderly Pts. and many with previous undiagnosed diabetes with mortality rate >40%
-Signs & Symptoms :
.polyuria
.volume depletion
.hemoconcentration (increases hematocrit)
.neurologic sign (visual changes)
.if untreated, will lead to death
-Diagnostic Criteria :
.blood glucose (>600 mg/dl)
.S. osmolarity (>340 mosmol/kg)
.arterial pH (>7.3)
.HCO3 (>18 mEq/L)
-Treatment :
.IV fluids (Most important)
.electrolyte replacement (Low K+)
.insulin
+Anti-glutamic acid decarboxylase (GAD) antibodies (Anti-GAD antibodies are usually positive in DM type1)
+Diabetes may be secondary to :
.Pheochromocytoma
.Glucagonoma
.Cushing's syndrome
.Thiazide therapy
.Acromegaly
.Pancreatic carcinoma
+Hypoglycemic agents :
.Glibenclamide
.Chlorpropamide
.Gliclazide
.Chlorpromazine
.Glipizide
+There is an association between the use of biguanide oral hypoglycemia agent metformin (Glucophage) and the development
of (Lactic acidosis)
DKA HONK
Age Any >60yrs
Mortality 5% 40%
Blood glucose High Very high (>900 mg/dl)
Osmolarity High Very high
Na Normal or decreased Normal or increased
HCO3 <15 mmol/L Normal or slightly low
Ketonuria Marked None/mild
**Insulinoma
-Is a tumor of the pancreas that produces excessive amounts of insulin / The tumor are usually small (<2cm) and solitary (single)
and may not appear on CT
-Pancreatic B-cell tumor and associated with MEN-1, can cause hypoglycemia-benign tumors
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-Signs & Symptoms :

.subacute or chronic hypoglycemia (low blood sugar)
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.blurred vision
.headache
.feeling of detachment
.slurred speech
.weakness
.symptoms occur in the early morning or late afternoon or after fasting or exercise
-Diagnosis :
.by measurements of blood sugar and insulin level in the blood (8 mg/mL or more in the presence of blood glucose values <40
mg/dL)
.CT scan,U/S and arteriography may also be useful in detecting the tumors
-Treatment :
.enucleation (surgical removal of a mass without cutting into or dissecting it) (BEST)
**Glucagonoma
-Is a rare tumor of the alpha cells of the pancreas, that results in the overproduction of the hormone glucagon
-Signs & Symptoms :
.DM (present in 80-90% of cases of glucagonoma - not responding to insulin)
.high blood glucose levels
.activation of anabolic and catabolic processes (gluconeogenesis and lipolysis)
.decreased blood levels of amino acids (hypoaminoacidemia)
.anemia
.diarrhea
.weight loss of 5–15 kg
.necrolytic migratory erythema NME (hyperglucagonemia)
+NME is a red, blistering rash that spreads across the skin. It particularly affects the skin around the mouth and distal
extremities; but may also be found on the lower abdomen, buttocks, perineum, and groin. It is strongly associated with
glucagonoma, a glucagon-producing tumor of the pancreas, but is also seen in a number of other conditions including liver
disease and intestinal malabsorption
-Diagnosis :
.blood serum glucagon (1000 pg/mL or greater is indicative of glucagonoma (the normal range is 50–200 pg/mL)
.plasma glucagon levels (ranging from 500 to 1000 pg/mL)
+Increased levels have been reported in cases of (decreased kidney function, acute pancreatitis, hypercorticism, liver diseases,
severe stress, extended fasting, and familial hyperglucagonemia)
.blood tests (may also reveal abnormally low concentrations of amino acids, zinc, and essential fatty acids)
.skin biopsies (may also be taken to confirm the presence of NME)
.CBC (low level of hemoglobin)
.MRI, CT
-Treatment :
.octreotide (somatostatin analog – inhibits GI secretion, which inhibits the release of glucagon)
+Only curative therapy for glucagonoma is surgical resection
**Adrenal Cortex
-The adrenal cortex produces steroids :
1.Glucocorticoids (cortisol)
2.Mineralocorticoids (which control potassium & sodium)
3.Androgens (sex hormones)
**Gynecomastia
-Is a common endocrine disorder in which there is a benign enlargement of breast tissue in males
+Decreased testosterone production and relatively high estrogen levels, leading to gynecomastia
-Causes :
.Physiologic (M.C)
.cirrhosis of the liver
.bronchogenic carcinoma
.testicular atrophy
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.digitalis therapy
.old age
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.hyperthyroidism (hyperparathyroidism is not) - hyperprolactinemia

.spironolactone, calcium channel blockers (used to treat HTN) (nifedipine, ketoconazole, methyldopa, cimetidine, digitoxin)
.drugs of abuse (alcohol, marijuana, heroin)
.puberty
.bronchogenic carcinoma
.klinefelter's syndrome
.testicular cancers
.CRF
.digoxin therapy
**Raynaud's Phenomenon
-Vasospastic disorder causing discoloration of the fingers, toes, and occasionally other areas
+Primary Raynaud's (Disease) – it often develops in young women in their teens and early adulthood + cold
+Secondary Raynaud's (Syndrome) :
.scleroderma (M.C.C)
.SLE
.rheumatoid arthritis
.Sjogren's syndrome
.dermatomyositis
.polymyositis
.mixed connective tissue disease
.cold agglutinin disease
.Ehlers-Danlos Syndrome
**Carpal Tunnel Syndrome CTS

-Compression of median nerve (paresthesia in lateral 3 digits + atrophy thenar muscle) / F > M
+Symptoms occur due to median nerve compression as it travels through the wrist at the carpal tunnel
-Signs & Symptoms :
.numbness, tingling, or burning sensations in the thumb and fingers
(middle fingers and radial half of the ring finger)
+Less-specific symptoms may include pain in the wrists or hands, loss of grip strength, and loss of manual dexterity
+Numbness and paresthesias in the median nerve distribution are the hallmark neuropathic symptoms (NS) of carpal tunnel
entrapment syndrome
.weakness and atrophy of the thumb muscles
.discomfort is usually worse at night and in the morning
+The main symptom is pain, numbness and tingling, in the thumb, index finger, middle finger, and the thumb side of the ring
fingers
-Causes (can be associated with any condition that causes pressure on the median nerve at the wrist) :
.obesity
.pregnancy
.amyloidosis
.oral contraceptives
.hypothyroidism
.arthritis
.diabetes
.pre diabetes (impaired glucose tolerance)
.trauma
.lipomas (is a benign tumor composed of adipose tissue - body fat)
.ganglion (is a nerve cell cluster or a group of nerve cell bodies located in the autonomic nervous system)
.vascular malformation
.repetitive activities of the hand and wrist
.acromegaly (causes excessive GH)
.cardiomyopathy
.polyneuropathy
-Treatment :
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.surgery
**Avitaminosis
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+Vit A deficiency causes (xerophthalmia or night blindness)

+Vit B1 (thiamine deficiency) causes (beriberi)
+Vit B3 (niacin deficiency) causes (pellagra) (diarrhea, dermatitis, dementia and death)
+Vit B12 deficiency leads to (megaloblastic anemia and subacute combined degeneration of spinal cord)
+Vit C deficiency leads to (scurvy) (easy bruising and petechiae, gum disease, loosening of teeth, poor wound healing)
+Vit D deficiency causes (rickets and osteomalacia)
+Vit K deficiency causes (impaired coagulation – bleeding)
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RHEUMATOLOGY
**Rheumatoid Arthritis RA
-Is a chronic, systemic inflammatory disorder that may affect many tissues and organs (multisystemic disease) / F > M (middle
age 40-50yrs) - but people of any age can be affected
+The hallmark of RA is inflammatory synovitis
+RA is considered a systemic autoimmune disease
+RA can also produce diffuse inflammation in the lungs, membrane around the heart (pericardium), the membranes of the
lungs (pleura) and white of the eye (sclera) and also nodular lesion, most common in subcutaneous tissue (DIP)
+The predominant infltrating call is the T lymphocyte (disease like HIV, in which T cells are decreased, will characteristically
improve preexisting RA; this is also the reason why RA is very rare in Pts. with HIV)
-Diagnostic Criteria (neef 4 of the folloing diagnostic criteria) :
.morning stiffness (>1h) (improve with movement of joint)
.>6wks symptoms
.symmetrical (bilateral)
.mainly affect small joints of hand and wrist
.>2 joints affected
.deforming arthritis
.swelling of wrists, MCPs, PIPs (for 6 wks)
.swelling of three joints (for 6 wks)
.joint erosion on x-ray
.RF positive
.rheumatoid nodules
+Summary of Criteria :
.RA is a chronic inflammatory symmetric arthropathy
.some joints are never involved in RA (DIPs – joints of the lower back) (DON'T affect distal interphalangeal joint)
.because RA is a systemic disease, tow-thirds of the Pts. present with constitutional symptoms (fatigue, anorexia, weight loss,
weakness-before the onset of the arthritis)
+Deformity Of Hand In RA :
.swan neck deformity
.Z-thumb
.wrist subluxation
.ulnar deviation
+Falty syndrome (RA, splenomegaly, neutropenia)
+Caplan syndrome (RA, pneumoconiosis)
-Signs & Symptoms :
+Joints (known as synovitis) - is inflammation of the synovial membrane that lines joints
.joint become swollen, tender and warm, and stiffness limites their movement
.the affected joints being swollen, warm, painful and stiff, particularly early in the morning on waking or following prolonged
inactivity and relieved by activity
.RA nearly always affects multiple joints (polyarthritis), most commonly small joints of the hands, feet and cervical spine
.In RA, the joints are often affected in a symmetrical fashion (bilateral) and may be asymmetrical
+Skin
.rheumatoid nodule (is the feature most characteristic of rheumatoid arthritis)
.erythema nodosum (painful, rash - anterior to tibia)
.lobular panniculitis
.atrophy of distal skin
.palmar erythema
+Lungs
.fibrosis of the lungs
.pleural effusions (exudate)
+Kidneys
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.renal amyloidosis
+Heart and Blood vessels
.atherosclerosis
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.risk of MI (heart attack) and stroke

.pericarditis
.endocarditis
.left ventricular failure
.valvulitis and fibrosis
+Ocular (eyes)
.keratoconjunctivitis episcleritis (Dry eye)
+Hepatic
.felty's syndrome (hepatosplenomegaly - pancytopenia)
+Hematological
.anemia
.neutropenia
.thrombocytosis
.lymphoma
+Neurological
.carpal tunnel syndrome (M.C problem)
+Constitutional symptoms
.fatigue
.low grade fever
.malaise
.morning stiffness
.loss of appetite
.loss weight
+Other
.Episcleritis may occur
.Amyloidosis is a recognized complication
-Causes :
.the cause of RA is unknown
.RA may be triggered as a reaction to an infectious agent (mycoplasma, parvovirus)
+Joints may be involved in RA :
.Proximal interphalangeal joints
.Knee joints
.Wrist joints
.Ankle joints
+Distal interphalangeal joints (don't affect)
-Diagnosis :
.X-rays (in RA, there may be no changes in the early stages of the disease)
.Blood tests (presence of rheumatoid factor RF / A negative RF does not rule out RA / Positive RF is bad prognosis (this test is
not very specific) / anti-CCP antibody is most specific for RA)
.high ESR / high CRP (C-reactive protein)
+RF (rheumatoid factor is + in 70% of RA / - in 30% of RA)
-Lab findings :
.RF or anti-CCP (cyclic citrullinated peptide)
.anemia
.ESR or CRP is high
.X-ray
.synovial fluid analysis
+RF (is also seen in other diseases) :
.sjogren's syndrome (Positive tests for RF commonly occur in Sjogren's syndrome)
.hepatitis C
.chronic infections
-Treatment :
.disease-modifying antirheumatic drugs (DMARDs) the best initial DMARDs is methotrexate MTX (to decreased deformity)
.NSAID (aspirin, cyclooxygenase) (to decreased pain and joint swelling)
.rest and physical activity
+Pharmacological such as (azathioprine, cyclosporin, D-penicillamine, gold salts, hydroxychloroquine ‘antimalarial’, leflunomide,
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methotrexate MTX, minocycline, sulfasalazine SSZ, cyclophosphamide)

+Deformity In RA :
.swan-neck deformity
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.Z-thumb
.wrist subluxation
.boutonniere deformity
.muscle atrophy or muscle rupture (Baker cyst)
.ulnar deviation
.Ahanto-axial joint subluxation which may cause spinal cord problem
**Systemic Lupus Erthematosus SLE

-Is a a systemic disease (autoimmune disease) in which tissue and multiple organs are damaged by pathogenic autoantibodies
and immune complexes (it is a type 3 hypersensitivity reaction caused by antibody-immune complex formation) (PIP & MCP)
+SLE most often harms (heart, joints, skin, lungs, blood vessels, liver, kidneys and nervous system)
+SLE is unknown etiology / F > M 9:1 (in young women 15-35yrs)
-Criteria (diagnostic criteria – need 4 to diagnose) :
.malar rash (rash on cheeks – butterfly rash)
.discoid rash (red, scaly patches on skin that cause scarring)
.serositis (pleuritis-inflammation of the membrane around the lungs)
.pericarditis (inflammation of the membrane around the heart)
.oral ulcers
.arthritis (tow or more peripheral joints, with tenderness, swelling or effusion – Non-deforming arthritis)
.photosensitivity
.blood / hematological disorder (hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia, neutropenia, pancytopenia)
.hypocomplementemia (decreased complement C3, C4)
.renal disorder (lupus nephritis) (M.C.C of death) / 20% of SLE Pts. have lupus nephritis – 50% of SLE Pts. have ESRD
.ANA test positive (antinuclear antibody) – in 95% of SLE but NOT specific / Anti dsDNA antibody (Most specific for SLE) +
Antismith antibody + Antiphospholipid antibody
.immunologic disorder (positive anti-smith, anti-ds DNA, antiphospholipid antibody, positive serological test for syphilis)
.neurological disorder (seizures, psychosis, depression)
-Summery Criteria :
.arthritis is identical to that of RA except that is non erosive
.all Pts. with renal involvement must undergo renal biopsy before treatment is initiated
.libman-sacks endocarditis is a non infectious endocarditis that is rarely seen in lupus Pt.
-Signs & Symptoms :
+Dermatological maifestations
.malar rash (butterfly rash)
.red scaly patches on the skin
.alopecia (hair loss)
.mouth, nasal, urinary tract and vaginal ulcers
+Musculoskeletal
.the small joint of the hand and wrist, although all joints are at risk
+Proximal interphalangeal joint (Don`t affect)
.SLE is less disabling and usually does not cause severe destruction of the joints (unlike RA)
+Hematological
.anemia, low platelet and WBC
.antiphospholipid antibody syndrome (high PTT / Recurrent abortion / Recurrent DVT)
.anticardiolipin antibody (positive test for syphilis)
+Cardiac
.pericarditis
.myocarditis
.endocarditis
.Noninfective (libman-sacks endocarditis)
+Pulmonary
.pleuritis
.pleural effusion
+Renal
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.hematuria
.proteinuria
.acute or end stage renal failure
+Neurological
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.headache
.depression
.seizures
.cognitive dysfunction
.mood disorder
.cerebrovascular disease
.polyneuropathy
.anxiety disorder
.psychosis
+Reproductive
.increased rate of fetal death in utero and spontaneous abortion
+Other
.Raynaud phenomenon
.fever
.malaise
.joint pains (myopathy)
.myalgias
.fatigue
.abdominal pain
+Signs Of Active SLE :
.anti ds-DNA antibody
.anti-smith antibody
.high EST / low CRP
.decreased C3, C4
-Diagnosis :
.a positive ANA supports the diagnosis but is not specific for SLE
.the dsDNA and anti-smith are specific antibodies for lupus (these occur only with lupus so if found, think lupus only)
.complement levels (C3, C4 or the more sensitive CH50 are decreased in Pts. with active lupus)
.elevated levels of ds-DNA antibodies when positive are seen with active lupus / the ds-DNA antibodies when positive are very
specific for diagnosis of lupus
.anti extractable nuclear antigen (anti-ENA) (serologic form testing for SLE)
+Pregnancy and SLE :
.fertility rates are normal in Pts. with SLE, but spontaneous abortions and are more common
.one reason for the spontaneous abortions in these Pts. may be anti-phospholipid antibodies, which cause placental infarcts
.this is treated with low-molecular weight heparin (LMWH) and aspirin during pregnancy
.all pregnant Pts. with lupus need to be screened for SSA/anti-Ro antibodies. These cross the placenta and are passively
transferred to the fetus, causing neonatal lupus and rarely permanent heart block
-Treatment :
.corticosteroids (cortisone) / immunosuppressive drugs / antimalarial drugs (cyclophosphamide, mycophenolate,
hydroxychloroquine)
.renal transplantation (for end-stage renal disease)
.neonatal lupus (most serious complication for neonatal lupus is heart block)
.wear protective clothing, sunglasses and sunscreen when in the sun
+SLE considered incurable, but highly treatable (is not curable but treatable)
+SLE can cause (Libman-Sack endocarditis) (Non-infectious endocarditis)
*Antiphospholipid Antibody Syndrome APLS

-Is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS provokes blood clots (thrombosis) in
both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, and severe
preeclampsia / 20-30% of SLE Pt. have antiphospholipid antibody
-Risk Factors :
+Primary APS
.genetic marker HLA-DR7
+Secondary APS
.SLE or other autoimmune disorders
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.genetic markers (HLA-B8, HLA-DR2, HLA-DR3)

.race (Blacks, Hispanics, Asians, and Native Americans)
-Causes :
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.recurrent thromboembolism (DVT, PE)

.recurrent abortion (miscarriage)
.low platelet (thrombocytopenia)
.livedo reticularis
.high PTT
-Treatment :
.low dose aspirin (or warfarin)
**Scleroderma SSc
-Is a chronic systemic autoimmune disease (primarily of the skin-skin thickening) (Mainly affect skin)
+Disease characterized clinically by thickening of the skin caused by accumulation of connective tissue and by involvement of
visceral organs (GI, lungs, kidneys / example ‘scleroderma renal crisis’ - has been used to characterize the renal involvement in
scleroderma)
+F > M (to develop scleroderma)
-Diffuse :
+GI gesture include (dysphagia, GERD, malabsorption)
+Pulmonary features include (pulmonary fibrosis with restrictive lung disease, cor pulmonale) – pulmonary involvement is now
the leading cause of death in SSc
+Renal features include (the scleroderma renal crisis in wich malignant hypertension develops and causes acute renal failure) –
this way the M.C.C of death
+Heart (HTN, heart failure)
-Antibody :
+Diffuse (anti-topoisomerase antibody)
+Limited (anti-centromere antibody)
-Types :
1.limited Systemic Sclerosis (CREST syndrome – affect hand, arm, face)
.scleroderma involves cutaneous manifestation that mainly affect the (hand, arm, face) and called CREST syndrome
.Pt. with limited scleroderma (the ANA test is positive)
.Scl-70 test (anti topoisomerase antibody) is negative in limited scleroderma and positive in diffuse ascleroderma
+CREST syndrome or Limited scleroderma
.Calcinosis (calcium deposits occur in soft tissue usually in the fingers)
.Raynaud (raynaud phenomenon)
.Esophageal dysfunction
.Sclerodactery
.Telangiectasias
+Raynaud's phenomenon (Raynaud Disease) is seen in : (vasospastic disorder causing discoloration of the fingers, toes)
.SLE
.SSc
.RA
.CREST
.Thoracic outlet syndrome
.Dermatomyositis
.Polymyositis
.Mixed connective tissue disease
.Ehlers-Danios syndrome
.Cold agglutinin disease
.Systemic sclerosis
.Cervical rip
+Primary Raynaud Disease (denotes a Pt. without an associated underlying disease / It often develops in young women in their
teens and early adulthood)
+Secondary Raynaud Disease (to describe Pt. with a defined secondary or associated disease - scleroderma)
+One test that allows the differentiation between primary & secondary Raynaud's (Nailfold capillaroscopy test)
+Treatment for Raynaud Disease is (calcium-channel blockers as nifedipine)
2.Diffuse Systemic Sclerosis
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.scleroderma is rapidly progressing and affects a large area of the skin and one or more internal organs (kidneys, esophagus,
heart, lungs)
-Complication from Scleroderma :
.heart (high Bp, irregular heart rhythm, enlargement of the heart lead to heart failure)
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.kidney (scleroderma renal crisis, malignant hypertension, acute renal failure)

.lung (shortness of breath, coughing, difficulty breathing, alveolitis, pneumonia, cancer, fibrosis)
.digestive (esophagus damage, acid reflux, malabsorption, dysphagia)
.skin & joints (carpal tunnel syndrome, muscle weakness, joint pain, stiffness)
-Treatment :
.D-penicillamine (for the skin manifestation)
+Treatment for Pt. with anaphylactic shock :
.Epinephrine
.Adrenaline
.IV fluids
.Steroids
+IgE mediated hypersensitivity reaction like bronchial asthma is (Type I hypersensitivity reaction)
**Sjogren's Syndrome
-Is a chronic autoimmune disease characterized by lymphocytic infiltration of the exocrine glands, resulting in xerostomia and
dry eyes
-Sjogren's Syndrome may be seen alone (primary) or in association with other autoimmune disease (secondary) such as RA,
primary biliary cirrhosis or SLE
-Sjogren's Syndrome progresses, it becomes a systemic disease involving major organs (lungs, kidneys, ect.) and may eventually
evolve into a lymphoproliferative disease (malignant lymphoma)
-Signs & Symptoms :
.itchy eyes
.sandy feeling under their eyes
.difficulty swallowing food
.also look for increase in dental caries and parotid enlargement
-Diagnostic tests :
.schirmer test
.ANAs will be positive and specifically anti-Ro (SSA) and anti-La (SSB)
+REMEMBER :
.all of the disease we just reviewed have an arthritis that is symmetrical and polyarticular (there are a few other disease that
may cause symmetrical polyarthropathy – know parvovirus B19 and hepatitis B) !
.RA is a disease that involves mostly the joints; the others, SLE, SSs and Sjogren's syndrome, usually have arthritis plus multiple
organ involvement
**Seronegative Arthropathies (Spondyloarthropathies)

-The spondyloarthropathies are a group of disorders that share certain clinical features and an association with the B-27 allele
-Seronegative Arthritis is an arthritis that is distinguished from RA due to absence of RF / Deforming arthritis
+Occurs more commonly in Pts. with tissue type HLA-B27
+RA is prevalent in the female population, whereas seronegative arthritis is more seen in males (M > F)
-Treatment :
.NSAIDs
.DMARDS (methotrexate)
+Types Of Seronegative Arthropathies :
.Ankylosing Spondylitis (seronegative ‘ANA negative – RF negative’)
.Reactive Arthritis (involve lower back and sacroiliac joints) (Richter Syndrome -transformation of chronic lymphocytic leukemia
- CLL)
.Psoriatic Arthritis (HLA-B27)
.Enteropathic Arthropathy (extra-articular manifestations – CD, UC)
*Ankylosing Spondylitis AS (Sacroiliitis)

-Is a chronic inflammatory disease of unknown etiology that affects primarily the axial skeleton and peripheral joints - the axial
skeleton with variable involvement of peripheral joints
+It many affects joints in the spine and the sacroiliac joint in the pelvis
+The majority of Pts. with AS exhibit the (HLA-B27) antigen and high levels of immunoglobulin A (IgA) in the blood
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+M > F (young males - very rare after 40 yrs of age) (90% of Pts. are positive for HLA B-27)
-Signs & Symptoms :
.chronic low-back pain (more in morning) and morning stiffness lasting at least 1h and improves with exercise in a young man
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(low back pain) (the cervical pain is rarely if ever affected and only late in the disease)
.entire spine (decreased spinal mobility – positive schober test)
.sacroiliac joint
-Diagnosis :
.X-ray studies of the spine (which show characteristic spinal changes and sacroiliitis - obliteration of the sacroiliac joints with
ossification in the spinal ligaments ‘bamboo-spine’)
+HLA B27 is associated with :
.Ulcerative colitis
.Crohn's disease
.Reiter's syndrome
*Reactive Arthritis (Reiter`s Syndrome) ReA

-Is a classified as an autoimmune condition that develops in response to an infection an another part of the body
+Triad (arthritis, urethritis, conjunctivitis)
-The manifestations of ReA :
.inflammatory arthritis of large arthritis (such as knee, causing pain and swelling)
.inflammation of the eyes in the form of conjunctivitis or uveitis
.urethritis in men or cervicitis in women
.is more common in men than in women (M > F), and more common in white than in black people
.M.C of which would be a genital infection with chlamydia trachomatis
.ReA usually manifests about 1-3 wks after a known infection (post chlamydia)
+20-40% of the men with the disease develop penile lesions (circinate balanitis)
.keratoderma blennorrhagica on the soles of the feet
.can develop cardiac manifestation, including (aortic regurgitation and pericarditis)
.ReA can be self-limiting, recurring, chronic or progressive
.the M.C triggers are intestinal infections (with Salmonella, Shigella or Campylobacter) and sexually transmitted infections (with
Chlamydia trachomatis)
*Psoriatic Arthritis (PsA)

-Develop in up to 30% of people who have the chronic skin condition psoriasis / Psoriatic arthritis is said to be a seronegative
spondyloarthropathy
-Signs & Symptoms :
.RF is not present in PsA
.pain, swelling or stiffness in one or more joints
.joints that are red or warm to the touch
.sausage-like swelling in the fingers or toes, known as (dactylitis)
.pain in and around the feet and ankles (tendonitis in the achilles tendon or plantar fasciitis in the sole of the foot)
.changes to the nails (pitting or separation from the nail bed)
.pain in the area of the sacrum (the lower back, above th tailbone)
-Diagnosis :
.family history
.negative test result for RF (blood factor associated with RA)
.arthritis symptoms in the (distal interphalangeal articulation of hand-this is not typical of RA)
.ridging and pitting of fingernails or toenails (onycholysis), and this associated with psoriasis and psoriatic arthritis
.radiologic images indicating joint change
*Enteropathic Arthropathy
-Occurs with ulcerative colitis and crohn disease; sometimes the arthritis occurs with flares of the inflammatory bowel disease
-The Pts. sometimes develop characteristic skin lesions: pyoderma gangrenosum and erythema nodosum
**Osteoarthritis OA
-Is the M.C joint disease in humans. The target tissue in OA is articular cartilage. OA, unlike RA, is not an inflammatory disease
+M.C joint to be affected is the knee, the 2nd M.C joint affected is the base of the thumb / in general, the major joints involved
in OA are the weight-bearing joints (hip and knee) and the small joints of the fingers (PIPs & DIPs)
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-Risk Factors :
.age
.female sex
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.genetic factors
.major joint trauma
.repetitive stress
.obesity
.gout
.endocrine disease (DM, acromegaly)
.deposition disease (hemochromatosis)
.exercise
-Lab tests :
.ESR and C-reactive protein (are always normal in OA) (if ESR is elevated, some other process is complicating OA, septic joints,
or it`s not OA)
.X-ray findings (osteophytes and unequal joint space)
+Bouchard`s nodes (when changes occur in the PIPs)
+Heberden's nodes (when changes occur in the DIPs)
-Diagnosis :
.clinical
.X-ray
-Treatment :
.NSAIDs
.COX-2 inhibitors (used in Pts. who are at high risk for GI complications)
.orthopedic surgery and joint arthroplasty
**Crystal-Induced Arthropathies
*Gout (podagra)
-Is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis (red, tender, hot, swollen
joints)
-The metatarsophalangeal joint MTP at r\the base of the big toe is the most commonly affected, other joints such as the heels,
knees, wrists and fingers / It may also present as tophi, kidney stones or urate nephropathy
+Acute attacks of gout rarely affect the shoulder
-Signs & Symptoms :
.recurrent attack of acute inflammatory arthritis
.pain usually begins over 2-4 hours and during the night
.elevated levels of uric acid may also lead to crystals precipitating in the kidneys,resulting in stone formation (uric acid stones)
.include a strong association with the consumption of (alcohol, fructose-sweetened drinks, meat, seafood, physical trauma,
surgery, coffe, vit C, dairy products)
.metabolic syndrome (abdominal obesity, hypertension, insulin resistance, abnormal lipid levels)
.diuretics have been associated with attacks of gout
.other medicines (niacin, aspirin ‘acetylsalicylic acid’)
.the immunosuppressive drugs (cyclosporine, tacrolimus)
-Causes :
.elevated levels of uric acid in the blood (hyperuricemia)
-Common Gout Triggers :
.regular, excessive alcohol intake (beer)
.surgery or a sudden, severe illness
.consuming large quantities red meat and shellfish
.a diet high in fructose
.radiation therapy
.crash diets, especially high-protein tad diets
.starting a uric acid-lowering treatment medicine
.taking the anti-rejection transplant medication cyclosporine (aspirin, duritics)
-Diagnosis :
.monosodium urate crystals in synovial fluid or a tophi (the most specific diagnostic finding ‘sodium urate crystals in synovial
fluid’)
.needle-like morphology
.negative birefringence mila
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-Treatment :
.NSAIDs (usual 1st line treatment for gout)
.colchicine (alternative for those unable to tolerate NSAIDs)
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.glucocorticoids
-Prophylaxis :
.xanthine oxidase inhibitor (allopurinol / allopurinol not treatment) and uricosuric (probenecid)
*Pseudogout (CPPD)
-M.C in knee; other joints commonly affected are the (wrist, shoulder and ankle)
+Is more common in elderly population and in people who have pre existing joint damage / Is caused by Ca urate
-Metabolic Abnormalities That Are Associated With CPPD :
.hemochromatosis
.hypophosphatemia
.hypomagnesemia
-Diagnosis :
.rectangular crystal
.rhomboid crystal
.positive birefringent crystals in synovial fluid evaluation
.radiography
-Treatment :
.is the same as gout
**Septic Arthritis (pyogenic arthritis)

-Is the purulent invasion (PUS) of a joint by an infectious agent which produces arthritis (Acute inflammation of a joint caused
by bacteria) (M.C in hip joint)
+M.C.C of infectious arthritis is gonorrhea (gonococcal arthritis), in Pts. younger than 40 yrs (F > M during pregnancy)
+M.C.C of infectious arthritis in older Pts. is staphylococcus aureus and occurs in Pts. with pre existing joint destruction from
other rheumatic disease
+Most infected joints with gonococcal will not have positive cultures and thr gram stain will be negative
-Risk Factors :
.Rheumatological disease (as A)
.DM (immunosuppression)
.prosthetic joint
.renal failure
-Causes arthritis :
.Staphylococcus
.Tuberculosis
.Gonococcal infection
.Lyme disease
-Diagnosis :
.joint aspiration for microscopy and culture is the gold standard
.X-ray (may be normal)
.CRP usually elevated (high CRP)
-Treatment :
.I.V antibiotics (that cover Staphylococcus aureus)
.if MRSA (methicillin resistant staphylococcus aureus) (vancomycin is the drug of choice)
**Vasculitis Syndromes
-Vasculitis is an inflammatory process involving the blood vessels that results in decrease of the lumen diameter and eventual
ischemia of the tissues supplied
*Wegener Granulomatosis
-Is a small vessel vasculitis that can involve any organ system but mainly affects the respiratory tract (sinuses, nose, trachea and
lungs) and kidneys
+The M.C sign of wegener granulomatosis is involvement of the upper respiratory tract
-Signs & Symptoms :
110
.rhinitis (common sign of the disease is chronic rhinitis that does not respond to usual treatment)
.sinusitis
.nasal ulcers
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.cough
.hemoptysis
.dyspnea
-Diagnosis tests :
.antineutrophil cytoplasmic antibodies (C-ANCA)
.positive ANCA test (is useful to support a suspected diagnosis of wegener g., it is never diagnostic). Also, the C-ANCA test may
be negative in some people with active wegener
.the only way to confirm the diagnosis is by performing a biopsy of an involved organ (usually the nasal septum)
-Treatment :
.is consists of high doses of corticosteroids and immunosuppressive drugs (cyclophosphamide)
*Polyarteritis Nodosa PAN

-Is a multisystem disease that may present with nonspecific complaints such as (fever, weight loss, malaise, anorexia and
abdominal pain)
+The disease can affect nearly any site in the body, except the lungs / Commoner in males / Mononeuritis multiplex , MI and
hypertension may occur
-Diagnosis :
.biopsy
-Treatment :
.is consists of high doses of corticosteroids and immunosuppressive drugs (cyclophosphamide)
*Churg-Strauss Syndrome
-This syndrome shares many of the clinical and pathologic features of PAN and can involve any organ
+The cardinal manifestations of churg-strauss syndrome are asthma, eosinophilia and lung involvement and the typical Pt. with
churg-strauss is a middle aged individual with new-onset asthma
-Signs & Symptoms :
.mononeuropathy
.transient pulmonary infiltrates on chest x-rays
.paranasal sinus abnormalities
.nasal polyps
.allergic rhinitis
*Temporal Arteritis TA (Giant Cell Arteritis)

-Is a vasculitis affecting the large arteries that supply the head, eyes and optic nerves
-New-onset headache in any Pt. older than 50 yrs prompt consideration of this diagnosis, which if left untreated may result in
permanent vision loss
-Signs & Symptoms :
.headache
.pain (that usually occurs in one or both temples)
.scalp tenderness (pain when combing hair)
.jaw claudication (jaw pain when chewing)
.decreased vision or blurry vision
.tongue numbness
.sudden loss of vision
.proximal stiffness (neck, arms, hips) due to polymyalgia rheumatica
-Diagnosis :
.ESR test (ESR increased in TA)
.diagnosis confirmed by biopsy
**Inflammatory Myopathies
-The inflammatory myopathies are inflammatory muscle disease that present with progressive muscle weakness
+They include polymyositis, dermatomyositis (treated by steroids) and body myositis (treated by immunosuppressive)
-The diagnosis is confirmed by muscle biopsy
**Nail Clubbing
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-Clubbing associated with :

+Lung Disease
.lung cancer (not seen in small cell lung cancer)
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.interstitial lung disease (sarcoidosis, fibrosis)

.complicated TB
.lung abscess, empyema, bronchiectasis, cystic fibrosis
.mesothelioma of the pleura
.arteriovenous fistula or malformation
+Heart Disease
.any disease featuring chronic hypoxia
.congenital cyanotic heart disease (M.C cardiac cause) (tetralogy of fallot, transposition of great vessels)
.subacute bacterial endocarditis
.atrial myxoma (benign tumor)
+GI and hepatobiliary
.malabsorption
.CD and UC
.cirrhosis (especially in primary biliary cirrhosis)
.hepatopulmonary syndrome (a complication of cirrhosis)
+Others
.hyperthyroidism (thyroid acropachy)
.familial and racial clubbing and “pseudoclubbing”
+COPD + Asthma (Don't cause clubbing)
+Causes Of Clubbing Of Fingers :
.Subacute bacterial endocarditis
.Pulmonary abscess
.Hepatic cirrhosis
.CD / UC
.Bronchiectasis
.Fibrosing alveolitis
.Bronchogenic carcinoma
.Tetralogy of Fallot
.Lung fibrosis
.Mesothelioma
.Aortic aneurysm
+Clubbing is not a feature of bronchial carcinoma
**Behçet's Disease
-It causes orogenital ulceration
-Colchicine and steroids is used in the management
-Arthritis is a feature, Superior vena cava obstruction may occur, Iritis, Thrombophlebitis, Neurological complications may
occur,Genital ulceration, Erythema nodosum / (HLA-B5, B1) An association with the GIMAP (GIMAP1, GIMAP2 and GIMAP4)
+Causes (auto-inflammation of the blood vessels)
+Vitiligo is associated with :
.Addison's disease
.Pernicious anemia
.Diabetes mellitus
.Thyrotoxicosis
**Erythema Nodosum EN
-Is an inflammatory condition characterised by inflammation of the fat cells under the skin
+Painful rash anterior to leg (Don't ulcerate)
-Causes :
.in about 30-50% of cases, the cause of EN is unknown – idiopathic (M.C.C)
.infections (HCV, TB, Streptococcal, Mycoplasma Pneumoniae, Yersinia, EBV)
.sarcoidosis, autoimmune disorders (inflammatory bowel disease or Behcet's disease)
.pregnancy
.medications (sulfonamides, oral contraceptives, bromides, indomethacin)
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.lepromatous leprosy
.RA
.arthralgia
.residual bruised appearance
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.tenderness of lesions
PULMONOLOGY
**Pleural Effusion
-Is excess fluid that accumulates between the tow pleural layers, the fluid-filled space that surrounds the lungs (accumulation of
fluid in the pleural cavity)
-Lymph is aspirated from the pleural cavity in chylothorax
-Signs Of Pleural Effusion :
.stony dullness on percussion
.diminished or absent breath sound
.deviation of trachea to opposite side
.bronchial breathing above effusion
-Diagnosis :
.confirmed by chest X-ray (costophrenic angle - 1st sign on CxR)
-Types :
+Transudative (low protein <25g/L) (increased hydrostatic pressure, decreased collcid osmotic pressure)
-Causes :
.heart failure
.constrictive pericarditis
.fluid overload
.meigs syndrome (ovarian fibroma + Rt. pleural effusion)
.nephrotic syndrome
.liver disease (cirrhosis)
.pulmonary embolism
.atelectasis
-Diagnosis :
.protein <25g/L (serum ratio <0.5)
.LDH <200 IU/ml (serum ratio <0.6)
.clear
-Treatment :
.chest tube
.tetracycline, bleomycin (pleurodesis)
.surgery
+Exudative (high protein 95g/L) (inflammation)
-Causes :
.bacterial pneumonia - empyema (parapneumonic effusions) (M.C.C of exudative pleural effusion)
.cancer (lung cancer, breast cancer and lymphoma - M.C.C of malignant pleural effusion)
.TB
.pulmonary embolism
.collagen vascular disease (RA, SLE)
.drug induced
.pancreatitis
-Diagnosis :
.protein >35g/L (serum ratio >0.5)
.LDH >200IU/ml (serum ratio >0.6)
.turbid
-Treatment :
.chest tube
.tetracycline, bleomycin (pleurodesis)
.surgery
**Obstructive Diseases (Obstructive Lung Disease – COPD, Asthma, Bronchiectasis, Cystic Fibrosis)
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*Asthma
-Is the common chronic inflammatory disease of the airways, characterized by variable and recurring symptoms, reversible
airflow obstruction and bronchospasm (hyperreactivity of the respiratory tree to various stimuli, resulting in reversible airway
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obstruction)
+Differentiates the asthma from COPD (Variability)
+Atopic Asthma (children – increased IgE) / Non-atopic Asthma (>40yrs – IgE normal)
+Pathophysiology :
.airway airway hyperresponsiveness (variability)
.bronchospasm
.inflammation (increased eosinophils)
.increased mucus production
-Signs & Symptoms :
.cough (M.C symptom)
.urticaria, allergic rhinitis and eczema
.wheezing
.shortness of breath (dyspnea)
.chest tightness and coughing
.worse at night or in the early morning or in response to exercise or cold air
.low PO2
.pulsus paradoxus
.cyanosis (severe asthma)
.restlessness
.silent chest (severe asthma)
.tachycardia (more than 130 per min)
.hypercapnia
+bradycardia and pulsus alternans are NOT
-Causes :
+Intrinsic (non-allergic) / Extrinsic (allergic)
.genetic factors (atopic, allergic – increased IgE type 1 and total this serum elevated, eosinophilia in children) (there is a positive
family history of allergic disease)
.environmental factor (Sudden change of air temperature)
.Beta-blocker medications ( propranolol), Cardioselective beta-blockers, ACE inhibitors, aspirin and NSAIDs (Paracetamol
injection) (M.C pharmacological stimulate is ASA, B-blockers, NSAIDs)
.viral and bacterial infections of the upper respiratory tract (M.C stimulate cause asthma is respiratory infections)
.psychological stress
.history of atopic disease (eczema, hay fever)
.dust
.smoking
.paint
.allergens perfumes
-Diagnosis :
.arterial blood gas (is severe asthma decreased Pao2, increased Pco2 and decreased pH)
.CXR findings are nonspecific in an asthmatic attack (the chest x-ray may be helpful in ruling out acute infection as the cause of
an acute attack)
.FEV <80%
-Treatment :
.O2
.bronchodilator (B2 agonist, anticholinergic, aminophylline)
.corticosteroids IV
.cromolyn sodium
.leukotriene antagonist
+For severe asthma - methylxanthine (aminophylline, theophylline, adrenalin IV)
+B2-agonist
.long acting beta-adrenoceptor agonist (formoterol, salmeterol) – NOT in emergency cases
.short acting beta-adrenoceptor agonist (salbutamol-ventolin, terbutaline) – FOR emergency cases (salbutamol NOT controller)
+Anticholinergic drugs
.long acting (tiotropium)
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.short acting (ipratropium bromide)

+Beta-blocker + NSAID (are contraindicated in ASTHMA)
+Severe asthma (peak flow <33% / PaO2 is high / silent chest / cyanosis / low Bp)
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+Acute severe asthma (peak flow 33-50% / respiratory >25 breaths per min. / heart rate >110 / unable to complete sentences in
one brath)
+Signs Of Sever-Life Threatining Asthma :
.inability to complete asentence in one breath
.HR >110 (tachycardia)
.RR >23 (tachypnea)
.silent chest
.Co2 retension (hypercapnia - respiratory acidosis)
.Po2 <60mmHg
.peak flow <33%
+Severity Of Asthma :
.intermittent (FEV1 >80% / Symptoms for <2wks / treated by inhaled cortisone + short acting B2-agonist as needed)
.mild persistent (FEV1 >80% / Symptoms for >2wks-but not daily / treated by inhaled cortisone + short acting B2-agonist every
4-6hrs)
.moderate persistent (FEV1 60-80% / Symptoms are daily / treated by inhaled cortisone + short-long acting B2-agonist)
.severe persistent (FEV1 <60% / Symptoms are throughout day / treated by oral cortisone + short-long acting B2-agonist)
+Cromolyn sodium / Leukotriene antagonist (zafirlukast – zileuton) – Alternatives for inhaled cortison (decreased frequency of
asthma attack)
++Asthma Medications :
+Rapid Relief Medications (short acting B2 agonist, short acting anticholinergic, systemic cortison - oral or IV)
+Long Term Controller Medications (inhaled cortisone, long acting bronchodilator, cromolyn sodium Na+, leukotriene
antagonist, systemic cortisone)
+Controller Asthma (inhaled cortisone, salmeterol, cromolyn Na+, tiotropium)
+Side Effect Of B2-agonist :
.hypotension
.tachycardia (reflex)
.tremor
.hypokalemia
*Chronic Obstructive Pulmonary Disease COPD

-Most people with chronic bronchitis have COPD
-Signs & Symptoms :
.shortness of breath (dyspnea is M.C symptom)
.cough + sputum (productive cough)
.hypoxia
.cyanosis
.hypercapnia (increased Co2)
.wheezing
.leg swelling
.chest tightness and tiredness
-Classifications (Types of COPD) :
1.chronic bronchitis (low Po2 / high Co2)
2.emphysema (low Po2 / low or normal Co2)
+Chronic Bronchitis (Type 1)
.clinical diagnosis (cough + sputum for 3 months-2yrs / hyperplasia of mucous + goblet cells in bronchus)
.low Po2 - hypoxia / high Co2 (type 2 respiratory failure)
.cyanosis
.blue-bloater
+Emphysema (Type 2)
.clinical diagnosis (M.C symptom is dyspnea / destruction of distal to terminal bronchioles / total lung capacity TLC is increased
115
in emphysema / surface area decreased (lung flat) / increased antero-posterior diameter-Barrel chest) / High FVC / Low FEV1 /
Decreased elasticity
.low Po2 - hypoxia / low or normal Co2 (type 1 respiratory failure)
.NO cyanosis
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.pink-puffer
+In emphysema (in <40yrs & non-smoker Pts.) / suspect alpha-1-antitrypsin deficiency (M.C.C of liver transplant)
-Causes :
.smoking (M.C.C)
.air pollution
.occupational exposures
.genetics (alpha 1-antitrypsin deficiency AAT)
.exacerbations (cold temperature, pulmonary emboli, exposure to personal smoke)
.asthma
.HIV/AIDS
.TB
.respiratory infections such as pneumonia
-Complications :
.cyanosis
.respiratory failure
.tension pneumothorax (rupture of bulla)
.lung cancer
.pulmonary HTN (cor pulmonale - Rt. side heart failure)
.Lt. ventricle failure
.polycythemia (high Hb)
+COPD (don`t cause finger clubbing)
+COPD cause of Rt. side heart failure (NOT Lt. side heart failure)
-Diagnosis :
.physical examination (in emphysema, distant breath sounds will be heard on auscultation, there may be evidence of rhonchi
and wheezes. Sign and symptoms of right heart failure ‘cor pulmonale’ and clubbing can also be seen on physical examination
in COPD) (cor pulmonale in COPD is associated with chronic pulmonary hypertension)
.CXR (in chronic bronchitis, increased pulmonary marking can be seen. In emphysema, hyperinflation of bilateral lung field with
diaphragm flattening, small heart size and increase in retrosternal space can be seen on X-ray)
.spirometry (pulmonary function test)
.FEV1 (forced expiratory volume in 1sr- FEV1<80%)
+COPD is not reversible (NOT variable)
+Exacerbations of COPD (acute dyspnea - M.C.C is chest infection)
+Recommended to give COPD Pts. (influenza pneumococcal vaccine)
+Antibiotics (Macrolide-azithromycin) should be given in acute exacerbation
-Treatment :
.bronchodilators (B2-agonist ‘ventalin, terbutaline, salbutamol’, anticholinergics ‘salmeterol, formoterol’, phosphodiesterase
inhibitor ‘theophylline’)
.corticosteroid
.antibiotics (macrolide)
.oxygen (60%) - NOT 100% O2
*Bronchiectasis
-Dilation of bronchi
-Signs & Symptoms :
.frothy productive cough with heavy sputum (M.C symptom)
.hemoptysis
.finger clubbing
.crepitation
.pulmonary hypertension
-Causes :
.post infection (TB, pneumonia, viral infection)
.congenital (cystic fibrosis, kartagener syndrome, immotile cilia syndrome)
.bronchial obstruction (tumor foreign body)
.idiopathic
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-Treatment :
.chest physiotherapy
.mucolytics
.antibiotics (M.C bacteria is pseudomonas)
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.bronchodilators
+A Large Round Mass In A CXR Might Be Due To :
.Hydatid cyst
.Bronchogenic carcinoma
.Tuberculoma
.Bronchogenic cyst
+The commonest symptom of bronchial carcinoma is Cough
+Pancoast tumor arises in Apex of the lung
+Ranges of hemoglobin saturation in arterial blood is 75-97%
+Regarding CXR :
.Rt. done of diaphragm is seen at the level of 6th anterior rib
.Visceral pleura cover the lung
.Rt. hilum is usually lower than the Lt.
.Pneumothorax appears radiolucent
+Hemoptysis is commonly associated with :
.Bronchiectasis
.Bronchial carcinoma
.Mitral stenosis
.Pulmonary infarction
.Pneumonia
.TB
.Lung trauma
.Goodpasture's syndrome
.Bronchial adenoma
.Aspergilloma
.Pulmonary infarction
.Cystic fibrosis
.Asbestosis
.Bronchitis
.Acute pneumonia
**Interstitial Lung Diseases ILD

-Is characterized by chronic inflammation and fibrosis of the interstitium and lung parenchymal (Diseases that affect lung
parenchymal)
-Causes :
.idiopathic pulmonary fibrosis
.infections (TB, viral, pneumonia)
.sarcoidosis
.asbestosis
.silicosis
.extrinsic allergic alveolitis
.drugs (bleomycin - can cause lung fibrosis)
.pneumoconiosis and occupational lung disease
.connective tissue or autoimmune disease – related pulmonary fibrosis
.hypersensitivity pneumonitis
.eosinophilic granuloma
.chronic eosinophilic pneumonia
.wegener granulomatosis
.idiopathic pulmonary obliterans
.bronchiolitis obliterans
.lymphangioleiomyomatosis
*Sarcoidosis
-Is a disease in which abnormal collections of chronic inflammatory cells (granulomas-Giant cell) form as nodules in multiple
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organs / Is a systemic disease of unknown cause, characterized histologically by the presence of nonspecific noncaseating
granulomas in the lung and other organs
+A chronic disease of unknown cause characterized by the enlargement of lymph nodes in many parts of the body and the
widespread appearance of granulomas derived from the reticuloendothelial system
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+Sarcoidosis most commonly affected young adults 20-40yrs (disease with a higher prevalence in nonsmokers) / The cause of
sarcoidosis is unknown
+Most often located in the (lungs or the lymph nodes) but any organs can be affected
-Sarcoidosis may be (asymptomatic or chronic) / It commonly improves or clears up spontaneously (asymptomatic Pt., usually in
the form of hilar adenopathy on a CXR)
-Signs & Symptoms :
.may be asymptomatic or chronic
.can affect any organ
.fatigue (unchanged by sleep)
.lack of energy
.weight loss
.aches and pains
.arthritis
.dry eyes
.swelling of the knee
.blurry vision
.dry cough
.skin lesions (erythema nodosum or lupus pernio-skin rash or face)
.anemia (occurs in 4-20% of Pts.) , leukopenia (low WBC)
.lymphadenopathy (bilateral hilar lymphadenopathy)
.hypergammaglobulinemia
.hepatosplenomegaly
.hypercalcemia
-Lab Findings :
.hypercalcemia or hypercalciuria (caused by increased circulation of Vit D produced by macrophages)
.elevation in angiotensin-converting enzyme (ACE) – it is nonspecific but can be used follow the course of the disease
.abnormalities in liver function tests
.skin anergy, PFTs may be normal
.uveitis and conjunctivitis are found in >25% of the cases
-Diagnosis :
.Biopsy (non caseating granuloma)
.tuberculin test PPD (negative)
+CxR (changes) are divided into for stages :
.stage 1 (bihilar lymphadenopathy)
.stage 2 (bihilar lymphadenopathy and reticulonodular infiltrates)
.stage 3 (bilateral pulmonary infiltrates)
.stage 4 (fibrocystic sarcoidosis typically with fibrosis - ground glass appearance)
-Treatment :
.corticosteroids (prednisolone) - It should always be treated with steroids
+The disease can remit spontaneously or become chronic, with exacerbations and remissions
+Pts. with sarcoidosis appear to be at significantly increased risk for cancer, in particular lung cancer, malignant lymphomas
+Good prognosis (young, white race, stage 1, erythema nodosum)
+Pad prognosis (old >40yrs, black race, stage IV, lupus pernio, organ involved, cardiac disease)
*Pneumoconiosis
-Is an occupational lung disease and a restrictive lung disease caused by the inhalation of dust (leads to fibrosis of the lung)
+A disease of the lungs due to inhalation of dust, characterized by inflammation, coughing, and fibrosis
+Usually appears 20-30yrs after constant exposure to finding agents (metal mining od gold, silver, lead, copper) but can develop
in <10yrs when dust exposure is extremely high (history is of primary importance is assessing possible occupational lung
disease)
-Signs & Symptoms :
.dyspnea
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.cough + sputum production

.cor pulmonale
.clubbing
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.hypoxemia is evident with an increased PAO2-PaO2 gradient

.CXR findings include (small irregular opacities, interstitial densities, ground glass appearance and honeycombing)
+Asbestosis
-Is an occupational lung disease caused by inhalation of asbestos dust
+Silicosis
- Is an occupational lung disease caused by inhalation of silica dust
**Pulmonary Embolism PE
-Is a blockage of the main artery of the lung or one of its branches
-Most commonly results from DVT, and some cases due to the embolization such as (air, fat, amniotic fluid)
+Arise from proximal (above the knee) DVT / Pulmonary embolism can infrequently occur with upper extremity, subclavian and
internal jugular vein thrombosis. This type occurs in Pts. when intravenous catheters are placed in the associated veins. Also in
the pregnant Pt., thrombosis may occur initially in the pelvic ceins rather than follow the usual course of starting in the distal
and then extending to the proximal veins
+Pulmonary embolism and DVT are considered one disease
+When to consider pulmonary embolism and DVTs (High-Risk Pts.) :
.recent surgery (especially orthopedic surgery-knee replacement surgery carries a 70% risk for DVT)
.cancer history (prostate, pelvic, abdominal and breast) (Pts. with unexplained DVT found that 15-20% of these Pts. developed
cancer within the first 2yrs after the diagnosis of a DVT)
.immobile Pts. (hospitalized) / Pts. with significant heart failure / long travel
.acquired thrombophilia
.inheriated thrombophilia
.pregnancy
-Signs & Symptoms :
.shortness of breath-dyspnea (M.C symptom)
.tachypnea (rapid breathing-Co2 is low – respiratory alkalosis)
.tachycardia
.hypoxia
.chest pain (pleuritic)
.hemoptysis
.cough
.pleural effusion
.loud 2nd heart sound (S2)
.raised jugular venous pressure (JVP)
+Signs On ECG :
.sinus tachycardia (M.C sign on ECG)
.Rt. bundle branch block
.Rt. venticular hypertrophy (Rt. axis deviation)
.S1, Q3, T3 (classical)
+Other Symptoms :
.cough (M.C symptom)
.cyanosis
.sudden death
.pleural effusion
.pleural friction rub
.DVT
.sudden onset dyspnea
.Rt. heart failure
.loud S2
.raised jugular venous pressure JVP
-Risk Factors :
.immobilization (after surgery, injury, pregnancy) (procoagulant)
.obesity (procoagulant)
119
.cancer (procoagulant)
-Diagnosis :
.CT pulmonary angiography (BEST)
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.normal D-dimer (is enough to exclude the possibility of thrombotic PE)

+ (-) excluded diagnosis / (+) isn't diagnosis
-Treatment :
.anti-coagulation
**Adult Respiratory Distress Syndrome ARDS

-Is characterized by increased permeability of the alveolar-capillary membrane and pulmonary edema, which eventually leads
to severe hypoxemia and decreased pulmonary compliance
+ARDS usually occurs within 5 days of the initiating event, and >50% will develop it within the first 24hrs
-Signs & Symptoms :
.dyspnea
.increased respiratory rate
.diffuse rales and rhonchi on auscultation
.CXR findings (diffuse interstitial or alveolar infiltrates; without of both lung fields may be seen)
.ABGs reveal decreased Pao2 and increased or normal Paco2
.swan-ganz catheter findings will reveal normal cardiac output and normal capillary wedge pressure but increased pulmonary
artery pressure
-Causes :
.sepsis
.trauma
.disseminated intravascular coagulation DIC
.drug overdose
.inhalation of toxins
.goodpasture syndrome
.systemic lupus erythematosus
.drowning
.period after bypass surgery
-Treatment :
.steroids (mortality rates are approximately 70%)
**Obstructive Sleep Apnea OSA / Pickwickian Syndrome (Obesity Hypoventilation Syndrome)

-Most important cause is obesity / Can occur episode of apnea during sleep
-Are provocative factors for obstructive sleep apnea :
.sleep deprivation (somnolence)
.alcohol use
.tobacco abuse
.CNS depressant medications
.obesity
.polycythemia
.hypoxia
-Symptoms :
.snoring
.day time sleeping (because of poor sleep)
.sleep apnea due to airway obstruction
-Complications :
.pulmonary HTN
.Rt. side heart failure (cor pulmonale)
-Diagnosis :
.sleep study (polysomnography)
.>10 episode of apnea in 1hr during sleep
-Treatment :
.weight loss (most important)
.avoid smoking, alcohol
.C-PAP (continuous positive airway pressure)
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**Lung Cancer
*Bronchogenic Carcinoma
-Is the leading cause of death because of malignancy in men and women
-Signs & Symptoms :
.cough (M.C)
.weight loss
.dyspnea
.hemoptysis
.chest wall pain
.repeated mnemonic processes (caused by post obstructive pneumonia)
-Causes :
.90% of cases of bronchogenic carcinoma are directly related to cigarette smoking in both men and women (the occasional non-
smoker who has lung cancer develops adenocarcinoma) (smoking is the major cause of lung cancer)
+The M.C lung cancers is Squamous Cell Carcinoma
-Diagnosis :
.sputum cytology (with the highest yield in Pts with squamous cell carcinoma)
.bronchoscopy (is best for centrally located lesions and helpful in staging)
.needle aspiration biopsy (should be performed if carcinoma is highly suspect and with pleural fluid aspirate)
**Atelectasis
-Is a collapse of part or the entire lung. It is seen most commonly in the immediate postoperative period. It occurs secondary to
poor inspiration or lack of coughing during this time. Mucous plug, tumor or foreign body can also lead to atelectasis
-Signs & Symptoms :
.tachycardia
.dyspnea
.fever
.hypoxemia
.on X-ray, upper lobe atelectasis can appear as tracheal deviation to the affected side
**Pleural Mesothelioma
-M.C malignant tumor of pleura / Most important risk factor is asbestosis
-Signs & Symptoms :
.chest pain
.weight loss
.pleural effusion (exudate)
.finger clubbing
-Diagnosis :
.biopsy (pleura)
+prognosis is poor
**Respiratory Failure
-Types :
1.low po2 / low or normal Pco2
-Causes :
.pneumonia
.pulmonary embolism
.pulmonary edema
.emphysema
.mild asthma
2.low Po2 / high Pco2
-Causes :
121
.severe asthma
.chronic bronchitis
.hypoventilation
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+The usual causes of low arterial oxygen tension (PaO2) :
.Right to left shunt
.Ventilation perfusion mismatch
.Impaired diffusion capacity
.Hypoventilation
**Hypercapnia
-High Co2
-Signs & Symptoms :
.headache
.vasodilation (warm extremities)
.tachycardia
.tachypnea
.large pulse volume (collapsing pulse)
.tremor (asterixis)
.papilledema
.coma
.altered level of consciousness
+Hyperventilation may be found in :

.DKA
.Acute attack of bronchial asthma
.Hysterical reaction
.Pulmonary embolism
**Interstitial Lung Disease

-Disease that affect lung parenchyma
-Example :
.idiopathic pulmonary fibrosis
.infections (TB, viral, pneumonia)
.sarcoidosis
.asbestosis
.silicosis
.allergic alveolitis
.drugs (bleomycin-can cause lung fibrosis)
+Causes of airspace disease :
.Right middle lobe pneumonia
.Pulmonary edema
.Lung contusion
.Lymphoma
**Cystic Fibrosis
-Autosomal recessive disease / Mutation on CFTR gene (chloride channels) or chromosome 7
-Signs & Symptoms :
+Infants (0-1yr)
.meconium ileus
.failure to thrive
.rectal prolapse
+Children
.recurrent chest infection
.bronchiectasis
.finger clubbing
.liver cirrhosis
.cyanosis
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.gallstones
.nasal polyp
.malabsorption (steatorrhea)
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-Diagnosis :
.sweat chloride test >60mmol/L (BEST)
-Treatment :
.chest physiotherapy
.pancreatic enzyme
.supplementation Vit (KEDA)
.antibiotics
.low fat diet
**Lung Infections
*Bronchitis
-Is an infection of the lung, which is limited to the bronchial tree with limited involvement of the lung parenchyma
-Acute Bronchitis is as acute inflammation of the tracheobronchial tube, are caused by (viruses, S.pneumoniae and H.influenza)
have not been implicated (smoking is M.C.C)
-Signs & Symptoms :
.cough often accompanied by sputum production
.a bacterial etiology is suggested by discolored sputum
.Pts. most commonly have clear lungs
.low-grade fever may be present, but Pts. are most commonly afebrile
-Diagnosis :
.signs of respiratory infection such as (cough and sputum, with a normal CXR confirm the diagnosis)
-Treatment :
.mild acute cases often do not require therapy because they are often caused by viruses that resolve spontaneously
.acute exacerbations of chronic bronchitis can be treated with amoxicillin, doxycycline or TMP/SMZ
.repeated infection or Pts. not responding to amoxicillin should be treated with any of the following amoxicillin/clavulanate,
clarithromycin, azithromycin, oral second-or third-generation cephalosporins, or the new fluoroquinolones, gatifloxacin,
levofloxacin or moxifloxacin
*Pneumonia
-Pneumonia is an inflammatory condition of the lung / Rates are greatest in children <5 yrs of age , and adults >75yrs of age
-Signs & Symptoms :
.productive cough
.fever (accompanied by shaking chills)
.chest pain during deep breaths (this chest pain worsened by inspiration) (pleuritic pain is associated with lobar pneumonia-
such as pneumococcus)
.increased respiratory rate RR
.high heart rate - tachycardia
.low oxygen saturation
.on physical examination, pneumonia presents with rales, rhonchi or signs of lung consolidation, including dullness to
percussion, bronchial breath sounds, increased vocal fremitus and egophony (E to A changes)
.sputum
.severe pneumonia of any cause may present with dyspnea
+Bacterial infections such as (streptococcus pneumoniae, haemophilus and klebsiella have significant purulent sputum
production)
+The sputum in Pts. with S.pneumoniae has been classically described as rusty (this rust is simply hemoptysis)
+Klebsiella pneumoniae has been associated with sputum described as being like currant jelly
+Interstitial infections such as those caused by pneumocystis pneumonia (PCP), viruses, mycoplasma and sometimes legionella
often give a non-productive or dry cough
-Causes :
+Bacteria - are the M.C.C of community acquired pneumonia (streptococcus pneumoniae)
.haemophilus influenza 20%
.chlamydophila pneumonia 13%
.mycoplasma pneumonia 3%
.staphylococcus aureus
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+Viruses – M.C.C in children <5yrs

.rhinoviruses
.coronaviruses
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.influenza virus
.RSV (M.C.C of pneumonia in children <5yrs)
.adenovirus
.parainfluenza
.HSV
+Fungi (Is uncommon-rare, but may occur with weakened immune system due to AIDS, immunosuppressive drugs)
+Common Causes :
.M.C.C of community acquired pneumonia is pneumococcus (S.pneumonia)
.M.C.C of hospital acquired pneumonia is staphylococcus aureus
.M.C.C of pneumonia in broncheitasis or cystic fibrosis is pseudomonas
.M.C.C of pneumonia in children <5yrs is viral pneumonia (RSV) (viral pneumonia)
.M.C.C of pneumonia in children >5yrs is viral pneumonia (pneumococcus)
.M.C.C of pneumonia in AIDS Pts. is (pneumocystis carinii pneumonia PCP) – Treated by (co-trimoxazole)
.M.C bacteria in alcoholic Pts. is (Klebsiella pneumonia)
.Aspiration pneumonia (anaerobic)
+Mycoplasma Pneumonia (can cause autoimmune hemolytic anemia, hemagglutination test)
+Legionella (from air conditioning system and can cause pneumonia + diarrhea, lymphopenia (decreased lymph) – Diagnosis by
(serology or urine)
-Diagnosis :
.physical examination of ohysical signs (cough + sputum + fever)
.CxR (S.pnumonia and other causes of typical pneumonia appears usually on CXR as lobar infiltration – single or bilateral)
.sputum culture (is diagnostic for typical pneumonia)
-Treatment :
.Pts. with more severe illness that must be treated with intravenous antibiotics as a hospitalized onpatient
.hospitalized Pts. with CAP should receive either levofloxacin, moxifloxacin or gatifloxacin pr a second- or third-generation
cephalosporin such as cefotaxime or ceftriaxone
+Outpatient (nonhospitalized) – 1st choice (macrolides-azithromycin, clarithromycin) (alternative - new fluoroquinolones -
levofloxacin, moxifloxacin, gatifloxacin)
+Inpatient (hospitalized) – (new fluoroquinolones - levofloxacin, moxifloxacin, gatifloxacin) (2nd or 3rd generation
cephalosporins – cefuroxime or ceftriaxone) combined with a marcolide or doxycyline) (Beta-lactam/beta-lactamase
combination drug – ampicillin/sulbactam, ticarcillin)
+Viral (neuraminidase inhibitors-tamiflu, may be used to treat viral pneumonia caused by influenza viruses – influenza A and B)
+Aspiration (clindamycin, a combination of a beta-lactam antibiotic and metronidazole, or an aminoglycoside-gentamycin)
+Pleural effusion, empyema and abscess (in pneumonia, a collection of fluid –pleural effusion, often forms in the space that
surrounds the lung-the pleural cavity . often requiring a chest tube / In severe cases of empyema, surgery may be needed)
.antibiotics are usually adequate to treat a lung abscess, but sometimes the abscess must be drained by a surgery
+Causes Of Empyema :
.Osteomyelitis of rib
.Pneumonia
.Perforation of the esophagus
.Subphrenic abscess
+Severity Pneumonia (indication for admission) :
.over 50yrs of age
.comorbidity
.altered mental status
.pulse >125/min
.RR >30/min
.systolic blood pressure <90mm Hg
.temperature <35C or >40C
.partial pressure of arterial O2 <60mm Hg (Po2 <60)
+Typical Pneumonia (bacterial)
.high fever
.productive cough
.looking ill
124
.CxR (lobar pneumonia-consolidation)

+Atypical Pneumonia (viruses, fungi, chlamydia, mycoplasma, legionella / treated by azithromycin)
.low fever
Page
.Pt. looking well

.dry cough
.CxR (patchy infiltrates)
+Atypical Pneumonia :
.The organism is mycoplasma pneumonia
.Treatment with clarithromycin
.Positive cold agglutination test
.Presence of cell wall responsible for resistance of penicillin
+TYPICAL agents (strep pneumoniae – haemophilus – moraxella )
+ATYPICAL agents (legionella – mycoplasma – chlamydia)
+Specific Predispositions Are As Follows :

.haemophilus influenzae (smokers, COPD)
.mycoplasma (young, otherwise healthy Pts / can cause autoimmune hemolytic anemia)
.legionella (epidemic infection in older smokers, particularly when located near infected water sources, such as air-conditioning
systems)
.pneumocystis jiroveci (formerly carinii) pneumonia (HIV-positive persons with <200 CD4 cells not on prophylaxis)
.coxiella burnetti (exposure to animals, particularly at the time they are giving birth)
.klebsiella (alcoholics)
.staphylococcus aureus (following viral syndromes or viral bronchitis, especially influenza)
.coccidioidomycosis (exposure to the deserts of the american southwest, particularly arizona)
.chlamydia psittaci (birds)
.histoplasma capsulatum (exposure to bat or bird droppings, spelunking)
.bordetella pertussis (cough with whoop and post-tussive vomiting)
.francisella tularensis (hunters, or exposure to rabbits)
.SARS, avian influenza (travel to southeast asia)
.bacillus anthracis, yersinia pestis and francisella tularensis (bioterrorism)
.M.C of aspiration pneumonia is Anaerobic
+Organism-Specific Presentations Are As A Follows :
.mycoplasma (dry cough and chest soreness, dyspnea is rare – Pts with mycoplasma pneumoniae rarely need to be admitted to
the hospital)
.legionella (CNS manifestations such as confusion, headache and lethargy. GI manifestations include (diarrhea and abdominal
pain)
.PCR (marked dyspnea, with chest soreness with cough in an HIV-positive person. Pts have AIDs with a CD4 count of <200/mL)
+Those Pts. who develop pneumonia after 5-7 days in the hospital are at increased risk of infection from drug-resistant, gram-
negative bacilli (pseudomonas, klebsiella, E.coli) or gram-positive bacilli such as (methicillin-resistant staphylococcus aureus
MRSA)
+Markers of severity are a high fever, hypothermia, leukopenia (WBC<4.000/mm), rapid pulse (>125/min), hyponatremia or
dehydration as determined by an elevated BUN
+Pneumococcal Vaccine (those who should receive the vaccine include all Pts older than the age of 65, as well as those with any
serious underlying lung, cardiac, liver or renal disease) (Immunocompromised Pts, such as those on steroids, HIV-positive
persons, splenectomized Pts, diabetics and those with leukemia or lymphoma should be vaccinated at the earliest possible
opportunity) / The Re-dosing in 5 yrs is only necessary for those with severe immunocompromised or in those who were
originally vaccinated before the age of 65yrs old / In generally healthy persons vaccinated above the age of 65, a single dose of
vaccine is enough to confer lifelong immunity
+(M.C bacteria is staphylococcus aureus) (in adult is lung cancer – in children is foreign body)
.treated by antibiotics (sometimes by surgery) / M.C complication of lung abscess is empyema
+Complication Of Pneumonia :
.pleural effusion
.chest tube
.empyema
+Rusty sputum is characteristic of Pneumococcal pneumonia
+Causes Of Aspiration Pneumonia :
.Gastroesophageal reflux
.Achalasia
.Phrenic nerve palsy
125
.Tracheoesophageal fistula
+Signs Consistent With Lobar Pneumonia :
.Reduced chest movement
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.Whispering pectoriloquy
.Pleural rub
.Bronchial breathing
+Viral Pneumonia :
.Amantadine is an effective medication for swine flue
.H1N1 virus is transmitted mainly through milk
.Viral pneumonia is more common than bacterial pneumonia
.Specific radiological findings is characteristic for viral pneumonia
*Lung Abscess
-Necrosis of the pulmonary parenchyma caused by microbial infection
-Signs & Symptoms :
.fever
.cough
.sputum production
.chest pain
.the features associated with lung abscesses are putrid, foul-smelling sputum
.weight loss
.anemia
.fatigue have usually been present prior diagnosis
-Causes :
.90% have at least some anaerobes involved
.the most commonly implicated anaerobes are peptostreptococcus, prevotella and fusobacterium species
.45% only anaerobic, 45% mixed with aerobes, 10% aerobes only
.aerobic bacteria, most frequently involved are S.aureus, E.coli, Klebsiella and Pseudomonas
.pulmonary infarction, cancer and vasculitis (like wegener granulomatosis) are three example of noninfectious causes of lung
cavities
+M.C.C of lung abscess in adults (lung cancer) / In children (foreign body)
+This is probably due to the delay of 1-2 weeks between the aspiration of oral contents and the development of necrosis and
cavitation
-Diagnosis :
.chest CT scan
*Tuberculosis TB
-Is an infectious disease usually caused by the bacterium Mycobacterium tuberculosis (MTB)
+Tuberculosis may infect any part of the body, but most commonly occurs in the lungs (known as pulmonary tuberculosis)
+Airborne transmission (TB is spread through the air)
+Hematogenous transmission can also spread infection to more distant sites, such as (peripheral lymph nodes, the kidneys, the
brain, and the bones)
+Mycobacterium tuberculosis is etiological agent of Pott’s disease
+Active infection occurs more often in people with HIV/AIDS and in those who smoke
+Severe form of TB disease and M.C in young children and those with HIV, is called (Miliary Tuberculosis)
-Signs & Symptoms :
.may infect any part of the body (most commonly occur in the lung)
.chronic cough with blood-containing sputum
.fever
.chills
.night sweats
.loss of appetite
.weight loss
.fatigue
.finger clubbing
+Typically found in the top of the lung (in active TB – upper lobe / latent – lower lobe)
-Vaccines :
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.Bacillus Calmette-Guerin (BCG) / The immunity is induced decreases after about 10yrs
-Diagnosis :
.CXR (upper low cavitation)
.mantoux tuberculin skin test PPD (previously immunized may have a false positive test)
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+>10mm induration (low risk) / >5mm (in high risk)

+PPD is sensitive but NOT specific
.sputum for (ziehl neelsen stain) – TB (acid fast bacilli AFB)
.sputum for culture
+Diagnosis of active TB is based on chest X-rays, as well as microscopic examination and culture of body fluids. Diagnosis of
latent TB relies on the tuberculin skin test (TST) or blood tests
-Treatment :
+Latent TB treatment usually employs a single antibiotic (I.N.H – Isoniazid, rifampicin for 2 months)
+Active TB disease is best treated with combinations of several antibiotics to reduce the risk of the bacteria developing
antibiotic resistance :
.ethambutol (can cause-side effect - optic neuritis)
.isoniazid is INH (can cause - peripheral neuropathy, hepatitis, Vit B6 deficiency ‘pyridoxine’)
.pyrazinamide (can cause – hepatotoxicity, hepatitis)
.rifampicin (can cause - change in the color of all body fluids to orange-red body secretion, red urine, red tears)
+Granulomatous Disease (sarcoidosis – TB)
+Anti TB Drugs :
.Isoniazid (INH)
.Rifampicin
.Pyrazinamide
.Ethambutol
.Streptomycin
.Isonicotinic acid hydrazide (INH)
+Contacts with a patient having TB who recently changed from negative to positive for PPD test should receive INH
+Isoniazid chemoprophylaxis may be given to selected high risk patients over 35yrs of age
+Warfarin
.Oral
.Mechanism (inhibit Vit K dependent, clotting factors II, VII, IX, X (1972), protein)
.Half life 1.5day
.Antidote (Vit K, FFP-plasma)
.Contraindicated in pregnancy (can cause cross placenta)
.PT, INR
+Heparin
.Subcutaneous or I.V
.Mechanism (activated antithrombin III)
.90min-1.5hrs
.Antidote (protamine sulfate)
.safe in pregnancy
.aPTT
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Anaphylaxis, Bites And Stings
**Anaphylaxis
-Syndrome of histaminergic release in which there are signs of severe injury such as urticaria, angioedema, hypotension,
tachycardia and respiratory compromise
-Signs & Symptoms :
.rash known as ‘hives’
.dyspnea
.stridor
.tachycardia
.hypotension
.hemodynamic collapse
-Treatment :
.antihistamine (diphenhydramine)
.for more sever symptoms of anaphylaxis with hemodynamic instability required (epinephrine injections, intravenous fluids,
antihistamines and systemic corticosteroids)
**Venomous Bites and Stings

*Cat And Dog Bites
-Dog bites (in the form of a puncture wound) / Infections are most often polymicrobial
-Cat bites are highly associated with (Pasteurella multocida)
-Dog bites are highly associated with (pasteurella, Eikenella and Capnocytophaga canimorsus)
-Treatment :
.exploration, debridement, irrigation and proper wound car
.antibiotics (amoxicillin and clavulanate) (a combination of clindamycin and either ciprofloxacin or
trimethoprim/sulfamethoxazole or azithromycin can be used in Pts. that are penicillin allergic)
*Human Bites
-The M.C organisms are anaerobic and aerobic bacteria
+Hepatitis B and HIV can also be transmitted through bites bu is much less common
-Treatment :
.clean and irrigate wound
.if bites <12hrs old, close loosely
.give counseling for tetanus, hepatitis B and prophylaxis
.initiate 5-7 days course of prophylaxis antibiotics
*Rabies
-Raccoons, rats, wild dogs, woodchucks, skunks, foxes
-Signs & Symptoms :
.incubation period up to 1yr
.prodrome of 2-10 days including (fever, paresthesias at the bite site)
.neurologic changes (aphasia, paralysis, hypersalivation and myoclonus)
-Diagnosis :
.viral cultures from saliva
.CSF
.serum
-Treatment :
.ribavirin (has been used in confirmed cases)
.prophylaxis with human rabies immunoglobulin (HR16), which gives immediate passive immunity
.human diploid cell vaccine (HDCV) should be given at 0, 3, 7, 14 and 28 days (5 shots total)
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*Snake Bites
-Snake venom contains numerous potentially dangerous substances, such as (hemolysis toxic, cardiotoxin, neurotoxin and
proteolytic enzymes. Some of these substances can result in neuromuscular blocked)
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-Factors that affect the severity of the bite :
.body size (the smaller the body, the worse the effects)
.location ob bite (trunk and face bites are worse than extremity bites)
.exercising after bite (Muscular activity helps spread the venom through the lymphatics)
.depth of injury (No poisoning occurs in 20-50% of bites because they are too superficial)
-Treatment :
.immobilize the Pt. (this will help to decrease the spread of venom through the lymphatics, which increases with muscular
contraction)
.apply compression bandage (this will decrease lymph flow)
.antivenin
.supportive (hypotension is managed with fluids)
.infective therapy (incision and suction of the bites) (tourniquets and ice immersion do not help and might be harmful)
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NEUROLOGY
**Cerebrovascular Accident CVA (Stroke)
-Is a sudden onset of a focal neurologic deficit, or brain attack (is when poor blood flow to the brain results in cell death) –
Ischemic or Hemorrhagia
-Types :
.Ischemic Strokes (M.C)
.Hemorrhagic Strokes (cerebral hemorrhage, subarachnoid hemorrhage)
.Transient ischemic attacks (TIAs) – Mini strokes (M.C.C is carotid artery stenosis)
-Diagnosis :
.the initial test of choice will always be a non contrast CT scan of the head (this test is done to distinguish between hemorrhagic
and ischemic stroke)
.CT scan is the most sensitive test for detecting blood in the brain
.CT scan are often negative for ischemia within the first 48hrs after symptoms onset
.MRI is the most accurate test for detecting cerebral ischemia
*Ischemic Stroke – Cerebral Ischemia – Cerebrovascular Ischemia

-Occur as a result of an obstruction within a blood vessel supplying blood to the brain – blood supply to part of the brain is
decreased, leading to dysfunction of the brain tissue in that area and to poor oxygen supply or cerebral hypoxia and thus to the
death tissue or cerebral infarction/ischemic stroke – Causes :
1. Cerebral thrombosis (refors to a thrombus – blood clot) (focal)
2. Cerebral embolism (obstruction due to an embolus) (focal)
3. Systemic hypoperfusion (in shock) (global)
4. Cerebral venous sinus thrombosis
-Types :
.focal ischemia (which is condined to a specific region of the brain)
.global ischemia (which encompasses wide areas of brain tissue)
-Symptoms :
.ischemia whithin the arteries branching from the internal carotid artery, may result in symptoms such as (blindness in one eye,
weakness in one arm or leg, weaknes in one antire side of the body)
.ischemia within the arteries branching from the vertebral arteries in the back of the brain, may results in symptoms such as
(dizziness, vertigo, double vision, or weakness on both sides of the body)
.difficulty speaking (slurred speech, loss of coordination)
.hemiplegia and muscle weakness of the face
.numbness
.altered smell, taste, hearing or vision
.weakness in tongue
.memory deficits
.loss of consciousness, headache, vomiting
+Other Causes :
.sickle cell anemia
.congenital heart defects
.irregular heartbeats
.myoamoya disease
.bacteria (usually from infectious endocarditis)
.cancer cells
.CHF
.DM
.hyperlipidemia
.homocysteinemia
.smoking
.HTN (M.C.C of intracranial hemorrhage)
.embolism (MI or atrial fibrillation) – Heart disease
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.thrombus (carotid artery)

.pulmonary embolism
.pericardial effusion
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.hypoxemia
.bleeding
.cerebral venous sinus thrombosis
*Hemorrhagic
-Types :
1. Cerebral hemorrhage or intracerebral hemorrhage (bleeding within the brain itself. Intraparenchymal hemorrhage – bleeding
within the brain tissue Or, Intraventricular hemorrhage – bleeding within the brain`s ventricular system)
2. Subarachnoid hemorrhage (bleeding that occurs outside of the brain tissue but still within the skull, between the arachnoid
mater and pia mater) (associated with polycystic kidney disease) (can cause hyponatremia)
+The blood supply to the brain is divided into tow major systems :
.the carotid (anterior) circulation
.the vertebrobasilar (posterior) circulation
+The major blood vessels comprise the anterior circulation include :
.the anterior cerebral artery ACA
.middle cerebral artery MCA
+Occlusion of the ACA (Anterior Cerebral Artery Stroke) presents with contralateral weakness in the arm and sensory loss in the
leg more than in the upper extremity. Urinary incontinence, confusion and behavioral disturbances are common
+Occlusion of the MCA (Middle Cerebral Artery Stroke) presents with contralateral hemiplegia, hemisensory loss and
homonymous hemianopia with eyes deviated toward the cortical lesion
**Convulsion (FIT)
-is a medical condition where body muscles contract and relax rapidly and repeatedly, resulting in an uncontrolled shaking of
the body
+Because a convulsion is often a symptom of an epileptic seizure, the term convulsion is sometimes used as a synonym for
seizure
+NOT all epileptic seizures lead to convulsions, and not all convulsions are caused by epileptic seizures
-Signs & Symptoms :
.brief blackout
.confusion
.drooling
.loss of bowel/bladder control
.sudden shaking of entire body
.uncontrollable muscle spasms
.temporary cessation of breathing
.symptoms usually last from a few seconds to around 15 minutes
-Causes :
.caused by some sort of electrical activity mishap in the brain
.chemicals in the blood
.infections like meningitis or encephalitis
.fevers
.head trauma
.stroke
.lack of oxygen to the brain
.genetic defects
.brain tumors
.by any type-1 diabetic, whose blood sugar is too low. Hypoglycemia can cause very bad convulsions until the person's blood
sugar is raised to normal level
+The M.C type of seizure is called a generalized seizure, also known as a generalized convulsion. This is characterized by a loss
of consciousness which may lead to the person collapsing. The body stiffens for about a minute and then jerks uncontrollably
for the next minute. During this, the patient may fall and injure themselves or bite their tongue and lose control of their
bladder. A familial history of this puts a person at a greater risk for developing them
**Seizures
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-Types :
.Epileptic seizure
.Non-epileptic seizure
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-Signs & Symptoms :

.sudden in onset
.with or without an aura
.disorientation
.sleepiness
.aching muscles for minutes to hours after the event
.Pt. may also experience incontinence
.tongue biting
.jerking of a finger or hand
.headache as a result of the seizure
-Causes :
.vascular (stroke, bleed, arteriovenous malformation AVM, cavernoma)
.infection (meningitis, abscess, encephalitis, cerebral malaria, neurocysticercosis)
.trauma (especially penetrating)
.autoimmune (CNS vasculitis)
.metabolic (hyponatremia, hypocalcemia, hypomagnesemia, hypoglycemia, hypoxia)
.idiopathic
.neoplasm (abscesses, tumors)
.psychiatric
.drug overdoses
.drug withdrawal
.drugs (antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine)
.multiple sclerosis
.people with celiac disease also have seizures
+Seizures may occur as a result of high blood pressure, known as hypertensive encephalopathy, or in pregnancy as eclampsia
when accompanied by either seizures or a decreased level of consciousness. Very high body temperatures may also be a cause
+Seizures in a person with a shunt may indicate failure
+Hemorrhagic stroke can occasionally present with seizures, embolic strokes generally do not (though epilepsy is a common
later complication); cerebral venous sinus thrombosis, a rare type of stroke, is more likely to be accompanied by seizures than
other types of stroke
+Head injury may cause non-epileptic post-traumatic seizures or post-traumatic epilepsy
+Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium
tremens
+In people with brain tumors (the frequency of epilepsy depends on the location of the tumor in the cortical region)
-Diagnosis :
.electroencephalogram is the test of choice fro the diagnosis of epilepsy
.diagnosis of idiopathic seizures is made only after secondary precipitating factors have been ruled out
.an abnormal EEG alone is not diagnostic of epilepsy
.CT scan and MRI of the head is usually indicated to rule out a structural lesion as the cause of seizure
*Epileptic Seizure
-Is a brief episode of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain. The outward
effect can vary from uncontrolled jerking movement (tonic-clonic seizure) to as subtle as a momentary loss of awareness
(absence seizure)
+A first seizure generally does not require treatment unless there is a specific problem on either electroencephalogram or brain
imaging
+The M.C type of seizures are convulsive (60%). Two-thirds of these begin as focal seizures and become generalized
+Focal Seizures (localized seizures)
.are often preceded by certain experiences, known as an aura sensory, visual, psychic, autonomic, olfactory or motor
phenomena
.Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a Jacksonian march
.these are known as automatisms and include simple activities like smacking of the lips or more complex activities such as
attempts to pick something up
+Generalized Seizures
.types of generalized seizures (tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures)
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1.Tonic-clonic seizures present with a contraction of the limbs followed by their extension, along with arching of the back for
10–30 seconds. A cry may be heard due to contraction of the chest muscles. The limbs then begin to shake in unison. After the
shaking has stopped it may take 10–30 minutes for the person to return to normal
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2.Tonic seizures produce constant contractions of the muscles. The person may turn blue if breathing is impaired
3.Clonic seizures involve shaking of the limbs in unison
4.Myoclonic seizures involve spasms of muscles in either a few areas or generalized through the body
5.Absence seizures can be subtle, with only a slight turn of the head or eye blinking. The person often does not fall over and
may return to normal right after the seizure ends, though there may also be a period of post-ictal disorientation
6.Atonic seizures involve the loss of muscle activity for greater than one second. This typically occurs bilaterally (on both sides
of the body)
-Duration :
.A seizure can last from a few seconds to more than five minutes, at which point it is known as status epilepticus
.Most tonic-clonic seizures last less than two or three minutes
.Absence seizures are usually around 10 seconds in duration
+Different Causes Of Seizures :
.During the neonatal period and early infancy the most common causes include hypoxic ischemic encephalopathy, central
nervous system (CNS) infections, trauma, congenital CNS abnormalities, and metabolic disorders
.The most frequent cause of seizures in children is febrile seizures, which happen in 2–5% of children between the ages of six
months and five years
.During childhood, well-defined epilepsy syndromes are generally seen
.In adolescence and young adulthood, non-compliance with the medication regimen and sleep deprivation are potential
triggers
.Pregnancy and labor and childbirth, and the postpartum, or post-natal period (after birth) can be at-risk times, especially if
there are certain complications like eclampsia.
.During adulthood, the likely causes are alcohol related, strokes, trauma, CNS infections, and brain tumors
.In older adults, cerebrovascular disease is a very common cause. Other causes are CNS tumors, head trauma, and other
degenerative diseases that are common in the older age group, such as dementia
*Non-epileptic Seizure
-Are paroxysmal events that mimic an epileptic seizure but do not involve abnormal, rhythmic discharges of cortical neurons
-Causes :
.Syncope (fainting) (reflex anoxic seizures)
.Breath-holding spells of childhood
.Cataplexy
.Hyperekplexia, also called startle syndrome
.Migraine
.Narcolepsy
.Non-epileptic myoclonus
.Opsoclonus
.Parasomnias, including night terrors
.Paroxysmal kinesigenic dyskinesia
.Repetitive or ritualistic behaviours
.Tics
.AADC Deficiency
*Febrile Seizure
-Is a seizure associated with a high body temperature but without any serious underlying health issue. They most commonly
occur in children between the ages of 6 months and 5 years. Most seizures are less than five minutes in duration and the child is
completely back to normal within sixty minutes of the event
+There Are Three Types Of Febrile Seizures :
.A simple febrile seizure is characterized by shorter duration (lasting less than 15 minutes), no focal features (meaning the
shaking is general rather than restricted to a part of the body such as an arm or leg), and if they do occur in series, the total
duration is less than 30 minutes (classically a generalized tonic-clonic seizure)
.A complex febrile seizure is one in which the seizure lasts longer than 15 minutes or multiple episodes occur within 24 hours
and generally does have focal features
.A febrile status epilepticus is a febrile seizure that lasts for longer than 30 minutes. It can occur in up to 5% of febrile seizure
cases
+Febrile seizures may run in families
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+The diagnosis involves verifying that there is not an infection of the brain, there are no metabolic problems, and there have
not been prior seizures that have occurred without a fever
+Febrile seizures without an intracranial infection or metabolic problems. They run in families. Several genetic associations have
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been identified. An association with iron deficiency has also been reported, particularly in the developing world
*Stokes Adams Attack (Syndrome)
-It is characterised by decrease in cardiac output and loss of consciousness due to a transient arrhythmia. For example,
bradycardia due to complete heart block
+The attacks are caused by lack of cardiac output due to antimony poisoning, cardiac asystole, heart block, Lev's disease or
ventricular fibrillation. The resulting lack of blood flow to the brain is responsible for the faint
-Signs & Symptoms :
.transient idiopathic arrhythmia (heart beats irregularly)
.occurs without warning leading to sudden loss of consciousness
.Pt. may be pale with hypoperfusion
.normal periods of unconsciousness last approximately thirty seconds (if seizures are present, they will consist of twitching after
15–20 seconds - seizures occur because of cerebral hypoxia)
.hypoxia
.breathing continues normally throughout the attack
-Treatment :
.isoprenaline (Isuprel)
.epinephrine (adrenaline)
*Epilepsy
-Is a group of neurological diseases characterized by epileptic seizures
+Epilepsy is characterized by a long-term risk of recurrent seizures. These seizures may present in several ways depending on
the part of the brain involved and the person's age
-Causes :
.broken bones
.brain-head injury
.toxic ingestion or metabolic problem
.stroke
.brain tumors
.infections of the brain (cerebral malaria, toxoplasmosis, toxocariasis)
.infections of CNS
.birth defects
.cerebral cavernous malformations
.arteriovenous malformations
.chronic alcohol use
.meningitis, herpes simplex encephalitis, pork tapeworm, neurocysticercosis
.genetic mutations (ion channels, enzymes, GABA, and G protein-coupled receptors, Down syndrome, Angelman syndrome)
.excessive and abnormal nerve cell activity in the cortex of the brain
.more common in among younger people
.malnutrition
.cerebral palsy
.spastic quadriplegia – spastic hemiplegia
.alzheimers disease, multiple sclerosis, tuberous sclerosis, autoimmune encephalitis
+Getting vaccinated does not increase the risk of epilepsy
*Syncope
-Treatment :
+Returning blood to the brain by positioning the person on the ground, with legs slightly elevated or leaning forward and the
head between the knees for at least 10–15 minutes, preferably in a cool and quiet place
.Beta blockers (β-adrenergic antagonists)
.Medications which may be effective include: CNS stimulants fludrocortisone, midodrine, SSRIs such as paroxetine or sertraline,
disopyramide, and, in health-care settings where a syncope is anticipated, atropine epinephrine (adrenaline)
+Vasovagal Syncope (M.C type)
-Is a malaise mediated by the vagus nerve and it leads to fainting. Is most commonly found in adolescents and in younger adults
-Signs & Symptoms :
134
.bradycardia
.emotion (fear, pain)
+Pt. with syncope (they will recover consciousness within several minutes of the event, and no physical exam will not have
evidence of incontinence or tongue biting)
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-Causes :
.Prolonged standing (standing too long) or upright sitting
.Hypoglycemia
.Anxiety (hyperventilation)
.Factitious syncope (temporary loss of consciousness caused by a fall in blood pressure)
.After or during urination (micturition syncope)
.Standing up very quickly (orthostatic hypotension)
.During or post-biopsy procedures.
.Stress directly related to trauma[8]
.Stress
.Postural orthostatic tachycardia syndrome (POTS)
.Any painful or unpleasant stimuli, such as (rauma - such as hitting one's funny bone, watching or experiencing medical
procedures - such as venipuncture or injection, high pressure on or around the chest area after heavy exercise)
.Severe menstrual cramps
.Sensitivity to pain
.Arousal or stimulants, e.g. sex, tickling, or adrenaline
.Sudden onset of extreme emotions
.Lack of sleep
.Dehydration
.Hunger
.Being exposed to high temperatures
.In health care, such as nursing care
.Use of certain drugs that affect blood pressure, such as cocaine, alcohol, marijuana, inhalants, and opiates
.The sight of blood
.Serotonin level / SSRI
.Swallowing
+Exertional Syncope
-Syncope with exercise, causes (aortic stenosis, hypertrophic cardiomyopathy)
**Dizziness
-Is an impairment in spatial perception and stability or loss of consciousness indicates a concussion has occurred
+Is defined as afalse sensation of mevement, i.e, the sensation of mevement in the absence of actual movement
-Classification :
.vertigo (~50%)
.disequilibrium (less than ~15%)
.presyncope (less than ~15%)
.lightheadedness (~10%)
+Vertigo is the sensation of spinning or having one's surroundings spin about them. Many people find vertigo very disturbing
and often report associated nausea and vomiting
.Pts. who experience vertigo will describe a sensation of movement without actually moving (Pts. will describe their
environment spinning around them). Sensation of tiling, swaying, or falling forward or backward are all consistent with vertigo.
These episodes are commonly associated with nausea and vomiting (tinnitus, hearing loss present in peripheral vertigo /
peripheral vertigo treated by meclizine or, in severe cases, diazepam – absent in central vertigo)
+Disequilibrium is the sensation of being off balance, and is most often characterized by frequent falls in a specific direction.
This condition is not often associated with nausea or vomiting
+Presyncope is Lightheadedness, muscular weakness and feeling faint as opposed to a syncope, which is actually fainting
.Pts. who complain of presyncope will describe their symptoms as ‘lightheadedness’ or ‘feeling like im going to back out’,
weakness, palpitations and shortness of breath
+It is essential to differentiate vertigo from presyncope because vertigo is usually a manifestation of neurologic disease,
whereas presyncope is a cardinal manifestation of cardiovascular disease
-Causes :
.benign paroxysmal positional vertigo
.traumatic vertigo
135
.cervical vertigo
.perilymphatic fistula
.vascular disease of the brainstem
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.drug overdose
.meniere's disease
.vestibular neuronitis
.labyrinthitis
.otitis media
.brain tumor
.acoustic neuroma
.motion sickness
.ramsay Hunt syndrome
.migraine
.multiple sclerosis
.pregnancy
.low blood pressure (hypotension)
.low blood oxygen content (hypoxemia)
.heart attack
.iron deficiency (anemia)
.low blood sugar (hypoglycemia)
.hormonal changes (e.g. thyroid disease, menstruation, pregnancy)
.panic disorder
.hyperventilation
.anxiety
.depression
.age-diminished visual, balance, and perception of spatial orientation abilities
+A stroke is the cause of isolated dizziness in 0.7% of people who present to the emergency room
+Non-specific dizziness is often psychiatric in origin. It is a diagnosis of exclusion and can sometimes be brought about by
hyperventilation
+Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner
ear, eyes, muscles, skeleton, and the nervous system
+Physiological Causes Of Dizziness :
.inadequate blood supply to the brain due to (a sudden fall in blood pressure) (heart problems or artery blockages)
.loss or distortion of vision or visual cues
.disorders of the inner ear
.distortion of brain/nervous function by medications such as anticonvulsants and sedatives
.result of side effect from prescription drugs, including proton-pump inhibitor drugs (PPIs) and Coumadin (warfarin) causing
dizziness/fainting
+Ménière's Disease
-Is a disorder of the inner ear that can affect hearing and balance. It is characterized by episodes of vertigo, tinnitus, and
hearing loss. The hearing loss comes and goes for some time, alternating between ears, then becomes permanent
-Signs & Symptoms :
.nausea, vomiting
.sweating
.unilateral (in one ear) or bilateral (both ears) hearing loss
.unilateral or bilateral tinnitus
.unilateral or bilateral sensation of fullness or pressure
.uncontrollable rhythmical and jerky eye movements
.migraine
+Other conditions can present themselves with Ménière's-like symptoms, such as (syphilis, Cogan's syndrome, autoimmune
inner ear disease, dysautonomia, perilymph fistula, multiple sclerosis, acoustic neuroma, and both hypo- and hyperthyroidism)
-Causes :
.Menière's disease is linked to endolymphatic hydrops
.membranous labyrinth
.related to swelling of the endolymphatic sac or other tissues in the vestibular system of the inner ear
.middle ear infection
.head trauma
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.upper respiratory tract infection

.from using aspirin
.smoking cigarettes, or drinking alcohol
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.HSV
+Is treated with low-salt diet and diuretics (in Pts. who fail medical therapy, you can consider surgical decompression)
+Labyrinthitis (otitis interna)

-Is inflammation of the inner ear. It results in vertigo and also possible hearing loss or ringing in the ears. It can occur as a single
attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea,
vomiting. Vestibular neuronitis may also be associated with eye nystagmus
.present with sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. The disease frequently
follows an upper respiratory tract infection
+Is treated symptomatically with meclizine and diazepam when the symptoms are severe (vertigo seconadry to labyrinthitis)
*Tremor
-Causes :
.multiple sclerosis
.stroke
.familial (relieved alcohol)
.hyperthyroidism
.traumatic brain injury
.chronic kidney disease
.neurodegenerative diseases (that damage or destroy parts of the brainstem or the cerebellum)
.parkinson's disease
.drugs (such as amphetamines, cocaine, caffeine, corticosteroids, SSRIs, B2-agonist-salbutamol) or alcohol, mercury poisoning
.withdrawal of drugs such as alcohol or benzodiazepine
.in infants with phenylketonuria (PKU), overactive thyroid or liver failure
.hypoglycemia
.lack of sleep, anxiety, lack of vitamins, or increased stress
.deficiencies of magnesium and thiamine
.spider bites (the redback spider)
.rhythmic shaking in the hands, arms, head, legs, or trunk; shaky voice; and problems holding things such as a fork or pen
**Disorders Associated With Headache

*Headache
-Is defined as pain located in the head, neck or jaw
-Causes :
+Primary headache syndrome include :
.migraine
.cluster
.tension headache
+Secondary headache syndromes include :
.intracranial hemorrhage
.brain tumor
.meningitis
.temporal arteritis
.glaucoma
-Clinical Presentation :
.A history of recurrent symptoms makes the diagnosis of a primary headache disorder more likely
.headache with fever and nuchal rigidity suggests meningitis as the underlying cause
.accompanied by nuchal rigidity without fever, suggests as intracranial hemorrhage is the underlying cause
.Pts. with brain tumors will present complaining of headache that is described as a deep, dull, aching pain that disturbs sleep
.the history of vomiting that precedes the onset of headache by a number of weeks, or a history of headache induced by
coughing, lifting or bending, is a typical of posterior fossa brain tumors
.Pts. with temporal arteritis complain of a unilateral pounding headache associated with visual changes, described as dull and
boring with superimposed lancinating pain. Pts. will also complain of polymyalgia rheumatica, jaw claudication, fever, weight
137
loss and scalp tenderness (difficulty combing hair or lying on a pillow). The scalp tenderness is from pain over the temporal
artery
.temporal arteritis is a disorder of the elderly, generally presenting in Pts. older than 50yrs of age. Temporal arteritis gives an
elecated sedimentation rate and is diagnosed with biopsy of the temporal artery. Do not wait for the biopsy results to initiate
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therapy with steroids

.Pts. with glaucoma will usually give a history of eye pain preceding the onset of the headachemn
-Diagnosis :
.Pts with severe, sudden onset of a first-time headache accompanied by strong evidence for an underlying cause on history or
physical examination should have a CT scan of the rule out any secondary cause
-Treatment :
.mild migraine (wich is defined as headache in the absence of nausea or vomiting – nonsteroidal anti-inflammatory
medications)
.the triptans are contraindicated in Pts with known cardio-vascular disease
.prophylactic treatment for migraine therapy should be initiated when Pts have acute migraine headache more than 3-4 times
per month (propranolol, timolol, valproic acid and topiramate)
+MIGRAINE THERAPIES :
.abortive (NSAIDs, aspirin, acetaminophen / triptans / ergotamine derivatives)
.prophylactic (beta blockers, calcium blockers, tricyclics, SSRIs, valproic acid, topiramate)
+Migraine Headaches
.F > M 2:1 (More in obese)
.are defined as a benign and recurrent syndrome of headache, nausea, vomiting and other varying neurologic dysfunction
.UNILATERAL headache (Attack lasr 4-72hrs)
.Pts. will describe the headache as pulsatile, throbbing, unilateral and aggravated by minor movement. Other associated
features include photophobia, phonophobia, nausea, vomiting and the time to maximal pain 4-72hrs
.typical triggers (triggers can be identified) include (alcohol, certain foods such as chocolate, various cheeses, monosodium
glutamate), hunger or irregular sleep patterns
.migraine without aura is a migraine without a preceding focal neurologic deficit
.migraine with aura (classic migraine) is a migraine headache that is accompanied by a preceding aura that consists of motor,
sensory or visual symptoms
.risk factors (cheese, OCP, travel, excercise)
.treated by (NSAIDs – aspirin, ketoprofen) / prophylaxis (if >2 attack per month) / B-blocker (propranolol) is decreased
frequency of attacks
+Tension Headache
.M.C type of headache
.BILATERAL headache
.described as tight, ‘band-like’ headache
.Pts. may also describe their headache as ‘vise-like’, and these headaches may be associated with tightness of the posterior
neck muscles / NO vomiting
.relieved by simple analgesic (paracetamol)
.movement will not generally exacerbate the headache
+Cluster Headache
.begin without warning and are typically described as excruciating, periorbital and peaking in intensity within 5min of onset
.UNILATERAL (around one eye)
.the attacks will last from 30min-3hrs and occur one to three times a day for a 4-8wks period
.symptoms associated with cluster headache include (rhinorrhea, reddening of the eye, lacrimation, nasal stuffiness, nausea
and sensitivity to alcohol)
.food and emotion rarely will trigger a cluster headache
.prophylaxis (verapamil-INN)
*Pseudotumor Cerebri (Idiopathic intracranial hypertension IIH / Benign intracranial hypertension BIH)
-Is an idiopathic increase in intracranial pressure also known as benign intracranial hypertension (can cause headache). The
disorder is 8-10 times more common in women (F > M)
+Is a neurological disorder that is characterized by increased intracranial pressure (pressure around the brain) in the absence of
a tumor or other diseases
+Respiratory irregularities, HTN, Bradycardia
-There is association with (epilepsy, brain masses, intracranial bleeding, obesity, chronic lung disease, addison disease, oral
contraceptive, long-term tetracycline use and Vit A toxicity)
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-Signs & Symptoms :

.headache
.visual disturbances such as (diplopia, sixth cranial nerve ‘abducens’ palsy)
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.papilledema
.enlargement of the blind spot on visual field testing
.worse in the morning
.associated with nausea and vomiting
.the pain may also be experienced in the neck and shoulders
.pulsatile tinnitus
.compression and traction of the cranial nerves, a group of nerves that arise from the brain stem and supply the face and neck
.papilledema (which is swelling of the optic disc, the spot where the optic nerve enters the eyeball)
.visual fields
+Most commonly, the abducens nerve (sixth nerve - This nerve supplies the muscle that pulls the eye outward) is involved
+The headache can be made worse by any activity that further increases the intracranial pressure, such as coughing and
sneezing
+Lumbar puncture is performed to measure the opening pressure, as well as to obtain cerebrospinal fluid (CSF) to exclude
alternative diagnosis / as a diagnostic LP (such as done in search of a CSF infection) (is contraindicated when pressure is
increased)
-Treatment :
.weight loss, removing offending agents such as oral contraceptive
.use of diuretics (acetazolamide or furosemide)
.steroids (prednisone) (used in severe papilledema – otherwise their use is controversial)
.repeated lumbar punctures may help (to exclude diagnosis)
.if this not effective and the disorder does not resolve, definitive treatment can be achieved with the placement of a surgical
shunt between the ventricles and the peritoneum)
+Acetazolamide (Diamox), which acts by inhibiting the enzyme carbonic anhydrase, and it reduces CSF production by six to 57
percent. It can cause the symptoms of hypokalemia (low blood potassium levels), which include muscle weakness and tingling
in the fingers. Acetazolamide cannot be used in pregnancy, since it has been shown to cause embryonic abnormalities in animal
studies. Also, in human beings it has been shown to cause metabolic acidosis as well as disruptions in the blood electrolyte
levels of newborn babies
*Trigeminal Neuralgia (TN or TGN)

-Is a neuropathic chronic pain disorder affecting the trigeminal nerve (also known as the fifth cranial nerve : a three-branched
nerve that carries sensations from the face to the brain and controls facial motor functions such as biting and chewing) /
paroxysm of severe stabbing pain, precipitated by facial sensory stimuli like shaving or washing with cold water / M > F – old
age >50 yrs
+TN is caused by loss of myelin from the sensory fibers within the nerve itself
+The classic presentation of TN (type 1) is characterized by episodes of sudden, explosive severe pain along the trigeminal
nerve, with periods of pain-free remission between attacks
+The atypical form of TN (type 2) presents with the paroxysmal pain of classic TN, but with the addition of a constant pain that
fluctuates from a dull aching to an excruciating roar
+The trigeminal nerve is a mixed cranial nerve responsible for sensory data such as tactician (pressure), thermoception
(temperature), and nociceptive (pain) originating from the face above the jawline; it is also responsible for the motor function
of the muscles of mastication, the muscles involved in chewing but not facial expression
+Is characterized by episodes of intense facial pain along the trigeminal nerve divisions
+The trigeminal nerve is a paired cranial nerve that has three major branches :
.the ophthalmic nerve (V1)
.the maxillary nerve (V2)
.the mandibular nerve (V3)
+One, two, or all three branches of the nerve may be affected. Trigeminal neuralgia most commonly involves the middle branch
(the maxillary nerve or V2) and lower branch (mandibular nerve or V3) of the trigeminal nerve
-Treatment :
.carbamazepine (of choice)
**Multiple Sclerosis MS
-Is an autoimmune inflammatory disease of the CNS white matter characterized by a relapsing or progressive course
+Is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged,
139
leading to demyelination and scarring as well as a broad spectrum of signs and symptoms
+Disease onset usually occurs in young adults (F > M) / MS being much less common in people living near the equator
+In MS, the body's own immune system attacks and damages the myelin particularly in the white matter of the brain and spinal
cord
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+The Types Of MS :
.relapsing (remitting) (good)
.progressive (worst)
+The Three Main Characteristics Of MS Are :
.the formation of lesions in the central nervous system (also called plaques)
.inflammation
.the destruction of myelin sheaths of neurons
-Signs & Symptoms :
.muscle weakness
.muscle spasms
.clonus
.difficulty in moving
.numbness, tingling
.Lhermitte's sign (electrical sensation that runs down the back when bending the neck)
.difficulties with coordination and balance (ataxia)
.problems in speech (dysarthria)
.dysphagia
.unsteadiness of a limb
.fatigue, acute or chronic pain
.bladder and bowel difficulties (urinary-stool incontinence, urgency or retention)
.visual problems (blurry - double vision, nystagmus, optic neuritis, transient loss of vision-amaurosis fungus)
.emotional symptoms (depression, unstable mood)
.paraplegia, paresthesia
+M.C affect spinal cord (Cervical)
+Rarely affect PNS (bad prognosis)
+Associated Conditions (Lhermitte's sign) :
.the cervical cord or of the caudal medulla
.transverse myelitis
.Behçet's disease
.trauma
.radiation myelopathy
.vitamin B12 deficiency (subacute combined degeneration)
.compression of the spinal cord in the neck from any cause such as (cervical spondylosis, disc herniation, tumor, and Arnold-
Chiari malformation)
.chemotherapy
+Symptoms may persist for several weeks or may resolve spontaneously over a few days
+Most Pts. will have a months-long to years-long disease-free period after their first exacerbation
+In some Pts. the progression of disease becomes more aggressive, so that a consistent worsening of function occurs (this form
of the disease is called secondary progressive disease)
+The diagnosis is made clinically when a young Pt. (usually less than 55yrs of age) presents with a history of multiple neurologic
complaints that cannot be explained by the presence of one CNS lesion (in other words, you should suspect the diagnosis when
a Pt. present with multiple neurologic deficits separated by time and space-anatomy)
+A number of triggers are known to exacerbate the disease. Infections or trauma may acutely worsen the disease. Pregnancy,
especially the 2-3 months following birth
-Causes :
+Is unknown; however, it is believed to occur as a result of some combination of genetic and environmental factors such as
infectious agents
+MS is not considered a hereditary disease / The cause of MS is thought to be multifactorial
.specific genes that have been linked with MS include differences in the human leukocyte antigen (HLA) system (a group of
genes on chromosome 6 that serves as the major histocompatibility complex - MHC)
+The association between multiple sclerosis and alleles of the MHC defined as DR15 and DQ6. Other loci have shown a
protective effect, such as HLA-C554 and HLA-DRB1*11
.infectious agents (hygiene hypothesis, HSV, ep virus, MMR)
.smoking, stress
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.gout (low levels of uric acid)

.inflammation (the inflammatory process is caused by T cells, a kind of lymphocyte that plays an important role in the body's
defenses)
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.the blood–brain barrier (is a part of the capillary system that prevents the entry of T cells into the central nervous system)
-Diagnosis :
.MRI (of the brain is the most accurate test to diagnose MS)
.McDonald criteria
.cerebrospinal fluid CSF analysis (by LP – high IgG) usually reveals a mild pleocytosis (usually less than 50 cells/ML), and total
protein that is mildly elevated (100mg/dL)
-Treatment :
.cortisone
.interferon-B1b and mitoxantrone (decreased frequency of attack)
+Good Prognosis (relapsing-remitting, female, optic neuritis, sensory symptoms-paresthesia, feq attacks, early age of onset-
younger)
+Pad Prognosis (male, progressive, spinal cord-paraplegia, diabetic, old age)
**Parkinson's Disease
-The motor symptoms of Parkinson's Disease result from the death of dopamine-generating cells in the substantia nigra, a
nigra, a region of the midbrain (Basal Ganglia) / Is a degenerative disorder of the central nervous system mainly affecting the
motor system
-Classifications :
1.primary or idiopathic
2.secondary or acquired
3.hereditary parkinsonism, and
4.Parkinson plus syndromes or multiple system degeneration
-Signs & Symptoms :
.movement-related (these include shaking, rigidity, slowness of movement and difficulty with walking and gait)
.later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease,
and depression being the most common psychiatric symptom. Other symptoms include sensory, sleep, and emotional problems
.tremor (pill rolling tremor) (rest tremor) – disappearing with voluntary movement and sleep
.bradykinesia - hypokinesia (Slowness of movement)
.rigidity (hypertonia – is stiffness and resistance to limb movement caused by increased muscle tone)
.lead-pipe rigidity and cogwheel rigidity
.mask-like face expression or small handwriting
.voice disorders (speech and swallowing disturbances)
.rapid shuffling steps and a forward-flexed posture
+Dementia (is late symptom)
-Causes :
.idiopathic
.drugs (neuroleptic agents-haloperidol, chlorpromazine / antiemetics-metoclopramide / alpha methyldopa / reserpine)
.poisoning from MPTP
.carbon monoxide
.cyanide
.structural lesion around the basal ganglia (trauma, tumor, abscess ,infarct)
+Parkinson + syndromes :
.parkinsonism + vertical gaze palsy = supranuclear palsy
.parkinsonism + prominent ataxia = olivopontocerebellar atrophy
.parkinsonism + prominent orthostatic hypotension = shy-Drager syndrome
-Diagnosis :
.medical history and a neurological examination
+Is a clinical one. It is important to identify any secondary causes of a Pts. parkinsonism that are potentially reversible. There is
no diagnostic test of choice that can identify Pts. with parkinson disease
-Treatment :
.dopamin - metabolite (treatment to decreased symptoms) (Monoamine oxidase B – MoaB)
+Upper Motor (hyper-reflexia, hypertonia, rigidity, NO atrophy, clonus, babinski sign +)
+Lower Motor (hyporeflexia, hypotonia-atonia, flaccid, atrophy of muscles, fasciculation, fibrillation)
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**Guillain–Barré syndrome GBS

-Is a rapid-onset muscle weakness caused by the immune system damaging the peripheral nervous system. The end result of
this autoimmune attack on the peripheral nerves is damage to the myelin
+GBS are autoimmune disease (schwann cells)
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+Many experience changes in sensation or develop pain, followed by muscle weakness beginning in the feet and hands and
migrating towards the trunk (Ascending paralysis)
+It can cause life-threatening complications, in particular if the respiratory muscles are affected (M.C.C of death) or if there is
autonomic nervous system involvement
-Signs & Symptoms :
.numbness, tingling, and pain, alone or in combination
.weakness of the legs and arms that affects both sides equally and worsens over time (the weakness can take half a day to over
two weeks)
+The muscles of the neck may also be affected, and about half experience involvement of the cranial nerves which supply the
head and face; this may lead to weakness of the muscles of the face, swallowing difficulties and sometimes weakness of the eye
muscles
.the weakness affects only the legs (paraplegia or paraparesis)
.Involvement of the muscles that control the bladder and anus is unusual
.back pain, painful tingling, muscle pain and pain in the head and neck relating to irritation of the lining of the brain
.symptoms of an infection in the 3–6 weeks prior to the onset of the neurological symptoms. This may consist of upper
respiratory tract infection (rhinitis, sore throat) or diarrhea
+In children, particularly those younger than six years old, the diagnosis can be difficult
.reduced power and reduced or absent tendon reflexes (hypo- or areflexia, respectively)
.weakness of the eye muscles (ophthalmoplegia) is more pronounced and may occur together with abnormalities in
coordination (ataxia)
.Bickerstaff brainstem encephalitis subtype may feature drowsiness, sleepiness, or coma
.respiratory failure
+This life-threatening scenario is complicated by other medical problems such as pneumonia, severe infections, blood clots in
the lungs and bleeding in the digestive tract
.the autonomic or involuntary nervous system (which is involved in the control of body functions such as heart rate and blood
pressure) is affected
-Causes :
.Campylobacter jejuni (M.C antecedent infection)
+Links between other infections and GBS are less certain :
.two other herpesviruses (Epstein–Barr virus/HHV-4 and varicella zoster virus/HHV-3) and the bacterium Mycoplasma
pneumoniae have been associated with GBS
.the tropical viral infection dengue fever has been associated with episodes of GBS
.Previous hepatitis E virus infection has been found to be more common in people with Guillain–Barré syndrome
.Zika virus has been linked to Guillain–Barré syndrome
.Some cases may be triggered by the influenza virus and potentially influenza vaccine. An increased incidence of Guillain–Barré
syndrome followed influenza immunization
-Diagnosis :
.made by nerve conduction studies NCS (BEST) and with studies of the CSF
+NCS and EMG electromyography (may show conduction slowing, conduction block)
+In the CSF (elevated protein level 100-1000mg/dL), without an accompanying increased cell count (albuminocytological
dissociation)
-Treatment :
.plasmapheresis
.administering intravenous immunoglobulins (IVIg)
.intubation - ventilation (needed when there is evidence of failure)
+Good Prognosis (80% of Pts. have a complete recovery within a few months to a year)
+Poor Prognosis (age over 40yrs, history of preceding diarrheal illness, requiring ventilator support, high anti-GM1 titre, poor
upper-limb muscle strength)
**Myasthenia Gravis MG
-Is an autoimmune neuromuscular disease leading to fluctuating muscle weakness and fatigability / young Pt.<40 yrs
+Antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction
+About 10% of MG Pts. are found to have tumors in their thymus glands (thymoma - benign tumor)
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-Signs & Symptoms :

.fatigability
.muscles become progressively weaker during periods of activity and improve after periods of rest
.weakness of the eye muscles (M.C) (ptosis)
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.dysphagia
.dysarthria
.asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision)
.myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation
+Crises may be triggered by (infection, fever, an adverse reaction to medication, or emotional stress)
+Reflexes and Feeling (sensation( are normal
+Since the heart muscle is only regulated by the (autonomic nervous system). It is generally Unaffected by MG
-Diagnosis :
.electromyography EMG (BEST and most sensitive(
.CT (for thymoma)
-Treatment :
.acetylcholinesterase inhibitors (neostigmine and pyridostigmine)
.immunosuppressive drugs (prednisone, cyclosporine, mycophenolate mofetil and azathioprine)
.plasmapheresis or IVIG (for emergency treatment)
.thymectomy (is a surgical method to treat MG)
**Lambert-Eaton Myasthenic Syndrome LEMS

.is a rare autoimmune disorder (muscle weakness of the limbs)
.antibodies (against presynaptic voltage-gated calcium channels in the neuromuscular junction)
.around 60% id those with LEMS have an underlying malignancy (M.C small cell lung cancer)
.can occur at any age, but M.C in Pts. >40 yrs of age
.signs and symptoms (weakness of LEMS involves the legs and arms) – Leg is more in MG, weakness of eye muscles in
Uncommon, dry mouth, constipation, blurred vision, sweating, orthostatic hypotension, in the advanced stages of the disease –
weakness of the respiratory muscles may occur, reflexes are reduced-hyporeflexia, NO fatigability)
.causes (associated with lung cancer, paraneoplastic syndrome)
.diagnosis (EMG)
.treatment (IVIG, chemotherapy, therapy, plasma exchange or plasmapheresis)
+NO response for acetylcholinesterase inhibitor
+MG (young <40yrs, antibody against nicotinic receptor, fatigability, eye muscle commonly affect, reflexes and sensation are
normal, associated with thymoma)
+LEMS (old >40yrs, antibody against Ca+2 channels-presynaptic, NO fatigability, rarely affect eye muscle, hyporeflexia,
associated with small cell lung cancer)
**Dementia
-Is a serious of global cognitive ability in a previously impaired person, beyond what might be expected from normal aging
+Alzheimer's Disease is still the most frequent cause
+Is far more common in the geriatric population, it can occur before the age of 65 yrs, in which case it is termed “early onset
dementia”
+Affected areas of cognition may be memory, attention, language and problem solving
+It is normally required to be present for at least 6 months to be diagnosed
+Delirium can be easily confused with dementia due to similar symptoms
+In Comparison :
.Delirium is characterized by a rapid-sudden onset, fluctuating course, a short duration (often lasting from hrs to wks)
.Dementia is characterized by a slow-gradual onset, NOT fluctuating course, as well as a progressive-longer duration (from
months to yrs) (slow decline of mental functioning)
-Causes :
+Irreversible (90%) / Reversible (10%)
.Alzheimer's Disease (M.C.C)
.vascular dementia
.traumatic brain injury
.strokes
.alcohol dementia (thiamine deficiency Vit B1 – Wernicke's encephalopathy)
.hypothyroidism
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.normal pressure hydrocephalus (ataxia, dementia, urinary incontinence)

.multi-infarct dementia (2nd M.C)
.Creutzfeldt-Jakob disease
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.chronic subdural hematoma

-Diagnosis :
.Mini-mental state examination
**Alzheimer's Disease AD
-It is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. The most common early
symptom is difficulty in remembering recent events (short-term memory loss)
-Signs & Symptoms :
.problems with language
.disorientation (including easily getting lost)
.mood swings
.loss of motivation
.not managing self care
.behavioural issues
-Causes :
.unknown
.amyloid hypothesis postulates that abeta-amyloid (beta A) deposits are the fundamental cause
+Support for this postulate comes from the location of the gene for the amyloid precursor protein APP on chromosome 21
+People with trisomy 21 (Down Syndrome) who have an extra gene copy almost universally exhibit AD by 40yrs of age
-Characteristics :
+Early
.impairment of learning and memory
.older memories of the person`s life are affected to a lesser degree than new facts or memories
+Moderate
.unable to perform most common activities of daily living
.speech difficulties (inability to recall vocabulary)
+Advanced
.completely dependent upon caregivers
.language is reduced to simple phrases or even single words, leading to complete loss of speech
.aggression and psychosis
-Treatment :
.acetylcholinesterase inhibitors (tacrine, rivastigmine, galantamine and donepezil)
+Life expectancy of the population with the disease is reduced / The mean life expectancy following diagnosis is approximately
seven years
+White Matter (myelinated neuron)

+Gray Matter (unmyelinated neuron)
+Cranial Nerves :
.I (olfactory nerve – smell)
.II (optic nerve – vision)
.III (oculomotor nerve – upper eye movement, medial eye movement, meiosis in pubic, upper eyelid)
(if injured – ptosis, mydriasis)
.IV (trochlear nerve – downward, eye movement – down Gaze)
.V (trigeminal nerve – face sensation, masticatory muscle)
.VI (abducens nerve, lateral eye movement) – M.C nerve affected by increased intracranial pressure
.VII (facial nerve – facial expression, taste sensation, salivary gland ‘except parotid’, lacrimal gland)
.VIII (vestibulo ocular nerve (hearing and balance)
.IX (glossopharyngeal nerve – taste for posterior tongue, parotid gland)
.X (vagus nerve)
.XI (spinal accessory nerve – supply sternocleidomastoid muscle + trapezius muscle)
.XII (hypoglossal nerve – tongue movement)
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Infectious Diseases
**Central Nervous System Infections
*Meningitis
-Is inflammation of the protective membranes covering the brain and spinal cord, known collectively as meninges
+The inflammation may be caused by infection with (Viruses – Aseptic) (Bacteria – Septic)
+Most cases of meningitis arise sporadically
-Signs & Symptoms :
.headache
.neck stiffness (increased neck muscle tone)
.fever (sudden)
.confusion or altered consciousness
.photophobia (inability to tolerate light) or phonophobia (loud noises)
.nuchal rigidity (neck stiffness, positive kernig's and brudzinski's signs) – Occurs in 70% of bacterial meningitis in adults
.nausea, vomiting
.altered mental status (is possible as well and can make a Pt. seem like they have encephalitis)
+Small children often exhibit only nonspecific symptoms, such as (irritability, drowsiness, decreased activity and feeding, look
unwell, seizure)
.any form of CNS infection can present with seizures
.focal neurologic deficits (M.C being visual field and cranial nerve deficits)
.the M.C long-term neurologic deficit from bacterial meningitis is damage to the 8th cranial nerve
+If a rash is present, it may indicate a particular cause of meningitis; for instance, meningitis caused by meningococcal bacteria
.rash is associated with several different types of meningitis (A petechial rash is suggestive of neisseria) (A rash on the wrists
and ankles with centripetal spread toward the body is suggestive of RMSF) (Facial nerve palsy is suggestive of lyme disease)
(Pulmonary symptoms or an abnormal CXR suggest TB)
-Causes :
.Streptococcus Pneumoniae is the M.C.C for all Pts. beyond the neonatal period in the past (Haemophilus influenza type B in
countries that do not offer vaccination)
.Neisseria Meningitidis (meningococcus) is spread by respiratory droplets and is the M.C.C of meningitis in adolescents (Older
children)
.Listeria Monocytogenes is more common in those with immune system defects, particulary of the cellular (T-cell) immune
system and sometimes neutrophil defects. These defects include (HIV, steroid use, leukemia, lymphoma and virous
chemotherapeutric agents)
.Staphylococcus Aureus is more common in those who have had any form of neurosurgery (because instrumentation and
damage to the skin introduce the organism into the CNS)
.Cryptococcus is more common in those who are HIV positive and who have profound decreases in their T-cell counts to levels
less than 100 cells
.Group B Streptococci (Streptococcus agalactiae) is the M.C.C of meningitis in the neonatal period (Premature babies and
newborns up to 3 months)
.Tuberculous Meningitis, which is meningitis caused by (Mycobacterium tuberculosis) (Is more common in people from
countries where TB is endemic, but is also encountered in persons with immune problems, such as AIDS)
+Viruses Causing Meningitis Include (enteroviruses, arboviruses ‘St.louis encephalitis virus, West nile virus’, HIV, herpes
simplex and lymphocytic choriomeningitis virus)
+Local Infections That Can Lead To Meningitis Include (otitis media, sinusitis, mastoiditis and dental infections). Hematogenous
spread could possibly occur from any infection but is more common with endocarditis and pneumonia
+Neonates and the elderly have decreased T-cell immune function; therefore, listeria is more common in the very young and
the very old. (however, it is critical to remember that evet with immune deficits, Streptococcus pneumoniae is still the M.C.C-it
is just that listeria is more common in these Pts, as compared to fully immunocompetent Pts.)
-Complications :
.sepsis
.low or abnormally low temperature (Hypothermia <35)
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.rapid breathing
.falling blood pressure
.fast heart rate
.DiC
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.hemorrhage of the adrenal glands (leading to Waterhouse-Friderichsen Syndrome) (Meningococcal)

.seizures
.abnormalities of the cranial nerves
.visual symptoms and hearing loss (To reduce complications of neurological disorders – Dexamethasone)
-Diagnosis :
.lumbar puncture is essential for establishing the diagnosis (CSF)
.CT scan of the head is the best initial diagnostic test if the Pt. has papilledema, focal motor deficits, new onset seizures, or
severe abnormalities in mental status, or is immunocompromised (HIV infection, immunosuppressive medications, post-
transplantation)
+CSF Findings In Different Forms Of Meningitis :
.Bacteria (Glucose – low / Protein – high / Cells – high PMN >300) (High pressure) (WBC – neutrophil)
.Virus (Glucose – normal / Protein – normal or high / Cells – mononuclear <300) (Normal pressure) (WBC – lymphocyte)
.Tuberculous (Glucose – low / Protein – high / Cells – mononuclear and PMN <300)
.Fungal (Glucose – low / Protein – high / Cells - <300)
.Malignant (Glucose – low / Protein – high / Cells – usually mononuclear)
+Gram staining of the sample may demonstrate bacteria in bacterial meningitis, but absence of bacteria does not exclude
bacterial meningitis as they are only seen in 60% of cases
+If non of the above is present, a lumber puncture can be safely done without doing a CT scan of the head first
+If the lumber puncture is delayed more than 20-30 mins for any reason, then the best initial step is to give as empiric dose of
antibiotics
+The most accurate test for bacterial meningitis on the lumber puncture is the culture of the CSF
+Pneumococcal – Contagious / Meningococcal – NOT
+Specific Diagnosis Of Non-bacterial Meningitis (is based on the nature of the organism) :
.lyme disease and RMSF are best detected with a specific immunological response and cytology
.cryptococcus neoformans is detected initially with an india ink test and then later with an elevation in the serum and CSF
cryptococcal antigen titer
.syphilis is confirmed by the presence of a positive VDRL or FTA on CSF
.TB is rarely detected by AFB smear
.culture for TB has a much higher yield, PCR can also aid in the diagnosis of TB
-Treatment :
.bacterial meningitis in adults is best achieved with (vancomycin)
+Vancomycin is used if you have definite or suspected pneumococcal resistance to penicillin or if there is a chance of
staphylococcal infection after neurosurgery
.ampicillin is added to those with immune defects to cover listeria and for Pts. over 50 yrs of age or <1 months old
.lyme disease is best treated with ceftriaxone
.cryptococcosis is treated with amphotericin
+Prophylactic (rifampin, ciprofloxacin or ceftriaxone)
+The M.C route of infection of most types of meningitis is the blood stream
+Post Traumatic Meningitis :
.Occurs within 2 weeks in most of the cases
.Most of the cases are associated with base skull fracture
.Antibiotics is the main line of treatment
.CSF fistula should be treated if present
.The most common organism in post traumatic meningitis is Pneumococcal
+A 15 months old child developed hydrocephalus following meningitis. The most likely causative organism is H.influenza
+The most common organism causing meningitis in toddlers (6 months - 3 years) is Haemophilus influenzae type B
+Incubation period meningococcal meningitis is usually 2-3 days
+Refusal of feeding is the earliest sign in a newborn with sepsis and meningitis
+Infection (meningococcal meningitis) is transmitted by droplet
+Indications For Lumbar Puncture :
.Diagnosis of meningitis
.Diagnosis of multiple sclerosis
.Benign intracranial hypertension
.Intrathecal injection of drugs
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*Encephalitis
-Is an infection of the brain. This includes both the meninges, as well as the brain parenchyma
-Signs & Symptoms :
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.fever and headache occur (nonspecific)

.altered mental status with fever and headache is the primary clue to the diagnosis
.any level of neurologic deficit may occur, ranging from slight confusion to lethargy or coma
.focal deficits of any kind can occur
.neck stiffness similar to that found in meningitis can occur (making it difficult to distinguish encephalitis from meningitis)
.seizures
-Causes :
.any bacterial, protozoal or rickettsial infection (the majority is caused by viruses)
.any virus can cause encephalitis, the M.C.C is herpes simplex, usually type-1 (HSV-1)
.varicella-zoster virus, CMV, enterocolitis, eastern and western equine encephalitis, ST.louis encephalitis, and west nile
encephalitis can also occur but are much less common than HSV
-Diagnosis :
.CT or MRI scan of the head should be performed
.for HSV (LP + PCR)
-Treatment :
.HSV encephalitis is best treated with intravenous acyclovir (famciclovir and valacyclovir have activity against HSV, they are not
available intravenously) (ganciclovir or foscarnet are active against CMV)
*Brain Abscess
-A collection of infected material within the brain parenchyma
-Signs & Symptoms :
.headache is the M.C symptom
.fever can be present
.focal neurologic deficits are the initial complaint in about 60% of Pts
.seizures may occur (as with any form of anatomic abnormality of the CNS) (all CNS infections can cause seizures)
-Causes :
.bacteria can spread into the brain from contiguous infections such as (otitis media, sinusitis, mastoiditis or dental infections)
.organisms may also spread through the bloodstream from endocarditis or pneumonia and seed the brain
.toxoplasmosis (can reactive in those with severe HIV disease when their CD4 counts are very low <50-100/mL)
.brain abscesses most commonly have (Streptococcus in 60-70%, bacteroides in 20-40%, enterobacteriaceae in 25-35% and
staphylococcus in 10% and are often polymicrobial)
-Diagnosis :
.the initial test is the CT scan
.MRI is even more accurate than is the CT scan
.no radiologic test alone can give the precise etiology (in the case of bacterial brain abscess, examination of the abscess fluid-
obtained by stereotactic aspiration or surgical excision of the abscess) for gram stain and culture is essential
.in HIV-positive Pts., 90% of brain lesions will be either toxoplasmosis or lymphoma
**Head and Neck Infections

*Otitis Media OM
-An infection of the middle ear between the eustachian tube and the tympanic membrane
-Signs & Symptoms :
.ear pain, fever and decreased hearing
.on physical examination you`ll find a red, bulging tympanic membrane with loss of the light reflex
.the most sensitive clinical finding is immobility of the membrane on insufflation of the ear with ear
.perforation of the tympanic membrane with diarrhea occurs rarely
-Causes :
.viral upper respiratory infection can cause edema of the eustachian tube, which often leads to middle ear infection
.M.C organisms are streptococcus pneumoniae, H.influenzae and moraxella catarrhalis
+This is roughly the same breakdown of organism type and frequency that occurs in bronchitis and sinusitis
-Diagnosis :
.physical examination of the ear is the chief means of establishing the diagnosis
.radiologic tests are not useful
.a specific bacteriological diagnosis can be obtained with tympanocentesis for culture, but this is rarely performed
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-Treatment :
.oral therapy with amoxicillin is still the best initial therapy
.amoxicillin-clavulanate is used if there has been recent amoxicillin use or if the Pt. does not respond to amoxicillin
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*Sinusitis
-An infection of the sinuses. The M.C site is the maxillary sinus, followed by ethmoid, frontal and sphenoid sinuses
-Signs & Symptoms :
.facial pain
.headache (is common and is worse when the Pt leans forward)
.postnasal drainage
.purulent nasal drainage
.fever
.tooth pain
-Causes :
.viruses are responsible for a large number of cases
.bacterial organisms cause disease with the same frequency as in otitis media described above
-Diagnosis :
.do not always need radiologic confirmation prior to treatment
.sinus x-ray are of little value, and routine imagine as a rule is not recommended
.CT scan of the sinuses is the test of choice
.sinus puncture is necessary to confirm a specific bacteriologic etiology
-Treatment :
.decongestants, such as (oral pseudoephedrine or oxymetazoline sprays) (for mild or acute uncomplicated sinusitis)
.antibiotics (for severe pain with discolored nasal discharge)
+Most cases of viral rhinosinusitis resolve in 7-10 days with asymptomatic management (antihistamines, NSAIDs and
decongestants)
*Pharyngitis
-The majority of pharyngeal infections are from viruses, the most important cause is from group A beta-hemolytic
streptococcus (S.pyogenes)
-Signs & Symptoms :
.sore throat with cervical adenopathy
.inflammation of the pharynx with an exudative covering is highly suggestive of S.pyogenes (Most viruses do not give an
exudate, although the Epstein-Barr virus can / Mild S.pyogenes infections may not give an exudate)
.hoarseness and cough are not suggestive of pharyngitis
-Diagnosis :
.rapid streptococcal antigen test are 60-100% sensitive but are >95% SPECIFIC
-Treatment :
.penicillin
*Influenza
-A systemic viral illness from influenza A or B, usually occurring in an epidemic pattern and transmitted by droplet nuclei
+Influenza can lead to damage to the respiratory epithelium, leading to sinusitis, otitis media, bronchitis and pneumonia
-Signs & Symptoms :
.fever
.myalgias
.headache and fatigue
.upper respiratory symptoms tend to predominate
.runny nose (coryza)
.nonproductive cough
.sore throat
.conjunctival injection
-Diagnosis :
.rapid antigen swabs or washings of nasopharyngeal secretions
.viral culture is the most accurate test but is usually not available rapidly enough to make it useful in acute Pt management
-Treatment :
.symptomatic therapy with acetaminophen and antitussives is useful
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.specific anti-viral medications for both influenza A and B are the (neuraminidase inhibitors oseltamivir and zanamivir) – they
should be used within 48hrs of the onset of symptoms to limit the duration of symptoms
+Influenza vaccine is contraindicated in those who are highly allergic to eggs and which would result in anaphylaxis
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**Gastrointestinal Infections
*Infectious Diarrhea/Food Poisoning
-Diarrhea (is the condition of having three or more loose or liquid bowel movements per day)
+Diarrhea is most commonly due to viral gastroenteritis with rotavirus, which accounts for 40% of cases in children under five
-Most infectious is caused by contaminated food and water, so the overlap between food poisoning and infectious diarrhea is
considerable
+There are several types of food poisoning, such as with Bacillus cereus or Staphylococcus aureus, that present predominantly
with vomiting, so the tow are not entirely synonymous
+Complications Of Diarrhea :
.dehydration
.acidosis (normal anion gap)
.electrolyte disturbances (decreased K+, increased Na+, decreased Cl-)
.hemoconcentration (increases hematocrit)
+Types Of Diarrhea :
1.Secretory (M.C.C of this type of diarrhea is a cholera toxin – that stimulates the secretion of anions, especially chloride ions)
2.Osmotic (can be the result of maldigestion – pancreatic disease or celiac disease) (it can be caused by osmotic laxatives)
(lactose intolerance – lactase deficiency)
3.Exudative (occurs with the presence of blood and pus in the stool)
4.Motility-related (is caused by the rapid movement of food through the intestinal – hypermotility) (diabetic neuropathy,
hyperthyroidism, increased peristalsis)
-Signs & Symptoms :
.the single most important feature of any person presenting with possible food poisoning is the presence or absence of blood in
the stool
.blood is most commonly associated with invasive enteric pathogens, such as (Salmonella, Shigella, Yersinia, invasive E.coli and
Campylobacter)
.ingestion of ciguatera toxin causes symptoms within 2-6 hrs, which includes (paresthesias, numbness, nausea, vomiting and
abdominal cramps). In severe cases they can be neurologic (weakness, reversal of hot-cold sensations), and cardiovascular
(hypotension) can develop
.Bacillus cereus and Staphylococcus predominantly present with vomiting 1-6hrs of their ingestion because they contain a
preformed toxin. They can give diarrhea later
.Giardia, Cryptosporidium, Cyclospora and most other protozoans do not give bloody diarrhea (the major protozoan associated
with blood in the stool is Entamoeba histolytica)
.Viruses can give voluminous watery diarrhea but do not result in bloody diarrhea
-Causes :
.Campylobacter (M.C)
.Salmonella (associated with contaminated poultry and eggs)
.E.coli (M.C.C of travelers` diarrhea)
.E.coli 0157:H7 (associated with eating under-cooked hamburger meat and with hemolytic uremic syndrome HUS)
.Shigella (associated with hemolytic uremic syndrome HUS)
.Bacillus cereus (associated with fried rice)
.Giardia lamblia and Cryptosporidiosis (are acquired from contaminated water sources that have not been appropriately
filtered, such as that ingested from fresh water on a camping trip)
.Cryptosporidiosis (associated with HIV, particularly when there is profound immunosuppression and the CD4 count has
dropped below 50 cells)
.V.parahaemolyticus (associated with contaminated shellfish, such as clams, oysters and mussels)
.V.vulnificus (from ingestion of raw shellfish) causes severe disease in those who have underlying liver disease. Is also
(associated with iron overload and the development of bullous skin lesions)
.viral infectious such as with rotavirus or Norwalk agents are most commonly (associated with outbreaks in children
.C.difficile (associated with previous antibiotic use)
.C.botulinum (associated with ingestion of infected canned foods)
.C.perfringens with meats that have been contaminated with spores by being unrefrigerated
.Campylobacter (rarely associated with Guillain-Baree Syndrome)
149
-Treatment :
.intravenous fluids and oral antibiotics (fluoroquinolone such as ciprofloxacin)
.Campylobacter (erythromycin)
.Giardia (metronidazole)
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.Cryptosporidium (control of the underlying HIV disease with antiretrovirals)

.Scombroid (antihistamines such as diphenhydramine)
*Gastroenteritis
-Viruses (rotavirus) and the bacteria (E.coli, Campylobacter) are the primary causes of gastroenteritis
+Rotavirus is the M.C.C of gastroenteritis in children's (VIRAL)
+Campylobacter jejuni is the M.C.C of gastroenteritis in adults (BACTERIAL)
+E.coli, Salmonella, Shigella, Campylobacter are the M.C types can cause gastroenteritis in children's (BACTERIAL)
+Toxigenic Clostridium Difficile is an important cause of diarrhea (associated with antibiotic use) (treated by vancomycin)
+Enterotoxigenic Escherichia coli (is most commonly isolated pathogen – Traveler's diarrhea) (Traveler's diarrhea is NOT bloody
diarrhea)
+Giardia lamblia, Entamoeba histolytica (treated by metronidazole) and (Cryptosporidium-M.C.C for diarrhea in AIDS Pts.)
(PARASITIC)
+Bloody Diarrhea (E.coli, Shigella, Salmonella, Campylobacter, ameba)
+Clostridium botulinum (associated with canned food) (appear 18-24hrs / after 24hrs)
+Clostridium perfringens (appear 18-24hrs / after 24hrs))
+Staphylococcus aureus (M.C.C for food poisoning) (appear 1-6hrs / after 24hrs)
+Bacillus cereus (associated with rice) (appear 1-6hrs / after 24hrs)
+Treatment (Antimotility agents - are drugs used to alleviate the symptoms of diarrhea) (loperamide) (loperamide is not
recommended in children or bloody diarrhea) / (Antiemetic - is a drug that is effective against vomiting and nausea)
(Ondansetron-zofran) (Metoclopramide-clopram, plasil)
+Food poisoning :
.Salmonella food poisoning is common
.Incubation period of salmonella food poisoning is 12-48 hours
.Incubation period of staphylococcal food poisoning is 1-8 hours
.Amanita poisoning is a type of mushroom poisoning
+Cause Food Poisoning By Causing Gastrointestinal Tract Infection :
.Salmonella
.Staphylococcus
.Vibrio parahaemolyticus
.Fungus
+Cause Food Poisoning By Producing Toxin :
.Staphylococcus
.Clostridium perfringens
.Clostridium botulinum
.Bacillus cereus
+Feature Of Staphylococcal Food Poisoning :
.Abdominal cramps
.Hypotension
.Vomiting
.Diarrhea
+Staphylococcal food Poisoning :
.Contaminated meats and confectionery constitute the most outbreak
.Vomiting and severe abdominal cramps are prominent symptoms
.The acute symptoms usually subside within 12 hours
.Majority of patients require no specific treatment
.Short incubation period
.It is a common source-type of epidemic
.Symptoms are usually of short duration
.The diseases is usually brief and only requires rest and sedation
+The incubation period of a food born salmonella outbreak is 1 day
+The characteristic incubation period for staphylococcus aureus food poisoning is 1-6hrs
+The incubation period of a food poisoning by chemical poisons is usually less than 1 hr
+Coliform organisms are used for routine testing of water
+Causes Of Invasive Diarrhea :
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.Salmonella
.Campylobacter
.Shigella
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.Amebiasis
++Common Drugs
+Vancomycin is the best treatment for pseudomembranous colitis (associated with antibiotics use)
+Erythromycin is bacteriostatic antibiotic
+Cefepime is active against pseudomonas infection
+Infections with Giardia lamblia are best treated with Metronidazole
+Penicillin the drug of choice for a child with pneumococcal pneumonia
+Antiviral Drugs :
.Acyclovir
.Vidarabine
.Ganciclovir
.Interferon
.Zidovudine
*Viral Hepatitis (Acute Viral Hepatic Infections)

-Viral hepatitis is an infection of the liver caused by one of the viruses hepatitis A, B, C, D or E
-Signs & Symptoms :
.jaundice
.dark urine
.light-colored stool
.fatigue
.malaise
.weight loss
.tender liver
.you cannot distinguish the precise viral etiology of the hepatitis by initial presentation alone
.hepatitis B and C can also give symptoms similar to serum sickness, such as (joint pain, rash, vasculitis and glomerulonephritis,
hey also lead to cryoglobulinemia)
.hepatitis B has been associated with the development of polyarteritis nodosa PAN
.hepatitis E has been associated with a more severe presentation in pregnant women
-Causes :
.hepatitis A and E are transmitted by contaminated food and water, and have an asymptomatic incubation period for several
weeks, and do not lead to either cirrhosis or hepatocellular carcinoma
.hepatitis B, C and D are transmitted by the parenteral route
.all forma of hepatitis can occasionally present with fulminant hepatic necrosis and acute liver failure
-Diagnosis :
.elevated total and direct bilirubin level
.elevation of both the ALT and AST (ALT greater than AST)
.the AST is usually more elevated with drug-and alcohol induced hepatitis
.the alkaline phosphatase and GGT are less often elevated
.the prothrombin time and albumin levels will be abnormal
.hepatitis A, C, D and E are diagnosis as acute by the presence of the IgM antibody to each of these specific viruses
.IgG antibody to hepatitis A, C, D and E indicates old, resolved disease
.hepatitis C activity can be followed with a PCR-RNA viral load level
.hepatitis B (HbsAg, HbeAg, IgM antibody)
+Hepatitis A (incubation period 2-6 weeks) (virus RNA) (onset - abrupt) (transmession - fecal/oral)
+Hepatitis B (4-26 weeks) (DNA) (insidious) (sexual > parenteral)
+Hepatitis C (2-20 weeks) (RNA) (insidious) (parenteral > sexual)
+Hepatitis D (4-8 weeks) (RNA) (abrupt) (parenteral, sexual)
+Hepatitis E (-) (RNA) (-) (fecal-oral)
+All Hepatitis virus are RNA, except HBV (hepatitis B) are DNA
+Incubation (A 2-4wks) (B 4-20) (C 2-26) (D 6-9) (E 3-8)
+Transmission (A-oral, saliva) (B-blood, sexual, vertical, saliva, via mother to child by breast feeding) (C-blood, saliva) (D-like
B) (E-oral)
+Vaccine (A-yes) (B-yes) (C-no) (D-prevented by) (E-no)
151
+Viral Hepatitis :
.Hepatitis B is transmitted by feco-oral route
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.Vaccination is available for hepatitis C

.Hepatitis D is a DNA virus
.Interferon treatment is required for hepatitis E
.Hepatitis B are not DNA viruses
.Hepatitis B vaccine is given in 2 doses
.Vaccine is protective for maximum 10yrs after administration
.Vaccine offers also partial protection against hepatitis C infection
.Vaccine should not be used in children younger than 10yrs of age
.The incubation period of infectious hepatitis is over 15 days
.Hepatitis A is the commonest
.All viruses are RNA except hepatitis B is DNA
.Hepatitis A and E don't produce chronic illness
.Hepatitis C is responsible for most chronic cases
.The greatest risk for infection transmitted by blood transfusion is present in one of the Hepatitis C
+Hepatitis A :
.Infectious before the appearance of jaundice
.Transmitted by feco-oral route
.Cause marked elevation on the liver enzymes
.The disease gives long life immunity
.Infectivity is high before the appearance of jaundice
.The vaccine is available after the age of one year
.In small children most cases are anicteric
.May present an anicteric in some cases less than 5yrs of age
.No specific treatment needed in most cases (prognosis is usually good)
+Hepatitis B :
.May be transmitted sexually
.Can cause chronic active hepatitis
.Hepatoma is recognized complication
.Vaccination is available
.Caused by DNA virus
.Produces chronic hepatitis in 5-10% of cases
.Infection has longer incubation period than hepatitis A
.Infection can be prevented by the use of vaccine
.May be transmitted sexually
.Hepatoma is recognized complication
.Vaccination is available
+Causes Of Chronic Hepatitis :
.Hepatitis B
.Hepatitis C
.Methyldopa
.Alpha-1-antitrypsin deficiency
+In Hepatocellular Carcinoma :
.It may lead to cirrhosis
.It leads to increased alfa feto protein
.It may cause fever
.It can be associated with polycythemia
**Genital Infections And Sexually Transmitted Infections (STIs)
*Syphilis
A systemic contagious disease caused by a spirochete; characterized by periods of active manifestations and by periods of
symptomless latency
-Signs & Symptoms :
1.Congenital
152
.early (symptomatic seen in infants up to two years)

.late (symptomatic, hutchinson teeth, scars of interstitial keratitis, bony abnormalities - saber shins)
2.Acquired
.early infectious syphilis (primary stage – chancre that appears within the 3rd week and disappears within 10-90 days.
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Lymphadenopathy is painless, rubbery, discrete and nontender to palpation. Primary chancres are usually found on the penis,
anus, rectum in men, and vulva, cervix, and perineum in women (may be found in other places such as lips, tongue, ect.)
(secondary stage – cutaneous rashes appear 6-12 weeks after infection, usually found symmetrically and more marked on the
flexor and volar surfaces of the body-pinkesh or pale red in white persons, pigmented spots, copper-colored macules in blacks /
lymphadenopathy, papules and alopecia can be seen)
.latent stage (may persist for life, and one-third of Pts. develop late or tertiary syphilis)
.late or tertiary syphilis (most commonly neurologic)
-Causes :
.Treponema pallidum
-Diagnosis :
.screening tests are the VDRL and RPR
.specific tests are the FTA-ABS, MHA-TP and dark field exam of chancre
-Treatment :
.penicillin (drug of choice for all stages of syphilis)
+A reaction called Jarisch-Herxheimer (general malaise, fever, headache, sweating rigors, and temporary exacerbations of the
syphilitic lesions 6-12hrs after initial treatment)
*Chancroid
-An acute, localized, contagious disease characterized by painful genital ulcers and suppuration of the inguinal lymph nodes
-Signs & Symptoms :
.small, soft, painful pimples that become shallow ulcers with ragged edges
.inguinal lymph nodes become very tender and enlarged
-Causes :
.Haemophilus ducreyi (Gram-negative bacilli)
-Diagnosis :
.made on clinical findings usually Gram stain initially with culture to confirm
.PCR testing is useful
-Treatment :
.azithromycin (single dose)
.ceftriaxone intramuscularly (single dose)
.erythromycin for 7 days or cipro for 3 days are alternative
*Genital Herpes
-Herpes virus, type 2, although type 1 can be seen in genital herpes
-Clinical Presentaion :
.vesicles develop on the skin or mucous membranes; they become eroded and painful and present with circular ulcer with a red
areola
.itching and soreness usually precede them
.the ulcer are scarring; there can be inguinal lymphadenopathy
.lesions are commonly seen in the penis in males and on the labia, clitoris, perineum, vagina and cervix in females
-Diagnosis :
.tzanck test and culture
-Treatment :
.acyclovir, famciclovir or valacyclovir
*Genital Warts
-Also known as condylomata acuminata or venereal warts
-Signs & Symptoms :
.commonly found on warm, moist surfaces in the genital areas
.they appear as soft, moist, minute, pink or red swelling that grow rapidly and become pedunculated, their cauliflower
appearance makes them unique in appearance
-Causes :
.papilloma virus
-Diagnosis :
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.clinical appearance
+Differentiation must be made between flat warts and condylomata lata of secondary syphilis
-Treatmetn :
.destruction (curettage, sclerotherapy, trichloroacetic acid)
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.cryotherapy
.podophyllin
.imiquimod (an immune stimulant)
.laser removal
**Urinary Tract Infections

*Cystitis
-Infection of the urinary bladder (F > M)
-Signs & Symptoms :
.dysuria, frequency, urgency and suprapubic pain are common
.hematuria, low-grade fever; foul-smelling and cloudy urine are less common
.on exam, suprapubic tenderness but no flank tenderness
-Causes :
.the same as for pyelonephritis
.any cause of urinary stasis or any foreign body predisposes
.tumors/stones/strictures/prostatic hypertrophy/neurogenic bladder
.sexual intercourse in women (honeymoon cystitis)
.catheters are a major cause, and the risk is directly related to the length of catheterization
.microbiology (E.coli M.C.C / Gram-negative bacilli such as, proteus, klebsiella, enterobacter, ect.) (enterococci occasionally, and
staphylococcus saprophyticus in young women)
-Diagnosis :
.best initial test is urinalysis for WBCs, RBCs, protein and bacteria; WBCs is the most important
.nitrites are indicative of Gram-negative infection
.a count of <5 WBCs is normal
.urine culture with >100,000 colonies of bacteria per mL of urine confirmatory but not always necessary with characteristic
symptoms and a positive urinalysis
-Treatment :
.for uncomplicated cystitis, 3 days of trimethoprim / sulfamethoxazole or any quinolone is adequate
.seven days of therapy for cystitis in diabetes
.quinolones should not be used in pregnancy
*Acute Bacterial Pyelonephritis

-An acute patchy, most often unilateral, pyogenic infection of the kidney
-Signs & Symptoms :
.chills
.fever
.flank pain
.nausea
.vomiting
.costovertebral angle tenderness
.increased frequency in urination
.dysuria
-Causes :
.infections usually occurs by ascension after entering the urethral meatus
.predisposing factors : obstruction due to strictures, tumors, calculi, prostatic hypertrophy or neurogenic bladder,
vesicoureteral reflux
.more common in women, in childhood, during pregnancy or after urethral catheterization or instrumentation
.E.coli is the most common pathogen, others include (klebsiella, proteus and enterococcus)
+Pts. who are immunosuppressed and subjected to indwelling catheters are more prone to candida
-Treatment (anof the antibiotics for Gram-negativie bacilli are effective) :
.antibiotics for 10-14 days (fluoroquinolone), or
.TMP/SMZ, or
.ampicillin and gentamicin, or
.third-generation cephalosporin
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**Skin Infections
*Impetigo
-A superficial, pustular skin infection seen mainly in children (ecthyma is an ulcerative form of impetigo), with oozing, crusting
and draining of the lesions
-Signs & Symptoms :
.more common on arms, legs and face
.may follow trauma to skin
.begins as maculopapular and rapidly progresses too vesicular pustular lesions or bullae
.the crusts are described as having a golden or yellow appearance and if untreated can progress to lymphangitis, furunculosis or
cellulitis and acute glomerulonephritis (due to gas)
-Causes :
.group A beta-hemolytic Streptococcus
.S.aureus (bullous impetigo)
-Treatment :
.oral first-generation cephalosporin or semisynthetic penicillin, oxacillin, cloxacillin, dicloxacillin (for severe or widespread
cases)
.topical mupirocin or bacitracin for mild cases
.penicillin-allergic Pts can be treated with macrolides such as clarithromycin or azithromycin
*Candidiasis
*Scabies
**Bone And Joint Infections

*Osteomyelitis
-Infection of any portion of the bone including marrow, cortex and periosteum
-Signs & Symptoms :
.pain
.erythema
.swelling
.tenderness over the infected bone
.with vascular insufficiency, there is often an obvious overlying or nearly ulceration or wound
.draining sinus tract is present
-Causes :
+Acute Hematogenous :
.occurs mostly in children in the long bones of the lower extremities and is secondary to a single organism 95% of the time
.the M.C organism is Staphylococcus aureus
.the most commonly involved bones are the tibia and femur and the location is usually metaphyseal due to the anatomy of the
blood vessels and endothelial lining at the metaphysis
+Secondary To Contiguous Infection :
.this can occur in anyone with recent trauma to an area or placement of prosthetic joint
.this is secondary to a single organism most of the time
.S.aureus is the M.C organism
+Vascular Insufficiency :
.majority is over the age of 50yrs, with diabetes or peripheral vascular disease, resulting in repeated minor trauma, which is not
noticed because of neuropathy and decreased sensation
.it is M.C in small bones of the lower extremities
.the single M.C organism is still S.aureus
-Diagnosis :
.the earliest tests to detect osteomyelitis are the technetium bone scan and the MRI (but the MRI can allow better
differentiation between the overlying soft-tissue infection and bone)
.x-ray (usually the initial test because it is more easily)
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.erythrocyte sedimentation rate ESR (nonspecific – it is useful to follow during treatment)

.CT scan, indium and gallium (all three can be normal in osteomyelitis, but none are as specific or sensitive)
-Treatment :
.acute hematogenous osteomyelitis in children can usually be treated with antibiotics alone
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.in adults (combination of surgical – wound drainage and debridement, removal of infected hardware) and antibiotic therapy
(treatment for 6-12 weeks)
.chronic osteomyelitis must be treated for as long as 12 weeks of antibiotics therapy, and in some cases, even longer periods of
antibiotics may be required
*Septic Arthritis
-Infection of a joint due to virtually any agent. The M.C etiology is bacteria (Neisseria gonorrhoeae, Staphylococci or
Streptococci) but (Rickettsia, Viruses, Spirochetes, ect. May also cause it). Generally, bacterial arthritis is divided into
Gonococcal and Non-Gonococcal types
-Pathogenesis :
.sexual activity is the only significant risk factor for gonococcal septic arthritis. Nongonococcal bacterial arthritis is usually
spread by the hematogenous route. Additional routes may include bites (animal or human), direct inoculation of bacteria into
the joint through surgery or trauma, or spread infection from surrounding structures such as bone
.even though both normal or damaged joints can get infected, any previous damage to a joint, such asa from rheumatoid
arthritis or osteoarthritis, previous surgery, prosthesis placement, gout, sickle cell disease, or the presence of certain risk
factors such as intravenous drug abuse, DM or HIV infection can predispose a joint to infection (any cause of bacteremia can
seed the joint because the synovium does not have a basement membrane)
-Presentation :
.Non-Gonococcal (monoarticular in >85%, with a swollen, tender, erythematous joint with a decreased range of motion. Knee is
the M.C. Skin manifestations are rare)
.Gonococcal (polyarticular in 50%; a tenosynovitis is much more common. Effusions are less common. Migratory polyarthralgia
are common. Skin manifestation with petechiae or purpura are common)
-Diagnosis :
.Non-Gonococcal (culture of joint aspirate fluid is positive in 90-95% and gram stain is positive in 40-70%. The cell count of the
synovial fluid is high >500.000 and is predominantly PMNs with a low glucose. Blood culture is positive in 50%)
.Gonococcal (much harder to culture. Only 50% aspirates have positive synovial fluid culture. Less than 10% of blood cultures
are positive. Other sites such as cervix, pharynx, rectum and urethra may also be positive. In the aggregate, culture of the other
sites has a greater yield than culturing the joint itself)
-Treatment :
.Non-Gonococcal (nafcillin or oxacillin vs vancomycin if MRSA is suspected)
.Gonococcal (ceftriaxone is the drug of choice)
*Gas Gangrene (Clostridial Myonecrosis)

-Tha necrotizing destruction of muscle by gas-producing organisms, associated with signs of sepsis / is uncommon
-Signs & Symptoms :
.<1-4 days of incubation after the wound and incubation pain, swelling and edema at the site of the wound
.hypotension, tachycardia and fever can occur
.crepitation over the site and renal failure are late developments, usually prior to death
-Causes :
.the spread of infection from wounds contaminated by (Clostridium perfringens)
**Carditis
*Infective Endocarditis
-Colonization of heart valves with microbial organisms causing friable infected vegetations and valve injury / Bacterial
endocarditis produces large vegetations and may affect any value in the heart, although left-sided lesions of the aortic and
mitral valves are common
-Signs & Symptoms :
.chills, sweats, fever, dyspnea, cough, stroke, skin lesions, nausea and vomiting, chest pain, malaise
.heart murmur or changing murmur
.splenomegaly
.septic complications
.mycotic aneurysm
156
.glomerulonephritis
.digital clubbing
.retinal lesions
.petechiae (streptococcus, staphylococcus)
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.splinter hemorrhages (streptococcus, staphylococcus)

.osler`s nodes (streptococcus)
.janeway lesions (staphylococcus)
.roth`s spots (streptococcus)
-Cuases :
.dental procedures that cause bleeding
.oral and upper respiratory tract surgery
.certain gastrointestinal procedures
.genitourinary surgery
.prosthetic heart valves
.virtually any valvular heart disease
.alimentation catheters in the right heart
.intravenous drug use
+Acute Infective Endocarditis
.caused by bacteremia
.S.aureus is the M.C.C of acute endocarditis
.produces large, bulky vegetations (2mm to 2cm) on the atrial side
.IV drug use the major risk factor
.rapid onset with fever and sometimes sepsis
.splenomegaly
.associated with invasion of myocardium (abscess cavities) and rapid valve destruction
+Subacute Infective Endocarditis
.4-5% have negative blood cultures
.risk factors (ventricular septal defect with shount/stenosis of any valve/prosthetic valves/indwelling catheters/bicuspid aortic
valve/mitral valve prolapse/marfan syndrome)
-Complications Of Infective Endocarditis :
.congestive heart failure (M.C.C of death)
.septic embolization (related to infarctions and metastatic infections); brain (mycotic aneurysm); spleen (greater with
subacute); kidneys; coronary arteries
.glomerulonephritis with nephrotic syndrome or renal failure (immune complex)
-Diagnosis :
.the major criteria for the diagnosis of endocarditis are a combination of positive blood cultures and an abnormal echo
.the minor criteria (fever, intravenous drug use, vascular phenomena, immunologic phenomena, microbiological evidence)
*Pericarditis
-Infection of inflammation of the pericardium
-Signs & Symptoms :
.sharp, pleuritic, retro-sternal (under the sternum) or Lt. precordial (Lt. chest pain)
.Pain is worse in the supine position or upon inspiration
.friction rub (auscultated on the cardiovascular examination usually on the lower Lt. sternal border)
.low-grade fever may also be present
.with tamponade (pulsus paradoxus)
-Causes :
+Pericarditis may be caused by (Viral, bacterial or fungal infection)
.M.C viral (Coxsackie-virus)
.M.C bacterail (Pneumococcus or tuberculous pericarditis)
+Others :
.idiopathic are probably viral
.immunologic conditions (SLE, RF) (SLE more in women)
.MI (Dressler's Syndrome) (2-6wks of MI)
.trauma to the heart
.uremia (uremic pericarditis) (treatment – dialysis)
.malignancy (as a paraneoplastic phenomenon)
.as side effect of some medications (isoniazid, cyclosporine, hydralazine, warfarin, heparin)
.radiation induced
157
.aortic dissection
.tetracyclines
.postpericardiotomy syndrome (usually after CABG surgery)
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-Diagnosis :
.ECG (diffuse ST segment elevation. The ST elevation progresses to T-wave inversion)
+Echo (may be normal in viral)
-Treatment :
.for viral or idiopathic pericarditis (inti-inflammatory medication like indomethacin, ibuprofen or naprosyn) (NSAIDs-aspirin)
*Myocarditis (Inflammatory Cardiomyopathy)

-Is inflammation of heart muscle
+It can cause a mild disease without any symptoms that resolves itself, or it may cause chest pain, heart failure, or sudden
death
+Good Prognosis (heart failure, even with a dilated left ventricle, acute myocardial infarction-like syndrome with normal
coronary arteries)
+Poor Prognosis (ventricular arrhythmias and high-degree heart block)
+Myocarditis is most often due to infection by common viruses, such as parvovirus B19, less commonly nonviral pathogens such
as Borrelia burgdorferi (Lyme disease) or Trypanosoma cruzi, or as a hypersensitivity response to drugs. Myocarditis can
sometimes be an autoimmune disease.
-Signs & Symptoms :
.dyspnea and fatigue (M.C)
.Pts may have a completely asymptomatic, subclinical infection or a rapid progression to chest pain, arrhythmia and death
.physical exam may be normal or may show on S3 gallop and murmurs
-Causes :
+Infections
.Viral (adenovirus, parvovirus B19, coxsackie virus, HIV, enterovirus, rubella virus, polio virus, cytomegalovirus, human
herpesvirus 6 and possibly hepatitis C)
.Protozoan (Trypanosoma cruzi causing Chagas disease and Toxoplasma gondii)
.Bacterial (Brucella, Corynebacterium diphtheriae, gonococcus, Haemophilus influenzae, Actinomyces, Tropheryma whipplei,
Vibrio cholerae, Borrelia burgdorferi, leptospirosis, and Rickettsia, Mycoplasma pneumoniae) (Bacterial myocarditis is rare in
patients without immunodeficiency)
.Fungal (Aspergillus)
.Parasitic (ascaris, Echinococcus granulosus, Paragonimus westermani, schistosoma, Taenia solium, Trichinella spiralis, visceral
larva migrans, and Wuchereria bancrofti)
+Toxins
.Drugs (alcohol, anthracyclines and some other forms of chemotherapy, and antipsychotics, e.g. clozapine, also some designer
drugs such as mephedrone)
+Immunologic
.Allergic (acetazolamide, amitriptyline)
.Rejection after a heart transplant
.Autoantigens (scleroderma, systemic lupus erythematosus, sarcoidosis, systemic vasculitis such as Churg-Strauss syndrome,
and granulomatosis with polyangiitis, Kawasaki disease)
.Toxins (arsenic, toxic shock syndrome toxin, carbon monoxide, or snake venom)
.Heavy metals (copper or iron)
+Electric shock
+Hyperpyrexia
+Radiation
-Diagnosis :
.ECG, CRP (C-reactive protein), ESR
.cardiac enzymes (Creatine kinase CK-MB, LDH, IgM and troponin) may be elevated
.the best diagnostic test is (endomyocardial biopsy), also this is rarely done
.nonspecific ST-T wave changes are the most common
.any degree of heart block is possible / viruses may be isolated from stool, saliva and nasopharyngeal washings
.echo (may demonstrate left ventricular systolic dysfunction)
**Acquired Immune Deficiency Syndrome AIDS / HIV

158
-AIDS is caused by the human immunodeficiency virus HIV

+This is typically followed by a prolonged period without symptoms
+More likely to get infections, including opportunistic infections and tumors CD4 <200
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+The primary mechanism of HIV is to infect a particular subset of T lymphocytes called CD4 cells, often just referred to as T
cells. Over time, HIV decreased the number of CD4 cells. As a person`s CD4 count drops, they become at increasing risk of
developing opportunistic infections and certain malignancies
-HIV is transmitted primarily via :
.unprotected sexual intercourse (anal and even oral sex) – heterosexual contacts, homosexual contacts (More risk)
.contaminated blood transfusions
.hypodermic needles
.from mother to child during pregnancy, delivery or breastfeeding
+Some bodily fluids, such as (saliva, tears) DO NOT TRANSMIT HIV
-Types :
.HIV-1 (more virulent, more infective)
.HIV-2
+Acute Infection (Acute HIV syndrome)
.develop an influenza-like illness or a mononucleosis illness 2-4wks post exposure
.some people also develop opportunistic infections at this stage
.the duration of the symptoms varies, but is usually 1-2wks
.symptoms (fever, large tender lymph nodes, throat inflammation, rash, headache)
.diagnosed by PCR (Elisa test -) (NO antibody)
.CD4 low, high viral load, NO seroconversion-NO antibody, highly infection
+Clinical Latency
.asymptomatic HIV
.chronic HIV
.antibody (+)
.CD4 normal
.without treatment, this 2nd stage of the natural history of HIV infection can last from about 3-20yrs
.symptoms (fever, weight loss, GI problems, muscle pains, persistent generalized lymphadenopathy-unexplained and non-
painful)
.diagnosed by PCR (Elisa test +) (Antibody)
+Acquired Immune Deficiency Syndrome AIDS
.is defined in terms of either a CD4* T-cell count below 200cells
.the M.C initial conditions that alert to the presence of AIDS are pneumocystis, pneumonia, cachexia in the form of HIV wasting
syndrome and esophageal candidiasis
.people with AIDS have an increased risk of developing various viral induced cancers including (Kaposi's sarcoma, Burkitt's
lymphoma, Primary central nervous system lymphoma and cervical cancer)
+Kaposi's Sarcoma (M.C cancer occurring in 10-20% of people with HIV)
+Burkitt's Lymphoma (2nd M.C cancer)
+Both these cancers are associated with human herpesvirus 8 – HHV 8
+Cervical Cancer (occurs more frequently in those with AIDS due to its association with human papillomavirus HPV)
-Diagnosis :
.primary HIV before seoconcersion is done by measuring HIV-RNA (PCR)
+M.C.C for pneumonia in AIDS is Pneumocystis pneumonia (CD4 <200/mL)
+M.C.C for diarrhea in AIDS is Cryptosporidium - Cytomegalovirus (CD4 <50/mL)
+M.C.C for esophagitis in AIDS is Candidiasis
+M.C.C for AIDS dementia complex ADC is Toxoplasmosis (CD4 <100/mL)
+700-1.500 (normal)
+200-500 (oral thrush, kaposi's sarcoma, TB, zoster, lymphoma)
+100-200 (pneumocystis carinii pneumonia, dementia, progressive multifocal leukoencephalopathy, disseminated
histoplasmosis and coccidioidomycosis)
+<100 (toxoplasmosis, cryptococcus, cryptosporidiosis, disseminated herpes simplex)
+<50 (cytomegalovirus, mycobacterium avium complex, progressive, multifocal leukoencephalopathy PML, CNS lymphoma)
-Other uses of the CD4 count are to determine :
.when to start prophylactic medications
.when to initiate antiretroviral medications
.adequacy of response to antiretroviral medications (the best test to monitor response to therapy os the HIV-RNA viral load)
159
-Viral Load Monitoring :

.viral load can be compared to glucose level for Pts. with diabetes
.monitoring of viral load is the best method to monitor adequate response to therapy when the Pts. is on antiretroviral
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medications and the goal is undetectable viremia

.a high viral load generally indicates that the level of CD4 cells is going to drop more rapidly
-Viral Sensitivity / Resistance Monitoring :
.is done to determine which antiviral medications will be effective in an individual Pt.
.sensitivity testing should always be done if a Pt is failing a combination of medications and a change in therapy is necessary
.it should also be done in any pregnant woman who has not been fully suppressed on the initial combination of medications
-Pregnant Pts. :
.pregnant women with serious disease (low CD4 or high viral load) should be treated fully for their HIV infection. That is, they
should get triple antiretroviral therapy as you would in a non pregnant person)
.C/S is only used routinely in those whose CD4 count and viral load are not controlled with medications (when viral load is
>1000 copies/mL of HIV-RNA at the time of delivery)
.zidovudine (AZT) treatment is indicated in all pregnant women. This should be used in combination with tow other
antiretroviral medications
-Breast Feeding :
.breast feeding is associated with transmission of virus to the infant. If a pregnant woman is already on antiretrivirals, she
should continue
.the majority of women can delivery with a normal vaginal delivery
+NOTES :
.It is associated with a very high viral load
.It occurs in at least 70% of HIV infection
.Maculopapular rash can occur in the upper trunk
.It is diagnosed by viral PCR
.It is transmitted by sexual contact
.It can be transmitted by blood transfusion
.The incubation period varying from one year to ten years
.Kaposi's sarcoma can occur
.Can be transmitted from mother to fetus
.Is caused by retrovirus
.Causes dementia
.Pneumocystis carinii pneumonia is a recognized complication
.May be transmitted through kidney transplantation
.Carriers are infectious
.Affects mainly the helper T-cells (T4)
.Affect the central nervous system
.Most common risk factors are MSM and heterosexual intercourse
.In women, the most common mode is heterosexual transmission
.There is often a 10-yrs lag between contracting HIV infection and developing the first symptoms. This is because CD4 cells drop
at a rate of 50-100/mL/yr without therapy
**Tetanus
-A severe infectious complication of wounds caused by the toxin of Clostridium tetani (neurotoxin); takes 1-7 days to develop;
spore forming, Gram-positive rod
-Signs & Symptoms :
.tonic spasm of voluntary muscles
.respiratory arrest
.difficulty in swallowing (dysphagia)
.restlessness
.irritability
.stiff neck, arms and legs
.headache
.lockjaw
.flexion of the arms and extension of the lower extremities, and high mortality rate
-Diagnosis :
.clinical
160
-Treatment (prophylaxis)
.tetanus toxoid – boosters every 10 yrs)
.immediate surgical care, debride wound
.antitoxin, tetanus immunoglobulin
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.penicillin 10-14 days

+NOTES :
.Trismus is characteristic
.The longer incubation period is better in the prognosis
.CSF is usually normal
.If the patient survives, recovery is complete
.It is the result of wound infection by gram-positive anaerobic bacilli of clostridia group
.These organisms live normally and actively in soil
.The usual cause of death in established tetanus is respiratory failure
.There are exotic noninvasive organism
.This disease is best prevented by active immunization and proper wound management
.The usual cause of death is established tetanus is respiratory failure
.Mild cases of tetanus can be treated with tetanus immunoglobulin IV or IM
.The cause of death in established tetanus is respiratory failure
.To prevent tetanus neonatorum women should be actively immunized by puberty
.Recommended for universal use regardless of age
.Important for workers in contact with soil, sewage or domestic animals
.For severe wounds, give a booster if more than 5Yrs have elapsed since the last dose
+Diseases May Be Water-Borne :
.Typhoid fever
.Bacillary dysentery
.Cholera
.Infectious hepatitis (hepatitis A)
.Tetanus (except)
**Toxic Shock Syndrome

-Signs & Symptoms :
.hypotension
.fever
.mucosal changes
.desquamative rash on hands and feet
.gastrointestinal
.renal
.hepatic
.muscular symptoms can also be present
-Causes :
.S.aureus (toxin TSST-1)
-Diagnosis :
.made mainly by clinical findings and history; hypocalcemia secondary to capillary leak
-Treatment :
.beta-lactamase stable penicillin is the choice (nafcillin / oxacillin)
+Staphylococcus aureus is the M.C.C of osteomyelitis

+Escherichia Coli is the M.C.C of pyelonephritis
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HEMATOLOGY
**ANEMIA
-A hematocrit (Hct) less than 41% in men / less than 36% in women
-A hemoglobin less than 13.5gm/dL in men / less than 12 mg/dL in women
+Microcytic (MCV <80) :
.iron deficiency
.thalassemia
.sideroblastosis
.lead poisoning
.anemia of chronic disease (can be either microcytic or normocytic)
+Mactocytic (MCV >100) :
.vit B12
.folic acid deficiency (but can also result from the toxic effects of alcohol)
.liver disease
.chemotherapeutic agents (methotrexate or zidovudine AZT or phenytoin)
.hypothyroidism
+Normocytic (normal MCV) :
.hemolysis
.aplastic anemia
+Hemolytic (Hymolysis) :
.Hereditary spherocytosis
.Hereditary elliptocytosis
.Sickle cell anemia
.Glucose-6-phosphate deficiency
+Hematocrit (Hct) (male 42%-54% / female 38%-46% / 1 year old age 20%-41%)
+Anemia is considered when RBCs count (< 4.5 million in males / < 3.9 million in females)
+Or Hemoglobin ( Hb ) content (< 13.5 gm % in males / < 11.5 gm % in females)
-Signs & Symptoms :
.fatigue
.tiredness
.poor exercise tolerance
.dyspnea on exertion and lightheadedness
.confusion and altered mental status may develop as oxygen delivery to the brain decreases
.death from anemia is most often from decreased oxygen delivery to the heart, resulting in the development of myocardial
ischemia
.a healthy young Pt. May have no symptoms at all with a hematocrit of 27-29%, whereas an older Pt. With heart disease may
develop dyspnea or anginal symptoms with the same hematocrit
-Diagnosis :
.once a diagnosis of anemia is determined based on a low hematocrit or hemoglobin
.MCV
.iron
.reticulocyte count
.peripheral smear
.red cell distribution of width (RDW)
.coombs test
.Vit B12
.folate levels
.bone marrow biopsy
-Treatment :
.a healthy young Pt. Can have transfusion withheld until the hematocrit is in the low 20%
.an older Pt. With coronary artery disease will need to be maintained above a hematocrit of 30%
162
**MICROCYTIC ANEMIA
Page
*Iron Deficiency Anemia

-Is defined as a decrease in the amount of red blood cells (RBCs) or hemoglobin in the blood due to not enough iron
+Is the commonest type of anemia in Jordan
+The average daily iron intake is 10-20 mg
+Iron absorbed in duodenum
+Alcohol increases iron absorption (tea drink are NOT)
+Ferrous iron absorbed better than ferric
-Signs & Symptoms (non-specific symptoms) :
.symptoms of fatigue and poor exercise tolerance may develop
.tachycardia
.palpitation
.dyspnea on exertion
.pallor develop
.older Pts. And those with coronary artery disease may become dyspneic at higher levels of hematocrit
.more severe anemia results in lightheadedness, confusion, syncope, and chest pain
.a systolic ejection murmur ‘flow murmur’ may develop in any Pt with moderately severe anemia
-Causes :
.is almost always caused by increased level of blood loss from the body
.the most common type of blood loss is gastrointestinal or menstrual
.a man requires about 1mg per day and a women about 2-3 mg per day on average
.it is difficult for the body to increase the level of iron absorption (occult blood in the stool, a heavier menstrual flow, or an
increased demand such as during pregnancy), the body is poorly equipped to increase its level of absorption to exceed 3-4 mg
per day
.other etiologies are increased urinary loss of blood, malabsorption, hemolysis and poor oral intake
-Symptoms specific to iron deficiency are very rare :
.brittle nails
.spoon shaped nails
.glossitis
.pica
+(iron def. Anemia as a specific diagnosis is determined by laboratory findings, not symptoms)
.High iron binding capacity
.Low serum ferritin
.Missed menstrual cycle
.Angular cheilitis (inflammatory lesions at the mouth's corners)
.Koilonychia (spoon-shaped nails) or nails that are weak or brittle
.Pruritus (itchiness)
.Insomnia
.Restless legs syndrome
-Treatment :
.oral therapy with ferrous sulfate tablets is the most common method of therapy
.parenteral iron is used in Pts with malabsorption, and in those who cannot tolerate oral therapy
.blood transfusion is the most effective method of delivering iron (but is not a standard method of correcting iron deficiency)
*Anemia Of Chronic Disease

-A defect in the ability to make use of iron sequestered in stores within the reticuloendothelial system. It can be either
microcytic or normocytic
-Signs & Symptoms :
.the symptoms are based on the severity of the anemia as described above
.the only other symptoms are based on the specifics of the underlying disease
-Causes :
.this is associated with many disease, including chronic infection (TB, osteomyelitis, vasculitis, rheumatoid arthritis, malignancy,
renal failure) (anemia can accompany virtually any chronic inflammatory, infectious or neoplastic condition)
-Diagnosis :
.the serum ferritin level (is normal or elevated)
.the serum iron level and total iron binding capacity (TIBC) (are both low)
.the reticulocyte count (is low)
163
-Treatment :
.iron supplementation and erythropoietin will not help, except in renal disease and anemia caused by chemotherapy or
radiation therapy for malignancies
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*Sideroblastic Anemia
-A microcytic anemia caused by a disorder in the synthesis of hemoglobin characterized by trapped iron in the mitochondria of
nucleated red blood cells
+Is a form of anemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes)
-Signs & Symptoms :
.the symptoms are related to the severity of the anemia as described above
.there is no specific presenting findings that will be sufficiency suggestive of sideroblastic anemia to allow a diagnosis without
significant laboratory evaluation
-Causes :
.the hereditary is from either a defect in aminolevulinic acid synthase or an abnormality in Vit B6 metabolism
.acquired forms are from drugs such as chloramphenicol, isoniazid or alcohol
.lead poisoning can cause sideroblastic anemia as well
.there is an association with myelodysplastic syndromes (MDS) and refractory anemia
.these can progress to acute myelogenous leukemia in a small percentage of Pts.
.alcohol use (M.C.C of sideroblastic anemia)
.genetic syndromes
-Diagnosis :
.the ferritin level is elevated
.the serum iron level is high
.TIBC total is low
.the most specific test is a Prussian Blue stain of red blood cells in the marrow (Marrow reticuloendothelial iron is strikingly
increased)
-Treatment :
.pyridoxine
.treat the lead poisoning
.some Pts. with the hereditary form will respond to pyridoxine therapy 2-4mg per day
*Thalassemia
-Is a form of inherited autosomal recessive blood disorder characterized by abnormal formation of hemoglobin
+The abnormal hemoglobin formed results in improper oxygen transport and destruction of red blood cells / Thalassemia are
not acquired anemia
+The hereditary underproduction of either the alpha or beta globin chains of the hemoglobin molecule resulting in a
hypochromic, microcytic anemia)
-Signs & Symptoms :
.in alpha thalassemia one gene deleted yields a normal Pt. The CBC is normal, the hemoglobin level is normal, and the MCV is
normal
.tow genes deleted have a mild anemia with hematocrit ranging from 30-40% with a strikingly low MCV
.three genes deleted have more profound anemia with hematocrit between 22-32% as well as the very low MCV
.four genes deleted Pts. die in utero secondary to gamma chain tetrads called hemoglobin barts
.Pts. with beta thalassemia major are homozygous for mutations of both genes coding for the beta hemoglobin gene, these Pts.
with beta thalassemia major, also known as cooley anemia, become severely symptomatic starting at 6 months of age (Pt.
becomes symptomatic in the second 6 months)
.they are severely symptomatic with growth failure, hepatosplenomegaly, jaundice and bony deformities secondary to
extramedullary hematopoiesis, cirrhosis, CHF
.beta thalassemia – ‘hair on end’ appearance (skull x-ray)
.hemolytic anemia resulting from imbalance of alpha and beta globin chains
-Causes :
.there are four genes coding for the alpha chain of hemoglobin. There can be deletions of one, tow, three, or all four genes
(alpha is more common in asian populations / chromosome 16)
.beta thalassemia can be mutated in either one or tow genes (is more common in mediterranean populations / chromosome
11)
-Diagnosis :
.beta thalassemia major has the severe symptoms, large spleen, and bone abnormalities described above
164
.both forms of thalassemia are diagnosed by having a microcytic anemia with normal iron studies
.beta thalassemia, there is an increased level of hemoglobin F and hemoglobin A2 (hemoglobin is a low as 3-4g/dL)
.those with alpha thalassemia will have normal amounts of hemoglobin F and A2
.tetrads of beta chains are called hemoglobin H (hemoglobin H is present in alpha thalassemia with three of four genes deleted)
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.RDW is normal in all forms because all of the cells are of the same size
-Treatment :
.beta thalassemia major Pts. require blood transfusions once or twice a month
.the chronic transfusions lead to iron overload, which requires treatment with deferasirox
.a small number of Pts can be treated with a bone marrow transplantation
**MACROCYTIC ANEMIA
*Vitamin B12 (cyanocobalamine) Deficiency
-Decreased absorption or intake of Vit B12 resulting in hematologic and/or neurologic abnormalities
-Signs & Symptoms :
.you cannot specifically determine that a Pt. has B12 deficiency only from the symptoms of anemia. Neurologic manifestations
may involve almost any level of the neurologic system
.Pts. may have peripheral neuropathy, position sense abnormality, viberatory, psychiatric, autonomic, motor, cranial nerve,
bowel, bladder and sexual dysfunction
.glossitis, diarrhea and abdominal pain may occur
.inadequate dietary intake of vitamin B12
.atrophic gastritis (in which case, the resulting megaloblastic anemia takes the name of "pernicious anemia"), or may result
from wide surgical resection of stomach
.resection of the terminal ileum (the principal site of vitamin B12 absorption)
.surgical removal of the small bowel
.long-term use of ranitidine hydrochloride
.Celiac disease
-Causes :
.the M.C.C of B12 deficiency is pernicious anemia
.the incidence of pernicious anemia increases with age. Gastrectomy and atrophic gastritis can also decrease intrinsic factor
production
.various forms of malabsorption such as sprue, regional enteritis, and blind loop syndrome can block absorption of Vit B12
.pancreatic insufficiency can result in the inability to absorb the Vitamin
.rarely, tapeworm infection with Diphyllobothrium latum can decrease absorption
.decreased intake is unusual and requires several years to produce disease
-Diagnosis :
.increased MCV, WBCs have hypersegmented neutrophils with a mean lobe count greater than four, RBCs are characterized by
macro-ovalocytes
.macrocytosis can occur with hemolysis liver disease and myelodysplasia
.reticulocyte count is reduced, although the bone marrow is hypercellular, pancytopenia may occur
.elevated LDH, bilirubin and iron level may occur but are nonspecific
.the most specific test is simply a low B12 level
.the Schilling test is occasionally used to determine the etiology of Vit B12 deficiency
.an elevated methylmalonic acid level occurs with B12 deficiency and is useful if the B12 level is equivocal
-Treatment :
.folic acid replacement can correct the hematologic abnormalities of B12 deficiency, but not the neurologic abnormalities
+Features Of Pernicious Anemia :
.Usually over 30 years, with blue eyes (elderly)
.Subacute combined degeneration of the cord can occur
.Optic atrophy can occur
.Weight loss is a common feature
.Subacute combined degeneration can occur
.Gastric atrophy with achlorhydria
+Significant in blood film is (hypersegmented neutrophils)
+The major difference between Vit12 and folate deficiency is (neuropathy-foot paresthesia)
*Folic Acid Deficiency

-Is a low level of folic acid in the body. Also known as vitamin B9, it is involved in adenosine,is absorbed throughout the small
intestine
165
-Signs & Symptoms :

.women with folate deficiency who become pregnant are more likely to give birth to low birth weight premature infants, and
infants with neural tube defects. neural tube defects
Page
.symptoms dependent on the severity of the anemia

-Causes :
.is almost due to some form of decreased dietary intake
.increased requirements from pregnancy, skin loss in disease like eczema, or increased loss from dialysis may occur and certain
anticonvulsants, such as phenytoin
.alcoholics have decreased folate intake
.crohn's disease, coeliac disease
.tetrahydrofolic acid
-Diagnosis :
.the hematologic presentation of folic acid deficiency is identical to B12 deficiency
.the diagnosis is based on a low RBCs, folic-acid level
-Treatment :
.replace folic acid, almost always orally
+About Megaloblastic Anemia :
.megaloblastic anemia secondary to folate deficiency
.serum folic acid and vitamin B12 are not normal
.manifestation may appear in the first year of life
.white blood cells and platelets are normal
.occasionally treatment is required for life
.in Jordan goat's milk may be a factor in its etiology
**HEMOLYTIC ANEMIA
-Is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels
(intravascular hemolysis) or elsewhere in the human body (extravascular)
-Signs & Symptoms :
.fatigue and weakness occur with mild disease
.dyspnea and later confusion occur with more severe disease
.jaundice and dark urine
.gallstones
.fever, chills, chest pain, tachycardia and backache may occur if the intravascular hemolysis is particularly rapid
.the major difference between hemolytic anemia and the micro-and macrocytic anemias is that hemolysis is more often the
etiology when the onset is sudden
-Causes :
.hemolytic anemia may either be chronic as in sickle cell disease, paroxysmal nocturnal hemoglobinuria, and hereditary
spherocytosis or acute such as in drug-induced hemolysis, autoimmune hemolysis, or G6PD deficiency
-Diagnosis :
.Pts. with hemolytic anemias generally have a normal MCV (but may be elevated)
.the LDH and indirect bilirubin are elevated (bilirubin levels above 4 are unusual with hemolysis alone)
.the peripheral smear shows fragmented cells, and the haptoglobin may be low with intravascular hemolysis
.hemoglobin may be present in urine when intravascular hemolysis is sudden and severe because free hemoglobin spills into
the urine
-Treatment :
.transfusion is needed as in all forms of anemia when the hematocrit becomes low
+Hemolysis May Occur In (Hemolytic Anemias) :
.Hereditary spherocytosis
.Thalassemia
.Sickle cell anemia
.Glucose-6-phosphate deficiency
.Hereditary elliptocytosis
*Sickle Cell Disease

-It is autosomal recessive disorder causing production of abnormal beta globin chains
166
-A hereditary form of chronic hemolysis ranging from asymptomatic to severe. It is characterized by irreversibly sickled cells and
recurrent painful crises
+More common in black / Increased incidence of salmonella osteomyelitis / Sickle cell tract are usually asymptomatic
-Signs & Symptoms :
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.chronic manifestations include (renal concentrating defect - isosthenuria)

.ulcerations of the skin of the legs
.bilirubin gallstones
.aseptic necrosis of the femoral head
.osteomyelitis
.retinopathy
.recurrent infections from Pneumococcus or Haemophilus
.growth retardation
.splenomegaly followed in adulthood by autosplenectomy
.the acute painful crisis consists of back, rib, chest and leg pain
.severe manifestations of sickling, include the acute chest syndrome consisting of (severe chest pain, fever, leukocytosis,
hypoxia and infiltrates on the chest x-ray
.pneumonia, stroke and TIA may also occur
.blindness and even MI and cardiomyopathy may also occur
.pregnant Pts experience increased rates of spontaneous abortion and low birth weight
.sickle trait gives a normal hematologic picture with no anemia and a normal MCV
.increased the frequency of UTI
-Causes :
.hemoglobin S is due to a substitution of a valine for glutamic acid as the 6th amino acid of the beta globin chain
.the heterozygous form (trait) is present in african-american population (homozygous disease)
.almost all of those with the trait are asymptomatic
.a sickle cell crisis is most often not associated with an increase in hemolysis or drop in hematocrit
.when increased hemolysis occurs, another etiology such as concomitant G6PD or acute splenic sequestration in a child should
be considered
.sudden drops in hematocrit may also be caused by parvovirus B19 infection or folate deficiency
.this drop in hematocrit is from acute aplasia (decrease in cell production), not hemolysis
-Diagnosis :
.normal MCV
.the reticulocyte count should always be elevated in the 10-20%
.they have folate deficiency or parvovirus B19 infection
.LDH and bilirubin are elevated as in all types of hemolytic anemia
.the hemoglobin electrophoresis is the most specific test
.the peripheral smear shows sickle cells
.the sickle prp (or sickledex) is a quick screening test used to diagnose evidence of sickle cell trait and cannot distinguish
between trait and homozygous disease
.the urinalysis usually has blood present, although it is often microscopic
.the WBCs count is often elevated in the 10.000-20.000 ranges
-Treatment :
.an acute sickle cell pain crisis is treated with fluids, analgesic and oxygen
.antibiotics are given with infection or even to Pts with fever and leukocytosis even if a definite site of infection has not been
documented
.ceftriaxone and cefotaxime are the two preferred agents because they cover Pneumococcus and Haemophilus influenza
.severe or life-threatening manifestations such as acute chest syndromes, CNS manifestations, priapism and acute cardiac
manifestations are managed with RBC transfusions if the hematocrit is low, and exchange transfusion if the hematocrit is high
.chronic management include folic acid replacement and vaccinations against Pneumococcus and influenza
.hydroxyurea is used to decrease the frequency of the vaso-occlusive pain crisis
.bone marrow transplantation can be curative but should still be considered experimental at this time
*Autoimmune, Cold Agglutinin, And Drug-Induced Hemolytic Anemia

-Various forms of acquired hemolytic anemias resulting from the production of IgG, IgM, or activation of complement C3
against the red cell membrane
-Causes :
.autoimmune destruction is often idiopathic
.known causes of autoimmune destruction are from antibodies produced in relationship to various forms of leukemia,
167
especially chronic lymphocytic leukemia, viral infections, lymphomas, collagen vascular disease like lupus, or in relationship to
drugs (the M.C drugs are the penicillins, cephalosporins, sulfa drugs, quinidine, alpha methyldopa, procainamide, rifampin and
thiazides
.cold agglutinin disease is an IgM antibody produced against the red cell in association with malignancies such as lymphoma or
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waldenstrom macroglobulinemia and infections such as mycoplasma or mononucleosis

.UC can also lead to autoimmune hemolytic anemia
-Diagnosis :
.autoimmune hemolysis gives a normocytic anemia, reticulocytosis, increased LDH, absent or decreased haptoglobin, and
increased indirect bilirubin
*Herediatery Spherocytosis
-A chronic mild hemolysis (autosomal dominant disorder) with spherocytes,jaundice and splenomegaly from a defect in the red
cell membrane
-Hemolysis occurs in the spleen, there is often splenomegaly and jaundice
-Severe anemia occasionally occurs from folate deficiency or parvovirus B19 infection such as in sickle cell disease. Bilirubin
stones often occur, leading to cholecystitis, often at a young age
-Treatment :
.folate replacement
.with more severe anemia, removal of the spleen
*Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency

-Also known as favism (after the fava bean) is an X-linked recessive genetic condition that predisposes to hemolysis
(spontaneous destruction of red blood cells) and resultant jaundice in response to a number of triggers, such as certain foods,
illness, or medication (the hereditary deficiency of an enzyme)
+G6PD deficiency is the most common human enzyme defect
-Signs & Symptoms :
.Pts. are normal until exposed to the stress
.a sudden severe, intravascular hemolysis can occur including (jaundice, dark urine, weakness and tachycardia)
.the history of recent drug ingestion is the main clue to the diagnosis
-Causes :
.the most common type of oxidant stress is actually from infections, not drugs
.the most commonly implicated drugs are (sulfa drugs, primaquine, dapsone, quinidine, nitrofurantoin)
-Diagnosis :
.the usual findings of an intravascular hemolysis include high LDH, bilirubin, and reticulocyte count with a normal MCV, low
haptoglobin and hemoglobinuria
.bite cell are seen on smear indicating the removal of the heinz bodies
-Treatment :
.there is no specific therapy beyond hydration and transfusion if the hemolysis is severe. The main therapy is to avoid oxidant
stress in the future
+Favism is a hemolytic anemia caused by deficiency of (Glucose-6-phosphate dehydrogenase)
*Aplastic Anemia
-Failure of all three cell lines produced in the bone marrow resulting in anemia, leukopenia and thrombocytopenia
(pancytopenia)
-Signs & Symptoms :
.Pts. most commonly present with bleeding from the thrombocytopenia, but may present with a combination of the findings
associated with deficiencies in all three cell lines
.fatigue from anemia and infections from neutropenia may also occur
.the clinical presentation may give a clue to presence of pancytopenia but is not sufficient to determine a true plastic anemia by
clinical manifestations alone
.the absence of a classical association such as benzene, radiation or chloramphenicol would most certainly not exclude a
diagnosis of a plastic anemia
.the most common single etiology is idiopathic
-Causes :
.there are many things that can cause bone marrow failure, the most common cause of true aplastic anemia is rarely precisely
determined
.radiation, toxins such as benzene, drugs such as nonsteroidal anti-inflammatory agents, chloramphenicol, alcohol and
chemotherapeutic alkylating agents
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.infiltration of the bone marrow with infections such as TB or cancer such as lymphoma can cause pancytopenia (but this is not
truly aplastic anemia)
.infections such as hepatitis, HIV, CMV, EBV and parvovirus B19 in immunocompromised Pts.
-Diagnosis :
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.pancytopenia on a CBC is the first test

.bone marrow biopsy confirms the diagnosis when alternative etiologies for a pancytopenia are not present (in other words, the
marrow is empty of almost all precursor cells as well as evidence of primary or metastatic cancer, infection or fibrosis)
.the marrow is hypoplastic and fat filled with no abnormal cells seen
-Treatment :
.bone marrow transplantation should be carried out whenever th Pt. is young and healthy enough to withstand the procedure
and there is a donor available
**ACUTE LEUKEMIA
-The rapid onset of bone marrow failure from the derangement of the pluiropotent stem cell resulting in the relentless
destruction of the normal production of the entire bone marrow. The blood cells lose the ability to mature and function
normally
-Signs & Symptoms :
.the M.C presentation results from the effects of the leukemic blast cells crowding out the normal marrow cells, resulting in
symptoms pf pancytopenia even if the total WBCs count is normal
.fatigue from anemia is the most common presenting complaint
.bleeding from thrombocytopenia occurs
.infections from the underproduction or abnormal function of white blood cells also occurs
.acute lymphocytic leukemia (ALL) is more common in children
.acute myelogenous leukemia (AML) is more common in adults
+ALL is more often associated with infiltration of other organs, but AML can do it as well
.enlargement of the liver, spleen and lymph nodes and bone pain are common at presentation
.disseminated intravascular coagulation DIC is associated with M3 promyelocytic leukemia
.CNS involvement resembling meningitis is present at the time of initial diagnosis in about 5% of Pts. (CNS involvement is most
characteristic of M4 and M5 monocytic leukemia)
.rarely, a syndrome of ‘leukostasis’ can occur when the white cell count is extremely elevated (resulting, in headache, dyspnea,
confusion and brain hemorrhage)
-Causes :
.most cases of acute leukemia arise with no apparent cause
.association with the development of acute leukemia, include (radiation exposure, benzene, chemotherapeutic agents such as
melphalan nad etoposide, as well as some retroviruses) (genetic disorders such as down syndrome and klinefelter can result in
an increased incidence of leukemia)
.myelodysplasia and sideroblastic anemia can also develop into acute leukemia
-Diagnosis :
.the CBC is the first clue to the diagnosis
.depression of all three cell lines is common at presentation
.the white cell count can be low, norma or elevated
.thrombocytopenia and anemia are usual
.many other disorders can present as pancytopenia similar to leukemia such as aplastic anemia, infections involving the
marrow, metastatic cancer involving the marrow, Vit B12 deficiency, SLE, hypersplenism and myelofibrosis
.a bone marrow biopsy showing greater than 20% blasts confirms the diagnosis of acute leukemia
.the presence of blasts tells you the Pt has acute leukemia (but blast analysis cannot be relied upon to always tell which type is
present)
.AML is characterized by the presence of Auer rods (Auer rods are most specific for M3), myeloperoxidase and esterase
.ALL is characterized by the presence of the common ALL antigen (CALLA) and terminal deoxynucleotidyl transferase TdT
.hyperuricemia and increased level of LDH
-Treatment :
.chemotherapy is used initially in all Pts. to induce a remission. Inducing a remission means a removal of over 99.9% of the
leukemic cells in the body
.the initial chemotherapy for AML is (cytosine arabinoside – AraC)
.the initial chemotherapy for ALL is (daunorubicin, vincristine and prednisone)
.promyelocytic leukemia is managed with the addition of the Vit A derivative all-trans-retinoic acit ATRA)
.all Pts must also undergo prophylaxis of the CNS to prevent relapse there. The best agent for this is intrathecal methotrexate
169
**CHRONIC LEUKEMIA
*Chronic Myelogenous Leukemia (CML)
-A chronic myeloproliferative disorder characterized by the massive overproduction of myeloid cells. These cells retain most of
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their function until later in the course of the disease

-Is a cancer of the white blood cells. It is a form of leukemia characterized by the increased and unregulated growth of
predominantly myeloid cells in the bone marrow and the accumulation of these cells in the blood
+M > F, and appears more common in the elderly with a median age at diagnosis of 65 years
-Signs & Symptoms :
.elevated white blood cell count can be found on routine blood count
.the most common symptoms are fatigue, night sweats and low-grade fever
.abdominal pain from massive enlargement of the spleen is common
.bone pain from infiltration with white cells can occur
.enlarged lymph nodes are rare
.infections and bleeding are uncommon
.rarely, a leukostasis reaction can occur from extremely elevated amounts of white cells (20.000-500.000)
-Causes :
.philadelphia chromosome is characteristic of the disease, the cause of the production of this chromosome is unknown
.the philadelphia chromosome is a translocation between chromosomes 9 and 22, resulting in a gene producing an enzyme
with tyrosine kinase activity
.five percent of cases are philadelphia chromosome negative
-Diagnosis :
.elevated white blood cell count
.neutrophils with a left shift
.blasts are either absent or present in very small amounts <5%
.the leukocyte alkaline phosphatase score (LAP) is diminished
.basophilia is characteristic of CML and all myeloproliferative disorders such as polycythaemia vera
.level B12 elevated (this not be enough to establish the diagnosis)
.philadelphia chromosome is a far more specific test for CML and should be done in a Pt with a markedly elevated white cell
count and a low LAP score
.platelet count can also be markedly elevated
-Treatment :
.the best initial therapy for CML is imatinib (Gleevec)
*Chronic Lymphocytic Leukemia (CLL)

-Massive overproduction of mature, but still leukemic, lymphocytes usually from the monoclonal production of B lymphocytes
-Signs & Symptoms :
.CLL can often present as an asymptomatic elevation of WBCs
.the Pts. are exclusively older with 90% being over the age of 50
.when the Pts. do have symptoms they are often nonspecific (fatigue, lethargy and uncomfortable enlargement of lymph
nodes)
.infiltration of of other parts of the reticuloendothelial system such as (the spleen, liver, and bone marrow) aslo occurs
.infection and bleeding are unusual presentations of the disease
.CLL can be associated with various autoimmune phenomena such as thrombocytopenia and autoimmune hemolytic anemia
-Causes :
.the etiology of CLL is unknown
-Staging for CLL is as follows :
.stage 0 (lymphocytosis alone)
.stage 1 (lymphadenopathy)
.stage 2 (splenomegaly)
.stage 3 (anemia)
.stage 4 (thrombocytopenia)
+Staging is important because the survival of untreated stage 0 and stage 1 disease is 10-12 yrs even without treatment
+the survival of stage 3 and stage 4 disease is 1-2yrs
-Treatmetn :
.early stage CLL with only an elevated white cell count or enlargement of lymph nodes is not treated
.Pts. with symptomatic disease always need to be treated
.those with more advanced-stage disease should receive initial therapy with (fludarabine)
.autoimmune hemolysis and thrombocytopenia are treated with prednisone
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.pentostatin is used in relapsed Pts.

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**PLASMA CELL DISORDERS
*Multiple Myeloma
-A clonal abnormality of plasma cells resulting in their overproduction replacing the bone marrow as well as the production of
large quantities of functionless immunoglobulins
-The disease is characterized by various systemic manifestations such as bone, kidney and infectious complications
-Signs & Symptoms :
.bone pain is the most common clinical manifestation, this is most commonly is the back and the ribs, secondary to pathologic
fractures
.radiculopathy from the compression of spinal nerve roots is also common
.infection particularly with encapsulated organisms such as (Pneumococcus and Haemophilus) is common
.renal failure and anemia are common
.the symptoms of hypercalcemia such as polyuria, polydipsia and altered mental status may occur
.weakness, fatigue and pallor are common
.rarely, symptoms of a hyperviscosity syndrome such as blurry vision, confusion and mucosal bleeding may occur
-Causes :
.the cause of multiple myeloma is unknown
-Diagnosis :
.normochromic, normocytic anemia is the most common laboratory findings (this is not specific for myeloma)
.a protein electrophoresis with a markedly elevated monoclonal immunoglobulin spike is present in almost all cases
.this is most commonly IgG, bu may be IgA, IgD, or rarely a combination of two of these
.plain x-ray of the skeletal system snd skull will reveal the plasma cells
.serum B2 microglobulin is elevated in 75% of Pts
.hypercalcemia from the destruction of bone is common, as is in elevation in the BUN and creatinine from the damage to the
kidney from the immunoglobulin
.bence-jones protein, calcium and hyperuricemia
-Treatment :
.younger Pts. should be treated with autologous bone marrow transplantation
.older pts. should receive a combination of melphalan and prednisone
.Pts. who are candidates for transplants should receive melphalan, prednisone and thalidomide
.hypercalcemia is treated initially with hydration and loop diuretics then with bisphosphonates such as pamidronate
*Monoclonal Gammopathy Of Uncertain Significance (MGUS)

-The overproduction of a particular immunoglobulin by plasma cells without systemic manifestations of myeloma such as bone
lesions, renal failure, anemia and hypercalcemia
-Signs & Symptoms :
.almost all Pts. with MGUS have no symptoms
.it is found on routine blood testing for other reasons
-Causes :
.tha cause of MGUS is unknown
.MGUS is a very common abnormality present in 1% of all Pts above the age of 50 and in 3% of those above age 70
-Diagnosis :
.an elevated monoclonal immunoglobulin spike of serum protein electrophoresis SPEP in amounts lower than found in
myeloma
.the creatinine, calcium and hemoglobin levels are normal
.an elevated total serum protein is the clue to the diagnosis
.there are no lytic bone lesions, and the bone marrow has <5% plasma cells
**LYMPHOMA
*Hodgkin Disease
-A neoplastic transformation of lymphocytes particularly in the lymph node characterized by the presence of Reed-Sternberg
Cells on histology and to spread in an orderly
-Signs & Symptoms :
171
.enlarged, painless, rubbery, non erythematous, non tender lymph nodes are the hallmark of the disease
.Pts may also develop what are labeled ‘B’ symptoms, which are drenching night sweats, 10% weight loss and fevers
.pruritus is common in the disease (it is not one of the ‘B’ symptoms)
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.cervical, supraclavicular and axillary lymphadenopathy are the most common initial signs of disease
.extralymphatic involvement is more common with non-Hodgkin lymphoma
-Causes :
.there are no clear environmental or infectious etiologies for the disorder
.hodgkin disease has bimodal age distribution (one peak in the 20s and 60s)
-Staging is as follows (the staging is the same for both Hodgkin as well as non-Hodgkin lymphoma) :
.stage 1 (one lymphatic group or single extra lymphatic site
.stage 2 (two lymphatic groups or extra lymphatic sites on the same side of the diaphragm)
.stage 3 (involvement of lymphatic groups on both sides of the diaphragm or involvement of any extralymphatic organ
contiguous to the primary nodal site
.stage 4 (widespread disease with involvement of diffuse extralymphatic sites such as the bone marrow or liver)
-Diagnosis :
.an excisional lymph node biopsy is the essential first step in determining the diagnosis
.after the initial diagnosis (biopsy), the most important step is to determine the extent of the disease because the stage will
determine the nature of the therapy, that is radiation versus chemotherapy
.a CXR or chest CT scan, abdominal CT scan, or MRI are used to determine if the disease is localized to the supraclavicular area
.lymphangiography and laparotomy are no longer routinely used for staging (laparotomy is used to definitively exclude more
widespread disease)
.CT scanning is sensitive enough to detect any involved lymph nodes
.if all of these tests are unrevealing and localized radiotherapy is contemplated
.a bone marrow biopsy is also sometimes used to definitively determine if the disease is truly localized
-Treatment :
.localized disease such as stage 1 and 2 is managed predominantly with radiation
.all Pts with evidence of ‘B’ symptoms as well as stage 3 or 4 disease are managed with chemotherapy
.the most effective combination chemotherapeutic regimen for Hodgkin disease is ABVD
+Types :
.Nodular sclerosis (M.C subtype)
.Mixed cellularity
.Lymphocyte predominant (Lymphocyte-rich)
.Lymphocyte depleted
*Non-Hodgkin Lymphoma (NHL)

-The neoplastic transformation of both B and T cell lineages of lymphatic cells
-NHL causes the accumulation of neoplastic cells in both the lymph nodes as well as more often diffusely in extralymphatic
organs and the bloodstream. The Reed-Sternberg cell is absent
-Signs & Symptoms :
.enlarged, painless, rubbery, non erythematous, non tender lymph nodes are the hallmark of the disease
.Pts may also develop what are labeled ‘B’ symptoms, which are drenching night sweats, 10% weight loss and fever
.NHL is the same as Hodgkin disease, the difference is that Hodgkin disease is localized to cervical and supraclavicular nodes 80-
90% of the time, whereas NHL is localized only 10-20% of the time
.NHL is far more likely to involve extralymphatic sites as well as to have blood involvement similar to chronic lymphocytic
leukemia
.CNS involvement is also more common with NHL / HIV- positive Pts often have CNS involvement
-Causes :
.there are a number of infectious and autoimmune disorders associated with the development of NHL (HIV, hepatitis C, Epstein-
Barr, HTLV-I and Helicobacter pylori predispose to the development of NHL) (EBV, HIV both more often associated with Burkitt
lymphoma) (HIV can also be associated with immunoblastic lymphoma)
-Treatment :
.localized disease such as stage 1 and 2 is managed predominantly with radiation
.all Pts with evidence of ‘B’ symptoms as well as stage 3 or 4 disease are managed with chemotherapy
.the initial chemotherapeutic regimen for NHL is still CHOP
.CNS lymphoma is often treated with radiation
**PLATELET DISORDERS
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*Idiopathiic Thrombocytopenia Purpura (ITP)

-Signs & Symptoms :
.the Pt. presents initially with signs of bleeding from superficial areas of the body such asa the skin, nasal and oral mucosa
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gastrointestinal tract, urine and vahina

.the Pt. is generally young, more often female, and complains of epistaxis, bruising, hematuria, dysfunctional uterine bleeding
and sometimes gastrointestinal bleeding
.petechiae, purpura and ecchymoses are often found in exam
.splenomegaly should be absent
-Causes :
.the idiopathic production of an antibody to the platelet, leading to removal of platelets from the peripheral circulation by
phagocytosis by macrophages
.the platelets are bound by the macrophage and brought to the spleen, leading to low platelet counts
.ITP is often associated with lymphoma, CLL, HIV and connective tissue diseases
-Diagnosis :
.thrombocytopenia is the major findings
.a normal spleen on exam and on imaging studies such as an U/S is characteristic
.antiplatelet antibodies have a high sensitivity but poor specificity
.the bone marrow should be filled with megakaryocytes indicating that there is a problem with platelet destruction and not
platelet production, the bone marrow will also exclude other causes of thrombocytopenia such as primary or metastatic cancer,
infiltration by infections such as TB or fungi, or decreased production problems such as drug, radiation or chemotherapy effect
on the bone marrow
.the peripheral smear and creatinine should be normal, excluding other platelet destruction problems such as hemolytic uremic
syndrome, thrombotic thrombocytopenic purpura, and DIC
-Treatment :
.prednisone is the initial therapy in most Pts.
.splenectomy is used in Pts in whom very platelet counts less than 10.000-20.000/mm
.RhoGAM – may be used in Pts. with profoundly low platelet counts <10.000mL or in a Pts. at risk for life-threatening bleeding
(RhoGAM may only used in RH-positive Pts.)
.refractory cases can be treated with rituximab
*Von Willebrand Disease (VWD)

-An increased predisposition to platelet-type bleeding from decreased amounts of von willebrand factor
-Signs & Symptoms :
.Pts. with vWD manifest platelet type bleeding such as that described above for ITP
.this is mucosal and skin bleeding such as epistaxis, petechiae, bruising and menstrual abnormalities
.both platelet problems as well as clotting factor abnormalities can result in gastrointestinal and urinary tract bleeding
.there is often a marked increase in bleeding after the use aspirin
-Causes :
.an autosomal dominant disorder resulting in a decreased amount of von willebrand factor
.this is the most common congenital disorder of hemostasis
.vWD results in a decreased ability of platelets to adhere to the endothelial lining of blood vessels
.in vWD, aggregation is normal, whereas adherence is abnormal
-Diagnosis :
.the platelet count and appearance are normal
.the bleeding time is increased particularly after the use of aspirin
.the level of von willebrand factor, also known as factor 8 antigen, is low
.the ristocetin platelet aggregation test, which examines the ability of platelets to bind to an artificial endothelial surface
(ristocetin), is abnormal
.the PPT may be elevated in some Pts. because of a concomitant decrease in levels of factor 8 coagulant portion
-Treatment :
.desmopressin acetate DDAVP is used for mild bleeding or when the Pt. must undergo minor surgical procedures
.factor 8 replacement is used if desmopressin is not effective and the bleeding continues
.Pts. should not use aspirin
.FFP os not useful
**Coagulopathy
+Causes of prolonged PT or PTT (prothrombin time or partial thromboplastin time) :
173
+Prolonged PT
.factor 7 deficiency
.Vit K deficiency
.liver disease
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.warfarin use
.factor 7 inhibitor
+Prolonged PTT
.vWf
.factor 8, 9, 11, 12 deficiency
.heparin
.antiphospholipid antibody
+Prolonged PT & PTT
.prothrombin, fibrinogen, factor 5, factor 10 or combined factor deficiency
.liver disease
.DIC
.supratherapeutic heparin or warfarin
.combined heparin and warfarin use
.direct thrombin inhibitors
.inhibitor of prothrombin, fibrinogen or factor 5, 10
*Hemophilia A and B
- The deficiency of factor 8 in hemophilia A and factor 9 in hemophilia B resulting in an increased risk of bleeding
-Signs & Symptoms :
.mild deficiencies (25% or greater activity) result in either the absence of symptoms or with symptoms only during surgical
procedures or with trauma
.more severe deficiency (<5-10% activity) can result is spontaneous bleeding
.type of bleeding found with factor deficiencies are (hemarthrosis, hematoma, gastrointestinal bleeding or urinary bleeding,
bruising and CNS bleeding may occur)
.severe hemophilia is obvious in most Pts by the age of two/ The disorder becomes apparent often at the time of circumcision
-Causes :
.both hemophilia A and B are x-linked recessive disorders resulting in disease in males
.females are carriers of the disease. Females do not express the disease because they would have to be homozygous, which is a
condition resulting in intrauterine death of the fetus hemophilia A is far more common than B
-Diagnosis :
.a prolonged PTT with a normal PT is expected
.a factor deficiency is strongly suspected when a 50:50 mixture of the Pts blood is created with a normal control and the PTT
drops to normal. This is known as a ‘mixing study’
.the mixing study will only tell you that a deficiency is present;it will not tell you which specific factor is deficient
.specific factor 8, 9 levels are necessary to determine a precise diagnosis. This is true of both hemophilia A and B
-Treatment :
.mild hemophilia can be treated with desmopressin DDAVP
.desmopressin can also be used prior to surgical procedures in mild hemophiliacs
.desmopressin works by releasing subendothelial stores of factor 8
.more severe deficiencies are treated with replacement of the specific factor
.desmopressin does not work for hemophilia B
*Vitamin K deficiency
-The deficiency of Vit K resulting in decreased production of factor 2, 7, 9 and 10
-Signs & Symptoms :
.bleeding may mimic that of hemophilia and may occur at any site. Look for oozing at venipuncture sites
-Causes :
.Vit K deficiency can be produced by dietary deficiency, malabsorption and the use of antibiotics that kill the bacteria in the
colon that produce Vit K
-Diagnosis :
.both Pt and PTT are elevates
.the PT usually elevates first and more severely
.a correction of the PT and PTT in response to giving Vit K is the most common method of confirming the diagnosis
-Treatment :
174
.severe bleeding is treated with infusions of fresh frozen plasma

.Vit K is given at the same tome to correct the underlying production defect
*Liver Disease
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-Coagulopathy from the decreased production of clotting factors by the liver

-Signs & Symptoms :
.bleeding may occur at any site, but the gastrointestinal tract is the most common site
-Causes :
.any severe liver disease or cirrhosis leads to a decreased production of the majority of clotting factors that are generally all
made in the liver, except for factor 8 and von willebrand factor. Factor 7 is first factor to be depleted
-Diagnosis :
.Pts. have an elevation of both PT and PTT, but the PT elevated first and is often more severely affected
.the disorder is clinically indistinguishable from Vit K deficiency except that there is no improvement when Vit K is given
.low platelet counts are often present from the hypersplenism that accompanies the liver disease
-Treatment :
.fresh frozen plasma is used acutely to correct severe bleeding such as melena
.long term management is based on the nature of the liver disease
*Disseminated Intravascular Coagulation (DIC)

-Is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of
blood clots in the small blood vessels throughout the body
-Signs & Symptoms :
.bleeding from any site in the body is possible because of a decrease in both the platelet as well as clotting factor levels
.thrombosis is loss common
.hemolysis is often present and may leaf to acute renal failure, jaundice and confusion
-Causes :
.although essentially an idiopathic disorder
.Gram negative septicemia
.Falciparum malaria
.solid tumors and blood cancers (particularly acute promyelocytic leukemia)
.obstetric complications: abruptio placentae, preeclampsia or eclampsia, amniotic fluid embolism
.trauma, burns, hyperthermia, rhabdomyolysis, extensive surgery
.sepsis (most commonly) or severe infection (bacterial infections are the most common): bacterial (Gram-negative and Gram-
positive sepsis), viral, fungal, or protozoan infections
.transfusion reactions
.severe allergic or toxic reactions (i.e. snake or viper venom)
.giant hemangioma (Kasabach-Merritt syndrome)
.large aortic aneurysms
.liver disease
.HELLP syndrome
.thrombotic thrombocytopenic purpura
.hemolytic uremic syndrome
.malignant hypertension
-Diagnosis :
.elevated in both PT and PTT with a decrease in the platelet count
.the fibrinogen level is often low because it has been consumed
.D-dimer and fibrin split products are present in increased amount
-Treatment :
.fresh frozen plasma FFP and sometimes platelet transfusions are necessary to correct the bleeding
.heparin is controversial and is rarely used except in those Pts. presenting predominantly with thrombosis
**BLOOD TRANSFUSION
-Complications Of Blood Transfusion / Potential Risk :
.Hypothermia
.Hypocalcemia
.Hyperkalemia
.Thrombocytopenia
.Hemolytic reactions
175
.Anaphylactic reactions
.Hepatitis C
.HIV infection
.Acute congestive heart failure
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.Transmission of infection
.Transfusion reaction
.Acidosis
.Impaired hemostasis
.Citrate toxicity
.Impaired oxygen delivery
.Incompatibility
.Noncardiogenic pulmonary edema
+The most fatal complication of blood transfusion is (Human error)
+Diseases Are Transmitted Through Blood Transfusion :
.Syphilis
.Malaria
.Hepatitis B and C
.Epstein-Barr virus
.Helicobacter Pylori (are NOT)
+In vascular injury the immediate response that produce hemostasis is (Vasoconstriction)
+Platelets normally have a half life of (7 days)
+In human being, normal red blood cell survival time is approximately (120 days)
+Generalized Increased Pigmentation May Be Seen In (skin) :
.Chronic liver disease
.Addison disease
.Hemochromatosis
.Ectopic ACTH secretion
.Nelson's syndrome
.Hemochromatosis
.Chronic renal failure
.Primary biliary cirrhosis
+Causes Of Hypopigmentation (skin) :
.Albinism
.Tuberous sclerosis
.Post inflammatory
.Vitiligo
176
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CARDIOLOGY
**Coronary Artery Disease (Atherosclerotic Heart Disease)
-Is a group of diseases that (Ischemic heart disease) :
.stable angina
.acute coronary syndromes (unstable angina, myocardial infarction, ST-segment elevation, non ST-segment elevation)
-Signs & Symptoms :
.typical chest pains
.retrosternal (central)
.heaviness (tightness)
.radiates to Lt. arm (or Lt. shoulder)
.pain aggravated by exertion
.pain relieved by rest
-Risk factors :
.smoking
.hypercholesterolemia (LDL)
.hypertension
.hyperglycemia (due to DM or otherwise)
.type A behavioural pattern
.lack of exercise
.stress
.alcohol, smoking
.obesity, diet rich in saturated fats (saturated fat – harmful / unsaturated fat – useful)
.men over 60; women over 65 (M > F) (in females – estrogen protect)
*Angina
1.Stable Angina
.is a classic type of angina related to myocardial ischemia
.a typical presentation of stable angina is that of chest discomfort and associated symptoms precipitated by some activity
(running, walking, etc.) / With minimal or non-existent symptoms at rest or after administration of sublingual nitroglycerin
2.Unstable Angina
.it occurs at rest (or with minimal exertion), usually lasting 3–5 minutes
.it is severe and of new onset (i.e., within the prior 4–6 weeks)
.it occurs with a crescendo pattern (distinctly more severe, prolonged, or frequent than before)
.is sometimes referred to as ‘preinfarction’ angina
-Diagnosis :
.ECG-electrocardiogram (normal or non-specific changes)
.cardiac enzymes (normal)
.exercise stress test (best test)/exercise ECG test “treadmill test” (stop it when – occur chest pain, ECG changes)
(contraindication – peripheral vascular disease, osteoarthritis, MI, unstable angina)
.cardiac catheterization (IS BEST)
-Treatment :
.Propranolol
.nitroglycerin (sublingual-at home)
.beta-blockers and calcium channel blockers (act to decrease the heart's workload)
.statins
.baby aspirin (100mg)
.stopping smoking
+In ER :
.O2
.nitroglycerin
.aspirin
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+Side Effect Of Nitroglycerin :

.headache (M.C)
.hypotension
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+Contraindications (Nitroglycerin) :
.systolic Bp <90
.sildenafil (viagra) <24hrs
.phosphodiesterase 5-inhibitor
**Myocardial Infarction
*NSTEMI (non ST-segment elevation MI) (Heart Attack) Vs STEMI (ST-segment elevation MI)
-Is considered to have occurred if ischemia produces damage detectable by biochemical markers of myocardial injury (troponin
or CK-MB) / If there are no detectable serum markers of myocardial injury 12-18hrs after symptoms onset,the Pt should be
diagnosed with UA
-Signs & Symptoms :
.chest pain
.pain radiates most often to the Lt. arm, but may also radiate to the lower jaw, neck
.difficulty in breathing (shortness of breath-dyspnea)
.nausea, vomiting
.sweating
.palpitation
+Silent MI is M.C in the elderly in Pts. with DM (epigastric pain)
-Risk factors :
.high serum cholesterol level
.elevated low density lipoprotein level (LDL)
.hypertension
.DM
.smoking
.male gender
.obesity
.increasing age
.family history
.excess alcohol and carbohydrates intake
.stressful life-style
+Complications Of Myocardial Infarction :
.DVT
.heart arrhythmia (M.C.C of death in the 1st hr post-MI)
.acute & Chronic heart failure (congestive heart failure) (M.C.C of heart failure is ischemic heart disease)
.cardiogenic shock (massive MI / inferior MI)
.papillary muscle rupture (mitral regurgitation)
.dressler’s syndrome - pericarditis (2-6wks after MI)
.ventricular aneurysm, (2-3 days, persistent ST-elevation)
.thromboembolism
.myocardial rupture (>1wk from MI)
-Diagnosis :
1.ECG
.The usual ECG findings of NSTEMI are (ST-segment depression) or (T-wave inversion)
2.CARDIAC MARKERS (Cardiac Enzymes – BEST)
.Cardiac Specific isoenzyme CK-MB (creatine kinase myocardial band) (starts to rise at 4-6 hours and falls to normal within 48-72
hours)
.Cardio Specific proteins (troponin-T) and (troponin-I) are rises in blood in NSTEMI (Troponin-T and troponin-I start to rise at 4-6
hours and remain high for up to two weeks)
+If cardiac enzyme (-) repeat after 6hrs
+Lipids (LDL, HDL, Triglyceride (TG), Cholestrol)
3.FULL BLOOD COUNT
.WBC / ESR / CRP (c-reactive protein) are elevated
4.CXR
178
.Signs of lung edema

5.ECHO
-Treatment :
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+Oxygen, aspirin, morphine and nitroglycerin (are usually administered as soon as possible)
.baby aspirin (antiplatelet therapy)
.heparin (antithrombin therapy – anticoagulant)
.glycoprotein (GP) Iib/IIIA inhibitors
.beta-blocker
.intravenous nitroglycerin (NTG) for refractory pain
.CABG (coronary artery bypass graft)
+Patients With NSTEMI Have A :
.normal physical examination
.abnormal ECG
.particularly dynamic ST-segment deviation
.T-wave inversion
+Cardia Enzymes :
.troponin I (most specific -1st)
.CK-MB (2nd)
.AST
.LDH (lactate dehydrogenase)
+Causes False Positive Troponin :
.Septic shock
.Pulmonary embolism
.Pulmonary edema
.Renal failure
+Causes Increased In Troponin :
.Pulmonary edema
.MI
.Congestive heart failure
.Myocarditis
+Stable Angina +MI

.after excessive or stress .at rest
.cardiac enzyme (-) .cardiac enzyme (+)
.ECG (non-specific changes) .ST-elevation
.5-15 minutes .>20 minutes
.relieved by nitroglycerin .not relieved by nitroglycerin
.no nausea, no vomiting, .may be associated with nausea, vomiting,
no sweating sweating
+Regarding Chest Pain Of Myocardial Infarction :

.duration more than 30 minutes
.associated with nausea
.relieved with sublingual nitrate
.Lt. shoulder radiation
*Arrhythmias (Cardiac Dysrhythmia or Irregular Heartbeat)

-Is a group of conditions in which the heart beats with an irregular or abnormal rhythm (too fast, or too slow)
+A heartbeat that is too fast (tachycardia) - above 100 beats per minute in adults
+A heartbeat that is too slow (bradycardia) - below 60 beats per minute
-Signs & Symptoms :
.palpitations or feeling a pause between heartbeats (M.C symptom)
.lightheadedness
.chest pain
+Many types of arrhythmia have no symptoms. When symptoms are present these may include palpitations or feeling a pause
between heartbeats
179
-Complications :
.stroke
.heart failure
.cardiac arrest
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-Types :
.extra beats (premature atrial contractions and premature ventricular contractions)
.supraventricular tachycardias (atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia)
.ventricular arrhythmias (ventricular fibrillation and ventricular tachycardia)
.bradyarrhythmias
-Classifications :
+Atrial
.Sinus bradycardia
.Premature atrial contractions (PACs)
.Wandering atrial pacemaker
.Atrial tachycardia
.Multifocal atrial tachycardia
.Supraventricular tachycardia (SVT)
.Atrial flutter
.Atrial fibrillation (Afib)
+Junctional arrhythmias
.AV nodal reentrant tachycardia
.Junctional rhythm
.Junctional tachycardia
.Premature junctional contraction
+Ventricular
.Premature ventricular contractions (PVCs)
.Accelerated idioventricular rhythm
.Monomorphic ventricular tachycardia
.Polymorphic ventricular tachycardia
.Ventricular fibrillation
.Torsades de pointes
+Heart blocks
.These are also known as AV blocks, because the vast majority of them arise from pathology at the atrioventricular node. They
are the M.C.C of bradycardia :
.First degree heart block, which manifests as PR prolongation
.Second degree heart block
(Type 1 Second degree heart block, also known as Mobitz I or Wenckebach / Type 2 Second degree heart block, also known as
Mobitz II)
.Third degree heart block, also known as complete heart block
+Sudden arrhythmic death syndrome (SADS)
.is a term used as part of sudden unexpected death syndrome to describe sudden death due to cardiac arrest brought on by an
arrhythmia in the presence or absence of any structural heart disease on autopsy
.The M.C.C of sudden death is coronary artery disease specifically because of poor oxygenation of the heart muscle, that is
myocardial ischemia or a heart attack
-Causes of SADS in young people :
.viral myocarditis
.long QT syndrome
.Brugada syndrome
.Catecholaminergic polymorphic ventricular tachycardia
.hypertrophic cardiomyopathy
.arrhythmogenic right ventricular dysplasia
-Treatment :
.beta blockers or agents that attempt to restore a normal heart rhythm such as procainamide
.Amiodarone IV
.Diltiazem IV
+Antiarrhythmics Drugs:
.Xylocaine
.Quinidine
180
.Amiodarone
.Procainamide
+Causes Of MI Without ACS (acute coronary syndrome) :
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.protein C deficiency
.polycythemia vera
.thrombocytosis
.coronary spasm
.coronary artery embolus
.SLE
.polyarteritis nodus
.kawasaki
+Causes Of Tachycardia :
.Amphetamine
.Anemia
.Antiarrhythmic agents
.Atrial fibrillation
.Atrial flutter
.Atrial tachycardia
.AV nodal reentrant tachycardia
.Brugada syndrome
.Caffeine
.Cocaine
.Exercise
.Fear
.Fever
.Hypoglycemia
.Hypovolemia
.Hyperthyroidism
.Hyperventilation
.Infection
.Junctional tachycardia
.Multifocal atrial tachycardia
.Nicotine
.Pacemaker mediated
.Pain
.Pheochromocytoma
.Sinus tachycardia
.Wolff-Parkinson-White syndrome
+Causes Of Bradychardia :
.Obstructive jaundice
.Recreational drug use or abuse (digoxin)
.metabolic or endocrine issues, especially in the thyroid
.Electrolyte imbalance
.Neurological factors
.Autonomic reflexes
.Situational factors such as prolonged bed rest
.Autoimmunity
.Cardiac causes (acute or chronic ischemic heart disease, vascular heart disease, valvular heart disease, or degenerative primary
electrical disease)
+In general, two types of complications result in bradycardias :
.disorders of the sinoatrial node (SA node)
.disorders of the atrioventricular node (AV node)
**Heart Failure (congestive heart failure CHF)

-Occurs when the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs
-Symptoms :
.shortness of breath (worse with exercise, while lying down, and may wake the person at night)
181
.excessive tiredness
.leg swelling
.chest pain (angina)
.hear failure symptoms are divided into "left" and "right" sided :
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1.Left sided heart failure
+The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic
circulation (the rest of the body except for the pulmonary circulation)
+Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as
well as fatigue due to insufficient supply of oxygenated blood
.pulmonary edema (fluid in the alveoli) (M.C)
.increased rate of breathing (respiratory distress)
.rales or crackles, heard initially in the lung bases
.cyanosis (hypoxemia)
.laterally displaced apex beat (which occurs if the heart is enlarged)
.gallop rhythm (additional heart sounds - third heart sound, triple rhythm) (S1, S2, S3)
.heart murmurs
.dyspnea (shortness of breath)
.orthopnea
.paroxysmal nocturnal dyspnea (PND)
.laterally displaced apex beat (which occurs if the heart is enlarged)
.fatigability, wheezing, dizziness, confusion
.cool extremities at rest
.pulsus alternans
.bilateral basal crepitations
.kerley B lines on CXR
2.Right sided heart failure
.peripheral edema
.ascites
.hepatomegaly
.jugular venous pressure (distended neck veins – increased TVP)
.coagulopathy
-Causes :
.ischaemic heart disease (M.C.C)
.dilated cardiomyopathy
.valvular heart disease
.hypertension
.anemia
.kidney diseases
.beriberi (vitamin B1/thiamine deficiency)
.hyperthyroidism
.Paget's disease
.arteriovenous fistula
.viral infections of the heart (can lead to inflammation of the muscular layer of the heart)
.chemotherapeutic agents (daunorubicin and trastuzumab)
.abuse of drugs (alcohol and methamphetamine)
.infiltrative disorders (amyloidosis)
.connective tissue diseases (systemic lupus erythematosus)
.decompensate (this most commonly results from an intercurrent illness such as pneumonia, myocardial infarction-heart
attack), abnormal heart rhythms, uncontrolled hypertension, or a patient's failure to maintain a fluid restriction, diet, or
medication)
.NSAIDs and thiazolidinediones
+Right heart failure compromises pulmonary flow to the lungs
+Left heart failure compromises aortic flow to the body and brain
+Mixed presentations are common; left heart failure often leads to right heart failure in the longer term
-Diagnosis :
182
.Echo
-Treatment :
.angiotensin-converting enzyme (ACE) inhibitors (1st line therapy for all HF Pts.)
+ACE (enalapril, captopril, lisinopril, ramipril)
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.angiotensin receptor blocker ARB (losartan, valsartan) (NO cough)

.beta-blockers (metoprolol, bisoprolol, carvedilol) (only this 3 drugs)
.digoxin (digitalis)
+Side effects of digoxin therapy :
.nausea, vomiting
.yellow vision
.AV block
.ventricular extrasystole
+Side effects of ACE-inhibitors :
.angioneurotic edema
.hyperkalemia
.dry cough
.hypotension
+Indications for the use of Beta-blockers :
.angina
.hypertension
.after myocardial infarction
.congestive heart failure CHF
.ischemic heart disease
.migraine
.anxiety
+Crepitations which are late inspiratory and unchanged with cough are typical of Pulmonary edema
**Hypertension HTN
-Normal Bp at rest is within the range of (100-140 mmHg systolic – top reading / 60-90 mmHg diastolic – bottom reading)
-Types :
.primary hypertension (90-95% of cases) (M.C)
.secondary hypertension (5-10% of cases)
-Causes Of Primary Hypertension :
.is rarely accompanied by any symptoms (and its identification is usually through screening)
-Causes Of Secondary Hypertension :
.Renovascular hypertension – Renal Artery Stenosis (M.C.C) (Fibromuscular dysplasia – in young females / Atheromatous
stenosis – in old age Pts.)
.Hypertension secondary to renal disorders (CRF / Glomerulonephritis)
.Hypertension secondary to endocrine disorders (Pheochromocytoma – caused by an excessive secretion of norepinephrine
and epinephrine which promotes vasoconstriction / Hyperaldosteronism – Conn's syndrome / Cushing`s syndrome – an
excessive secretion of glucocorticoids causes the hypertension / Hyperparathyroidism / Hyperthyroidism – systolic HTN /
Hypothyroidism – diastolic HTN / Acromegaly)
.Hypertension Secondary To Other Causes (Pregnancy, Drugs, Liquorice, Coarctation Of Aorta)
-Complications :
.MI
.stroke
.left ventricular hypertrophy
.hypertensive cardiomyopathy
.hypertensive encephalopathy
.hypertensive retinopathy
.hypertensive nephropathy
-Treatment :
.diuretics (1st drug is thiazide)
.beta-blockers (atenolol, metoprolol, propranolol) (post MI)
.mixed (alpha + beta-blocker ‘labetalol’) (in pregnancy)
.alpha-blockers (tamsulosin, doxazosin, alfuzosin) (pregnancy)
.ACE inhibitors (captopril, enalapril) (for heart failure)
.angiotensin receptor blocker ARB (losartan, valsartan)
183
.calcium channel blockers (amlodipine, nifedipine, diltiazem, verapamil) (contraindicated in HF)

.vasodilators (sodium nitroprusside, hydralazine, minoxidil) (they are only used in hypertensive emergencies)
+Choice Of Initial Medications :
.thiazide diuretics – increased absorption of Ca+2 (1st line drug for HTN) (kidney stones)
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.ACE inhibitors and angiotensin receptor blockers ARB (renal and retinal complications of DM) (decreased nephropathy and
retinopathy)
.ACE inhibitors (decreased mortality in HF)
.alpha-blocker (bening prostatic hyperplasia)
.alpha-methyldopa, labetalol (pregnancy)
.beta-blocker (post-MI)
+Thiazide can cause (hypercalcemia, hypocalcemia)
*Hypertensive Crisis (Hypertensive Emergency or Malignant Hypertension)

-Severe increase in blood pressure that can lead to a stroke. Extremely high blood pressure — a top number (systolic pressure)
of 180 (mm Hg) or higher or a bottom number (diastolic pressure) of 120 mm Hg
+Systolic over 180 or diastolic over 120 / HTN 180/120 + one or more organ damage
-Signs & Symptoms :
.the eyes may show retinal hemorrhage or an exudate
.papilledema - hypertensive retinopathy (must be present before a diagnosis of malignant hypertension can be made)
.the brain shows manifestations of increased intracranial pressure, such as (headache, vomiting, and/or subarachnoid or
cerebral hemorrhage)
.the kidneys will be affected (resulting in hematuria, proteinuria, and acute renal failure)
.chest pain
.arrhythmias
.headache
.epistaxis
.dyspnea
.faintness or vertigo
.severe anxiety
.agitation
.altered mental status
.paresthesias
.vomiting
-Causes :
.discontinuation of antihypertensive medications
.autonomic hyperactivity
.collagen-vascular diseases
.drug use (particularly stimulants, especially cocaine and amphetamines and their substituted analogues)
.glomerulonephritis
.head trauma
.neoplasias
.preeclampsia and eclampsia
.renovascular hypertension
Systolic Pressure (mm Hg) Diastolic Pressure (mm Hg)

+Normal < 120 < 80
+Pre-hypertension 120-139 80-89
+Hypertension stage 1 140-159 90-99
+Hypertension stage 2 ≥ 160 ≥ 100
+Hypertensive crisis – emergency ≥ 180 ≥ 110
**Infective Endocarditis
-Inflammation, of the inner tissue of the heart, such as its valves
+M.C bacteria-Organism in infective endocarditis is (Streptococcus Viridans)
+M.C bacteria in I.V drugs abusers is (Staphylococcus Aureus)
+The site of endocarditis in drug abusers is (Tricuspid Valve)
+M.C bacteria in prosthetic valve is (Staphylococcus Epidermidis)
184
+Streptococcus Bovis, associated with colon cancer

+M.C valve-affected (mitral valve)
-Signs & Symptoms :
.fever
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.clubbing
.weight loss
.heart murmur
.roth's spots (on the retina)
.Osler's nodes (painful subcutaneous lesions in the distal fingers)
.janeway lesions (painless hemorrhagic cutaneous lesions on the palms and soles)
.intracranial hemorrhage
.conjunctival hemorrhage
.splinter hemorrhage (nail hemorrhage)
.renal infarcts
.splenic infarcts or splenomegaly
.vascular phenomena (septic embolism – causing thromboembolic problems such as stroke in parietal lobe of the brain or
gangrene of fingers
.anemia
.malaise
.fatigue
.hematuria
.anorexia
-Causes :
.bacteremia (Streptococcus viridans, Staphylococcus aureus)
+Bacteremia caused by (dental procedures and I.V drug abusers)
-Classifications :
.subacute bacterial endocarditis SBE (M.C is Streptococcus viridans)
.acute bacterial endocarditis ABE (M.C is Staphylococcus aureus)
-Diagnosis :
+Major criteria include :
.positive blood culture
.positive echo + vegetation
+Minor criteria include :
.predisposing factor (known cardiac lesion, recreating drug injection)
.fever >38c
.evidence of embolism (arterial emboli, pulmonary infarcts, janeway lesions, conjunctival hemorrhage)
.immunological problems (glomerulonephritis, Osler`s nodes)
-Treatment :
.high dose antibiotics (2-6 weeks)
+Fever Of Unknown Origin :
.Infectious (endocarditis, TB, Brucella, Typhoid, Malaria)
.Malignancy (leukemia, lymphoma)
**Rheumatic Fever
-Is an inflammatory disease that occurs following a Streptococcus pyogenes infection caused by antibody cross-reactivity that
can involve the heart, joints, skin, and brain
+The disease typically develops 2-4 weeks after a throat infection (occur post-Streptococcal infection - tonsillitis)
+Acute rheumatic fever commonly appears in children between the ages of 6-15 age
-Signs & Symptoms :
+Major Criteria
.polyarthritis, arthritis
.carditis
.erythema marginatum (itchy rash)
.sydenham's chorea
.subcutaneous nodules
+Minor Criteria
.fever
.arthralgia
185
.raised ESR
.C-reactive protein, leukocytosis, WBS elevated
.erythema nodosum
.ECG (prolonged PR interval)
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+Others
.multiple painful joints
.involuntary muscle movements
.atrial fibrillation
.infection of the valves
.abdominal pain
.nose bleeds
-Diagnosis :
.evidence (Anti-streptolysin O - ASO or ASLO) + 2 major criteria, OR
.evidence (ASO titer + 1 major + 2 minor), OR
.evidence (ASO titer + Chorea)
+Chorea - a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and
face
-Treatment :
.high dose antibiotics (pencillin)
.NSAID (Aspirin)
.erythromycin, prednisone
+Lipid lowering agents :
.statine
.fibrates (gemafibrozil)
.bile acid binding
.nicotinic acid
.fish oil (omega-3)
**Syncope
-Is defined as a short loss of consciousness and muscle strength, characterized by a fast onset, short duration and spontaneous
recovery
-Cardiac Syncope (is sudden without warning and complete recovery / last for 1-2min)
-Causes of cardiac syncope :
.arrhythmia (bradycardia and tachycardia)
.obstructive cardiac lesion (Aortic stenosis and mitral stenosis)
.acute aortic dissection
.pericardial tamponade
.pulmonary embolism
.pulmonary hypertension.
.hypertrophic cardiomyopathy
+Contraindications Of Exercise Electrocardiogram (Stress Test) :

.unstable angina
.recent MI (within 10 days)
.sever hypertrophic cardiomyopathy
.sever aortic stenosis
.malignant HTN
.heart failure
+We Stop Exercise Electrocardiography (Exercise Stress Test), When :
.chest pain
.ECG pain
.decreased in Bp >20 mmHg
.HTN >140/110
.arrhythmia
+Causes Of Atrial Fibrillation :
.ischemic heart disease (IHD)
.rheumatic heart disease
186
.idiopathic
.hyperthyroidism
.pneumonia
.pericarditis
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.cardiac surgery
.alcohol
.congenital heart disease
+Wolf Parkinson White Syndrome (WPW) :
.ECG (delta wave)
.usually associated with atrial fibrillation
.drug to choice is (amiodarone)
+Atrial Flutter :
.ECG (saw-tooth appearance)
.management like atrial fibrillation
+Homocystinuria + Lipoproteinemia (risk factor for IHD)
+Lipoproteinemia - A disorder in which the proteins that carry fat around the body are defective
+Homocystinuria - It is an inherited autosomal recessive trait, which means a child needs to inherit a copy of the defective gene
from both parents to be affected (is an inherited disorder of the metabolism of the amino acid methionine, often involving
cystathionine beta synthase)
**Pulmonary Edema
-Signs & Symptoms :
.dyspnea
.wheezing
.tachycardia
.cyanosis
.cough with expectoration (pink frothy sputum)
.gallop rhythm
.crackles
-Causes :
.Lt. sided HF (M.C)
.MI
.mitral regurgitation
.mitral stenosis
.aortic regurgitation
.arrhythmia
+Pulmonary edema is caused by :
.Fallot Tetralogy
.Acute glomerulonephritis
.Aspiration of hydrocarbons
.Left to right shunt
-Diagnosis :
.CXR (bilateral shadow - butterfly)
.Kerley B lines
-Treatment :
.Pt. in sitting position
.oxygen (60%)
.furosemide I.V (40-80%)
.morphin
.aminophylline
.C-PAP
**Valvular Heart Disease

*Mitral Stenosis
-Characterized by the narrowing of the orifice of the mitral valve of the heart
-Signs & Symptoms :
.increased Lt. atrial pressure (left atrial enlargement)
187
.pulmonary edema
.hemoptysis
.hoarseness of voice
.malar flush
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.diastolic murmur (loud S1)

.thromboembolism + atrial fibrillation
.opening snap (S2)
.pre-systolic murmur
.rumbling mid-diastolic murmur
.dyspnea, orthopnea
.systemic embolism
.Rt. sided heart failure (hepatomegaly, ascites, peripheral edema)
-Causes :
.rheumatic fever (M.C.C)
.rheumatic heart disease
.calcification
.CHD
.mitral valve (it is the most common valvular heart disease in pregnancy)
.infective endocarditis
.endomyocardial fibroelastosis
.malignant carcinoid syndrome
.systemic lupus erythematosus
.whipple disease
.fabry disease
.rheumatoid arthritis
.hurler' disease
.hunter's disease
.amyloidosis
*Mitral Regurgitation
+The symptoms associated with MI / F > M
-Signs & Symptoms :
.congestive heart failure (shortness of breath, pulmonary edema, orthopnea, and paroxysmal nocturnal dyspnea)
.symptoms of cardiogenic shock (shortness of breath at rest)
.cardiovascular collapse with shock (cardiogenic shock)
.infective endocarditis of the mitral valve
.holosystolic murmur
.loud S3
.tachycardia
-Causes :
.rheumatic fever (M.C.C)
.Marfan's syndrome
.hyperthyroidism
.mitral valve prolapse (MVP)
.myxomatous degeneration
.Ehlers Danlos Syndrome
.Ischemic heart disease
.chordae tendineae
.pulmonary edema
.Lt. atrial enlargement
.pansystolic murmur (late systolic click)
+Rheumatic heart disease affects most commonly Mitral valve
*Tricuspid Regurgitation (TR)

-Signs & Symptoms :
.Rt. sided heart failure (such as ascites and peripheral edema)
.pansystolic heart murmur
.loud S3
188
-Causes :
.Rt. ventricular dilation (right ventricular infarction, inferior myocardial infarction, and cor pulmonale)
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.endocarditis
.pulsatile liver
.increased JVP
.rheumatic
.myxomatous
.ebstein anomaly
.endomyocardial fibrosis
.traumatic (blunt chest injury)
.LV dysfunction or valve disease
.chronic lung disease
.pulmonary thromboembolism
.RV ischemia
.Left to right shunt
**Aortic Valve Disease

*Aortic Stenosis
-M.C.C is (in old age calcification) (bicuspid aortic valve in children)
-Signs & Symptoms :
.angina
.syncope
.heart failure
.left ventricular hypertrophy
.sudden death
.slow rising pulse (decreased pulse pressure)
.early systolic murmur (ejection systolic murmur)
.S4 gallop
.A2 decreased, S2 single
.aortic ejection click
.carotid thrill
-Treatment :
.surgery if <0.75cm
*Aortic Regurgitation
-Can cause pulmonary edema
-Signs & Symptoms :
.causes wide pulse pressure
.head nodding
.collapsing pulse
.diastolic murmur
.pulse pressure (systolic increased-diastolic decreased)
.left ventricular impulse
.pistol shot femoral pulses
**Cardiomyopathy
-"heart muscle disease" is the measurable deterioration for any reason of the ability of the myocardium (the heart muscle) to
contract, usually leading to heart failure
-Signs & Symptoms :
.dyspnea
.peripheral edema
.irregular heart rate
-Types :
1.Dilated Cardiomyopathy DCM
.is a condition in which the heart becomes enlarged and cannot pump blood efficiently (M.C form)
189
.causes heart failure & arrhythmia

2.Hypertrophic Cardiomyopathy HCM
.is a primary disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophied
(thickened) without any obvious cause, creating functional impairment of the cardiac muscle
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.familial (autosomal dominant)

.M.C.C of sudden death in young athletes
3.Restrictive Cardiomyopathy RCM
.is a form of cardiomyopathy in which the walls are rigid, and the heart is restricted from stretching and filling with blood
properly
.M.C.C is amyloidosis
4.Constrictive Pericarditis
.is a medical condition characterized by a thickened, fibrotic pericardium, limiting the hearts ability to function normally
.M.C.C is idiopathic
-Other Causes :
.TB
.sarcoidosis
.Rt. side heart failure
.lower limbs edema
.ascites
.hepatomegaly
.chronic renal failure
.post-myocardial infection
.post-viral pericarditis
.chronic pericarditis
.heart surgery
+Contraindication for thrombolytic therapy :
.stroke (within 2 months)
.HTN (uncontrolled)
.surgery (within 6 days)
.bleeding disorder
.non-STEMI
.post MI (>12hrs)
**Coarctation Of Aorta CoA

-Is a congenital condition whereby the aorta narrows in the area where the ductus arteriosus (ligamentum arteriosum after
regression) inserts
-Signs & Symptoms :
.Bp in upper limb increased / Bp in lower limp decreased
.lower limb atrophy
.radio-femoral delay
.systolic murmur in ventricular hypertrophy
.CxR (notching of ribs)
.associated with turner's syndrome (45 XO)
By Dr.Mohammad Z. abu sheikha@

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Internal Medicine

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MEDICINE

By Dr.Mohammad Z. abu sheikha@

gastric acid production)

By Dr.Mohammad abu sheikha@

.infections (candida esophagitis, HSV)

.pneumatic balloon dilation

.pneumatic dilation or surgery (surgical myotomy)

**Diffuse Esophageal Spasm (DES)

**Gastroesophageal Reflux Disease GERD

-Signs & Symptoms :

.heartburn and regurgitation (M.C symptoms of GERD)

**Benign Esophageal Stricture

.webs and rings

**Tumors Of The Esophagus (Esophageal Cancer)

cisplatin and 5-FU are used)

**Plummer–Vinson Syndrome (PVS)

.the acute abdomen (appendicitis, cholecystitis, pancreatitis, intestinal obstruction)

**Zollinger-Ellison Syndrome (ZES)

**Peptic Ulcer Disease PUD

.gastroesophageal reflux disease (GERD)

*Duodenal Ulcers (DU)

release digested food and acid into the duodenum)

*Gastric Ulcer (GU)

+H. pylori Can Lead To :

+Drugs Are Used For H. Pylori Eradication :

**Cancer Stomach (Gastric Cancer)

.diffuse (no glands)

**Inflammatory Bowel Disease (IBD)

.colonoscopy and biopsy

+Upper endoscopy (Are NOT)

+Signs And Symptoms CD UC

*Irritable Bowel Syndrome

.can lead to tricuspid insufficiency and pulmonic stenosis

+Vitamins (AKED) dependent on bile salts for its absorption

esophageal ulcers, Mallory-Weiss tear)

NSAIDs), dieulafoy's lesions)

.0-5 months (25-40) (30)

.3-5 yrs (20-30) (25)

*Lower Gastrointestinal Bleeding (LGIB)

+Pain with defecation occurs with hemorrhoids and anal fissure

+Drugs May Produce GI Bleeding :

*Wilson`s Disease (Hepatolenticular Degeneration)

**Alpha 1-antitrypsin Deficiency (A1AD)

.high protein diet

**Hemochromatosis (Bronzed diabetes)

**Iron Overload (Hemochromatosis)

prolonged haemodialysis, and post-portacaval shunting

**Celiac Disease (Gluten enteropathy)

**Diseases Of The Pancreas

.Hematocrit (fall) decrease >10%

+Amylase + lipase - protein (enzyme) value is NOT one of Ranson`s criteria

-Encapsulated collection of pancreatic fluid

**Juvenile Polyposis JPS

-Signs & Symptoms :

.blood in the stool

+M.C site of distant (hematogenous) metastasis from colorectal cancer is liver

+Colon cancer is M.C.C of Large bowel obstruction

*Colonic And Rectal Polyps (Colorectal Polyps)

.total proctocolectomy and ileostomy

+With FAP, other tumor must be looked for is (duodenal tumors)

**Diverticular Disease Of The Colon

.autoimmune liver disease