GI

ESOPHAGUS DISORDERS
GERD
 A condition that develops when the reflux of stomach contents causes troublesome symptoms/complications
 One of the most common GI complaints. Positive relationship with increasing BMI
 Most commonly occurs due to relaxation or hypotension of the lower esophageal sphincter (LES) caused by caffeine,
alcohol, fat, chocolate, smoking, estrogen, meds
 Heartburn (pyrosis) often exacerbated by meals, increased intra-abdominal pressure, bending over and nocturnal symptoms
associated with reclining
 Less common symptoms  regurgitation of acid or nonacid fluid and water brash, odynophagia, globus, dysphagia, nausea,
vomiting, bronchospasms, hoarseness, chronic cough, chronic laryngitis, sore throat, noncardiac chest pain, sleep
disturbances, halitosis, dental erosions and bronchitis
 Alarm symptoms  odynophagia or progressive dysphagia, unexplained weight loss, recurrent vomiting, occult or gross GI
bleeding, jaundice, palpable mass or adenopathy, family history of GI malignancy, advanced age and anemia
o Diagnosis:
 Clinical  if no alarm symptoms
 EGD  if alarm symptoms present, not responsive to 4-8 week trial of PPI, multiple risk factors for
esophageal adenocarcinoma, pts with GERD 5 years or more
 Double contrast barium swallow (should not diagnose GERD), ambulatory 24 hour pH/impedance
monitoring (most sensitive test), manometry (cannot diagnose GERD), RUQ US, EKG and stress test (must
rule out ACS), CBC (check for anemia)
o Treatment:
 Mild/intermittent (fewer than 2 episodes per week)  lifestyle changes +/- low dose H2RA +/-
antacid
 2nd choice  normal dose H2RA x2 weeks, 3rd choice  low dose PPI and increase as needed
 Severe/frequent (2+ episodes per week)  normal PPI dose and decrease to low dose or H2RA once
mild and intermittent
 Lifestyle modifications  STOP eating spicy/acidic/chocolate/greasy foods, STOP tobacco and
alcohol use, STOP caffeinated beverages, citrus juices, vinegar, tomato sauces, chocolate,
peppermints, weight loss, loose fitting clothing, DON’T eat within 2-3 hours of laying down and sleep
with head of bed elevated 30 degrees
 Surgery  fundoplication
COMPLICATIONS OF GERD
REFLUX ESOPHAGITIS
 Damage to esophageal mucosa from caustic gastric reflux
o Diagnosis: EGD
o Treatment:  PPI. Consider fundoplication
BARRET ESOPHAGUS
 Stratified squamous epithelium replaced w/ metaplastic columnar epithelium in distal esophagus
 Increased in GERD patients with truncal obesity
 Increased risk of cancer (esophageal adenocarcinoma)
o Diagnosis: EGD + biopsy to confirm
o Treatment:  PPI + lifestyle changes. Consider fundoplication
ESOPHAGEAL ULCER
 Severe erosion causes ulcer
 Odynophagia, upper GI bleeds
o Diagnosis: EGD
o Treatment: PPI. Fundoplication
ESOPHAGEAL STRICTURE
 Most commonly a fibrosis or scar tissue formations that narrows the lumen of the esophagus
 Slow progression of dysphagia with solids and intermittent esophageal obstruction over months to years
 Reflux/pyrosis decreases once stricture forms because it provides a barrier structure & most are located at the GE junction
o Diagnosis: barium swallow AND EGD (to rule out carcinoma)
o Treatment: Dilation. Long term PPI
SCHATZKI’S RING
 Ring of smooth mucosal and submucosal tissue
 Episodic dysphagia, sensation that food “sticks” while swallowing (especially poorly chewed food)
 Pts with this almost always have hiatal hernias
o Diagnosis: barium swallow
o Treatment: Esophageal dilatation. PPI
ESOPHAGITIS
EOSINOPHILIC ESOPHAGITIS
 Chronic immune or allergy mediated condition of eosinophils infiltrating esophageal epithelium
 Most commonly seen in kids or young adults
 History of allergies, atopy
 Adults presentation  dysphagia for solids, episode of food impaction, pyrosis
 Children presentation  abdominal pain, vomiting, chest pain, failure to thrive
o Diagnosis: labs (eosinophilia or elevated IgE), EGD + biopsy (reveals small concentric rings, vertical
furrowing/shearing, white plaques/exudates or can appear normal in 1/3 of patients)
o Treatment:
 Dietary elimination or reduce environmental triggers
 Symptom control  topical corticosteroid or oral corticosteroid inhaler w/out spacer swallowed
instead of inhaled
 Dilation of strictures (w/ great caution, increased risk of perforation)
 Referral to allergist
INFECTIOUS ESOPHAGITIS
 General  immunosuppressed pts
o Odynophagia and dysphagia, +/- substernal cp
 Diagnosis: EGD with biopsy and brushings
 Treatment: treat empirically
 Candidal  most common in HIV pts
o May be asymptomatic, 75% have thrush, but 20-25% have thrush with viral esophagitis
 Diagnosis: EGD  diffuse yellow-white plaques
 Treatment: empirically with PO fluconazole x 14-21 days, if no response in a week do EGD
 Cytomegalovirus (CMV) 
o Can affect colon and retina
 Diagnosis: EGD (1+ large, shallow, superficial ulcerations)
 Treatment: ganciclovir or valganciclovir
 Herpetic  typically HSV1, most common in transplant pts
o Herpes labialis
 Diagnosis: EGD (multiple, small, deep ulcerations)
 Treatment: acyclovir or famciclovir or valacyclovir (immunosuppressed pts), self-limited or
acyclovir (immunocompetent pts)
DYSPHAGIA
NEUROGENIC DYSPHAGIA
 Difficulty transferring food/drink/saliva from mouth to pharynx because of “swallowing center” in medulla and pons OR
enteric nervous system
 Most commonly from a stroke
 Dysphagia, drooling, swallow induced coughing, nasal regurgitation, aspiration, choking on food, weight loss
o Diagnosis: needs URGENT evaluation, history (guide diagnosis & etiology), videofluoroscopy, manometry,
nasoendoscopy
o Treatment:
 Treat the problem
 Improve food transfer & prevent aspiration  dietary modification, swallow therapy, non-oral
feeding if necessary
ZENKER’S DIVERTICULUM
 Rare. Restricted opening during swallowing
 Dysphagia, halitosis, regurgitation of undigested food, nocturnal choking, coughing or sore throat, may have protrusion in
neck if retaining food
o Diagnosis: modified barium swallow (VFSE)
o Treatment:
 Diverticulectomy or endoscopic diverticulotomy. Referral
ESOPHAGEAL ATRESIA +/- TRACHEOESOPHAGEAL FISTULA (TEF)
 Most common esophageal malformation
 Failure of the esophagus to form properly, typically failure of union of proximal and distal portions (frequently w/
tracheoesophageal connection/fistula)
 Drooling, choking, respiratory distress, recurrent pneumonias, failure to thrive, gastric distention (if fistula between trachea
and distal esophagus)
 o Diagnosis: prenatal  routine 2nd or 3rd trimester US (polyhydramnios, nonvisualized or collapsed stomach, dilated
proximal esophageal pouch), postnatal  catheter passage into stomach, AP CXR (curled catheter in esophageal
pouch), fluoro-guided contrast to confirm if needed, TEF  lateral CXR, bronchoscopy/endoscopy or CT
o Treatment:
 Surgical repair
VASCULAR RINGS: PEDIATRIC DYSPHAGIA
 Rare, congenital anomalies from aortic arch development, encircling trachea, esophagus or both
 Associated with congenital heart defects like tetralogy of fallot
 Dysphagia, feeding problems, vomiting, respiratory symptoms
o Diagnosis: CXR, echocardiogram, MRI/MRA, CT
ACHALASIA
 Loss of peristalsis in distal 2/3 of esophagus, impaired relaxation of LES due to denervation of esophagus from loss of
inhibitory neurons in myenteric plexus
 Gradual dysphagia for solids and liquids, postprandial substernal discomfort/fullness, regurgitation undigested food, weight
loss
o Diagnosis: barium swallow (absence of peristalsis, poor esophageal emptying, esophageal dilation, symmetric
bird’s beak tapering of distal esophagus, high LES pressure), EGD (rule out carcinoma or distal stricture),
manometry (confirmed diagnosis)
o Treatment:
 Smooth muscle relaxants. Botulinum toxin injection into LES. Pneumatic dilation*. Surgical myotomy*
DIFFUSE ESOPHAGEAL SPASM
 Esophageal contractions that can occur simultaneously, rapidly or in an uncoordinated manner
 Intermittent dysphagia, regurgitation, substernal pain, may be triggered by hot/cold food/drink
o Diagnosis: high resolution manometry (best for pts with frequent symptoms), barium swallow (“corkscrew
esophagus”)
o Treatment: 1st line  CCBs and nitrates
SCLERODERMA
 Autoimmune, females, 30-50 yrs
 Progressive deposition of collagen in esophagus, causes hypomotility and LES incompetence
 Chronic GERD, dysphagia, choking, hoarseness, cough after swallowing
 Limited symptoms: CREST  calcinosis, Raynaud’s phenomenon, esophageal dysfunction, sclerodactyly, telangiectasias
o Diagnosis: manometry (low or no peristalsis, low LES tone), EGD (check for complications), barium swallow
(“waterfall esophagus”)
o Treatment: PPI
CARCINOMAS
ESOPHAGEAL CARCINOMA
 Two types 
o Squamous cell carcinoma  most common esophageal cancer worldwide; middle 1/3rd of esophagus; risk factors
 chronic alcohol and tobacco use, achalasia, caustic-induced stricture, pts with head/neck cancer, HR-HPV; poor
prognosis 30% have distant mets
o Adenocarcinoma  most common esophageal cancer in US; distal 1/3rd of esophagus; risk factors  chronic
GERD, obesity, smoking
 Progressive dysphagia, weight loss, +/- odynophagia, mild GI blood loss from tumor
o Diagnosis: EGD + biopsy, CT (evaluation for distant mets), endoscopic US (if no mets and for detailed image of mass)
o Treatment: Surgical resection. Chemotherapy. Radiation

MALLORY WEISS TEAR

 Longitudinal mucosal tear (non-penetrating) at the GE junction. Most common risk factor  alcoholism
 Hematemesis +/- melena, strain/retching
o Diagnosis: EGD (shows 0.5-4 cm linear mucosal tear at GE junction)
o Treatment:
 Resuscitate if needed
 Generally ablates spontaneously
 Endoscopic local epinephrine, cauterization therapy or endoscopic clipping
 Surgical intervention

HIATAL HERNIA
 Abdominal cavity contents herniating through the esophageal hiatus of the diaphragm
 Most common is type I or sliding hiatal hernia
 Type I  caused by trauma, malformation or iatrogenic, typically asymptomatic or if larger, GERD
  Types II-IV  caused by complication from surgery, asymptomatic or epigastric/substernal pain or postprandial fullness;
nausea (intermittent)—GERD symptoms less common
 Size of hernia correlates with severity of reflux symptoms
o Diagnosis: Type I  not pursued but found during w/u of GERD normally, EGD, barium swallow; Types II-IV 
barium swallow most sensitive
o Treatment:
 Sliding  if symptomatic, manage GERD symptoms and consider referral for surgery if refractory to meds
 Paraesophageal  if symptomatic, surgical repair

ESOPHAGEAL VARICIES
 Enlarged submucosal veins with propensity to bleed, typically at distal end of esophagus
 Caused by portal HTN, most commonly from cirrhosis
 Hematemesis or melena, may have unstable vitals d/t hemorrhagic shock
o Diagnosis: EGD
o Treatment:
 Resuscitate if needed
 Acute hemostasis  endoscopic band ligation, sclerotherapy, + octreotide, balloon tamponade (if
needed for short term control)
 Antibiotic
 Prevention  beta blockers plus series of endoscopic variceal ligation procedures

NAUSEA & VOMITING

 MCC of acute N/V is viral gastroenteritis
 Acute/ no pain: food poisoning, infectious gastroenteritis, drugs, systemic illness
 Acute/ severe pain: peritoneal irritation, gastric or intestinal obstruction, pancreaticobiliary disease
 Persistent vomiting: pregnancy, gastric outlet obstruction, gastroparesis, dysmotility, psychogenic, CNS or systemic disorders
 Timing of nausea/vomiting:
o First thing in am, prior to breakfast  pregnancy, increased ICP, alcohol intake, uremia, nocturnal GE reflux
o Immediately after meals  bulimia, infection, or psychogenic, IBS
o 1-3 hours after meals  gallstones (digested food), gastroparesis or gastric outlet obstruction (undigested)
 ALWAYS ASK  Neurologic symptoms  Headache, Stiff neck, Vertigo, Visual changes, Focal weakness or paresthesias
 PE  Hypotension & tachycardia indicate significant dehydration (assess skin turgor, mucous membrane hydration, cap
refill) & In children  significant dehydration (>5%loss of body wt.) is shown by abnormal cap refill, abnormal skin turgor,
no tears, & abnormal respirations
o Diagnosis: serum electrolytes, liver enzymes, lipase, amylase, abdominal XR, CT, UGI series or upper
endoscopy, nuclear scintigraphy, head CT or MRI, LP
o Treatment:
 Mild, self-limiting  clear liquids, small amounts of dry food, Avoid fatty, fried meals
 Severe  hospitalization and IV fluids for dehydration, correction of electrolyte disturbance,
administration of antiemetic medication, NG suction if needed
 IVF: typically 0.45%-0.9% NS with 20 meq KCL/L (K added after initial fluid boluses usually)
 Commonly prescribed  dopamine receptor antagonists: Promethazine , Prochlorperazine,
Metoclopramide, Trimethobenzamide
 Other meds  neurokinin receptor antagonists, corticosteroids, dexamethasone, serotonin 5-HT3
antagonists (Ondansetron), antihistamines and anticholinergics (Hydroxyzine, Meclizine,
Dimenhydrinate), cannabinoids, benzodiazepines, phosphorated carbohydrate solutions

DIARHHEA  increase in stool frequency (over baseline, typically 3+ stools/day) or decrease in solidity ( increased fluidity, often
“watery” or unformed feces) and often both
ACUTE DIARHHEA  < 2 weeks
 Noninflammatory Presentation  Periumbilical cramps, bloating, N/V, watery and NOT bloody diarrhea, Fecal leukocytes
NOT present (no tissue invasion)
 Inflammatory Presentation  Fever & bloody or pus in diarrhea: Dysentery, Small volume diarrhea since typically from the colon
(<1L/day), Left lower quadrant cramps, urgency, tenesmus, Fecal leukocytes usually ARE present, pos. lactoferrin if invasive
 Acute Infectious (Viral) Gastroenteritis  Intestinal “flu”, sudden onset N/V/D, Generally noninflammatory, Usually mild,
self-limited, resolves within a few days in healthy individuals
 Protozoal 
o Amebiasis: Often carrier, asymptomatic state, If symptomatic, onset 2-4 weeks, Gradual onset abd pain and
diarrhea. Associated abd distension, hepatomegaly, hyperperistalsis, tenderness, Severe cases – dysentery, with 10-
20 bloody stools/day, high fever, hypotension, fulminant 40% mortality
  Diagnosis: serology, imaging for liver abscess severe presentation
o Giardiasis: due to Giardia lamblia, occurs after ingestion of cysts, 1-3 weeks, contaminated water, food, may be
asymptomatic. With symptoms: loose stool, cramps, N/V, flatus, bloating, pain, may be chronic
 Diagnosis: ova & parasite exam, serotyping
o Treatment:
 Noninflammatory oral rehydration, antidiarrheal drugs
 If worsens or lasts longer than 7 days  stool samples sent off
 Inflammatory  symptomatic care, no antibiotics needed but if STEC, immunocompromised, sig.
dehydration drug of choice is fluoroquinolones
 Viral gastroenteritis  supportive care, fluid & electrolyte replacement, antibiotics NOT indicated
and loperamide, Lomotil, bismuth preparations
 Amebiasis  metronidazole or tinidazole + intestinal amebicide (luminal agent: iodoquinol,
paromomycin, diloxanide furoate)
 Giardiasis  metronidazole or tinidazole
FOOD POISONING
Staphylococcus
 Incubation: 1-8 hrs, symptomology w/in 2-12 hrs. Sudden onset N/V lasting up to 24 hrs
 Associated foods: meats, dairy, & bakery products. Diagnosis: Clinical. Testing for toxin possible. Treatment: supportive care
Bacillus cereus  emetic toxin
 Preformed toxin, Incubation: 1-8 hrs. Acute onset severe N/V x 24 hrs
 Foods: reheated fried rice, high starch foods. Diagnosis: Clinical usually, can test for toxin. Treatment: supportive care
Bacillus cereus  diarrheal toxin
 Incubation: 10-16 hours (small intestine). Abd cramps, watery diarrhea, nausea x 24-48 hrs
 Foods: toxin found in meats, stews & gravies. Diagnosis: Clinical usually, can test for toxin.. Treatment: supportive care
Clostridium perfringens
 Incubation: 8-16 hrs. Sudden onset, profuse diarrhea, abd cramps, nausea, rare vomiting. Resolution 24-48 hrs.
 Foods: grows in rewarmed meat, poultry; produces enterotoxin
o Diagnosis: clinical diagnosis, stool culture, test for enterotoxin available. Treatment: supportive care
Clostridium botulinum
 Onset: 12-72 hrs. Vomiting, diplopia, dysphagia, dysphonia, respiratory compromise x days – mos.
 Foods: canned foods, fermented fish, foods kept warm for long periods
o Diagnosis: culture, test for toxin. Treatment: airway stabilization, mechanical ventilation, polyvalent antitoxin
Clostridium difficile
 Onset: usually post abxs (typically 7-10d)Also often hospital acquired. Abrupt onset diarrhea, possibly bloody. Possible fever.
 Foods: -. Meds: antimicrobials, especially clindamycin, beta-lactams. More severe strains with fluoroquinolones.
o Diagnosis: test for toxin (stool). Treatment: oral vancomycin or fidaxomicin, probiotics; fecal transplant for
recurrent infections  Add metronidazole for fulminant disease
Enterohemorrhagic E. coli (includes Shiga toxin producing O157:H7 (STEC))
 Onset: 1-8 days. Sudden, bloody diarrhea & abd. pain. Self-limited in adults X 5-10 d. Children: HUS.
 Foods: undercooked beef, especially hamburger; unpasteurized juice, milk; raw fruits & vegetables
o Diagnosis: culture, test for toxin. Treatment: supportive, plasma exchange for HUS.
Enterotoxigenic E. coli (ETEC)
 Onset: 1-3d. Watery diarrhea, abd cramps X 3-7d. Foods: water & foods with fecal contamination
o Dx: stool culture. Test for toxin. Tx: for travelers’ diarrhea (MCC ETEC), fluoroquinolones lessen symptoms and duration.
Vibrio parahaemolyticus
 Onset: 2-48 hrs.. Sudden onset, watery diarrhea, abd cramps, N/V x 2-5 d
 Foods: undercooked or raw seafood
o Diagnosis: clinical unless severe symptoms, then stool culture
o Treatment: supportive care, consider antibiotics for severe symptoms (Doxycycline, Fluoroquinolones)
Vibrio cholera
 Onset: 24-72 hrs. Sudden profuse watery diarrhea (endemic regions). Foods: contaminated water, fish, shellfish, street food
o Diagnosis: stool culture, molecular and rapid tests
o Treatment: PO or IV rehydration –replacement of fluids and electrolytes. Tetracycline, azithromycin reduce
infectivity, shorten duration of diarrhea, reduce volume of stool losses by up to 50%
Campylobacter jejuni
 Onset: 2-5 d. Fever, possibly bloody diarrhea, abd cramps x 2-10d
 Foods: raw or undercooked poultry, unpasteurized milk or contaminated water. Diagnosis: stool culture on special medium
o Treatment: usually self-limited; azithromycin or fluoroquinolones –severe case.
 Late-onset complication: Guillain-Barre syndrome  May have neg stool studies, can use serologic test
Shigella
  Onset: 24-48 hrs. Sudden onset diarrhea, bloody with pus in stool, abd. cramps, tenesmus, lethargy, fever. May be mild, self-limiting.
 Spread: contaminated food or water (human feces), person-to-person. Diagnosis: stool culture
o Treatment: Usually self-limiting, if still symptomatic after documented infection; treat with Fluoroquinolones.
Avoid opioids and intestinal antimotility drugs.
Salmonella
 Onset: 1-3 d. Sudden or gradual onset, low-grade fever and diarrhea
 Foods: eggs, poultry, unpasteurized milk, cheese, juices, raw fruits & vegetables
o Diagnosis: stool culture. Treatment: supportive. No antibiotics unless high risk, then fluoroquinolones
Yersinia entercolitica
 Onset: 24-48 hrs. Severe abd pain, diarrhea, fever  Polyarthritis & erythema nodosum (children)
 Foods: undercooked pork, unpasteurized milk, tofu, contaminated water
o Diagnosis: stool culture, special medium. Tx: severe  tetracycline or fluoroquinolones. Mild  supportive. Lasts 1-3 weeks
Rotavirus
 Onset: 1-3 d, Most common in infants and young children. Acute onset, fever, vomiting and watery diarrhea x 4-8 d
 Foods: contaminated food (feces), and food touched by infected individuals
o Diagnosis: immunoassay (stool) depending on severity. Treatment: supportive care
Noroviruses, other caliciviruses
 Onset: 12-48 hrs. N/V (children), diarrhea (adults), fever, abd cramps, myalgias X 12-60 hrs.
 Foods: shellfish & fecally contaminated foods
o Dx: Clinical. Stool cultures neg. PCR pos. Tx: supportive care, unless severe in pediatric pt, then hospitalize for rehydration

CHRONIC DIARRHEA > 4 weeks

 Osmotic diarrhea stool volume decreases with fasting, increased stool osmotic gap (> 100 mosm/kg)
 Secretory diarrhea large volume watery stool, secretion exceeds absorption, no significant change with fasting, normal
stool osmotic gap (< 50 mosm/kg)
 Inflammatory diseases fever, hematochezia, abdominal pain, sometimes pus
 Meds caused by SSRIs, cholinesterase inhibitors, NSAIDs, PPIs, ARBs, metformin, allopurinol
 Malabsorption syndromeswt loss, osmotic diarrhea, abnormal labs, fecal fat >10 g/24h (foul smelling stool that “floats” due to
steatorrhea)
 Motility disorders lower abdominal pain, altered bowel habits (IBS)
 Chronic infections constant or intermittent symptoms, relationship to meals, occurrence at night or related to meals or when
fasting, stool appearance greasy, malodorous, watery, bloody, or with pus & abdominal pain. MCCIBS, lactose intolerance, meds
o Treatment: Loperamide. Diphenoxylate w/ atropine. Codeine, tincture of opium. Clonidine. Octreotide.
Cholestyramine/colestipol/colesevelam

STOMACH DISORDERS
DYSPEPSIA
 Acute, chronic, or recurrent upper abdominal pain and discomfort. Sometimes referred to as “indigestion”
 Functional dyspepsia (idiopathic or nonulcer) 75% of cases. Bothersome epigastric pain or burning, bothersome early
satiety, and/or bothersome postprandial fullness w/ no evidence of structural/organic disease to explain symptoms
 Underlying/organic cause Food or drug intolerance, Luminal GI tract dysfunction, H. pylori infection, Pancreatic disease,
Biliary tract disease
 Alarm Features  Unintentional weight loss, Anemia, Hemorrhage, Early satiety, Progressive dysphagia, Odynophagia, Palpable
mass/lymphadenopathy, Fam hx of upper GI cancer, New onset of symptoms age >60, Recurrent/persistent vomiting
o Diagnosis: Initial labs: CBC, CMP, Lipase, and Amylase should be performed in all pts
 If > 60y/o  upper endoscopy & biopsy to rule out h. pylori, additional eval: US or CT
 If < 60 y/o  test and treat for h. pylori, additional eval: biopsy of duodenum (to rule out celiac disease or
inflammatory conditions)
o Treatment:
 If > 60 y/o 
 If H. pylori is present, treat w/ eradication therapy and treat underlying dz process (PUD)
 If symptoms persists after H. pylori eradication, trial of PPI for 4-8 weeks
 If symptoms persists after PPI, trial of TCA for 8-12 weeks  If improvement, continue for
6 mths and discontinue. Resume if symptoms recur
 If symptoms persists after TCA, trial of prokinetic for 4 weeks  If improvement,
discontinue prokinetic. If symptoms recur, repeat 4 week course
 If persistent symptoms after above Re-evaluate symptoms. Assess gastric emptying in pts
w/ N/V predominant symptoms. Trial of psychotherapy in pts w/functional dyspepsia
 If < 60 y/o 
  Pts who are H. pylori negative or have symptoms after eradication therapy  Treat with
antisecretory therapy with a PPI for 4-8 weeks
 If no improvement after 8 weeks of PPI Treat w/therapeutic trial of TCA 8-12 weeks
 If no improvement on trial of TCA Consider prokinetic agent x 4 weeks
GASTRITIS
 Conditions with histologic evidence of inflammation of epithelium or endothelium of stomach
 Erosive and hemorrhagic type  caused by stress, NSAIDs, alcoholics & critically ill pts or those with portal HTN
o Epigastric pain, N/V, hematemesis but often asymptomatic . Diagnosis: endoscopy
o Stress gastritis  mucosal erosions and subepithelial hemorrhages
 Tx: prophylactic  IV H2-receptor antagonist or PPIs, sulcrafate; Once bleeding starts  give continuous
IV infusion of PPI (pantoprazole 80 mg IV bolus then 8 mg/h continuous infusion) and endoscopy
o NSAID gastritis  using COX-2 inhibitors decrease ulcer incidence
 Treatment: endoscopy, withdrawal/decrease NSAID (always take w/meals), PPI
o Alcoholic gastritis  dyspepsia, nausea, emesis, mild hematemesis
 Treatment: H2-receptor antagonist or PPI, sucralfate for 2-4 weeks, alcohol cessation
o Portal HTN gastritis  chronic GI bleeding, acute significant bleeding but is often asymptomatic
 Treatment: propranolol or nadolol
 Nonerosive, nonspecific gastritis  h. pylori, pernicious anemia or eosinophilic gastritis
o H. pylori gastritis  asymptomatic (most pts), mild diffuse gastritis, inflammation of gastric antrum but sparing
gastric body and few pts have inflammation primarily of the gastric body
o Pernicious anemia gastritis  autoimmune disorder of fundic glands results in: achlorhydria (lack of acid secretion),
decreased IF secretion and vitamin B12 malabsorption
 Treatment: endoscopy with biopsy at diagnosis with periodic surveillance
o Eosinophilic gastritis  rare, anemia from mucosal blood loss, abdominal pain, early satiety, vomiting after eating
 Treatment: corticosteroids
o Infections  bacterial, viral, fungal, parasitic
 Acute bacterial  treat with broad spectrum antibiotics, possibly emergency gastric resection
PEPTIC ULCER DISEASE
 Erosive change that extend through muscularis mucosa to submucosa. 5 times more common in duodenum
 Dyspepsia, bleeding, pain (localized to epigastrium, not severe, described as gnawing, dull, aching or “hunger-like”), nausea
and anorexia (with gastric ulcers), may have positive FOBT, tarry stools or coffee ground emesis
 Constant pain (penetration or perforation) and pain that increases w/ meals with N/V or undigested food (gastric outlet obstruction)
 Symptoms exacerbated by food, “classic” pain occurs 2-5 hours after a meal and at night between 11 PM and 2 AM
 PE epigastric tenderness (MC), RUQ pain, tachycardia/orthostasis, severe tenderness and guarding, succussion splash
o Diagnosis: labs (normal), anemia, leukocytosis, upper endoscopy (procedure of choice), UGI – barium study (alternative)
o Treatment:
 Test & treat for h. pylori is present. Avoid NSAIDs
 PPI 
 Active, complicated duodenal ulcer  4-8 weeks
 Active gastric ulcer  8-12 weeks
 NSAID induced ulcer  minimum 8 weeks
 Non h. pylori and non NSAID ulcer  4-8 weeks
 Prevention  PPI (minimum 8 weeks), COX-2 selective NSAID, misoprostol 200 mcg orally 4 times daily
H PYLORI
 Gastritis, Possible PUD (duodenal or gastric), May lead to development of gastric adenocarcinoma or gastric lymphoma, Dyspepsia
o Diagnosis: biopsy test, urea breath test, stool antigen test (monoclonal antibodies), serologic assay (for IgG)
o Treatment: Bismuth quadruple combination (preferred)  PPI and 2-3 antimicrobial agents for 14 days
ZOLLINGER-ELLISON SYNDROME
 Non-B islet cell tumor (gastrinoma) of pancreas or duodenum
 Over 80% of tumors are located in gastrinoma triangle: Junction of cystic and common bile ducts superiorly, 2nd and 3rd parts of
duodenum inferiorly, and neck and body of pancreas medially
 Over 60% of tumors are malignant
 Peptic ulcer disease (over severe) in 95%, elevated serum gastrin with gastric acid hypersecretion, abdominal pain, diarrhea,
GERD, esophagitis, ulceration, strictures, Barrett’s, nausea, weight loss, GI bleeding
 MEN1 in 25%  look for parathyroid, pancreatic/duodenal, and pituitary tumors Increased risk for carcinoid tumors
o Diagnosis: serum gastrin level >1000 pg/mL, secretin test, stop PPI 7 day before testing + put pt on H2 blocker, stomach
acid pH < 2.0 (diagnostic), other labs: calcium, imaging: endoscopic US, radioactive somatostatin analog study, CT, MRI
o Treatment: High dose oral PPI  omeprazole 60-120 mg/day. Octreotide. Chemotherapy. Surgical resection
GASTRIC OUTLET OBSTRUCTION
 MCC in adults  pancreatic adenocarcinoma, MCC in young children  pyloric stenosis
Edema or cicatricial narrowing of pylorus or duodenal bulb
N/V (usually partially digested food contents), epigastric pain or fullness, early satiety, abdominal distention, weight loss, dilated and
atonic stomach (chronic obstruction), malnutrition, dehydration, metabolic alkalosis, hypokalemia, succussion splash in epigastrium
o Dx: abd. XR, nasogastric aspiration (aspiration of >200 ml of foul smelling fluid = dx), EGD, water-soluble or barium
contrast studies, CT. Tx: NPO, adequate fluid and electrolyte replacement, NG tube. IV PPI. Treat underlying cause
GASTROPARESIS Delayed gastric emptying. MCC is idiopathic
 Postprandial fullness or early satiety, N/V 1-3 hours after meals of undigested/partially digested food, upper abd. discomfort, possible
small bowel manifestations (abd. distention, bloating, diarrhea, malnutrition, malabsorption), colonic involvement (constipation or
alternating constipation and diarrhea)
o Dx: plain film XR (dilation of esophagus, stomach, small intestine, colon), gastric scintigraphy (best test of gastric emptying)
o Treatment:
 No specific tx NG suction and IVF, frequent small meals (low in fiber, milk, gas forming foods and fat), liquid
enteral supplements prn. Avoid meds that decrease GI motility. Optimize glycemic control
 Stop amylin and GLP-1 analogs
 Prokineticsmetoclopramide 5-20mg PO or 5-10mg IV/SQ qid + erythromycin 50-125mg PO tid before meals
 Antiemetics prn to help control nausea and vomiting
PYLORIC STENOSIS
 Non-bilious vomiting (starts at 2-4 weeks of age), pathognomonic projectile vomiting (sometimes blood streaked), not ill-
looking but are hungry after episodes of vomiting, dehydration, poor weight gain, fretfulness, malnutrition, metabolic
alkalosis, apathy, abdomen may be distended after feeding with prominent gastric peristaltic waves, Hypertrophic muscular
sphincter- palpable oval mass 5-15 mm long, in RUQ “pyloric olive”
o Diagnosis: hypochloremic alkalosis, hypokalemia, elevated Hgb and Hct, mild unconjugated bilirubinemia, US (shows
hypoechoic muscle ring > 4 mm thick with hyperdense center), barium upper GI series, “double track” of barium
o Treatment:
 Refer for surgery  pyloromyotomy
 Treat dehydration & electrolyte abnormalities before surgery
 IV cimetidine before surgery
GASTRIC TUMORS  Majority are adenocarcinomas
 Early onset asymptomatic, abdominal discomfort/pain (often vague postprandial abdominal heaviness), early satiety, nausea,
vomiting, anorexia, dysphagia, GI hemorrhage, later symptoms of weight loss and palpable mass (usually diagnosed late)
o Diagnosis: positive FOBT, anemia, elevated CEA, endoscopy and gastric biopsy, double contrast XR
o Treatment: Surgical resection of tumor, adjacent tissue, regional lymph nodes. Chemotherapy. Prevention 
Mediterranean diet, aspirin use, allium vegetable consumption

PANCREAS DISORDERS
ACUTE PANCREATITIS MC inpatient primary GI diagnosis in US. MCC = gallstones and 2nd MCC = alcohol
 3 phases initial, second and third
 Abd. pain (major complaint; may be mild discomfort to severe, constant & incapacitating; usually constant, “boring,” in epigastrium
+ periumbilical area, pain may radiate to back, chest, flanks, lower abd.; pain lessened by leaning forward), N/V, abd. distention
 PE distressed, anxious, low grade fever, tachycardia, hypotension, shock (not uncommon), jaundice, erythematous skin nodules,
pulm. basilar crackles, atelectasis, pleural effusion, abd. tenderness and rigidity, BS decreased/absent, cullen’s, grey turner’s
o Diagnosis: serum amylase and lipase (3x above normal established dx) CBC (leukocytosis), hyperglycemia,
hypocalcemia, hyperbilirubinemia, liver enzymes elevated, hypoxemia, US, CT abdomen
o ANY severe acute pain in abdomen or back suggests possible acute pancreatitis
o Diagnosis generally confirmed by 2 of 3 criteria:
 typical abdominal pain in epigastrium that may radiate to back
 3x or > elevation in serum lipase and/or amylase
 confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging (CT, US, MRI)
o Treatment:
 Mild acute self-limited, improves w/in 3-7 days, fluid resuscitation, IV analgesics, O2 via NC 2L, initial
NPO + oral intake resumed if pt is hungry/has normal bowel function/no N/V, liquid diet or low fat solid diet
 Moderate severe acute  prolonged hospitalization, ICU step down
 Severe acute  CT or MRI (assess for necrosis or complications), prophylactic abx NOT rec, ICU admission
 MOST important treatment  safe and aggressive fluid resuscitation
 NPO, IV narcotic analgesics, supplemental oxygen
 IVF  Lactated Ringer’s or normal saline: initial bolus of 15-20 mL/kg (1050-1400 mL), then 3 mL/kg/hr.
(200-250 mL/h) to maintain urine output > 0.5 mL/kg/hr.
 Serial bedside evaluations every 6-8 hours. Measure Hct and BUN every 8-12 hours
 Necrosismay require antibiotics IV, pancreatic debridement, transgastric drainage
 PreventionAvoidance of excess alcohol, remove gallstones, Treat hypertriglyceridemia
CHRONIC PANCREATITIS  Progressive fibroinflammatory process of pancreas
 Permanent structural damage leads to impaired exocrine and endocrine function. MCC is alcohol abuse
 Primary manifestations  abdominal pain & pancreatic insufficiency
 Abdominal pain Epigastric, radiates to back, Steady, boring pain, occasionally associated with N/V, May be relieved partially by
sitting upright or leaning forward, often worse 15-30 minutes after eating, initially often as “attacks” of pain; with disease
progression becomes continuous, some patients with chronic pancreatitis have NO PAIN
 Pancreatic insufficiency  > 90% pancreatic function is lost, loose, greasy, foul smelling stools that are hard to flush
(steatorrhea), malabsorption of fat soluble vitamins, weight loss, glucose intolerance
o Diagnosis: labs (normal), “classic triad”  pancreatic calcifications (imaging), steatorrhea and DM, dx confirmed
with one of the following  calcifications in the pancreas on plain abd XR or CT, abnormal pancreatogram with
beading of the pancreatic duct (ERCP or MRCP) or abnormal secretin pancreatic function test
o Treatment:
 For pain  treat underlying cause, cessation of alcohol, small meals low in fat and stay hydrated,
supplement with medium chain TG, stop smoking, add H2 blocker or PPI
 Continued pain management  analgesics
 Amitriptyline and nortriptyline
 Short courses of opiates with low dose amitriptyline 10 mg qhr x 3 weeks and NSAID
 Some pts require chronic opioids  long acting with addition of pregabalin
 Steatorrhearestrict fat intake, enzyme supplementation, vit supplementation (calcifediol), medium
chain triglycerides
 For glucose intolerance  annual fasting glucose levels, if abnormal will need insulin
 Patient education  NO alcohol or smoking and diet low in fat
PANCREATIC NEOPLASMS
 4th leading cause of cancer related death, nearly all will die from it, 85% of tumors adenocarcinomas, 5 year survival rate of only 6%
 Two types endocrine (MEN1 NET, insulinoma, gastrinoma) & exocrine (maj. of tumors, adenocarcinomas, acinar cell carcinomas)
 2/3rds arise in head or uncinated process of the pancreas
 Early symptoms vague and nonspecific, pain (epigastrium usually), jaundice, early satiety, anorexia, nausea/vomiting
 PEweight loss, icterus, possibly palpable GB
o Diagnosis: very few cancers diagnosed when still localized, abdominal US, staging, contrast abdominal CT, PET
o Treatment: Surgical resection. Palliative procedures. Chemotherapy

GALLBLADDER DISORDERS
CHOLELITHIASISGallstones. 80% are cholesterol stones. No inflammation.
 Often asymptomatic, biliary “colic” (characteristic complaint, sudden onset lasting 15 min-5 hrs that resolves quickly or gradually,
precipitated by eating often w/ intake of a fatty meal and occurs shortly afterwards, visceral pain severe, constant ache or fullness,
normally in RUQ or epigastric area; pain radiates to R scapula/interscapular area/shoulder; may be nocturnal), N/V
 PE tenderness of RUQ and sometimes a positive murphy’s sign
o Diagnosis: elevated GGT > 90 U/L, US (imaging of choice), plain abdominal XR, HIDA, abdominal CT, ERCP
o Treatment: Ursodeoxycholic acid (Ursodiol). Laparoscopic cholecystectomy (surgical gold standard)
ACUTE CALCULUS CHOLECYSTITISAcute GB wall inflammation, generally occurring after cystic duct obstruction by gallstone
 Triggered by large/fatty meal, biliary pain that is constant, progressively worsens, localized to RUQ or epigastrium, may subside
slowly over 12-18 hrs, may radiate to R scapula/interscapular area/shoulder, peritoneal signs (pain w/ jarring or deep inspiration),
anorexia, N/V, low grade fever, tender RUQ possibly w/ palpable enlarged GB (+ murphy’s sign, rebound tenderness, jaundice)
o Dx: clinical (classic triad of sudden onset RUQ pain, fever, leukocytosis), bilirubin elevated, transaminases,
amylase, US (shows stones, GB wall thickening, dilated bile duct, pericholecystic fluid), HIDA (nonvisualized GB
with filling of common bile duct/duodenum seen)
o Treatment: Hospitalization, NPO, IV abx (cephalosporins, penicillin or fluoroquinolones), fluids, NSAIDs
(ketorolac), opioids (preferred for pain, morphine, hydromorphone). Laparoscopic cholecystectomy preferred
ACUTE ACALCULOUS CHOLECYSTITIS
 5-10% of pts with acute cholecystitis, no stones found at time of diagnosis that are obstructing duct
 Usually critically ill, fever may be only sign, palpable RUQ mass, rarely jaundice, may present w/ sepsis, shock and
peritonitis or may present similar to calculous cholecystitis (fever, severe RUQ pain w/ positive murphy’s sign)
o Diagnosis: US (preferred initially), CT (enlarged, tense GB with poor motility and emptying, no stones present)
o Treatment: Cholecystectomy. Gallbladder drainage. Antibiotics (always)
CHRONIC CALCULUS CHOLECYSTITIS  Secondary to chronic inflammation of the GB wall
 Clinical manifestations do NOT correlate with symptoms of acute cholecystitis
 Minimal symptoms, GB wall firm and thickened w/ lymphocytic infiltration. Tx: If symptomatic  cholecystectomy

FUNCTIONAL GALLBLADDER DISORDER Acalculous cholecystopathy

 Disorder gallbladder motility  produces biliary pain when no stones are present
 oDiagnosis: abnormal CCK nuclear cholescintigraphy with EF < 40%, CCK infusion reproduces patient’s pain, normal liver
enzymes, conjugated bilirubin & amylase/lipase. Treatment: Can resolve spontaneously. Cholecystectomy
CHOLEDOCHOLITHIASIS Common duct stones
 Asymptomatic, mild epigastric/RUQ tenderness, biliary pain, jaundice, episodic cholangitis, pancreatitis, N/V, pruritis (due to long
standing obstruction, worse in warm weather, worse on extremities than trunk, much MC in neoplastic obstruction than stones)
o Diagnosis: elevated WBCs, elevated bilirubin, elevated alkaline phosphatase and GGT, elevated liver
transaminases, transabdominal US (imaging study of choice), ERCP, EUS and MRCP
o Treatment: Laparoscopic cholecystectomy. Choledochotomy incision. Endoscopic sphincterotomy
GALLSTONE PANCREATITIS
 Risk of stone causing pancreatitis is inversely proportional to its size. Symptoms of pancreatitis
o Diagnosis: US of biliary tree
o Treatment:
 If severe  ERCP with sphincterotomy and stone extraction then cholecystectomy
 If mild  stone has passed, proceed with cholecystectomy and cholangiogram for detecting CBD
stones, stone removal during cholecystectomy
ACUTE CHOLANGITIS  Bacterial infection of bile ducts
 Charcot’s Triad  fever, epigastric or RUQ pain, jaundice
 Reynold’s pentad  fever, RUQ pain, jaundice, septic shock (hypotension, tachycardia), mental status changes (confusion)
 Abdominal exam: same as for acute cholecystitis
o Diagnosis: leukocytosis, hyperbilirubinemia, elevated liver transaminases and alkaline phosphate, US/helical CT,
ERCP (diagnostic test of choice), PTC, helical CT/MRI
o Treatment:
 1st line admit, IV abx, fluid resuscitation, analgesics for pain control, vasopressor support if needed
 2nd line when stable, biliary decompression
 Endoscopic drainage. Percutaneous transhepatic drainage. Surgical drainage
PRIMARY SCLEROSING CHOLANGITIS
 Chronic liver disease characterized by a progressive course of cholestasis with inflammation and fibrosis of intrahepatic and
extrahepatic bile ducts
 Up to 90% cases have ulcerative colitis. Progressive disease leading to secondary biliary cirrhosis
 Intermittent jaundice, fatigue, weight loss, pruritus, abdominal pain
o Diagnosis: elevated alkaline phosphatase and bilirubin, ERCP vs MRCP (“beading”), liver biopsy
o Treatment:
 No known effective medical therapy or cure. Refer to GI
 Short term treatment with dilatation and stents. Surgical resection
 Liver transplantation  in advanced disease
GALLBLADDER CARCINOMA
 Most common GI malignancy. Most commonly is adenocarcinoma
 Asymptomatic, Abdominal pain, Anorexia, nausea, vomiting, Palpable gallbladder, jaundice
o Diagnosis: CT/MRI abdomen and pelvis (test of choice), percutaneous transhepatic cholangiography, MRCP
o Treatment:
 Refer to GI. Surgery  laparotomy (for staging), open cholecystectomy or extended cholecystectomy
 Chemotherapy. Radiation
CHOLANGIOCARCINOMA
 Bile duct carcinoma. Tumors of biliary tree, exclusive of gallbladder and ampulla of Vater
 >90% are adenocarcinomas, nodular is MC and highly invasive
 Painless jaundice (MC), pruritis, mild RUQ pain, fever, fatigue, weight loss, anorexia, clay colored stools, dark urine, cholangitis
o Diagnosis: elevated alkaline phosphate, elevated GGT, CA 19-9 > 129 U/mL, CEA (normal or elevated), AFP normal,
total bilirubin > 10 mg/dL, US or CT then refer for MRI, MRCP, ERCP
o Treatment:
 Refer to GI. Surgery  resection of biliary system (including GB if limited disease), hepatic lobectomy
 Palliative procedures if unresectable disease
AMPULLARY CARCINOMA  Periampullary neoplasms that develop near ampulla of Vater
 Obstructive jaundice (MC), diarrhea (fat malabsorption resulting in steatorrhea), mild wt loss, fatigue, abdominal pain, fever, N/V
o Dx: US (first step to eval for obstructive jaundice but unlikely to show tumor), abdominal CT, ERCP (decompression and
confirmation of tumor), MRCP
o Tx: Refer to GI. Surgery Whipple procedure. Papillectomy, laser ablation, photodynamic therapy

SMALL INTESTINE & COLON DISORDERS

CONSTIPATION
 Unsatisfactory defecation w/ either infrequent stools, difficult stool passage or both
  Rome IV criteria for functional constipation:
1. Must include 2 or more of the following:
 Straining during ≥ 25% defecation
 Lumpy or hard stools in ≥ 25% of defecation (Bristol 1-2)
 Sensation of incomplete evacuation in ≥ 25% of defecation
 Sensation of anorectal obstruction/blockage in ≥ 25% of defecation
 Need for manual maneuvers to achieve defecation in ≥ 25% BM
 Fewer than 3 spontaneous bowel movements per week
2. Loose stools are rarely present without laxatives
3. IBS criteria not met
 Above criteria x 3 + months, symptom onset 6+ months prior to dx
 Infrequent bowel movements and abdominal bloating. Excessive straining. Sense of incomplete evacuation. Need for digital
manipulation. Decreased appetite. Nausea and vomiting. Paradoxical “diarrhea” (with fecal impaction). Firm stool
 Alarm symptoms  45-50+ yrs. old with no previous colon cancer screening. Change in stool caliber “pencil-thin stools”.
Iron-deficiency anemia. Obstructive symptoms. Recent onset of constipation. Rectal prolapse. Hematochezia, + FOBT.
Weight loss. Positive family hx of colon cancer or inflammatory bowel disease. No response to empiric treatment
o Diagnosis: history, physical exam w/DRE, FOBT, 2 week bowel diary very helpful, CBC (anemia), serum
electrolytes (hypokalemia, hypercalcemia), serum glucose, TSH (hypothyroidism), FOBT (GI bleed), colonoscopy
(if alarm symptoms), abdominal XR, barium enema, anorectal manometry, balloon expulsion testing, colonic transit
studies, defecating proctography
o Treatment:
 First line 
 Lifestyle modifications  high fiber diet, exercise, adequate water intake, routine bowel
training, never ignore need to defecate
 Fiber supplements  Psyllium (Metamucil), Methylcellulose (Citrucel), Calcium polycarbophil
(FiberCon)
 Stool surfactant agents (stool softners)  mineral oil, Docusate sodium (Ducolax, Colace)
 Second line  osmotic laxatives (mangesium hydroxide, lactulose, polyethylene glycol powder (MiraLax))
 Third line  stimulant laxatives (bisacodyl (ducolax), senna) and others (lubuprostone (amitiza),
linaclotide (linzess))

ACUTE & CHRONIC LAXATIVE ABUSE

 #1 cause for factitious diarrhea
 Acute  watery, high volume diarrhea, abdominal cramping, 10-20 bowel movements a day. Pt may be dehydrated,
underweight, malnourished, orthostatic hypotension, fatigue
 Chronic  metabolic alkalosis, cathartic colon (enlarged colon with loss of haustra)
o Diagnosis: Laxative screen of stool specimen: magnesium and phosphorus levels, stool osmolality, ESR, CRP,
CMP, stool studies
o Treatment: Correct electrolytes, dehydration and malnutrition. Referral to psychiatrist
ILEUS
 Neurogenic failure or loss of motility of GI tract in absence of obstruction
 Commonly seen post-op
 Abdominal discomfort (mild, generalized, continuous), Nausea/vomiting, Bloating, Delayed passage of or inability to pass
flatus, Inability to tolerate an oral diet
 PE  Distention. Bowel sounds diminished or absent. Mild TTP, no peritoneal irritation
o Diagnosis: abdominal XR (Upright and supine films. Distended gas-filled loops of small and large bowel. Air-fluid
level possible), CT (rule out small bowel obstruction), serum electrolytes (hypokalemia)
o Post-op Diagnosis: symptoms persist for more than 3-5 days, in absence of mechanical bowel obstruction or other
causes that could lead to post-op abd distention and decreased bowel activity
o Treament:
 NPO. IV fluids & electrolytes
 AVOID opioid analgesics  use NSAID or Tylenol instead
 Chewing gum post-op
 If prolonged  NG suction, parenteral nutrition
 Prevention post-op  avoid IV opioids, ambulate early, start clear liquids
SMALL BOWEL OBSTRUCTION
 Normal flow in lumen is interrupted
 MCC is post-op adhesions
 Abdominal pain (Typically periumbilical, intermittent, crampy  Simple obstruction; If pain becomes focal, constant 
peritoneal irritation from ischemic or necrotic bowel; Sudden, severe pain  perforation; Colicky pain occurring for shorter
 time associated with bilious vomiting  Proximal obstruction; Progressive pain lasting longer (days) with distension 
Distal obstruction), Nausea & vomiting (vomiting more severe with proximal obstructions), Duodenum, proximal
jejunum, Diarrhea (early), Constipation/Obstipation (late), absence of BM/flatus
 PE  Abdominal distension, High-pitched “tinkling” hyperactive bowel sounds early followed by hypoactive bowel sounds,
Abdominal TTP, Tachycardia, orthostatic hypotension, decreased urine output dehydration is hallmark sign of SBO, Fever
(indicates complication: abscess, ischemic/necrotic bowel)
o Diagnosis: serum electrolytes (hyponatremia, hypokalemia), elevated BUN and creatinine levels (indicate dehydration),
CBC (anemia, elevated WBC, increased hematocrit), elevated lactic acid, UA, type and crossmatch, plain abdominal
XR (first test to order  Supine and upright required. Dilated small-bowel loops with air-fluid levels. Absent or
minimal colonic gas, “String of pearls”), CT (best test to order for etiology and specific location of blockage)
o Treatment: Aggressive fluid resuscitation. NG suction. Analgesia and antiemetic. Early surgical consultation
LARGE BOWEL OBSTRUCTION
 Loss of normal flow of intraluminal contents. Less common than SBO but is an EMERGENCY. MC benign etiology is volvulus
 Tumor (colon cancer) (most common in US)
 Volvulus (sigmoid volvulus -- most common cause of LBO in developing world)
 Gradual onset  Malignancy and diverticulitis, Acute onset  Volvulus, Lack of BM or flatulence, Abdominal distention,
Nausea and Vomiting (more likely if proximal), Crampy abdominal pain (intermittent, paroxysmal), Change in caliber of
stool (gradual, less acute onset)
 PE  Bowel sounds normal early on but progress to no bowel sounds, Very tender abdomen, fever, rigidity = peritonitis with
perforation, Mass may be palpated on digital rectal exam if very distal obstruction, Observe for hernias
o Diagnosis: KUB radiograph (dilation of bowels, coffee bean sign, northern exposure sign), standing XR (free air
under diaphragm, concern for perforation), contrast enema (birds beak, contraindicated in peritonitis/suspicion for
perforation), CT, flex/rigid endoscopy, labs (CBC, CMP, UA, lactate, type and crossmatch)
o Treatment: IV fluid and electrolytes resuscitation. Early surgical consult. NG tube if vomiting present
INFLAMMATORY BOWEL DISEASE
ULCERATIVE COLITIS
 Diffuse mucosal inflammation—rectum and extends proximally through colon (does not affect small bowel)
o Diffuse friability and erosions, contiguous. Not transmural like Crohn’s
 3 times more common than Crohn’s disease
 Insidious onset, Bloody diarrhea is the hallmark, Frequent stools, Mucous discharge, Tenesmus (urge to go to bathroom),
Lower abdominal pain, Fulminant (Severe symptoms with signs of toxicity)
 Extracolonic features Uveitis, Pyoderma gangrenosum, Pleuritis, Erythema nodosum, Ankylosing spondylitis,
Spondyloarthropathies, Primary sclerosing cholangitis
 Physical Exam  Normal & in more severe disease  Fever , Tachycardia, Abdominal tenderness, no peritoneal signs unless
complicated colitis, Weight loss, nutrient deficient
 UC usually spares anus and involves rectum
o Diagnosis: CBC (anemia), CMP (hypoalbuminemia, hypokalemia, hypomagnesemia, increased alkaline
phosphatase), elevated ESR and CRP, pANCA (positive in up to 70% of pts), chronic diarrhea > 4 weeks and
evidence of active inflammation on endoscopy and chronic biopsy changes, stool assays (exclude other diseases),
ileocolonoscopy (DO NOT perform if fulminant signs/symptoms due to risk of perforation), colonoscopy (lesions
isolated to colon. Lesions contiguous. Inflammation limited to mucosa/submucosa), XR
o Treatment:
 For mild  5-ASA (mesalamine, sulfasalazine, azo compounds)
 For moderate to severe  corticosteroids, immunomodulating drugs (mercaptopurine, azathioprine,
methotrexate)
 For fulminant disease  admit, NPO, IV corticosteroids, fluids, abx +/- cyclosporine or infliximab
 Anti-TNF therapies
 Surgery referral
CHRONS DISEASE
 Chronic, recurrent disease characterized by patchy transmural inflammation involving any segment of the GI tract from
mouth to anus (skip lesions)
 Lesions most commonly found in terminal ileum and perianal area
 Higher prevalence among smokers
 Low grade fever, prolonged diarrhea, abdominal pain RLQ, +/- bleeding, fatigue, weight loss, perianal lesions (skin tags, anal
fissures, perianal abscesses, fistulas), usually spares the rectum
 If obstruction  postprandial bloating, cramping pain, loud borborygmi
 Extra intestinal manifestations  arthralgias, arthritis, iritis or uveitis, pyoderma gangrenosum, or erythema nodosum,
gallstones, nephrolithiasis, aphthous lesions
o Diagnosis: labs and stool studies same as UC, colonoscopy and tissue biopsy (ulcers, strictures, segmental
involvement with areas of normal appearing mucosa adjacent to inflamed mucosa; non-necrotizing granulomas,
 hyperemia and edema then ulcerations & production of lymphoid tissue causes cobblestone appearance), ASCA,
barium enema, upper GI barium series, CT and MRE (becoming more standard of care), wireless capsule endoscopy
(if CT enterography or SBFT is positive)
o Treatment:
 Similar to UC if solely in colon
 Mild ileocecal disease  PO budesonide or PO mesalamine
 Moderate ileocecal disease  PO budesonide + PO mesalamine (if first presentation), anti-TNF (if relapse)
 Severe ileocecal disease  IV steroids (first presentation), anti-TNF (if relapse)
 Surgery referral, Admit
 Patient education  Smaller more frequent meals, Increase fluid intake to offset diarrhea, Trial of
cutting out dairy (lactose intolerance is high)

IRRITABLE BOWEL SYNDROME

 Chronic (>6 months) functional disorder characterized by abdominal pain or discomfort with alterations in bowel habits not
explained by the presence of structural or biochemical abnormalities
 Usually in late teens/early twenties, 2/3 are women
 Recurrent abdominal pain on average at least one day per week in the last 3 months, with at least two of the following of
Rome IV criteria  related to defecation, associated with a change in frequency of stool, associated with a change in
form/appearance of stool (abnormal form: lumpy or hard, loose or watery)
 Passage of mucus (uncommon), bloating or feeling of abdominal distention, dyspepsia, heartburn, chest pain, headaches,
fatigue, myalgias, urologic dysfunction, gynecologic symptoms, anxiety, or depression
 Irritable bowel syndrome with diarrhea (IBS-D)  Patient reports that abnormal bowel movements are usually diarrhea (type
6 and 7 in the BSFS)
 Irritable bowel syndrome with constipation (IBS-C)  Patient reports that abnormal bowel movements are usually
constipation (type 1 and 2 in the BSFS)
 IBS with mixed bowel habits (IBS-M)  Patient reports more than 1/4 of all abnormal bowel mvmts were constipation and
more than 1/4 were diarrhea
 IBS unclassified  Patients who meet diagnostic criteria for IBS but cannot be categorized into one of the other three subtypes
 PE  normal typically, maybe some mild lower abdominal tenderness
o Diagnosis: subjective and based on the exclusion of similar disorders, CBC, ESR, CRP (can help rule out anemia),
IBD, stool exam, colonoscopy (all pts 50 or older with no previous test, to exclude malignancy), celiac testing (if has
IBS with diarrhea), food allergy testing (rule out lactose intolerance)
o Treatment:
 Reassurance , Decrease stress
 Diet  fatty food/caffeine poorly tolerated, trial of lactulose free and fructose free diet, trial of
probiotics, fiber may help
 IBS-C 
 Without pain/bloating:
o 1. Lifestyle changes + laxatives: polyethylene glycol (Miralax)
o 2. Lifestyle changes + lubiprostone (Amitiza) or linaclotide (Linzess)
 With pain/bloating:
o 1. Lifestyle changes + laxative + Antispasmotic: hyoscyamine, dicyclomine
o 2. Lifestyle changes + SSRIs: paroxetine, citalopram + Linaclotide or Lubiprostone
 IBS-D 
 Without pain/bloating:
o 1. lifestyle changes + antidiarrheals (loperamide, cholestyramine)
o 2. other antidiarrheals: alosetron*, eluxadoline (Viberzi)
 With pain/bloating:
o 1. lifestyle changes + antidiarrheals + antispasmotics
o 2. lifestyle changes + tricyclic antidepressants (desipramine, amitriptyline, doxepin)
 IBS-M 
 Without pain/bloating: 1. lifestyle changes + prn laxatives + prn loperamide
 Psychological therapy  cognitive behavioral therapy, relaxation techniques, hypnotherapy
CELIAC DISEASE
 Permanent, systemic autoimmune disorder in response to gluten that results in diffuse damage to the proximal small intestinal
mucosa  leading to malabsorption of nutrients
 Celiac disease only develops in people with HLA-DQ2 (95%) or -DQ8 (5%) class II molecules
 Gluten peptide (wheat, rye, barley) stimulates an inappropriate immunologic response
 Typical Symptoms  Weight loss, Chronic diarrhea, Abdominal discomfort, Bloating, Growth retardation- kids, Failure to
thrive- kids, Anemia (IDA typically or megaloblastic from low B12), Flatulence, Osteoporosis, Fatigue, Vitamin def.
  Atypical  Dermatitis herpetiformis, Depression, Delayed puberty
 PE  Normal in mild cases, Signs of malabsorption, Loss of muscle mass or subcutaneous fat, Pallor due to anemia, Easy
bruising due to vitamin K deficiency, Hyperkeratosis due to vitamin A deficiency, Bone pain due to osteomalacia,
Neurologic signs (peripheral neuropathy, ataxia) due to vitamin B12 or severe vitamin E deficiency, Abdominal examination
may reveal distention with hyperactive bowel sounds, Dermatitis herpetiformis (Pruritic papulovesicles over the extensor
surfaces of the extremities and over the trunk, scalp, buttocks, and neck (autoimmune, not HSV))
o Diagnosis: IgA-tTG (titer will typically be above normal range), Also measure total IgA, Keep pt. on gluten and refer
for endoscopic biopsy (most specific and sensitive test, histology will show intraepithelial lymphocytes, villous atrophy
and crypt hyperplasia), CBC (anemia), CMP (malabsorption deficiencies), vitamin panel, bone density scan
(osteoporosis), skin biopsy (if evidence of dermatitis herpetiformis), antibodies (undetectable after 3-12 months of gluten)
o Treatment:
 Removal of ALL gluten from diet (wheat, rye, barely)
 Dietician referral, patient support groups, dietary guides
 Initially need vitamin supplements
 Treat other diseases (osteoporosis)
DIVERTICULAR DISEASE
 Diverticulosis – presence of diverticula, herniations of colonic mucosa and submucosa through muscularis. Pseudodiverticula
 Almost always have involvement in the sigmoid (highest intraluminal pressure) and descending colon
 Diverticulitis occurs when diverticulum/diverticula become inflamed, possibly due to infection
 Abdominal pain LLQ (MC complaint), fluctuating bowel habits (constipation more common than diarrhea), chronic constipation
 PE  usually normal, depends on severity, may have LLQ tenderness, may feel thickened sigmoid or mass (uncommon),
fever, GI bleeding, N/V, localized guarding, rigidity and rebound tenderness if severe or complications from diverticulitis
o Diagnosis: usually discovered incidentally at endoscopy, clinical diagnosis, CBC (leukocytosis), abdominal CT (best
test for dx and if no improvement with empiric antibiotic therapying 2-4 days), FOBT may be positive, colonoscopy
(after resolution of symptoms typically 6-8 weeks)
o Treatment:
 Uncomplicated/asymptomatic  high fiber diet
 Acute diverticulitis  clear liquid of low residue diet, oral antibiotics for 7-10 days
 Amoxicillin/clavulanic acid (875mg/125mg) BID
 Metronidazole, 500 mg TID PLUS Ciprofloxacin 500 mg BID
 Trimethoprim-sulfamethoxazole 800mg/160mg BID PLUS Metronidazole 500mg TID
 Moxifloxacin 400mg daily (allergy to metronidazole and beta lactam agents)
 For 7–10 days or until the patient is afebrile for 3–5 days
 Analgesia  acetaminophen is best
 Admit  Increasing pain, Inability to tolerate oral fluids, Severe diverticulitis (high fevers, leukocytosis,
or peritoneal signs), Elderly or immunosuppressed or who have serious comorbidities, CT scan showing
complicated disease (abscess, perforation), In the hospital give nothing by mouth, start intravenous fluids,
antibiotics and NG tube if ileus present, Failed outpatient treatment after 2-3 days
 Surgical consult  failure to improve in 72 hours or complicated diverticulitis
MECKEL’S DIVERTICULUM
 Diverticulum (true) in small bowel from embryologic remnant
 Most common congenital anomaly of GI tract
 Occurs in mid-distal ileum
 Asymptomatic, bleeding and obstruction (most common complaints), small bowel obstruction (currant jelly stools)
 When to suspect it  Child with painless GI bleeding, Child with recurrent small bowel intussusception, Pt with recurrent
appendicitis symptoms, s/p appendectomy, Adults with GI bleed but negative EGD and colonoscopy
 Rule of 2’s  2% of population has them, Located 2 feet from the ileocecal valve, 2 inches long, 2:1 male to female ratio
(for symptomatic pts), Presents within first 2 yrs. of life
o Diagnosis: Meckel’s scan (technetium-99m, pertechnetate radioisotope scanning, must have 1.8 cm2 of ectopic
gastric mucosa to test positive), mesenteric arteriography, plain film XR, CT, CBC
o Treatment: Symptomatic patients  surgery
HEMORRHOIDS
 Hemorrhoidal veins are in submucosa of rectum
 Internal vs. external or mixed
 Classification 
o Grade I hemorrhoids are visualized on anoscopy and may bulge into the lumen but do not prolapse below dentate line
o Grade II hemorrhoids prolapse out of the anal canal with defecation or with straining but reduce spontaneously
o Grade III hemorrhoids prolapse out of the anal canal with defecation or straining, and require manual reduction
o Grade IV hemorrhoids are irreducible and may strangulate
  Hematochezia (BRBPR, classically “on toilet paper” or outside of stool, rarely significant bleeding, painless bleeding),
pruritis (over cleaning, prolonged fecal content on skin, mucus from columnar cells on skin), fecal soilage, protrusion (pt can
see or feel hemorrhoid), pain and palpable perianal lump (if thrombosed)
o Diagnosis: history and PE (DRE + Valsalva, anoscopy), colonoscopy (if hematochezia is significant, iDA, >40 y/o
or concern for colorectal cancer or IBD)
o Treatment:
 For ALL hemorrhoids  lifestyle changes
 Treat underlying constipation/diarrhea, avoid straining, avoid over cleaning, avoid
prolonged sitting on toilet, sitz baths, daily fiber, water, exercise, avoid prolonged sitting or
standing
 Grade I & external hemorrhoids  Lifestyle changes +/- topical corticosteroid
 Grade II  + rubber band ligation (best)
 Grade III  + rubber band ligation (best)
 Grade IV  Surgical hemorrhoidectomy
 Thrombosed hemorrhoids  If in acute pain, hemorrhoidectomy, If >72 hrs from onset, conservative
therapy, Incisional thrombectomy if needed but not preferred
ANAL FISSURE
 Painful, linear tear in the distal anal canal (anoderm, distal to dentate line)
 90% occur at posterior midline of anal canal
 Pain with bowel movements (“passing broken glass”), minimal bleeding (bright red blood on toilet paper), irritation/pruritis,
visualize tear (acute), chronic appearance would include hypertrophied anal papilla at the proximal end of the fissure and a
sentinel pile or skin tag at the distal end
o Diagnosis: clinical, anal manometry (elevation in anal resting pressure, sawtooth deformity w/ paradoxical
contractions of sphincter muscles is pathognomonic)
o Treatment:
 Acute  conservative treatment with stool softeners, increased fiber, topical analgesic, sitz baths (is
usually adequate for tx) + topical nitroglycerin or nifedipine
 Chronic  refer, Botox injections, surgery (anal sphincterotomy)
RECTAL ABSCESS
 Acute phase collection of purulent material in subcutaneous tissue of perianal area (simple abscess)
 Severe pain in anorectal area (constant, not only with bowel movements), induration, fluctuance, erythema in perianal area,
fever, malaise, palpable perirectal mass, +/- purulent discharge if drainage has begun
o Diagnosis: clinical, CT or MRI (if mass not palpable or clinical picture not clear)
o Treatment:
 I&D (even if not fluctuant)
 Antibiotics  only if patient is diabetic, immunosuppressed, has valvular heart disease, extensive cellulitis
 Culture  if abx indicated, concern for resistant bacteria, pt on multiple abx courses & to
differentiate between rectal abscess and soft tissue abscess
 Refer for complex abscesses to be drained in OR
ANAL FISTULA
 Communicating connection b/t the infected crypt gland (abscess) to the perirectal skin or (infrequently) to other organs
 Most commonly at dentate line. MCC is rectal abscess
 Perianal pain (especially pain w/ moving, sitting, defecating, coughing), fever (not very common), fluctuant mass (if abscess present)
o Diagnosis: physical exam, labs (appear septic), +/- wound culture, anoscopy, MRI (best imaging study), CT (for
large intrapelvis abscess), fistulography
o Treatment:
 Fistulotomy (mainstay of treatment)
 Stool bulking agents
 Non-narcotic pain meds
 Sitz baths
 Antibiotics  reserved for those with overlying cellulitis or evidence of sepsis
RECTAL PROLAPSE
 Protrusion through anus of some or all layers of rectum
 Complete (full thickness) vs. partial (mucosal)
 Usually caused by surgical or traumatic injury
 Mucous/stool discharge, Feel/see the prolapse through anus, History of this initially, but it would correct itself after
defecation was complete, Difficulty initiating or completing bowel movement, Abdominal discomfort, Incomplete bowel
evacuation, Note that rectal pain is not a common presenting complaint
o Diagnosis: clinical, concentric rings of rectal mucosa protruding from anus (HALLMARK), Colonoscopy or rigid
proctosigmoidoscopy (to assess for other lesions in the rectum because prolapse has to be caused by something)
 o Treatment:
 Surgical repair (mainstay of treatment)
 Not a surgical candidate  treat constipation, pelvic floor PT, biofeedback, taping (last resort for
bedbound or elderly)
PILONIDAL DISEASE
 MC in males, age 20
 Painful, fluctuant mass in the sacrococcygeal region (natal cleft), Purulent discharge may be present
o Diagnosis: clinical
o Treatment:
 Incision, drainage, and curettage of the abscess cavity to remove hair nests and skin debris
 Clean daily in Sitz bath
 Keeping the hair shaved around the area to prevent reinfiltration
 Refer for surgery*
FECAL IMPACTION
 Stool hardens and becomes fixed in the anal canal. Typical in elderly
 Decreased appetite, Nausea & Vomiting, Abdominal pain, Abdominal distention, Possible paradoxical diarrhea as liquid
leaks around impacted stool, Firm feces palpable on DRE
o Diagnosis: clinical, DRE, abdominal XR (helpful if impaction is proximal rectum or sigmoid colon)
o Treatment:
 Enema. Digital disruption of impacted fecal material. Stool softeners after impacted feces removed
HERNIAS
 Abdominal cavity contents protruding through abdominal wall via fascial defect
 Ventral  anterior abdominal wall hernias
 Umbilical  from increased intraabdominal pressure, common in African American infants
 Inguinal  most common type of abdominal hernias in males and females
o Indirect  more common to strangulate than direct, leaves empty peritoneal sac in inguinal canal, bowel can fill
this, Passes through the inguinal ring
o Direct  Typically do not contain bowel, passes through Hesselbach’s Triangle (Inguinal ligament (inferior border),
Inferior epigastric vessels (lateral border) & Lateral boarder of rectus abdominus (medial border))
 Femoral  passes through femoral canal, highest risk for incarceration, more common in women
 Incisional  iatrogenic cause
 Asymptomatic (until mass noted), acute pain, bulge with straining or lifting, abdominal pain (in femoral hernias), mass
reduced upon laying down
 PE  palpable mass upon straining or at rest, indirect (touches tip of finger), direct (touches side of finger), have patient
raise head to increase abdominal pressure or cough if standing
o Diagnosis: physical exam, US or CT (if unable to detect on PE)
o Treatment:
 Uncomplicated hernias  observed
 Symptomatic  refer for surgical repair
 Strangulation  emergency repair
 Contraindicated for surgery  fitted with a truss
SMALL BOWEL BENIGN NEOPLASMS
 Rare and often remain asymptomatic. Adenomas  3 types (villous  significant potential for malignant transformation ;
tubular  MC in duodenum; Brunner’s gland  rare
 Leiomyomas  arise in submucosal layer of wall of small intestine, causing necrosis, ulceration and bleeding into bowel lumen
 Lipomas  2nd MC benign tumor of small bowel, adipose tissue or serosal fat
o Treatment: Refer to GI for medical management if symptomatic
SMALL BOWEL MALIGNANT NEOPLASMS
 Abdominal pain (most common symptom, intermittent and crampy in nature), weight loss, N/V, GI bleeding, intestinal obstruction
 Majority of symptomatic small bowel tumors are malignant
 Disease usually advance when patient becomes symptomatic  regional lymph nodes or distant mets
o Diagnosis: CPE, CBC, FOBT, CMP, CT, small bowel series, enteroclysis, endoscopic, urinary excretion of 5-HIAA
(if suspected carcinoid syndrome), surgical exploration (most sensitive diagnostic modality in evaluating a patient
w/ high suspicion of having a small bowel neoplasm)
o Treatment: Refer to GI or general surgeon

COLON POLYPS
 A protuberance into the lumen from colon mucosa
 Often asymptomatic, but may bleed or cause tenesmus, or rarely an obstruction
  Hyperplastic polyps  normal histology, no dysplasia, non-neoplastic, MC in rectosigmoid colon, normally < 5 mm, repeat
colonoscopy in 10 years
 Adenomas  2/3 of all colon polyps, dysplastic, most colon cancers arise from adenomas
COLORECTAL CANCER
 2nd leading cause of cancer deaths in US. Screening is critical to prevent adenomas from progressing to CRC. ~95%
adenocarcinomas. Lynch Syndrome  Most common inherited syndrome that predisposes CRC
 Familial Adenomatous Polyposis (FAP)  Inherited autosomal dominant gene, Nearly 100% of patients have CRC by age
50, At risk pts, start flex sigmoidoscopy at 10-12 yrs old & All end up needing colectomy
 Iron def. anemia causes fatigue and weakness (right side colonic cancers), obstructive symptoms w/ colicky abdominal pain
and change in bowel habits to pencil-thin stools (left sided colon), constipation alternating with inc. frequency and loose
stools, tenesmus/urgency/recurrent hematochezia (in rectal cancers), weight loss (sign of advanced disease)
 PE  normal, palpable mass in abdomen, FOBT positive, hepatomegaly, ascites
o Diagnosis: CBC (anemia), LFTs (mets), CEA, colonoscopy (diagnostic test of choice) with biopsy, CT (for staging)
o Treatment:
 Referral for surgical resection
 Chemotherapy
 Radiation
 *depends on location & staging of tumor
 Patient education  daily aspirin for at least 5 years & removal of adenomatous polyps reduces risk
 Screening  colonoscopy ages 50-75 every 10 years (best option), start screening at 40 IF single first
degree relative with CRC or advance adenoma diagnosed before age 60 OR two first degree relatives
LIVER DISORDERS
HEPATITIS A
 International travel is a leading risk factor for Hep A in USA
 Onset may be abrupt or insidious, Malaise, Myalgia, Arthralgia, Easy fatigability, Upper respiratory symptoms, Anorexia,
Distaste for smoking, N & V frequent, Low-grade fever (which breaks as jaundice begins), Abdominal RUQ pain,
Aggravated by jarring or exertion, Hepatomegaly <50% , Liver tenderness, Splenomegaly 15%, Soft, enlarged lymph nodes
(especially in the cervical or epitrochlear areas is possible)
o Diagnosis: WBC (normal to low), Strikingly elevated ALT or AST levels occur early then, elevations of bilirubin and
alkaline phosphatase, IgM anti-HAV appears early, IgM and IgG anti-HAV are detectable in serum soon after onset
o Treatment:
 Self-limited
 Bed rest
 IV 10% glucose
 Palatable meals as tolerated
 AVOID strenuous physical exertion, alcohol, hepatotoxic agents
 Oxazepam (small doses)
 Admit  if encephalopathy, INR > 1.6 or unable to maintain hydration
HEPATITIS B
 Sexual contact and is present in saliva*, semen, and vaginal secretions
 Prodrome of anorexia, N/V, malaise, aversion to smoking. Fever, enlarged and tender liver, jaundice, Serum sickness-like
rash + arthritis may occur early & precede onset of liver symptoms, Clay-colored stools, dark urine
o Diagnosis: WBC (normal to low), markedly elevated aminotransferases early in course, Liver biopsy (shows
hepatocellular necrosis and mononuclear infiltrate but is rarely indicated)
 Does not have Hepatitis B immunity
o Not been infected, but at risk for possible future infection
o Negative HBsAg, negative anti-HBc and negative anti-HBs
o Encouraged to get the vaccine.
 Immunity from Hepatitis B infection
o Has surface antibodies present due to recovery from a prior Hepatitis B infection
o Negative HBsAg, positive anti-HBc and positive anti-HBs
 Immunity from Hepatitis B vaccine
o Has surface antibodies present due to the Hepatitis B vaccination
o Negative HBsAg, negative anti-HBc and positive anti-HBs
 Acute Hepatitis B infection Has positive HBsAg, positive anti-HBc, positive IgM anti-HBc and negative anti-HBs
 Chronic Hepatitis B infection  Has positive HBsAg, positive anti-HBc, negative IgM anti-HBc and negative anti-HBs
o Treatment:
 Acute  supportive (high calorie diet)
 Chronic  antiviral therapy (entecavir, tenofovir)
HEPATITIS C
 Transmitted via blood predominately. 50% of cases are transmitted by injection drug use
Clinical illness is often mild, usually asymptomatic, and characterized by waxing and waning aminotransferase elevations, If
any symptoms present will be similar to HAV
o Diagnosis: EIA for anti-HCV, HCV viral levels and genotype, Waxing and waning aminotransferase elevations
o Treatment:
 Viral clearance
 For select pts  peginterferon for 6-24 weeks & ribavirin may be added after 3 months if HCV fails
to clear
 Patient education  testing donated blood, safe sex, vaccination for HAV and HBV, test for HIV, no
alcohol or drug use
HEPATITIS D
 Only in association with HBV infection
 The only antigen is HDAg
o Diagnosis: detection of antibody to hep D antigen (anti-HDV) and, where available, hep D antigen (HDAg) or HDV
RNA in serum
o Treatment: No specific treatment & no vaccine. Interferon alpha
HEPATITIS E
 Waterborne hepatitis outbreaks, fecal/oral. Uncommon in US
 Arthritis, pancreatitis, and neurologic complications
o Treatment: Self-limited
HEPATITIS G
 Percutaneously transmitted and associated with chronic viremia lasting at least 10 years
 Does not appear to cause important liver disease. HGV coinfection may improve survival in pts w/ HIV infection
CHRONIC HEPATITIS
 Chronic necroinflammation of liver of > 3–6 months duration demonstrated by persistently elevated serum aminotransferase
levels or characteristic histologic findings
 In absence of advanced cirrhosis, pts usually have mild, nonspecific symptoms, Hx of previous hepatitis, categorized by
underlying etiology
 Chronic HBV  develops in 25-50% of children, Rise in serum HBV DNA levels and possible progression to cirrhosis
 Chronic HCV  develops in 85% of patients w/ acute hepatitis, looks like every other chronic hep, coffee slows progression
o Diagnosis: antibody tests and viral nucleic acid in serum
o Treatment: Refer for liver biopsy and antiviral treatment
AUTOIMMUNE HEPATITIS
 Usually seen in young to middle-aged women
 Insidious, chronic hepatitis, may follow viral illness or exposure to drug/toxin, exacerbations postpartum, amenorrhea
 PE  Multiple spider angiomas, cutaneous striae, acne, hirsutism, and hepatomegaly
 Extrahepatic features  Arthritis, Sjogren syndrome, thyroiditis, nephritis, ulcerative colitis, Coombs-positive hemolytic anemia
o Diagnosis: positive for HLA-B8 and HLA-DR3 (younger pts), positive for HLA-DR4 (older pts), liver biopsy
(interface hepatitis), aminotransferase levels > 1000, total bilirubin elevated, serum gamma globulin levels elevated,
ANA antibodies detected and multiple other antibodies
o Treatment:
 Prednisone 30 mg orally daily with azathioprine 50 mg orally daily
 Azathioprine
 Liver transplant  if non-responsive
 Admit  if hepatic encephalopathy, INR > 1.6
ALCOHOLIC HEPATITIS
 80% of patients with alcoholic hepatitis have been drinking 5 years or more before symptoms
 Asymptomatic, Recent period of heavy drinking, complaints of anorexia and nausea, and the demonstration of hepatomegaly and
jaundice, Abdominal pain (RUQ) and tenderness, splenomegaly, fever, and encephalopathy may be present
o Diagnosis: AST is usually elevated but usually not above 300 units/L, AST is greater than ALT, usually by a factor of 2 or
more, serum bilirubin increased (> 10 mg/dL), alk phos increased, anemia, leukocytosis, thrombocytopenia, serum albumin
decreased, gamma-globulin increased, folic acid deficiency, US (exclude biliary obstruction), CT w/ IV contrast or MRI
(for masses), liver biopsy
o Treatment:
 Abstinence from alcohol
 Nutritional support & folic acid/thiamine/zinc administration (if deficient)
 Naltrexone, acamprosate or baclofen
 Methylprednisone 32 mg/d PO
 Refer  for liver biopsy
 Admit  if encephalopathy, INR > 1.6, total bilirubin > 10, inability to maintain hydration
DRUG & TOXIN INDUCED HEPATITIS
 Nonsteroidal anti-inflammatory drugs and antibiotics are most frequent offenders of liver disease
 Minocycline and nitrofurantoin, most commonly associated with Hepatitis
 Coadministration of a second agent may increase the toxicity of the first--Isoniazid and rifampin. Acetaminophen and alcohol
 Mimics viral hepatitis
o Diagnosis: history, histologically & clinically similar to autoimmune hepatitis, portal tract neutrophils & hepatocellular
cholestasis
o Treatment: Refer  when require liver biopsy. Admit  pts w/ liver failure
NONALCOHOLIC FATTY LIVER DISEASE
 Caused by Obesity, Diabetes or Insulin resistance, Hypertriglyceridemia
 Mostly asymptomatic, Mild right upper quadrant discomfort, Hepatomegaly is present in up to 75%, Clinical signs of chronic
liver disease are uncommon
o Dx: mildly elevated aminotransferase & alkaline phosphatase levels (may be normal in 80% of pts), antinuclear or smooth
muscle antibodies, elevated serum ferritin, US, CT or MRI, liver biopsy (diagnostic, macrovesicular steatosis and fibrosis)
o Treatment:
 Lifestyle changes  remove offending factors, weight loss, dietary fat restriction, exercise
 Various drugs under study  thiazolidinediones, vitamin E, bariatric surgery
CIRRHOSIS
 Mexican Americans and African Americans have a higher frequency
 Micronodular vs. macronodular
 Usually insidious onset of symptoms; asymptomatic for a long time, Fatigue, Disturbed sleep, Muscle cramps, Weight loss,
Menstrual abnormalities (usually amenorrhea), erectile dysfunction, loss of libido, sterility, and gynecomastia in men, hematemesis,
glossitis and chelitis, splenomegaly
 Advanced: Anorexia is usually present and may be extreme, N/V, Reduced muscle strength and exercise capacity
 Encephalopathy  Day–night reversal sleep pattern (Disruption in diurnal rhythm of melatonin), Asterixis, Tremor, Dysarthria,
Delirium, Drowsiness, Ultimately coma
o Diagnosis: CBC (macrocytic anemia, thrombocytopenia), elevation of AST and alkaline phosphatase, elevation of
bilirubin, decreased albumin, gamma-globulin increased, vit D deficiency, US (detects size), contrast CT or MRI (if
nodules found), liver biopsy, US elastography and magnetic resonance elastography (measure liver stiffness)
o Treatment:
 Abstinence from alcohol, adequate calorie intake, sodium reduction, vitamin supplements, vaccinations up
to date, liver transplantation, pharmacologic treatments
 Treatment of complications
 Refer  for liver biopsy, before MELD score > 14 or endoscopy
 Admit  Gastrointestinal bleeding, Stage 3–4 hepatic encephalopathy, Worsening kidney function, Severe
hyponatremia, Serious infection, Profound hypoxia
PRIMARY BILIARY CHOLANGITIS
 Chronic disease of the liver characterized by autoimmune destruction of small intrahepatic bile ducts and cholestasis
 Middle-aged women
 Asymptomatic for years, Insidious of fatigue and pruritus, As it progresses  Hepatosplenomegaly, Xanthomatous lesions on
skin, tendons, and eyelids, Jaundice, steatorrhea, and signs of portal hypertension are late findings, Orthostatic hypotension,
Cognitive dysfunction
o Diagnosis: Elevation of alkaline phosphatase, cholesterol; bilirubin elevates later, Antimitochondrial antibodies are
present in most, serum IgM levels are elevated, liver biopsy (for staging)
o Treatment:
 Cholestyramine 4 g three times daily
 Ondansetron 4 mg orally three times daily prn & sertraline 75-100 mg/d orally
 Ursodeoxycholic acid 13-15 mg/kg/d one or two doses
 Colchicine 0.6 mg orally twice daily & methotrexate 15 mg/wk orally
 Refer  liver biopsy, liver transplant evaluation
 Admit  GI bleed, stage 3-4 hepatic encephalopathy, worsening kidney function, severe hyponatremia,
profound hypoxia
HEMOCHROMATOSIS
 The body absorbs too much iron from food, supplements, or cast iron cookware, and this results in the level building up in the body
 Autosomal recessive disease caused in most cases by a mutation in the HFE gene on chromosome 6
 Early symptoms of fatigue and arthralgia, later  arthropathy, hepatomegaly, skin pigmentation (slate-gray, brown or bronze),
cardiac enlargement, DM, erectile dysfunction
o Diagnosis: mildly abnormal liver tests, elevated plasma iron, elevated serum ferritin, HFR mutations (testing indicated in
any pt with evidence of iron overload), MRI, liver biopsy
o Treatment:
  Avoid foods rich in iron, alc, vitamin C, raw shellfish, supplemental iron & avoid cooking in cast iron pans
 Weekly phlebotomies  removal of 1-2 unit of blood to reduce ferritin levels then as needed
 Chelating agents
 Refer  for liver biopsy and initiation of therapy
WILSONS DISEASE
 Hepatolenticular degeneration
 Rare autosomal recessive disorder that usually occurs in persons under age 40
 Genetic defect effecting ATP7B in the liver and leads to copper accumulation and oxidative damage
 Hepatitis, Splenomegaly with hypersplenism, Coombs-negative hemolytic anemia, Portal hypertension, Neurologic or
psychiatric abnormalities, brownish or gray-green Kayser-Fleischer ring (pathognomonic), renal calculi, RTA,
hypoparathyroidism, infertility, hemolytic anemia, lipomas, aminoaciduria
o Diagnosis: alkaline phosphatase to total bilirubin ratio >4, AST to ALT ratio > 2.2, increased urinary copper excretion, low
serum ceruloplasmin level (< 5 mg/dL is diagnostic), elevated hepatic copper concentration, coombs- negative, MRI
(increased copper), molecular analysis of ATP7B mutations (diagnostic)
o Treatment:
 Restriction of dietary copper (shellfish, organ, nuts, mushrooms, chocolate)
 Oral penicillamine 0.75-2 g/d taken 1 hr before or 2 hr after food  DRUG of CHOICE
 Oral pyridoxine 50 mg per week
 Trientine 250-500 mg three times a day  if penicillamine not tolerated
 Zinc acetate or gluconate  asymptomatic or pregnant pts
 Refer  all pts with diagnosis
 Admit  Acute liver failure, Gastrointestinal bleeding, Stage 3–4 hepatic encephalopathy, Worsening
kidney function, Severe hyponatremia, Profound hypoxia
HYPERBILIRUBINEMIA
 Excess of bilirubin in the body tissues
 Conjugated hyperbilirubinemia almost always implies liver or biliary tract disease
 Hyperbilirubinemia due to the reflux of conjugates back into the plasma
CRIGLER-NAJJAR SYNDROME
 Buildup of unconjugated bilirubin in the blood
 Autosomal recessive
 Jaundice at birth, kernicterus
o Treatment: Type 1  light therapy 10-14 hours per day. Liver transplant
HEPATOCELLULAR CARCINOMA
 Associated with cirrhosis in 80% of cases
 Cachexia, weakness, weight loss, sudden appearance of ascites
 PE  tender enlargement of liver, palpable mass, bruit or friction rub over the tumor
o Diagnosis: CBC (leukocytosis, anemia), elevation of serum alkaline phosphatase, HBsAg, Anti-HCV, alpha-fetoprotein
levels elevated (tumor marker for HCC), multiphasic helical CT and MRI with contrast (preferred imaging), liver biopsy
(diagnostic)
o Treatment:
 Screening  Ultrasonography and alpha-fetoprotein testing every 6 months
 Refer  all patients
 Admit  complications of cirrhosis, severe pain, for surgery and other interventions

ABDOMINAL DISORDERS
ABDOMINAL AORTIC ANEURYSM
 Dilation of the aorta >3cm
 90% of abdominal atherosclerotic aneurysms originate below the renal arteries
 Most ruptures occur at >5cm
 Asymptomatic until rupture mostly, mid abdominal discomfort radiating to the lower back (ripping or tearing, constant or
intermittent, exacerbated by gentle pressure)
 Rupture  Severe abdominal or back pain, Palpable mass, Hypotension, Syncope, Periumbilical ecchymosis (Cullen sign) or flank
ecchymosis (Grey Turner sign)
o Diagnosis: abdominal US (diagnostic study of choice), CT (if ruptured)
o Treatment:
 Screening  males 65-75 with history of smoking
 Refer  if > 4 cm or tender
 Elective repair  > 5.5 cm, rapid expansion of > 0.5 cm in 6 months, new symptoms of pain or tender
 Admit  signs of rupture
ISCHEMIC BOWEL DISEASE
  Reduction in intestinal blood flow of the mesenteric circulation
 Most commonly as a result of occlusion, vasospasm, or hypoperfusion
 Small bowel is surgical emergency
 Acute & Chronic
ACUTE MESENTERIC ISCHEMIA
 Severe, acute, unremitting abdominal pain strikingly out of proportion to the initial physical findings, Abdomen may
be soft; either nontender or minimally tender, Distention is often the first sign, peritonitis (esp if infarction or gangrene has
occurred), nausea, emesis, & transient diarrhea due to urgent bowel evacuation, Occult blood
 Consider in patients >50 years who present with sudden onset of severe abdominal pain lasting >2 hours, especially if a
history of cardiovascular disease (congestive heart failure, myocardial infarction, arrhythmia) is present
o Diagnosis: leukocytosis, lactic acidosis, hemoconcentration, raised serum aminotransferase levels, XR (to exclude other
causes), CT angiography (gold standard)
o Treatment:
 Restore blood flow
 Correction of precipitating cause
 Emergent laparotomy  if suspicion of perforation or gangrene
CHRONIC MESSENTERIC ISCHEMIA
 result of reduced blood flow due to atherosclerotic narrowing of at least two of three major vessels (ie, celiac axis, SMA, or IMA)
 The classic diagnostic triad  Postprandial abdominal pain, Weight loss, Abdominal bruit, Pain from abdominal
angina (typically recurrent, dull, crampy, epigastric, and periumbilical & occurs 10–30 minutes after meals and lasting 1–3
hours), Nausea, emesis, and early satiety
 PE  Soft abdomen without tenderness during episodes of pain & Classic description of pain disproportionate to physical findings
 Average duration of symptoms prior to dx is 1 year
o Diagnosis: CT angiography
o Treatment: Restore mesenteric arterial flow. Refer  aortomesenteric grafting
COLONIC ISCHEMIA
 75% of all intestinal ischemia, mainly in elderly
 Abrupt onset of crampy LLQ abdominal pain, mild to moderate rectal bleeding or bloody diarrhea (within the first 24 hours),
Cardiovascular disease is common (hypotension, cardiovascular surgery (coronary artery bypass grafting, aortic aneurysm
repair)), dialysis, and dehydration
 PE  mild to moderate abdominal tenderness over affected bowel (most often left-sided)
o Diagnosis: XR (nondiagnostic, thumbprinting), abdominal CT w/contrast or angiography, colonoscopy (confirms
diagnosis), stool studies, conventional catheter-based arteriography
o Treatment: Bowel rest, NPO. Serial abdominal exam. Broad spectrum IV antibiotics are recommended . NO
antithrombotic therapy for most pts. STOP vasoconstrictors. Rectal tubes and NG decompression if
necessary. Surgery referral
APPENDICITIS
 Peak incidence between 10-30 years of age, Most common etiology of atraumatic abdominal pain in children >1 year old
 Initial vague abdominal pain (periumbilical or central), then more inflammation causes localized pain in RLQ at McBurney’s
point, Early  nonspecific symptoms of general malaise, indigestion, or bowel irregularity
 Atypical  diarrhea in the elderly
o Diagnosis: clinical, CBC (elevated WBC), elevated CRP and ESR, UA and pregnancy test (always w/ abd pain),
early surgical consultation, US (in children & pregnant females, thickened, noncompressible appendix >6 mm in
diameter), CT (best imaging modality)
o Treatment: Appendectomy. NPO, fluid resuscitation, antiemetics, analgesia. Perioperative antibiotics
INTUSSUSCEPTION
 Invagination of one segment of intestine into another segment  Think telescope
 Most frequent cause of intestinal obstruction in the first 2 years of life
 85% of cases are idiopathic
 >6yo - lymphoma
 starts just proximal to ileocecal valve & extends for varying distances into the colon
 Previously healthy infant 3–12 months of age develops recurring paroxysms of abdominal pain with screaming and drawing
up of the knees, Vomiting and diarrhea, Bloody bowel mvmts with mucus “currant jelly stools”, Lethargic between
paroxysms and may be febrile, Abdomen is tender and often distended & Sausage-shaped mass palpated
o Diagnosis: abdominal US (“bull’s eye” or “coiled spring”)
o Treatment: May resolve spontaneously. Barium enema & air enema (diagnosis AND treat) if done within 24
hours. Surgery
VOLVULUS
 Rotation of the gut on its vascular pedicle leading to obstruction, ischemia and infarction if untreated
 80% occur in first month of life and 90% within the first year . *Ladd’s bands
  Presents w/abrupt onset of constant abdominal pain, bilious vomiting, abdominal distention, and irritability, Typically
ill appearing and may have signs of shock, Abdomen is diffusely tender and distended & may be rigid, absence of fever
(distinguishes from sepsis)
o Diagnosis: upper GI series with contrast (test of choice), plain XR (done first to rule of perforation, “bent inner-
tube” appearance, single long air-fluid level present on upright or decubitus radiographs)
o Treatment:
 Surgical emergency  resuscitation & immediate surgery consult (sigmoid colectomy)
 Soft rectal tube  for sigmoidoscopic or colonoscopic decompression
TOXIC MEGACOLON
 potentially lethal complication of inflammatory bowel disease (IBD) or infectious colitis  characterized by total or
segmental nonobstructive colonic dilatation plus systemic toxicity
 Severe bloody diarrhea (most common symptom), altered metal status, tachycardia, fever, postural hypotension, lower
abdominal distention and tenderness with or w/o signs of localized/generalized peritonitis
o Diagnosis: plain abdominal XR
o Treatment: Fluid resuscitation . Broad spectrum antibiotics . IV corticosteroids  if crohn’s or UC.
Complete bowel rest. NG tube. Surgical consultation. Oral vancomycin AND IV metronidazole  if c. diff