Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

GASTROINTESTINAL DISORDERS
Signs & Sx of GI Distress abd pain, distension, bloating, chest discomfort, indigestion, dysphagia; anorexia, N/V, wt gain or loss; diarrhea & constipation, tenesmus; jaundice; hemoptysis, hematemesis (vomiting bld), hematochezia (the passage of bld in the feces); melena (dark, tarry stools containing decomposing bld; indicative of bleeding in the upper part of the GIT) RED FLAGS

progressive wt loss, night sweats & fevers possible malignancy bright red bld from rectum diverticular disease, UC, tumour blood in stool hemorrhoids, colorectal CA, diverticular dis, UC, tumour dizziness, nausea, sweating, hypotension GI bleeding melena complicated esophageal ulcer, peptic ulcer disease (PUD) 4X more common than bleeding from the lower GI major cause of morbidity & mortality Lab Dx: Hb, BUN:creatinine ( w/ UGIB >36 in pt w/out renal insuff), coagulation profile, platelet count (<50 requires platelet transfusion), LV fxn test, plasma fibrinogen, electrolytes DDx: btwn gastric/duodenal ulcer, gastric/esophageal varices, Mallory-Weiss tear, esophagitis, neoplasm, hemorrhagic gastritis Lab Dx: see above; xray in suspected obstruction DDx: food poisoning, ectopic preg, MI, LU dis, acute pancreatitis, appenditis, peritoneal inflm, cholecystitis, cholelithiasis or KI stone, bowel obstructn, testicle/ovary torsion, rupture of aortic aneurysm Keynotes: DRE may reveal peritoneal inflm bc anterior rectum has peritoneal surface include preg test & pelvic exam to rule out ectopic preg

UPPER GI BLEEDING

alcohol abuse LV cirrhosis portal

HTN esophageal varices (potential source for UGIB) NSAID use may lead to gastric bleeding

ABDOMINAL PAIN

Categories: Visceral: arises from abdominal organs Parietal: arises from outside layer of abdominal organs; pain more localized Superficial abd wall pain: asstd w/ injuries to mm or inflm of the skin as in Herpes zoster Referred pain

Extraperitoneal causes: - pneumonia, MI, empyema, rheumatic fever, leukemia, SCA, SC tumour, Herpes zoster, nephritis, prostitis..many many more (see pp 2 pkg 1)

- Observe position of the pt: - flexed right hip < extension appendicitis - fetal acute pancreatitis - pain < mvmt peritoneal inflm - pain > mvmt ureteral stone, cholecystitis - Abdominal exam: - palpation, rebound tenderness - Murphys sign (+) acute cholecystitis - Grey-turners sign (+) retroperitoneal bleed - Cullens sign (+) Quality of pain Sudden 15-45min; > antacids & food Several hours Several days Acute/chronic diarrhea Cramping, intermittent, stabbing Squeezing, steady Perforation, rupture, torsion PUD Biliary colic Pancreatitis Obstruction, spasm, dilation Biliary colic

painful soft abd in elderly

IBD point tenderness suggests appendicitis, diverticulitis, cholecystitis

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

DISEASES OF THE ESOPHAGUS

DYSPHAGIA
- subjective awareness of difficulty swallowing dt impaired progression of matter to ST Mechanical/Obstruction Pre-esophageal or esophageal origin:

1)Intrinsic narrowing: inflamed

esophagus becomes swollen diameter 2)Extrinsic compression: external compressive forces Motor/Neurological 1)Diff swallowing dt oral lesions, paralysis of tongue, oropharyngeal anesthesia

solids only obstruction solids & liquids motor dysfunction intermittent lower esophageal ring
(Schatzki)

DDx: hiatal hernia, GERD + complications (Barretts metaplasia, esoph stricture), esoph web (PVS), ring (Schatzkis), carcinoma

progressively worsens carcinoma

NB: Rule out globus hystericus: feeling of having a lump in throat unrelated to swallowing; asstd w/ anxiety & grief

2)Dysfxn of peristalsis dt
impairment of striated esophageal mm a.r.o. CVA or myopathy of smooth mm as in achalasia & diffuse spasms

Mechanical Obstructive Disorders of the Esophagus

HIATAL HERNIA
- A portion of the ST prolapses through the diaphragmatic esophageal hiatus - 2 types:

- caused by factors that intraabd P such

as: constipation, preg, ascites, obesity - asstd w/ GERD & its complications

Sx: usually asymptomatic

1)Paraesophageal hernia:
widened esoph hiatus permits fundus of ST to protrude into chest,; GE jxn remains below the diaphragm preventing acid reflux

2)Sliding hiatal hernia: MC, GE

jxn migrates into the chest thru the esoph hiatus; as LES moves up into chest it is less effective as a sphincter allowing acid reflux

GASTROESOPHAGEAL REFLUX DISEASE (GERD)

reflux of gastric contents into esophagus dt incompetence of LES

Causes:

Sx:

infection, drugs, corrosive chemicals,

pregnancy, scleroderma

Heartburn (epigastric/substernal burning)

occurs w/I an hour or two after meals & last minutes to hours; radiates up & down thorax (DDx: angina: pain radiates from across chest into back, lasts minutes unless MI develops

agents that LES P : caffeine,

chocolate, alcohol, nicotine, fats

Dx: endoscopy w/ biopsy confirms GERD; esophageal manometry to determine the P & strength of the LES; esophageal pH monitoring, barium swallow

Disease

Definition

Etiology, Pathogenesis & Complications

Complications: esophagitis strictures, ulcerations w/chronic inflammation scarring pulmonary aspiration lasts hours)

Signs & Sx

Dx & DDx

Chest pain: substernal that may radiate into

back, neck, arms, jaw; independent or co-existent w/ heartburn

Barretts esophagus/ Metaplasia

Regurgitation of gastric contents Dysphagia for solids w/ full feeling in throat

(may indicate developing stricture) Persistent non-productive cough bloating, belching

< lying down after meal, bending over, at night

or when fasting angina-like pain d/t stretching and stimulation of visceral afferent fibers of esophagus burning, squeezing hoarseness, repetitive clearing of throat

BARRETTS ESOPHAGUS/ METAPLASIA

- A metaplastic change of normal

squamous epith of the esoph to abnormal columnar epithelium dt chronic irritation

- Specialized metaplastic cells

secrete mucous & histologically resemble cells in ST & intestine

Tx: - dont lay down after eating or elevate head, acid suppressing med (antacids, proton pump inhibitors, histamine rec antagonists)

- wt loss to intraabd P - diet: avoid acid forming

- most pts asymptomatic and unaware of their condition until found during an endoscopy or barium swallow foods, eat smaller meals Dx & Lab Dx: see pp 2 pkg 2 DDx: congenital, PlummerVinson syndrome, chronic inflm, caustic ingestion, autoimmune dis, celiac sprue

ESOPHAGEAL WEBS, RINGS, STRICTURES

Plummer-Vinson Syndrome **Web

Web: smooth, eccentric 2-3mm wide, extension of normal esoph T consisting of mucosa & submucosa Ring: smooth, concentric 3-5mm wide extension of T consisting of all 3 layers Stricture: about 1-4cm long; develops a.r.o scarring from acid reflux - A thin mucosal memb covered by normal squamous epith that grows across the inside of the esophagus from the mucosa (at the level of the cricoid)

- Fe def anemia: depletion of Fe dependent enzymes changes in muscles involved in swallowing mech atrophy of esophageal mucosa web formation - asstd w/ AI conditions such as: RA, pernicious anemia, celiac, thyroiditis probably present at birth correlated to GERD, pill induced esophagitis, congenital

Sx: difficulty swallowing solids

Tx: perforation of webs, treat underlying anemia & webs will disappear on their own

Schatzkis Ring **Ring

- lower esophageal ring located at the junction of esoph & ST

Sx: - intermittent non-progressive dysphagia for solids

DDx: carcinoma, dysphagia is permanent and progressive Tx: esophageal dilation w/ intention of fracturing ring, chew food well Tx: esophageal dilation, chew

develops when lumen < 12mm (normal

3-4cm)

Peptic Esophageal

- inflm & ulcer formation scar

- a result of GERD induced esophagitis

Disease

Definition

Etiology, Pathogenesis & Complications

(accounts for 70-80% of strictures) - some congenital Histological changes - edema, cellular infiltration, basal cell hyperplasia, deposition of collagen on healing

Signs & Sx

Dx & DDx

Stricture **Stricture

formation stricture formation

food well, long term proton pump inhibitors, avoid substances that LES P

ESOPHAGEAL DIVERTICULA Zenkers Diverticulum (pharyngoesophageal) CARCINOMA OF THE ESOPHAGUS

congenital or acquired outpouchings at any level of the esophageal wall most common diverticula just behind cricoid cartilage at approx. the upper esophageal sphincter obstructive (mechanical esophageal disorders) adenocarcinoma, or squamous cell carcinoma contains all layers of wall prolonged stasis of trapped food w/I the diverticulum increases risk of squamous cell carcinoma men tobacco smoking alcoholism vit A & C deficiency lye ingestion achalasia Barretts esophagus Celiac sprue

often asymptomatic, but may cause dysphagia

& regurgitation

Sx: progressive, persistent dysphagia for solids

pain indicates extension of tumor beyond

wall of esophagus dysphagia for liquids, cough, hoarseness, and weight loss are symptoms of advanced esophageal carcinoma

Motor Neurological Disorders of the Esophagus

Achalasia

primary esophageal motility

disorder char by failure of the LES to relax & absence of esophageal peristalsis cardiospasm, or megaesophagus, or esophageal aperistalsis

neurogenic disorder: pts have imbalance

(excitatory > inhibitory) in neurotransmissn from scarring of Auerbachs plexus

Sx: dysphagia for both liquids and solids weight loss (90%) Associated symptoms: chest pain, regurgitation

LES doesnt relax when swallowing =

obstruction loss of peristaltic activity secondary dilation of esophagus above

Dx: birds beak appearance of lower esoph; esophageal manometry; pH monitoring to rule out GERD; endoscopy to rule out tumour & malignancy Tx: Ca channel blockers & nitrates to LES P

nocturnal cough d/t dilated lumen increased

sputum aspiration pneumonia, bronchiectasis Sx: intermittent dysphagia for both liquids & solids occasional chest pain, globus hystericus, regurgitation of food odynophasia esp w/extremely cold or hot food chest pain d/t spasm (pain similar to angina location * c/b relieved by nitroglycerin) Sx: hematemesis Sx: sudden onset of severe chest pain in lower thorax & upper abd - SOB

Esophageal Spasm

strong, uncoordinated, nonpropulsive contractions food doesnt travel down neural defect accompanied by incomplete relaxation of LES similar to achalasia

Esophageal Tears & Varices

Mallory-Weiss Syndrome Boerhaaves Syndrome
- non-transmural tears at the GE jxn - transmural perforation of the esophagus - caused by intraabdominal P dt forceful vomiting and failure of the LES to relax - typically occurs after forceful vomiting; repeated episodes of retching & vomiting Tx: surgery to repair tears; females w/ MWS rule out preg Tx: *EMERGENCY surgery and drainage required; most lethal perforation of the GIT - best prognosis w/ early dx & surgery w/in 12h

- < swallowing, no hematemesis (DDx: MWS

has hematemesis) - tachycardia, sweating, fever, HTN

Disease

Definition

Etiology, Pathogenesis & Complications

- seen in pts w/ portal HTN (ie cirrhosis of the LV) bld flow thru vessels leading to esophagus chance of rupture & bleeding

Signs & Sx

Dx & DDx

Esophageal Varices

- dilated bld vessels w/in the wall of the esophagus

*Vessels may rupture causing life-threatening hemorrhage

DISEASES OF THE GALLBLADDER, BILE DUCTS, & DISORDERS OF THE PANCREAS

Congenital Abnormalities

- includes abnormalities in
position, number, size & shape Ectopia: abn position stasis dt compression gallstone formation Double GB: abn number & shape Segmentation: abn size & shape

BILIARY CALCULI

presence of calculi in the GB (cholelithiasis) or in the biliary ducts (choledocholthiasis)

more freq in women & some ethnic groups risk factors: western diet, family hx Formation depends on: 1) Lithogenic bile production 2) GB motility 3) Cyrstallization of CHOL (termed nucleation of gallstones

three types of stones: cholesterol, pigment, and mixed stones (80%); up to 3cm in diameter CHOL rich stones result from: LV not providing enough bile salts & lecithin, LV synthesis of CHOL, supersaturation of bile w/ CHOL lithogenic bile, slow emptying of GB Tx: oral bile acids biliary secretion of CHOL in CHOL saturation of bile Complications: infection (cholecystitis), obstruction, acute pancreatitis, perforation gall stone ileus, stricture biliary cirrhosis, malignancy Symptoms occur only when stones migrate Dx: ultrasound CHOLELITHIASIS/ gallstones in the gallbladder genetic, sex, obesity, rapid wt loss to obstruct:
CHOLEDOCHOLITHIASIS
gallstones in the common bile duct rapid in biliary chol saturation, high caloric diet, regional enteritis, CF, Type IV hyperlipidemia, diabetes, long-term parenteral nutrition, Crohns, bowel resection pigment gallstones associated w/chronic hemolytic anemia, chronic LIV dz, cirrhosis, biliary infection, obstruction/ anomalies of the GB or bile ducts Complications:

cystic duct obstruction: (50%) biliary colic common bile duct obstruction: (10-20%)
biliary colic, jaundice, inflammation of hepatic bile ducts (cholangitis), or pancreatitis from ascending bacterial infn SX: Pain: Dx: ultrasound, abd xray only shows 10% of stones, cholangiogram, alkaline phosphatase, slightly transaminases and/or acute inflammation of GB

BILIARY COLIC

pain produced by contraction of

biliary tree d/t sudden obstruction & increased intraluminal pressure in bile duct

- risk of GB CA w/ cholelithiasis - asymptomatic stones in the common

bile duct are more life-threatening and should be removed

sudden onset, severe, steady, lasts up to

3hrs, maximal in RUQ & epigastrum radiates to interscapular area, right scapula,

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

shoulder, back (rare) episodes are longer than intestinal colic slightly > flexed posture vomiting does not relieve pain

consistent relief only w/ narcotics

Other features: N&V often cold sweats

DDx: 1) Gastric ulcer/food poisoning: pain relieved by vomiting 2) LV disease 3) Hepatitis: v. high transaminases Tx: surgery, chemical dissolution, oral bile acids

fever and chills (asstd w/ acute obstruction & jaundice, pruritis uncommon
dark urine & light stools abdomen is soft, may dev local tenderness bacterial infection)

ACUTE CHOLANGITIS

bacterial inflammation of the bile

ducts close-space infection usually complicated d/t bacteria than ascend from the intestine

biliary colic jaundice shaking chills w/fever

SCLEROSING CHOLANGITIS

inflammation of hepatic bile duct progressive narrowing of bile duct

men 3x >women

pruritus

right abd pain

jaundice fatigue nausea Sx: pain is followed a few hours later by N/V patient lies motionless vomiting does not relieve pain pain is mild or severe biliary colic pain in RUQ, referred to interscapular region, right shoulder associated w/pulmonary edema and inflammation Other symptoms

Lab Dx: elevated serum ALP, ERCP

ACUTE CALCULUS CHOLECYSTITIS

- inflammation of the GB caused by calculi

women>men associated findings:

Hx of biliary sx
fatty food intolerance constipation during attack

Dx: ultrasound best initial method, leukocytosis present, xray, cholecystogram during acute attacks

fever jaundice not present in simple

cholecystitis local tenderness in RUQ

m/b pruritis (d/t bile build up)

sx may be mild or masked in elderly & pts taking corticosteroid/immunosuppressive therapy

cutaneous hyperesthesia (+) Murphys sign pain & inspiratory arrest

while palpating RUQ, (+) Courvoisiers sign palpable GB, (+) Boas sign tenderness around R scapula Complications of calculous cholecystitis

CHRONIC CHOLECYSTITIS

recurrent subacute inflm of GB

and sx d/t gallstones

single episode of biliary colic, acute

cholecystitis chronic inflammatory changes

empyema: suppurative infn in which GB fills

w/ purulent material sepsis *BAD* perforation of GB

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

perforation: days to 1 week after acute

cholecystitis; 25% mortality; sx of acute peritonitis

hydropic gallbladder: obstructed cystic duct

GB filled w/ clear, mucous white bile

fistula: erosion of GB from gallstones

fistula to duodenum, colon, ST

gallstone ileus: migration of gallstone thru

fistula into intestinal tract; may cause colonic obstruction if >2cm acute pancreatitis

ACALCULUS CHOLECYSTIS CANCER OF GALLBLADDER

abnormal thickening of GB wall women 3x >men

2-10% of cases of acute cholecystitis operations, severe trauma, acute medical illness, Strep, diabetes mimic those of acute or chronic cholecystitis

palpable mass in RUQ

signs of obstructive jaundice

Sister Mary Joseph lesion: erythematous,

ACUTE PANCREATITIS

acute inflammation of pancreas in main cause: alcohol binge drinking,

which pancreatic enzymes autodigest the gland gallstones

less common cause: post-op

pancreatitis, abd trauma, hyperlipidemia, drugs, uremia, PUD w/penetration of pancreas, viral infections, biliary colic Complications - inflm can spread easily & can evolve into hemmorhagic or necrotizing pancreatitis

retracted excoriated umbilical metastasis Sx: pain in epigastrium/abdomen (RUQ), sometimes in periumbilical region pain radiates to back

Lab Dx: serum amylase, lipase, trypsinogen

N/V abdominal tenderness < supine (+) Cullens sign retroperitoneal bleeding
that causes hematoma at umbilicus, or flank ((+) Turners sign )

diminished/absent bowel sounds (d/t pain)

CHRONIC PANCREATITIS

persistent histological changes

after etiologic agent has been removed

alcohol

cystic fibrosis common cause in children

scarring

decreased breathing, bloating decreased BM (not a classic sign) SX: Pain

in the epigastrium after eating, radiates to

back < supine several days to week, usually relieved only by narcotics recurrent attacks often precipitated by alcohol excess Other features

malabsorption in association w/ steatorrhea

Lab Dx: Xray: pancreatic calcification, m/b left pleural effusion ERCP: diffuse ductal dilatation, irregular beaded appearance Peritoneal aspirate: very high amylase (final stage) US: enlarged pancreas and/or abscess CT: pancreatic calcification

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

ADENOCARCINOMA OF THE PANCREAS

Men > women, 55-65 yrs

and clay color, floating, bulky & foul smelling stool jaundice diabetes Associated findings: vomiting wide-ranging temp shock w/cold clammy skin tenderness in lower epigastrium abdomen is slightly rigid abdominal distention, transient adynamic ileus Cullens sign, Grey-Turners sign Sx:

Lab: increase serum amylase Only 10-20% are respectable at time of dx. 3 months survival w/out resection

70% in head of pancreas, 30% in tail risks: hereditary pancreatitis, smokers,

diabetics, long term exposure to insecticide DDT, chronic pancreatitis

constant abd pain (after meals) or

periumbilical discomfort pain radiates to back, relieved by sitting up or bending knees jaundice (65%) weight loss (60%) palpable gallbladder (Courvoisiers sign) palpable epigastric mass

DISEASES OF THE STOMACH & DUODENUM

H. Pylori Infection
- responsible for 90% of duodenal ulcers & 80% of gastric complaints - can survive in mucus layer of ST dt secretion of enzyme urease which creates a more alkaline env for itself - only found in gastric mucosa Asstd w/: - acute gastritis, PUD, MALTomas, GERD, Fe def anemia, skin dis, rheumatic conditns

ACUTE GASTRITIS

inflammatory lesions
gastric mucosa diffuse/localized usually self-limited

of the

drugs (aspirin, NSAIDs, steroids) accidental ingestion of caustic substance (lye, sulfuric acid) stress (eg., trauma w/added shock, sepsis, organ failure)

Sx: asymptomatic in 30%

Dx: endoscopy

2 Types: 1) Erosive hemorrhagic, superficial/deep erosions 2) Non-erosive H.pylori infn

infections (H.pylori, M. tuberculosis,

Candida, herpes)

sx usually hemorrhage epigastric burning pain N/V

st

H.pylori culture
serologic testing for anti-Abs urease test (breath or biopsy) Tx: transfusion, anti-secretory ulcer meds, vasoconstrictors Dx: endoscopy CBC (anemia)

occult GI bleeding, when severe associated

w/ hematemesis chronic bleeding anemia melena Symptoms similar for Type A & B: burning epigastric pain dyspepsia/indigestion

CHRONIC GASTRITIS

characterized by: superficial

lymphocyte infiltrate in the lamina propria, progressive inflammatory changes

prolonged use of alcohol, aspirin, etc radiation, thermal injury

infections (H. pylori) association w/gastric polyps, gastric

ulcer, and gastric cancer (Type B > Type

N/V
Type A sx:

Type A: less common, involves

Disease

Definition

Etiology, Pathogenesis & Complications

A)

Signs & Sx

Dx & DDx

body & fundus; AI dis that leads to inflm & atrophy of mucosa; achlorhydria is diagnostic, lack of IF pernicious anemia

plasma Abs to intrinsic factor & parietal cells

hypochlorydria, achlorhydria

sx of pernicious anemia (pts have few GI

complaints) hypergastrinemia hypothyroidism, DM, vitiligo occur more frequently in Type A Type B sx:

Type B: more common, involves

antrum in younger pts, entire ST in elderly; 90% have H.pylori infection, HCl production not affected if only antrum involved bc HCl produced in body of ST

gastric acid level is normal/slightly reduced

gastrin cell Abs

gastric secretions
PEPTIC ULCER DISEASE
- A circumscribed ulceration of the mucous membrane that penetrates the muscularis mucosa - Occurs in areas exposed to acid & pepsin 2 Types of Ulcers: Gastric Ulcers: MC occur along lesser curvature of ST, develop later in life, hyposecretion of HCl, chance of malignancy, < food Duodenal Ulcers: w/in first few cm of duodenum (bulb), smaller ulcerations, hypersecretion of HCl, benign, > food Can occur at any age, intermittent dis

Family hx of H.pylori, steroids and

NSAID,

Stress impairs mucosal defense

mechanisms excess HCl secretion personality type A, Zollinger-Ellison syndrome

serum gastrin elevated Sx: burning epigastric pain or RUQ pain, bloating, N/ mb V, anemia may present only w/bleeding (melena, pallor, tachycardia, low BP) Duodenal ulcers: pain >w/meals, but <2-3hrs after meals weight gain pain may awaken from sleep hypersalivation increased HCl Gastric ulcers: rarely in pts <40yoa pain < eating weight loss - tend to have normal/reduced HCl Sx:

Dx: endoscopy, xray, family hx Tx: goal is to neutralize or gastric acidity, tx for H.pylori infn

< smoking; healing

complications of PUD: hemorrhage, perforation, penetration of adjacent organ, gastric-outlet obstruction, malignancy (gastric ulcers) RED FLAG: *Emergency

inflm of peritoneum: rigid abd,

sounds, occult bld

bowel

GASTRIC CARCINOMA

4 Types: 1) Protruding: polyp type 2) Penetrating: tumour has sharp, well demarcated borders, mb ulcerated 3) Spreading: along mucosa or thru wall; edges of ulcers fibrotic Leather bottle ST 4) Misc

possible etiologic factors: tobacco use,

Vit C def., consumption of preserved food, pernicious anemia Risk factors: H.pylori infn, atrophic gastritis, gastric dysplasia, polyps men > women, 60-75yrs Stages of carcinoma: I: confined to muscularis propria II: muscularis & serosal invovl III: gastric & nodal involve IV: residual dis V: metastatic Diffuse fatty change: - alcoholism, obesity, diabetes

weight loss, anorexia

epigastric pain early satiety

Dx: endoscopy w/ biopsy and brush cytology; serum carcinoembryonic Ag

- achlorhydria irt stimulation

indicates malignancy Tx: surgery, chemo

vomiting ( weakness & fatigue (2 to bld loss)

gross GI bleeding dysphagia

palpable left supraclavicular node (Virchows

node) suggestive of metastatic disease in chest & abdominal cavity *RED FLAG Sx: non-tender, asymptomatic hepatomegaly may present w/ RUQ pain & jaundice Dx: mild in ALP or transaminase (AST/ALT)

DISEASES OF THE LIVER

FATTY LIVER DISEASE
- excessive accumulation of lipidin hepatocytes

Disease

Definition

Etiology, Pathogenesis & Complications

- other causes: malnutrition (PEM, kwashiorkor), metabolic disorders, drugs, systemic illnesses w/ fever (Reyes syndrome) Focal Fatty change: - less common; presents as a space occupying lesion in the LV - asstd w/ alcoholism, obesity, diabetes Major Factors: - Quantity & duration of consumption - nutritional status of the pt - genetic & metabolic traits Prognosis related to the amt of cirrhosis and LV cell necrosis - fibrosis is a common response to hepatocell injury or necrosis - caused by: infections, storage disorders, toxic metabolite accum, chemicals & drugs, disturbances in LV bld flow, obstruction of bile flow - fibrosis develops from depostition of collagen irt injury, inflm, necrosis in hepatic fxn 4 Stages: see pp 11 pkg 5 - presents insidiously - 90% in women aged 35-70 - commonly asstd w/ AI diseases such as RA, scleroderma, sicca cplx, autoimmune thyroiditis - slow progression longer survival

Signs & Sx

Dx & DDx

- most common LV response to

injury

- alcoholic fatty LV mb accompanied by inflm, necrosis & permanent damage (cirrhosis)

- hyperlipidemia - US/CAT show fat deposits - Gold standard = biopsy Tx: reversible if underlying cause removed;

ALCOHOLIC LIVER DISEASE

- spectrum of clinical sx &

pathologic changes caused by EtOH - progresses to symptomatic alcoholic hepatits - widespread fibrosis & nodule formation w/in the LV

Sx: - variable clinical picture; becomes apparent in pts 30s, severe prob in 40s - LV may be enlarged, smooth, tender - Cirrhosis may be present & asymptomatic

Lab Dx: glutamyl transpeptidase (GGT) Tx: stop drinking EtOH..duh! - supportive tx

CIRRHOSIS

Sx: - pruritis - portal HTN w/ variceal bleeding, ascites

- LV failure renal failure coma

- Weakness, anorexia, malaise, wt loss

Lab Dx: serum albuin, prothrombin time, serum globulin, transaminase, ALP normal or , bilirubin normal

- Obstruction of bile flow jaundice, pruritis,

xanthelasmas - LV may be palpable - normocytic or microcytic anemia Sx: - 50% asymptomatic w/ abnormalities detected during bld test Dx: biopsy, ultrasound DDx: - extrahepatic biliary obstruction, chronic hepatits, primary sclerosing cholangitis, drug induced cholestasis

PRIMARY BILIARY CIRRHOSIS

- dis of unknown cause char by chronic cholestasis & by progressive destruction of intrahepatic bile ducts

- pruritis, non-sp fatigue

enlarged, firm, non-tender LV (50%) splenomegaly (25%) skin xanthomas clubbing, metabolic bone dis, peripheral neuropathy in some

Changes in Liver Function UNCONJUGATED HYPERBILIRUBINEMIA

Loss of LV fxn : urea synthesis, bld ammonia hepatic encephalopathy albumin synthesis ascites clotting factors bleeding Causes: increased formation of bilirubin - hemolysis, Gilberts syndrome, Crigler(hemolytic anemia) Najjar syndrome, neonatal jaundice, drugs impaired hepatic uptake (d (rifampin, chloramphenical) glucoronyl transferase activity) neonatal jaundice (immature glucoronyl transferase)

increased formation of bile does not lead to pruritus impaired hepatic uptake N ranges of LFTs, absence of urinary bile, characteristic bili fractionation, N LIV histology < stress, excessive exercise, fasting

neonatal jaundice bili (not bound to

albumin) deposits in brain tissue permanent neurological injury may occur & possibly death

CONJUGATED BILIRUBINEMIAS

4 categories: hepatocellular (eg., hepatitis,

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

cirrhosis) obstructive

infiltrative (eg., fat LIV)

ACUTE HEPATITIS
space-occupying lesion (eg., tumor, cyst, abscess) - a systemic infection affecting predominantly the LV 4 stages of acute hepatitis: 1. incubation period 2. preicteric phase 3. icteric phase 4. convalescent period Typical symptoms of hepatitis include: jaundice less than 1/3 of pts common cold nausea, fatigue, anorexia, loss of appetite slight fever diffuse muscle pain decreased desire to smoke Lab Dx: ALP

transaminase AST + ALT serum bilirubin

heaviness/fullness/discomfort in RUQ
(inflamed, swollen LIV glysons capsule stretched pain ascites In icteric phase: dark urine cutaneous jaundice lasts several weeks Extrahepatic sx: joint pain (symmetric) small hand and wrist joints

diffuse adenopathy (enlarged LIV)

skin rash Frequently, the infection is asymptomatic and anicteric!

Hepatitis A

RNA enterovirus

fecal-oral contamination
incubation: 15-49d present in stool 2 weeks after infection

N & V
jaundice (50% develop) malaise, fever anorexia

Anti-HAV (total)+ IgM anti-HAV+

Prior infection:

Anti-HAV (total)+ IgM anti-HAVIgG anti-HAV+ HBsAg+, IgM anti-HBc+

Prior infection:

Hepatitis B

DNA virus

Identified in almost every body fluid (saliva, sweat, blood, breast milk, tears, semen, etc) Risk: sexual contact, sharing razors, breast-feeding, etc Incubation: mean 70-80d Present in blood 2 months after infections

Appear at about 3 months; may be asymptomatic, or symptomatic: Arthralgia N & V jaundice (not every case) May progress to fulminant hepatic failure & death (2%) Chronic carrier risk for early death from cirrhosis or hepatocellular carcinoma

HBsAgAnti-HBs+ Anti-HBc+
Chronic carrier

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

In severe cases of Hep B + C:

encephalopathy- toxic involvement of

present w/I 2wks confused

brain

HBsAg+ IgM anti-HBcHep B vaccine

psychomotor slowing, pt is disoriented and flapping tremor wrist becomes dorsiflexed

when asked to spread fingers fulminant severe LIV failure

HBsAgAnti-HBs+ Anti-HBc-

Hepatitis C

RNA virus

parenteral exposure

milder than other hepatitis viruses

incubation period: mean 50d

more than 50% infected ppl become chronic carriers risk of chronic hepatitis, cirrhosis, hepatocellular carcinoma

similar to those of Hep B, except arthralgias

less common infreq other manifestations porphyria cutanea tarda, cryoglobulinemia

Hepatitis D Hepatitis E CHRONIC HEPATITIS

defective RNA virus RNA virus liver cell necrosis and inflammation lasting > 6-12months

occurs only in presence of Hep B incubation: 30-18-d

symptoms more severe fulminant hepatic

failure and death in up to 20% pts mild in most pts

anti-HD+

transmitted by RNA virus

alcohol intake over many years accounts for majority of chronic cases

20% mortality if acquired during pregnancy jaundice (variable)

Terrys nails (white nails) spider nevi (angiomas) sign of damaged estrogen metabolism gynecomastia atrophic testes excessive decrease in weight ascites from portal hypertension Sx: - abd pain, wt loss, palpable RUQ mass, unexplained deterioration in a pt w/ cirrhosis - fever - first manifestation is an acute abdominal emergency caused by rupture of tuour - painful, growing hepatomegaly, hepatic friction rub, bruit

HBV, HBC also major causes (injury

caused by Immune-med host rxn to viral infection)

DDx: - alcoholic LV dis, acute viral hepatitis, primary biliary cirrhosis - biopsy needed for definitive dx

Wilsons disease in children & young

HEPATOCELLULAR CARCINOMA
- LV tumour arising from malignant hepatocytes adults - HBV & HCV carriers at greater risk - environmental carcinogens - alcoholic cirrhosis

Dx: alpha-fetoprotein, biopsy

Fibrolamellar carcinoma, Cholangiocarcinoma, Hepatoblastoma

- other primary LV cancers

Dx: based on histology; therapy is of little value and prognosis is poor

DISEASES OF THE SMALL INTESTINE & COLON

Healthy Bowel Flora
- Benefits of healthy flora: - Synthesis & excretion of vitamins (K,B12, & other B vit) - Prevent colonization of disease causing pathogens through competition for attachment - Stimulate the dev of immune & lymphatic T in the GIT (Peyers patches)

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

- Stimulate the production of cross-reactive Abs - Abs produced against the antigenic cpts of the normal flora cross react w/ certain pathogenic bacteria preventing infn

Intestinal Dysbiosis

an harmful overgrowth of intestinal bacteria/pathogenic bac (more than 104 ml of tissue)

- caused by: ABC use, poor diet ( fat, sugar, fiber), compromised GIT (Crohns, IBS) hypochlorydia ( HCl)

- gas, bloating, diarrhea, N/V

Dx: Stool analysis measures digestion & maldig thru fecal chymotrypsin, pH, fiber; intestinal abs thru fecal LCFA, SCFA, CHOL

Maldigestion & Malabsorption

- inability to break down lrg molecules in the lumen of the SI - inability to transport molecules across the intestinal mucosa

1. Inadequate digestion dt - pancreatic insufficiency - bile salt def - inadequate mixing of chime, bile, pancreatic enzymes - 2nd to LV dis, terminal ileal disease impaired enterohep recycling 2. Mucosal Disorders dt - gluten enteropathy/food sensitiv - intestinal ischemia - leaky get syndrome - intest lymphoma - inadeq absorptive surface dt bowel resection, Crohns - fibrosis dt systemic sclerosis, radiation enteritis

Manifests as: - Fat soluble vitamin def (ADEK) Sx: night blindness, dry skin, hemolytic anemia in children, neurological prob (CN 2, 7, 9, 10) & bleeding disorders - Iron Fe abs in duodenum & upper jejunum; malabs leads to Hb, serum Fe & ferritin; Sx: anemia, glossitis, koilonychias (spooned nails) - Calcium Ca abs in duod & upper jejunum; binds to Ca binding PRO in cells (CBP by Vit D; abs serum Ca & Mg; Ca def leads to metabolic bone disease; Sx: tetany, parethesias; Dx: measure serum Ca & Mg, bone scan for bone mineralization Folic acid Abs in jejunum; abs RBC folate; Sx: glossitis, megaloblastic anemia; may see folic acid with bacterial overgrowth Vitamin B12 Def caused by terminal ileal dis; Sx: pernicious anemia; prolonged def degeneration of the spinal cord, peripheral neuropathy, dementia; Dx: Schilling Test CHO Sx: generalized malnutrition, wt loss, flatus; Dx: D-xylose test PRO Sx: malnutrition, wt loss, amenorrhea, libido; Dx: measure serum albumin FAT Sx: malnutrition, wt loss, steatorrhea; Dx: fecal fat excretion

DIVERTICULAR DISEASE
Complications:

diverticulitis (NB: little to no bleeding) bleeding (NB: diverticula bleed often) peptic ulceration perforation neoplasm obstruction: strangulation, invagination = incarceration, twisting, intussusception

Duodenal diverticula Jejunal diverticula

w/in 1-2cm of the papilla of Vater

saccular outpouchings

common bile duct obstruction may occur

dt outpouchings interfering w/ its emptying malabsorption

asymptomatic in most pts rarely causes upper GI bleeding diarrhea, bloating, distention, flatus

- found during endoscopy/autopsy Tx: surgical removal of multiple or large diverticuli

steatorrhea: bulky & greasy

stool

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

anorexia (d/t build up of toxins

from undigested food) glossitis (d/t vit def)

anemia; pernicious anemia +

neuropathy ascites & edema (protein def) osteopenia (Vit D def), osteoporosis & tetany d/t Ca def

Meckels diverticulum

true diverticulum as it involves all

layers of bowel wall

most freq congenital anomaly of the GI

tract; represents the remnant of the viteline duct Complications: - peptic ulceration from HCl prod, perforations, bowel obstruction, neoplasm, GIT strangulation, twisting, incarceration Pathogenesis:

DDx: 1) Acute appendicitis:

average 5-7cm long w/i 60-90cm

of ileocecal valve of terminal ileum may contain ST or pancreatic T which may produce HCl

Colonic diverticulum

outpouchings of mucosa only

(not true diverticula) herniation of mucosa/submuc thru the muscular layer; along the teniae at the site of penetratn of mesenteric vsls

Low-fiber diets: intraluminal P especially in the sigmoid colon mucosal herniation outpouching at focal wall weakness ** vegetarians have a 1/3 incidence of diverticuli

asymptomatic in uncomplicated diverticula Sx: crampy abd pain in LLQ, pain alternates w/diarrhea and constipation; > BM; bloating

Tx: stool bulk intraluminal P; regulate bowel frequency

Chronic constipation dt hard, dry fecal matter; also caused by lack of exercise, ignoring the urge, stress/anxiety, drugs, pregnancy

DIVERTICULITIS

complication of diverticulosis

inflammation of diverticular sacs

usually involves the R side of the colon

retention in the diverticula of undigested

food residues and bacteria hard mass called a fecalith

Sx: crampy LLQ pain, fever,

constipation/diarrhea, N/V, tenderness, pain < BM

compromises bld supply suscept to

invasion by colonic bact, perforation w/ peridiverticular abscesses Complications:

Dx: made on the basis of clinical sx; CT scan performed during acute phases of diverticulitis NB: colonoscopy & barium enema are CI during acute phase dt risk of perforation - after resolution of acute, endoscopy to visualize damage and rule out IBS DDx:

- bowel obstructn, abscess formation

peritonitis L-sided appendicitis

1)
2)

fistula to bladder or vagina may develop

(< 25%)

bleeding is rare (see next line)

Diverticulosis: multiple non-inflamed diverticuli often bleed from the R side of the colon, while inflamed diverticuli do not IBS:

Tx: ABC, IV fluids, bowel rest (NPO)

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

Complication of Diverticulitis: BLEEDING

- occurs in 20-25% of cases - 80% spontaneously stop w/ only supportive tx; 20% rebleed

Dt erosion of a penetrating artery at the

dome of the diverticulum

Sx: acute and brisk, painless w/impressive episodes of bright red blood per rectum and not associated w/straining

Dx: colonoscopy (after acute bleeding stops), arteriography or rapid sequence nuclear scanning to localize the bleeding portion of the colon Management of bleeding: - initially, IV fluids & bld replacement; after rebleeding surgical resection

MEGACOLON - Definition: massive distention of colon accompanied by constipation & obstruction Hirschsprungs Disease Congenital malformation of Peristalsis absent in aganglionic (Aganglionic ganglia in the colonic submucosa segment unable to pass stool Megacolon) (Meissners) & myenteric functional obstruction at most distal
(Aurbachs) plexus inability to defecate Usually involves sigmoid colon segment proximal colon dilation

- apparent after birth when infant doesnt pass meconium, abd distension follows; may occur later in life w/mild sx Sx: severe constipation & vomiting, absence of stool in rectum Sx: chronic constipation, abd distention

Dx: DRE reveals absence of stool in rectum, X-ray shows a dilated proximal segment & a narrow distal segment, biopsy of mucosa/ submuc to confirm Tx: surgical resection of aganglionic seg; or bypass of contracted seg by attaching normal colon to just above the internal sphincter Dx: barium enema shows entire megacolon is distended & filled w/ stool; no narrow segment found DDx: 1) Hirschsprungs: DRE in CIM reveals feces in rectum (feces absent in Hirschsprungs); no narrow segment & normal ganglia found in CIM Tx: enemas until pt acquires normal BM DDx: 1) Hirschsprungs: onset is during childhood; acquired megacolon occurs later in life; empty rectum in congenital megacolon Tx: aimed at identifying underlying cause; use of purgatives that act by irritating the mucosa or by direct stimulation of the plexuses

1/5000 live births; MCly in males,

familial, asstd w/ other congenital abnorm Complications: enterocolitis, perforation

Chronic Idiopathic Megacolon

psychogenic megacolon

onset at time of toilet training

Acquired Megacolon

Causes: schizophrenia, depression cerebral atrophy spinal cord injury Parkinsons scleroderma narcotic drugs (morphine & codeine) esp in bedridden pts

obstipation (constipation d/t obstruction) massive colonic dilatation rectum distended w/feces

infection by Trypanosoma cruzi

(Chagas disease) destruction of ganglion cells in colon;

INTESTINAL OBSTRUCTION 1) Mechanical obstruction 2) Non-mechanical obstruction Mechanical Obstruction Extrinsic Lesions: - adhesive bands, internal & *Dynamic ileus
external hernias Intrinsic Lesions:

- MC causes: carcinoma, sigmoid diverticulitis, volvulus (account for 90% of cases) - extreme prolonged contraction of

Disease

Definition

Etiology, Pathogenesis & Complications

intestine d/t heavy metal poisoning, uremia, extensive intestinal ulcerations - compensatory contraction of bowel above obstruction twisting, strangulation, etc - Occurs to some degree after abdominal operation; only lasts 2-3 days Causes: post-op narcotics, retroperitoneal hematomas asstd w/ vertebral fractures, thoracic dis (fractured ribs, pneumonia, MI), electrolyte imbalance (part K+), intestinal ischemia Complications: peritonitis d/t d

Signs & Sx

Dx & DDx

- carcinoma, diverticulitis, Crohns, gallstone obstruction, intussesception, volvulus (twisting causing obstruction)

Non-mechanical Obstruction *Adynamic ileus

- Mediated by H from the sympathoadrenal system

Small Bowel Obstruction

Hallmark: abd distention caused by accumulation of stool, gas, fluid w/in obstructed segment

Sx depend on whether obstruction is complete/ incomplete, transient/ persistent Sx: cramping, paroxysmal mid-abd pain; pain < the higher the obstruction; btwn intervals of pain, pt is relatively comfortable

N/V = very severe; earliest sx; more profuse

the higher the obstruction; constipation & abd distention follows vomiting Complete obstruction = cessation of passage of gas or stool via rectum Onset of acute pain may occur over a week Sx: colicky abd pain w/ spasms that may last a few minutes, pain localized in hypogastrium (midline), vomiting m/b absent but nausea is constant and severe, constipation & abd distention; local tenderness w/ rigidity on palpation

Dx: Xray shows air-fluid levels & absence of gas Physical exam: abd distension dt accumulation of gas & fluid; abd is soft & tender; distension is localized not general; visible peristalsis of ST and small bowel DDx: 1)Large Bowel Obstructn: LBO nausea absent

Large Bowel Obstruction

- #1 cause : left-sided carcinoma of rectum ; also caused by volvulus of sigmoid or cecum, diverticulitis

IRRITABLE BOWEL SYNDROME (IBS)

motility disorder involving the entire hollow GI tract enhanced visceral activity dysregulation of CNS function (motor, sensory)

recurrent abd pain, usually LLQ

altered freq of defecation w/hard stool (constipation), or watery stool (diarrhea) sense of incomplete evacuation

exclusion of other conditions

relation of sx to environmental
and emotional stress

feeling of abd distention after food intake

excess flatus

tender sigmoid full w/feces may be palpated

in LLQ

sx always occur in waking state, < stress

(depression, anxiety), ingestion of food (indigestion)

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

ACUTE APPENDICITIS - normal appendix (7cm long x 1cm wide); derived from the cecum - usually lies along anterior surface of cecum, but position is variable leading to difficulties in dx of appendicitis - inflammation of the appendix - primary event is obstruction of the Sx: pain: initially, periumbilical &/or Acute appendicitis
appendiceal lumen by fecalith (67%), inflammation, foreign body or neoplasm ischemia, 2nd bacterial infection - recent studies: ulceration of mucosa is initial event

epigastric pain soon localized to RLQ at McBurneys point, anorexia, in some case N/V - localized abd pain on coughing , light percus - abd tenderness w/in Sherrens triangle (formed by umbilicus, right ASIS, symphysis pubis), rebound tenderness - low-grade fever (37.7-38.3) Variability dt position of appendix: Retrocecal appendix: pain and rigidity of abdomen is less Pelvic appendix: if located low, abd wall is not rigid urinary frequency, diarrhea rectal exam will cause pain & inflamed appendix felt as fullness or mass With rupture:

Dx: based on clinical s/sx - (+) Rovsings sign, psoas sign, obturator sign - leukocytosis; absence of leukocytosis present in some cases; leukocytes indicates a risk for perforation DDx: 1) Meckels diverticulum: clinically mimics acute appendicitis

generalized peritonitis diffuse rigidity and tenderness distention and abd sounds

INFLAMMATORY BOWEL DISEASE (IBD)

- a motility disorder involving the whole GIT - chronic, non-specific disorder of unknown cause

- MC GI dis in practice; women > men - Upper and lower GI sx from abnormal intestinal motility & spasms, visceral sensitivity to certain foods Pathogenesis: genetic predisposition, disturbed immune regulation, certain infectious dis, cigarette smoking

abscess formation win /localized mass & tenderness can be found 3 major clinical manifestations:

abdominal pain (LLQ) diarrhea rectal bleeding

Physical exam: significant abd tenderness & distension unusual; sigmoid C tender & full on palpation Dx: (made by exclusion) chronic intermittent nature of sx w/ out obvious signs of physical deterioratn; relation of sx to env or emotional stress - sigmoidoscopy: reveals prominent vascular pattern, mm spasms, excess normal looking mucous - colonoscopy to exclude inflame or neoplasm - barium enema may reveal spasticity of sigmoid & accentuated haustra

Sx: recurrent abd pain, altered freq of defecation w/ constipation & diarrhea, sense of incomplete evacuation, abd distention after eating, pain > BM, flatus characteristic passage of mucous NB: sx almost always occur on waking, < stress or indigestion, sx are variable depending on whether inflam is acute/ chronic, mucosal/transmural, & if it

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

involves the SI/LI DDx: - parasites, candida, diverticular dis, infectious diarrhea, lactose/food intol, celiac, tumour/neoplasm Tx: exercise, diet mod, dietary fiber w/ spastic colon & constipation Dx: - based on clinical sx w/ findings of ulcerations, long strictured segments (string sign), & skip lesions; - colonscop, biopsy shows granulomas formation Xray:

CROHNS DISEASE

- alternating areas of normal & involved mucosa w/ transmural inflammation skip lesions - may occur anywhere in GI tract (from buccal mucosa to colon) - Crohns of the small bowel: regional enteritis

- ileum involved most often - granulomatous disease - longitudinal, deep ulcers Complications of transmural inflm:

- periods of exacerbation & remission Sx: Pain: colicky, steady, often in RLQ (ileum), after meals; not relieved by defecation (in contrast to IBS) - tender mass in RLQ - diarrhea, steatorrhea, occult blood, melena Other features:

fistula formation: 1. enterocolonic btwn diff parts of GI, 2. enterovesical adjacent hollow viscus, 3. colovaginal, 4. enterocutaneous (btwn GI & skin) stricture formation 2 to scar formatn bowel obstruction & intraabd abscess

cobblestone appearance d/t

alteratn in ulcers & mucosa DDx:

systemic symptoms: fever, weight loss,

malaise, anorexia

intestinal obstruction (25%), massive GI

bleeding (2-3%) pseudopolyps uncommon, anal fistula & perirectal abscess common Extraintestinal manifestations: anemia hepatobiliary disorders increased risk of gallstones peripheral arthritis, ankylosing spondylitis skin problems: erythema nodosum

1)IBS has abd pain, diarrhea,

bloating, but symptoms are more prolonged w/absence of bleeding

2)Xray: deep ulcerations, long

strictured segments, skip areas incontrast to UC & other inflamm conditns

3) UC: shallow ulcers, dilation of

colon

4)Colonoscopy: inflm in contrast to

IBS Tx: anti-inflm, B12 inj, supplemental Vit D, Ca ; anti-diarrheals, probiotics, bowel rest w/ IV fluid; surgery may be necessary for obstruction, fistulas, perforation, growth retardation in children; responds poorly to surgery Dx: clinical s/sx; exclusion of infectious diarrhea, parasites, neoplasm; stool exam shows mucous, bld & WBC - Rectal sigmoidoscopy: friability, edema, hyperemia of mucosa & ulcerations; biopsies must be taken - Barium enema CI in severely ill or toxic pts dt risk of perforation DDx:

pyoderma gangrenosum (deep ulceratn

w/ necrotic center)

oral lesions apthous ulcers, stomatitis

ocular problem: iritis, episcleritis, uveitis blurred vision & H/A

ULCERATIVE COLITIS * see chart in notes pkg 7 page 27 DDx btwn UC & Crohns

Chronic, relapsing inflammatory disorder of rectum and colon

Etiology, pathogenesis similar to Crohns Pathology: microabscesses of the crypts of Lieberkuhn (70%); shallow lesions inflammation is limited to mucosa & submucosa (Crohns = long, deep lesions that are transmural) - confined to rectum and sigmoid colon - continuous lesions, beginning at rectum (Crohns has skip lesions)

Sx: bloody diarrhea (more pronounced in Crohns) - pain > defecation (aot Crohns pain not relieved by defecation) - pseudopolyps common - anal fistula & perirectal abscess uncommon - wt loss, fever, LLQ cramping pain - nocturnal passage of a small volume of blood and mucus - abd may or may not be tender

Disease

Definition

Etiology, Pathogenesis & Complications

Signs & Sx

Dx & DDx

- severe anemia dt bleeding Complications - risk of colon CA depending on duration & extent of dis; severity not a risk factor - **Toxic megacolon: pt presents w/ fever, tachycardia, anemia, leukocytosis, abd pain; mid-transverse colon dilated to <6-7cm; perforation & peritonitis may follow - pericholangitis

1) IBS: stool of IBS has inflammatory changes & mucus is abnormal 2) Crohns: inflm is transmural as opp to UC (inflm in crypts of lieberkuhn); discontinuous skip lesions (UC has continuous ulceration confined to colon); pseudopolyps uncommon, anal fistula & perirectal abscess common 3) Infectious diarrhea & parasites: stool sample Tx: (similar to Crohns) surgery is indicated for toxic megacolon **, ileoanal anastmosies, massive hemorrhage, carcinoma

ACUTE DIARRHEA Condition Viral or Bacterial Gastroenteritis Rotavirus Salmonella, Shigella Pseudomembranous colitis Laxative use
Age - All ages Signs & Sx - abrupt onset, lasts > 1wk; fever, N/V - crampy abd pain - may lead to severe dehydration in children - vomiting, fever - no pain - vomiting, abd pain - high fever - severe colitis w/ pseudomembrane formation - life threatening diarrhea - mm weakness, lassitude Clinical Dx & Lab Dx - stool culture, CBC

- MC < 3 yrs - MC 1-4 yrs - hx of ABC usage (eg Clinamycin)

- peak incidence in winter - stool culture - Clostridium difficile super infection seen asstd w/ clindamycin use - stool culture for NaOH for phenolphthalein - barium enema - lytes for hypokalemia - bioassay of toxins in bld, stool, food - bld & T culture - leukocytosis, thrombocytosis - stool examination for WBC (+) send for stool culture - high fever bld culture

- usually seen in women

Toxins: Clostridium botulism Staphylococcus Dysentary syndrome

- All ages

- hx of prior good health

- severe vomiting & diarrhea 2-4hrs after eating contaminated food (meat, dairy) - neurological sx (diplopia, dysarthria, dysphagia, paralysis) - gastrointestinal sx only - acute, watery diarrhea (may contain bld & mucous) - abd cramps, HA, N/V, fever, malaise

CHRONIC DIARRHEA
IBS
- most common cause of chronic diarrhea - MC in young women; high stress individuals - intermittent D alternating w/ constipation - mucous in stool - incomplete evacuation - < morning asstd w/ urgency - tender abd to palpation - abd distention, gas

Disease

Definition

Etiology, Pathogenesis & Complications

- 1st episode lasts 2wks w/potential recurrence in following weeks & months - wt loss, bloody stools, fever, arthralgia, anemia - inability to gain wt in children - flatulence, vomiting, anorexia - failure to thrive in children - neurological sx - acute/gradual onset of 1-3wks; may persist for wks to months - flatulence, foul smelling, explosive, watery diarrhea - mucous in stool - anorexia & wt loss - Peutz-Jeghers syndrome: polyposis of SI Complications: - GI carcinoma before age 40 - risk for extraintestinal carcinomas

Signs & Sx

Dx & DDx

Crohns & UC

- Adults & children

- proctoscopy, colonoscopy, GI radiographs

Lactase Deficiency Diabetes Giardiasis

- infants <1yr - African/Mediterranean decent

- hikers & campers

- lactose intolerance test - mucosal biopsy - fasting bld GLU - colony count of gastric contents - microscopic stool analysis & duodenal aspirate for giardia

TUMOURS OF THE SMALL & LARGE INTESTINE

BENIGN TUMORS OF THE SMALL INTESTINE

adenomas, lipomas, leiomyomas

Sx: - polyps appear firm and lobulated, 2-3cm in diameter; pedunculated or sessile - m/b associated w/ obstruction or bleeding but are mostly asymptomatic - mucocutaneous pigmentation (perioral skin, lips, buccal mucosa, hands, feet)

MALIGNANT TUMORS OF THE SMALL INTESTINE *rare

Types of tumours

adenocarcinomas (duodenal) carcinoid tumors (appendix,

ileum) - carcinoid tumours grow v. slowly pt may live for years even if metastatic

most common primary small bowel tumor is symptomatic carcinoid, found in appendix

may be metastatic from breast, KI,

ovaries/testes, melanomas endocrine cell tumors neuroendocrine neoplasms pts almost always have extensive LIV metastasis precursors of adenocarcinoma

Sx: bleeding, bowel obstruction, malabs - Carcinoid syndrome: caused by prod of vasoactive amines (serotonin, histamine, bradykinin) by tumour; sx: cutaneous flushing, cyanosis, diarrhea, abd pain, wheezing Tx: surgery, poor prognosis

lymphomas (appendix & ileum)

leiomyosarcomas

BENIGN TUMORS OF THE LARGE BOWEL

adenomatous polyps

risk when polyps are larger than 2cm,

villous vs tubercular, sessile vs pedunculated

Sx: rectal bleeding; large polyps may cause sx of abd obstruction

Dx: barium enema, endoscopy of colon Tx: surgery Tx: if colonectomy not performed adenocarcinoma by age 40

FAMILIAL POLYPOSIS

multiple adenomas w/in the colon

multiple adenomas carpet the colon

lesions usu <1cm in diameter w/ tubular

histology Risk factors: Hx of adenomatous polyps

Gardners syndrome: when osteomas

or soft tissue tumors are present

by time sx occur, 2/3 pts developed

carcinoma Sx: asymptomatic symptomatic: sx vary depending on location and size

MALIGNANT TUMORS

- 98% of all colorectal carcinomas

Disease

Definition

Etiology, Pathogenesis & Complications

UC > Crohns familial polyposis hx of other malignancy

Signs & Sx

Dx & DDx

OF LARGE BOWEL: ADENOCARCINOMA OF THE COLON

MC symptoms: GI bleeding (m/b occult, associated w/Fe def anemia)

st

fam hx of colon CA in 1

relative

change in bowel habits

abdominal pain anorexia/weight loss (advanced)

Strong positive associations: high animal fat consumption (red meat) low fiber consumption obesity ethanol refined sugar cigarette smoking Metastasis usu involves LIV; however, bone, LUs, and brain also m/b affected - once symptomatic, prognosis is poor - survival rate: identified in early stage (95% 5yr), metastatic stage (<10% 5yr)

external palpation of abd, or digital

exam, may feel mass

CANCER OF THE ANUS & RECTUM

Sx: painless, inconsistent rectal bleeding, palpable internal/external mass, may have ulcers, polyps, verrucous warts

Dx: anoscopic exam; if cause of bleeding not identified, further testing req **High incidence of colorectal CA in pts w/ rectal bleeding

COLORECTAL CANCER

Sx: asymptomatic Left-sided tumors: alternating D/C; risk of obstruction, bld in stool, wt loss, flat lesions that grow in napkin ring fashion Right-sided tumors: discomfort after eating, Fe def anemia, bld in stool, wt loss, grow as a polyploidy mass

Dx : tests for colorectal neoplasm : - Fecal occult bld testing: sensitivity & specificity (sen & sp) 50% - Sigmoidoscopy: lower sens than barium enema & colonoscopy - Barium enema: sensitivity - Colonoscopy: gold standard DDx: Crohns, UC, IBS, diverticulitis, bowel obstruction, infn, PID, ischemic colitis