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Esophagus
Gastroesophageal Reflux Disease (GERD)
Definition
condition in which the stomach contents (solid or liquid) leak backwards from the stomach into Epigastric discomfort = postprandial
the esophagus (the tube from the mouth to the stomach) fullness, early satiety, epigastric pain
or burning.
Etiology
inappropriate transient relaxations of lower esophageal sphincter (LES) most common
low basal LES tone (especially in scleroderma)
contributing factors include: delayed esophageal clearance, delayed gastric emptying, increased
intra-abdominal pressure
acid hypersecretion (rare): Zollinger-Ellison syndrome (gastrin-secreting tumour)
hiatus hernia worsens reflux, does not cause it (see General Surgery, GS22)
Management
PPIs are the most effective therapy and usually need to be continued as maintenance therapy
on-demand: antacids (Mg(OH)2, Al(OH)3, alginate), H2-blockers or PPIs can be used for NERD
diet helps symptoms, not the disease; avoid alcohol, coffee, spices, tomatoes and citrus juices
only beneficial lifestyle changes are weight loss (if obese) and elevating the head of bed (if
nocturnal symptoms)
dyspepsia may recur if therapy is discontinued
Complications
esophageal stricture disease scarring can lead to dysphagia (solids)
ulcer
bleeding
Barretts esophagus (see below) and esophageal adenocarcinoma gastroscopy is recommended
for patients with chronic GERD or symptoms suggestive of complicated disease (e.g. anorexia,
weight loss, bleeding, dysphagia)
Barretts Esophagus
Definition
metaplasia of normal squamous esophageal epithelium to abnormal columnar epithelium
containing intestinal metaplasia
Up to 25% of patients with Barretts
esophagus do not report symptoms of
Etiology GERD.
thought to be acquired via long-standing GERD and consequent damage to squamous epithelium
Epidemiology
in North America and Western Europe, 0.5-2.0% of adults are thought to have Barretts Updated Guidelines 2008 for the Diagnosis,
esophagus Surveillance and Therapy of Barretts Esophagus
up to 10% of GERD patients will have already developed BE by the time they seek medical Am J Gastroenterol 2008;103:788-797
attention Screening of the general population is not
recommended and needs to be individualized
more common in males, age >50, Caucasians, smokers, overweight, hiatus hernia and long based on risk factors. Role of esophageal
history of reflux symptoms capsule endoscopy for screening is currently
under investigation.
Pathophysiology Surveillance interval is based on grade of
dysplasia. If no dysplasia confirmed on two
endoscopy shows erythematous epithelium in distal esophagus; diagnosis of BE relies on biopsy endoscopies within the year, then q3y. For low
demonstrating the presence of specialized intestinal epithelium of any length within the esophagus grade dysplasia (LGD), repeat endoscopy within
BE predisposes to premalignant changes in abnormal columnar epithelium, characterized as low- 6 mo to ensure there is no high grade dysplasia
or high-grade dysplasia (HGD) and if none, then q1y until no dysplasia
on two consecutive endoscopies. If HGD, repeat
endoscopy within 3 mo to ensure there is no
Significance adenocarcinoma and recommend intervention
rate of malignant transformation is approximately 0.12% per year for all BE patients prior to (endoscopic resection) or intensive surveillance
dysplasia (endoscopy q3m).
Diagnosis using alternative imaging
risk of malignant transformation in high-grade dysplasia is significantly higher; studies have techniques (fiberoptic, chromoendoscopy) and
reported a 32-59% transformation rate over 5-8 yr of surveillance biomarkers (DNA content abnormalities, loss of
increased gastric acid secretion is more frequently associated with Barretts esophagus as heterozygosity or methylation of specific genes)
opposed to reflux alone are being investigated but none are currently
ready for routine clinical use.
Treatment of reflux symptoms with PPI
Management decreases the development of dysplasia. Surgery
acid suppressive therapy with high-dose PPI indefinitely (or surgical fundoplication) (fundoplication) for patients without major
endoscopy every 3 yr if no dysplasia co-morbidities and whose reflux symptoms are
controlled on PPI has a 20% failure rate at 5 yr
high grade dysplasia: regular and frequent surveillance with intensive biopsy, endoscopic and has not shown to decrease progression to
ablation/resection, or esophagectomy produce similar outcomes; however, evidence increasingly adenocarcinoma.
favouring endoscopic ablation with mucosal resection or radiofrequency ablation Prognosis: 5 yr risk of esophageal
if low grade dysplasia, both surveillance and endoscopic ablation/resection are satisfactory adenocarcinoma in high grade dysplasia is
>30%.
options Management in high grade dyslasia,
surveillance with intensive biopsy, endoscopic
ablation, or esophagectomy produce similar
outcomes and thus should be individualized to
patient preference and local expertise.
G8 Gastroenterology Esophagus Toronto Notes 2014
Eosinophilic Esophagitis
Definition
inflammatory condition with prominence of eosinophils on esophageal biopsy
most commonly found in children, but increasingly recognized in adults
Etiology
unknown; may be an allergic disorder in children
cytokines cause edema and fibrosis
Clinical Features
odynophagia or dysphagia (solids); history often dates back to childhood
first presentation may be to ER with food bolus impaction
allergies common
Investigations
endoscopy may reveal multiple rings or crepe-paper appearance
biopsy showing increased eosinophils is necessary to confirm diagnosis
Management
corticosteroid (e.g. fluticasone) spray (swallowed not inhaled)
budesonide in a matrix to increase contact time with esophageal mucosa
leukotriene B4 inhibitors (e.g. Montelukast)
rule out food allergies: elimination diets have been an effective therapy in children
Complications
increased risk of perforation with endoscopic dilatation procedures
Dysphagia
Definition
difficulty swallowing, sensation of food sticking after swallowing
Key Questions in Dysphagia
Dysphagia Difficulty in starting swallowing?
Associated symptoms? (regurgitation,
change in voice pitch, weight loss)
Solids, liquids or both?
Oropharyngeal Esophageal
(difficulty initiating swallowing choking, (inability to move food down esophagus) Intermittent or progressive?
coughing, nasal regurgitation) History of heartburn?
Change in eating habits/diet?
Neurological* Muscular Structural Solid food only Solid foods and liquids
Cortical Muscular dystrophy Zenkers diverticulum
Bulbar Polymyositis Thyromegaly
Peripheral Myasthenia gravis Cervical spur Mechanical obstruction Neuromuscular disorder
Cricopharyngeal Dysphagia = Difficulty in swallowing
Odynophagia = Pain on swallowing
Progressive Intermittent Intermittent Progressive
Esophageal Diverticula
Definition
outpouchings of one or more layers of the esophageal tract
Clinical Features
commonly associated with motility disorders
dysphagia, regurgitation, retrosternal pain, intermittent vomiting, may be asymptomatic
Classification
classified according to location
pharyngoesophageal (Zenkers) diverticulum
most frequent form of esophageal diverticulum
posterior pharyngeal outpouching most often on the left side, above cricopharyngeal
muscle and below the inferior pharyngeal constrictor muscle
symptoms: dysphagia, regurgitation of undigested food, halitosis
treatment: endoscopic or surgical myotomy of cricopharyngeal muscle surgical excision
of sac
mid-esophageal diverticulum
secondary to mediastinal inflammation, motor disorders
usually asymptomatic; no treatment required
just proximal to LES (pulsatile type)
usually associated with motor disorders
usually asymptomatic; no treatment required
Treatment
endoscopic dilatation and indefinite PPI
anti-reflux surgery if above treatment unsuccessful
G10 Gastroenterology Esophagus/Stomach and Duodenum Toronto Notes 2014
Esophageal Carcinoma
see General Surgery, GS14
Clinical Features
asymptomatic with lumen diameter >12 mm, provided peristalsis is normal
dysphagia with large food boluses
Plummer-Vinson (or Patterson-Kelly syndrome)
upper esophageal web with iron deficiency, plus cheilosis (dry scaling and fissuring of the Plummer-Vinson Syndrome Triad
lips) and koilonychia (concave outer nail surface) Fe Deficiency anemia
usually in middle-aged females (>40 yr) Dysphagia
Esophageal webs
elevated risk of hypopharyngeal carcinoma
Schatzkis ring
mucosal ring at squamo-columnar junction above a hiatus hernia
causes intermittent dysphagia with solids
treatment involves disrupting ring with endoscopic bougie
Infectious Esophagitis
Definition
severe mucosal inflammation and ulceration as a result of a viral or a fungal infection
Risk Factors
diabetes
chemotherapeutic agents
immunocompromised states
Symptoms
characteristically odynophagia, less often dysphagia
diagnosis is via endoscopic visualization and biopsy
Appearance
Candida (most common): whitish-yellow plaques without visible ulceration or inflammation
Herpes (second most common), CMV: focal ulcers
Red Flags of Dyspepsia
Treatment (raise suspicion of gastric malignancy):
Candida: nystatin swish and swallow, ketoconazole, fluconazole Unintended weight loss
Herpes: often self-limiting; acyclovir, valacyclovir, famciclovir Persistent vomiting
CMV: IV gancyclovir, famciclovir or oral valganciclovir Progressive dysphagia
Odynophagia
Unexplained anemia or iron deficiency
Hematemesis
Stomach and Duodenum Jaundice
Palpable abdominal mass or
lymphadenopathy
Family history of upper GI cancer
Dyspepsia Previous gastric surgery
Definition
intermittent epigastric discomfort, characteristically develops after eating
The most common cause of dyspepsia
is functional (idiopathic) dyspepsia
History and Physical Neither clinical impression nor
history: most important are age, associated symptoms (such as weight loss and vomiting), and computer models can adequately
drugs (especially NSAIDs) distinguish between organic disease and
physical examination: adenopathy, abdominal mass/organomegaly, Carnetts sign (if pain is due functional disease in patients referred
for endoscopic evaluation of dyspepsia.
to abdominal wall muscle problem then the pain will increase during muscle contraction, such
as during a sit-up) JAMA 2006;295:1566-1576
Investigations
laboratory: usual (CBC, liver enzymes, glucose, Cr, etc.) plus amylase, albumin
consider trial of empiric anti-secretory drug therapy, non-invasive testing for H. pylori infection, Key Questions to Ask
endoscopy, barium radiography Dysphagia
Weight Loss
G11 Gastroenterology Stomach and Duodenum Toronto Notes 2014
Cl HCO3
CO2 + H2O H2CO3
Histamine +
HCO3
H+ H2R H2R antagonist
cAMP Gastrin +
Gastrin ( in ZE syndrome)
Intrinsic receptor
factor
ACh +
H+ Protein
PPIs Ca2+ ACh R
kinases (M3) Anticholinergic
K+
K+
PGE2/PGI2,
Cl PG Misoprostol
cAMP receptor
NSAIDs
K+
Na+
Tobi Lam 2012
Gastric
lumen inhibition decrease acid secretion Interstitial fluid
+ increase acid secretion
Gastritis
Definition
defined histologically: inflammation of the stomach mucosa
Etiology
some causative agents may play a role in more than one type of gastritis and an individual
patient may have histopathological evidence of more than one type of gastritis
Clinical Features
non-erosive gastritis is asymptomatic (except in certain rare causes like Crohns Disease);
difficult to diagnose clinically or endoscopically
erosive gastritis can cause bleeding (pain only if progresses to ulcers rare); can be seen
endoscopically
Management
determined by etiology (see H.Pylori section, G13, NSAID section, G14 and Stress-Induced
Ulceration section, G14)
non-pharmacological: avoidance of mucosal irritants such as alcohol, NSAIDs and foods that
trigger symptoms
Treatment
specific management depends on etiology; (see H.Pylori section, G13, NSAID section, G14 and
Stress-Induced Ulceration section, G14)
eradicate H. pylori if present, chief advantage is to lower ulcer recurrence rate
stop NSAIDs if possible
start PPI: inhibits parietal cell H+/K+-ATPase pump which secretes acid
heals most ulcers, even if NSAIDs are continued
other meds (e.g. histamine H2-antagonists) less effective
discontinue tobacco
no diet modifications required but some people have fewer symptoms if they avoid caffeine,
alcohol and spices
G13 Gastroenterology Stomach and Duodenum Toronto Notes 2014
Post-Endoscopy
Resume clear fluids 6 hours post-endoscopy
Test for H. pylori
Counsel re: most likely causes (NSAIDs, anti-platelet agents)
If re-bleeding: repeat endoscopy with aim of hemostasis
Consult interventional radiology or surgery if needed
Epidemiology
H. pylori is found in about 20% of all Canadians
highest prevalence in those raised during 1930s
infection most commonly acquired in childhood, presumably by fecal-oral route
high prevalence in developing countries, low socioeconomic status (poor sanitation and
overcrowding)
Outcome
gastritis (non-erosive) in 100% of patients but asymptomatic
peptic ulcer in 15% of patients
gastric malignancy [gastric carcinoma and mucosal associated lymphomatous tissue (MALT)
lymphoma in 0.5% of patients]
most are asymptomatic but still worthwhile eradicating to lower future risk of peptic ulcer/
gastric malignancy and prevent spread to others (mostly children <5 yr of age)
G14 Gastroenterology Stomach and Duodenum Toronto Notes 2014
Investigations
NSAID-Induced Ulceration
NSAID use causes gastric mucosal petechiae in virtually all, erosions in most, ulcers in some
(25%)
erosions bleed, but usually only ulcers cause significant clinical problems
most NSAID ulcers are clinically silent: dyspepsia is as common in patients with ulcers as in
patients without ulcers; NSAID-induced ulcers characteristically present with complications
(bleeding, perforation, obstruction) If at high risk for development of ulcers,
prophylaxis with PPI indicated
NSAIDs more commonly cause gastric ulcers than duodenal ulcers
may exacerbate underlying duodenal ulcer disease
Pathophysiology
direct: erosions/petechiae are due to local (direct) effect of drug on gastric mucosa The David Y Graham Lecture: Use of
indirect: systemic NSAID effect (intravenous NSAID causes ulcers, but not erosions), inhibits Nonsteroidal Anti-inflammatory Drugs (NSAID)
in a COX-2 Restricted Environment
mucosal cyclooxygenase, leading to decreased synthesis of protective prostaglandins, thus Am J Gastroenterol 2008;103:221-227
leading to ulcers This short article reviews the current understanding
of NSAID risks, emphasizing (1) with the possible
Risk Factors For NSAID Causing Peptic Ulcer exception of naproxen, all NSAIDs increase
previous peptic ulcers/UGIB cardiovascular/cerebrovascular risk, especially the
COX-2 specific inhibitors (2) low-dose Aspirin,
age now used widely to decrease these risks, increases
high dose of NSAID/multiple NSAIDs being taken the likelihood of upper GI tract bleeding and may
concomitant corticosteroid use not abrogate the cardiovascular risk of NSAIDs (3)
concomitant cardiovascular disease/other significant diseases clopidogrel is no safer than Aspirin in patients
with high risk of upper GI tract bleeding (4) add a
PPI to NSAID if there is an increased risk of upper
Treatment GI events.
prophylactic cytoprotective therapy with a PPI is recommended if any of the above risk factors
exist concomitantly with ASA/NSAID use
lower NSAID dose or stop all together and replace with acetaminophen
combine NSAID with PPI or misoprostol
enteric coating of Aspirin (ECASA) provides minor benefit since this decreases incidence of
erosion, not incidence of ulceration
Stress-Induced Ulceration
Definition
ulceration or erosion in the upper GI tract of ill patients, usually in ICU
lesions most commonly in fundus of stomach
Pathophysiology
unclear: likely involves ischemia; may be caused by CNS disease, acid hypersecretion, Cushing
ulcers
physiological stress (e.g. fever, severe illness, complex post-op course) causes ulcers and erosions
G15 Gastroenterology Stomach and Duodenum/Small and Large Bowel Toronto Notes 2014
Risk Factors
mechanical ventilation severe surgery/trauma
anti-coagulation CNS injury (Cushings ulcers)
multi-organ failure burns involving more than 35% of body surface
septicemia
Clinical Features
UGIB (see Upper Gastrointestinal Bleeding, G25)
painless
Treatment
prophylaxis with gastric acid suppressants (H2-blockers or PPI) decreases risk of UGIB, but may
increase risk of pneumonia
treatment same as for bleeding peptic ulcer but often less successful
Gastric Carcinoma
see General Surgery, GS18
Acute Diarrhea
Definition
passage of frequent unformed stools for <14 d
Etiology Useful Questions in Acute Diarrhea
most commonly due to infections Those Fads Wilt
most infections are self-limiting and resolve within 7 d Travel
Homosexual contacts
Risk Factors Outbreaks
food (seafood, chicken, turkey, eggs, beef) Seafood
medications: antibiotics, laxatives Extra-intestinal signs of IBD
others: high risk sexual activity, infectious outbreaks, family history (IBD) Family history
Antibiotics
Diet
Classification Steatorrhea
broadly divided and classified into inflammatory and non-inflammatory diarrhea Weight loss
mechanisms: Immunosuppressed
stimulation of intestinal water secretion and inhibition of water absorption (i.e. secretory Laxatives
problem) Tumour history
in inflammatory diarrhea, organisms and cytotoxins invade mucosa, killing mucosal cells,
further perpetuating the diarrhea
Investigations
stool cultures/microscopy (C&S/O&P) are required only if diarrhea is inflammatory, severe, or
for epidemiological purposes (day care worker, nursing home resident, etc.)
C&S only tests Campylobacter, Salmonella, Shigella, E. Coli Stool Osmotic Gap
other organisms must be ordered separately Stool osmolality is normally about 290
flexible sigmoidoscopy: useful if inflammatory diarrhea suspected mOsm/kg and can be approximated by
biopsies are the most useful method of distinguishing idiopathic IBD (Crohns disease and the calculated stool osmolality
ulcerative colitis) from infectious colitis or acute self-limited colitis (2 x [Na+]stool + [K+]stool)
In osmotic diarrhea, measured stool
C. difficile toxin: indicated when recent/remote antibiotic use, hospitalization, nursing home or osmolality > calculated stool osmolality
recent chemotherapy In secretory diarrhea measured stool
osmolality = calculates stool osmolality
Treatment
fluid and electrolyte replacement orally in most cases, intravenous if severe extremes of age/coma
anti-diarrheals
antimotility agents: diphenoxylate, loperamide (Imodium); contraindicated in mucosal
inflammation
side effects: abdominal cramps, toxic megacolon S. typhi has a rose spot rash (transient
maculopapular rash on anterior thorax,
absorbants: kaolin/pectin (Kaopectate), methylcellulose, activated attapulgite upper abdomen), and a prodrome of
act by absorbing intestinal toxins/micro-organisms, or by coating intestinal mucosa high fever, bradycardia, headache and
much less effective than antimotility agents abdominal pain. Diarrhea is not the initial
modifiers of fluid transport: bismuth subsalicylate (Pepto-Bismol) may be helpful presentation.
antibiotics: rarely indicated
risks
prolonged excretion of enteric pathogen (especially Salmonella)
drug side effects (including C. difficile infection)
development of resistant strains
renal failure/hemolysis (enterohemorrhagic E. Coli O157:H7)
indications for antimicrobial agents in acute diarrhea:
septicemia
prolonged fever with fecal blood or leukocytes
clearly indicated: Shigella, V. cholerae, C. difficile, travellers diarrhea [enterotoxigenic
E. coli (ETEC)], Giardia, Entamoeba histolytica, Cyclospora
situational: Salmonella, Campylobacter, Yersinia, non-enterotoxigenic E. coli
Salmonella: always treat Salmonella typhi (typhoid or enteric fever); treat other Salmonella
only if there is underlying immunodeficiency, hemolytic anemia, extremes of age,
aneurysms, prosthetic valve grafts/joints, sickle cell disease
Travellers Diarrhea
see Infectious Diseases, ID14
Chronic Diarrhea
Definition
passage of frequent unformed stool for >14 d
approach is similar to that of acute diarrhea except that the majority of cases are non-infectious
Etiology/Classification
see Differential Diagnosis of Common Presenting Complaints, G4
Investigations
guided by history
stool analysis for: C. difficile toxin, C&S, O&P fecal fat, WBC
blood for: CBC, electrolytes, CRP, TSH, celiac serology (anti-tTG, protein electrophoresis, IgA)
colonoscopy and ileoscopy with biopsy
upper GI endoscopy with duodenal biopsy
wireless small bowel endoscopy capsule (last resort very costly)
trial of lactose free diet
caveat: may delay diagnosis of IBD and celiac disease
G17 Gastroenterology Small and Large Bowel Toronto Notes 2014
Investigations
transglutaminase serology/protein electrophoresis and abdominal imaging are most useful
because celiac disease and chronic pancreatitis are the two most common causes of steatorrhea
72 h stool collection (weight, fat content) documents steatorrhea
serum carotene, folate, Ca2+, Mg2+, vitamin B12, albumin, ferritin, serum iron solution, INR/PTT
stool fat globules on fecal smear stained with Sudan (rarely used)
other tests specific for etiology (e.g. CT scan/MRI to visualize pancreas)
trial of therapy with pancreatic enzymes
Treatment
dependent on underlying etiology
Epidemiology
more common in women
family history: 15% of first-degree relatives
may present any time from infancy (when cereals introduced) to elderly
peak presentation in infancy
Clinical Features
classically: diarrhea, weight loss, anemia, symptoms of vitamin/mineral deficiency, failure to
thrive; now more commonly bloating, gas, iron deficiency
improves with gluten-free diet, deteriorates when gluten reintroduced
disease is usually most severe in proximal bowel
thus iron, calcium and folic acid deficiency more common than vitamin B12 deficiency
gluten enteropathy may be associated with dermatitis herpetiformis skin eruption, epilepsy,
myopathy, depression, paranoia, infertility, bone fractures/metabolic bone disease
Investigations
small bowel mucosal biopsy (usually duodenum) is diagnostic with:
villous atrophy and crypt hyperplasia
increased number of plasma cells and lymphocytes in lamina propria
increased intraepithelial lymphocytes
villous atrophy also seen in small bowel overgrowth, Crohns, lymphoma, Giardia, HIV
consider CT enterography to visualize small bowel to rule out lymphoma
evidence of malabsorption (localized or generalized)
steatorrhea
low levels of ferritin/iron saturation, Ca2+, Fe, albumin, cholesterol, carotene, B12 absorption
improvement with a gluten-free diet; should not be started before anti-tTG and biopsy
serological tests
Gluten Microchallenge with Wheat-based
serum anti-tTG antibody, IgA, is 90-98% sensitive, 94-97% specific Starch Hydrolysates in Celiac Disease Patients
IgA deficient patients have false-negative anti-tTG Aliment Pharm Therap 2008;28:1240-1248
thus measure serum IgA concomitantly (via serum protein electrophoresis) Study: Randomized, placebo-controlled,
fecal fat >7% prospective study with 24 wk follow-up.
Participants: 90 patients with celiac disease in
remission.
Treatment Intervention: Patients either received glucose
dietary counselling syrups, maltodextrins or placebo.
gluten free diet: avoid barley, rye, wheat Primary Outcome: Small bowel mucosal
morphology and inflammation, symptoms, celiac
oats allowed if not contaminated by other grains serology and malabsorption.
rice and corn flour are acceptable Results: There were no significant differences
iron, folate supplementation (with supplementation of other vitamins as needed) between the intervention and control group in
if poor response to diet change, consider: small-bowel morphology and inflammation,
gastrointestinal symptoms, serology or
alternate diagnosis malabsorption parameters.
non-adherence to gluten-free diet Conclusion: Celiac patients can safely continue
concurrent disease (e.g. microscopic colitis, pancreatic insufficiency) to consume wheat-based starch hydrolysates,
glucose syrups and maltodextrins.
G19 Gastroenterology Small and Large Bowel Toronto Notes 2014
Prognosis
associated with increased risk of lymphoma, carcinoma (e.g. small bowel and colon)
risk of malignancy may be lowered by dietary gluten restriction
Pathophysiology
poorly understood
sustained response of the immune system, perhaps to enteric flora in a genetically predisposed
individual
current hypothesis: lack of appropriate down-regulation of immune responsiveness
Genetics
increased risk of both UC and CD in relatives of patients with either disease, especially siblings,
early onset disease
familial risk greater if proband has CD rather than UC
likely polygenomic pattern: 9 gene loci described to be associated
CARD15/NOD2 gene mutation associated with CD (relative risk in heterozygote is 3, in
homozygote is 40), especially Ashkenazi Jews, early onset disease, ileal involvement, fistulizing
and stenotic disease
CARD15 gene product modulates NFB, which is required for the innate immune response
to microbial pathogens, best expressed in monocytes-macrophages
Clinical Features