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USMLE Step 2 (Fach) / Gastroenterology (Lektion)

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  • Celiac disease Epidemiology:- Bimodal distribution: At 8-12 months and at third to fourth decade of life- Prevalence: in the US ∼ 1:3000- More common in individuals of northern European descent Etiology:- Association with HLA-DQ2 (90-95%) and HLA-DQ8 (5-10%)- Consuming gliadin from grains such as wheat, rye, and barley- Associated with autoimmune diseases Clinical features:- Chronic or recurring diarrhea: steatorrhea- Flatulence, abdominal bloating, and pain- Nausea/vomiting - Malabsorption symptoms: fatigue, weight loss, vitamin deficiency, iron deficiency anemia, osteoporosis, hypocalcemia- Dermatitis herpetiformis- Peripheral neuropathies, headache, ataxia, depression, irritability- Gynecological associations: reduced fertility or infertility- Associated chromosomal syndromes: Turner syndrome Diagnostics:- Lab tests: IgA (anti‑)tissue transglutaminase antibody (tTG); IgG deamidated gliadin peptide (in IgA deficiency), anti-endomysial antibody (EMA); stool fat assays- Endoscopy with small intestine biopsy: confirmatory test Treatment: - Lifelong gluten-free diet- Iron and vitamin substitution, supplementation of calcium and vitamin D to prevent bone loss
  • Whipple disease Epidemiology: very rare, mainly males 30-60 years of age Clinical features:- Malabsorption syndrome, abdominal pain- Enteropathic arthritis (60% of cases), sacroiliitis (40% of cases)- Cardiac symptoms (e.g., valve insufficiencies)- Neurological conditions (myoclonia, ataxia, impairment of oculomotor function) Diagnostics:- Small intestine biopsies: detection of PAS-positive macrophages- PCR testing and immunohistochemistry staining- If neurological complaints occur → liquor diagnostics, potentially MRI Treatment:- IV ceftriaxone for 2 weeks- Maintenance treatment with oral trimethoprim-sulfamethoxazole for 1 year
  • Tropical sprue Epidemiology: occurs in residents of the tropics or in travelers returning from these areas (after trips lasting several weeks) Etiology: Bacterial infection that leads to structural damage of the intestinal mucosa Clinical findings:- Chronic diarrhea with steatorrhea- Abdominal cramps- Progressive weight loss- Fatigue- Malabsorption Diagnostics:- Blood tests: megaloblastic anemia, hypoalbuminemia, hypocalcemia, vitamin D deficiency- Serology for antibodies to rule out celiac disease- Stool analysis: Fecal fat 10-40 g/d- Rule out infection with pathogens (e.g., Giardia lamblia, Entamoeba histolytica)- Endoscopy of the small bowel and biopsy: villous atrophy, elongated crypts, presence of inflammatory cells (plasma cells, lymphocytes, eosinophils) Treatment: Tetracycline and folic acid for 3-6 months
  • Crohn's disease Risk factors:- Nicotine abuse- Familial predisposition (e.g., mutation of the NOD2 gene, HLA-B27 association) Clinical features:- Typically non-bloody, chronic diarrhea- Abdominal pain, typically in the RLQ- Malabsorption: Weight loss, anemia, steatorrhea, gallstones, kidney stones, vitamin ADEK deficiency- Abdominal mass- Enterocutaneous fistula formation, typically seen in the perianal region- Clinical features of abscesses (∼ 50% of cases)- If intestinal stenosis/strictures: possible signs of bowel obstruction (vomiting, obstipation)- If perforation → signs of peritonitis- Joints: enteropathic arthritis (e.g., sacroiliitis)- Eye: iritis, episcleritis, uveitis- Liver/bile ducts: primary sclerosing cholangitis (PSC; less common than in UC)- Dermatologic disease: Erythema nodosum, acrodermatitis enteropathica, pyoderma gangrenosum Diagnostics:- Initial testing: Blood and stool tests (↑ CRP, ↑ ESR, ↑ thrombocytes, ↑ leukocytes, anemia, ↑ ASCA, calprotectin, rule out C. difficile)- Confirm with endoscopy and/or radiographic imaging and/or biopsy- Perform contrast radiological studies and/or ultrasonography to assess extent, severity and complications (i.e., abscesses, fistulas or stenoses) Treatment:- Antidiarrheal agents: Loperamide- Acute therapy:→ Mild to moderate disease: Oral budesonide, 5-ASAs, antibiotics (metronidazole, ciprofloxacin)→ Moderate to severe disease: Systemic corticosteroids (30-60 mg prednisone daily)→ Steroid-refractory disease: TNF-α antibodies ± azathioprine (or 6-mercaptopurine)- Maintenance therapy:→ First-line treatment: 5-ASAs→ Alternatives: Azathioprine, 6-mercaptopurine, methotrexate, TNF-α antibodies
  • Ulcerative colitis Clinical features:- Bloody diarrhea with mucus- Abdominal pain and cramps- Tenesmus- Uveitis, iritis, episcleritis- Primary sclerosing cholangitis (PSC)- Joints: arthritis, ankylosing spondylitis, sacroiliitis- Skin manifestations: erythema nodosum, pyoderma gangrenosum- Episcleritis- Aphtous stomatitis- Fatigue, fever Diagnostics:- Lab tests: ↑ ESR, ↑ CRP, leukocytosis, anemia, ↑ perinuclear ANCA (pANCA); in case of PSC ↑ GT- Stool analysis: Test for bacteria to rule out other causes; calprotectin, lactoferrin- Colonoscopy- Imaging: Radiography, CT, MRI, ultrasound Treatment:- Antidiarrheal agents: loperamide- Mild: Topical 5-ASAs- Moderate: Oral and topical 5-ASAs- Severe: High‑dose oral and topical 5-ASAs and oral corticosteroids- Steroid-refractory: Cyclosporine Complications:- Toxic megacolon- Fulminant colitis- ↑ Risk of cancer → Colonoscopies with biopsies every 1-2 years are recommended 8-10 years after the initial diagnosis 
  • Clostridium difficile infection Pathogen: Clostridium difficile = Gram-positive rod-shaped bacillus, obligate anaerobe- Forms environmentally resistant spores (capable of withstanding heat and acid) Etiology:- Route of infection: fecal-oral transmission of ubiquitous bacteria - Antibiotic treatment: clindamycin, cephalosporins, fluoroquinolones, and less commonly, penicillin- Risk factor: Gastric acid suppression (e.g., with proton pump inhibitors) Clincial features:Symptoms of C. difficile-associated diarrhea usually develop during antibiotic treatment or 2-10 days following its initiation; however, 25-40% of cases may manifest as late as 10 weeks following treatment.- Watery diarrhea, characteristically foul-smelling→ May have traces of mucus or occult blood- Cramping abdominal pain, nausea, anorexia- Fever and dehydration (especially in severe cases)- Fulminant colitis: abdominal distention and severe hypovolemia- Recurrent disease: reoccurrence of symptoms following end of treatment (10-40% of cases) Diagnostics:- History: Treatment with antibiotics in the last 3 months; recent hospitalization- Stool tests: → PCR for C. difficile genes alone OR→ Enzyme immunoassay (EIA) for C. difficile glutamate dehydrogenase antigen AND → EIA for C. difficile toxins A and B- Blood tests: Leukocytosis, ↑ creatinine, ↓ albumin, electrolyte imbalance, ↑ lactate- Abdominal x-ray/CT scan: detection of toxic megacolon, abscesses, perforation, or evidence of pseudomembranous colitis Treatment:- Discontinue the precipitating antibiotic- Fluid replacement- Avoid antidiarrheals (e.g., loperamide)- Nonsevere cases→ 1st-line: oral vancomycin or oral fidaxomicin→ 2nd-line: oral metronidazole- Severe cases: 1st-line: oral vancomycin and IV metronidazole- Refractory: Fecal transplant Control measures:- Gloves and protective gown (change after each patient); a mask is not necessary- Hand hygiene (applies to caregivers, patients, and contact persons): thorough washing with soap and water- Consistent disinfection of possibly contaminated surfaces with sporicidal oxidants, such as peracetic acid or sodium hypochlorite
  • GI Bleed - Management 1. Stabilize patient- 2 Large Bore IVs- IVF, Type and Cross, blood pressure, Coags/FFP 2. Determine if the bleeding is UGIB or not- EGD⊝ for blood → LGIB⊕ for blood → UGIB 3. UGIB → Endoscopy 4. LGIB → CBC ± Transfusion rate- Brisk bleed → Arteriogram- Slow bleed → Colonoscopy
  • Surveillance following polypectomy - Hyperplastic polyp < 10 mm in size in the rectum or sigmoidRecommended interval until next control colonoscopy = 10 years - Low risk adenoma: 1-2 tubular polyps < 10 mm in size and without intraepithelial neoplasia (IEN)Recommended interval until next control colonoscopy = 5-10 years - High risk adenoma: 3-10 tubular polyps, 1 polyp ≥ 10 mm, 1 villous or tubulovillous polyp, 1 tubular polyp with high-grade dysplasiaRecommended interval until next control colonoscopy = 3 years - More than 10 adenomasRecommended interval until next control colonoscopy = < 3 years; depends on the case (i.e., family history)
  • Diverticulitis - Complications Abscess (most common complication):- Peridiverticular localization; causes similar symptoms to acute diverticulitis- Suspect an abscess in patients with persistent fever and abdominal pain despite antibiotic treatment- Fluid collection < 3 cm can be treated with IV antibiotics and observation- Fluid collection > 3 cm should have CT-guided percutaneous drainage Perforation: symptoms of acute abdomen caused by- Rupture of an inflamed diverticulum → free communication with the peritoneum, generalized fecal peritonitis- Rupture of a diverticular abscess → generalized purulent peritonitis Fistulas:- Colovesical (most common): Symptoms: pneumaturia and fecaluria; may cause recurring urinary tract infections, including urosepsis- Diagnosis: CT with oral contrast→ Localized thickening of colon and bladder→ Air or contrast material in the bladder- Treatment: Primary anastomosis; Antibiotics if surgery is not possible Intestinal obstruction:- Causes: inflammatory swelling, compression through abscesses, ileus caused by localized irritation- Symptoms: abdominal pain and distension, constipation, nausea, vomiting, acute abdomen
  • Ranson's criteria Assesses the severity and predicting the prognosis of acute pancreatitis Consists of 11 parameters (five factors are assessed at admission and the other six during the next 48 hours) that are used to create a prognostic score On admission- Age > 55 years- Leukocytosis > 16.000/μL- Hyperglycemia > 200 mg/dL- ↑ LDH > 350 U/L- ↑ AST > 250 U/L After 48 hours:- ↓ Hematocrit by ≥ 10%- ↑ Blood urea nitrogen by ≥ 5 mg/dL despite fluids- ↓ Calcium < 8 mg/dL- ↓ pO2 < 60 mmHg- Sequestration of fluids > 6 L- Base deficit > 4 mmol/L or mEq
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  • Metabolic syndrome Presence of ≥ 3 of the following conditions (or already receiving medical treatment for them)- Insulin resistance: fasting glucose ≥ 100 mg/dL- Elevated blood pressure: ≥ 130/85 mm Hg- Elevated triglycerides: ≥ 150 mg/dL- Low HDL-C: in men < 40 mg/dL; in women < 50 mg/dL- Abdominal obesity: waist circumference ≥ 102 cm in men; ≥ 88 cm in women
  • Hepatorenal syndrome Deterioration of kidney function in patients with advanced liver disease. The condition is caused by renal vasoconstriction resulting in hypoperfusion of the kidneys. Triggers: loss of volume- Drainage of ascites- Gastrointestinal bleeding- Forced diuresis- Excess use of laxatives (lactulose) Symptoms:- Oliguria up to anuria with progressive kidney failure- Clinically associated with decompensated cirrhosis- Renal water retention leads to edema and hydrops (ascites, pleural, or pericardial effusion) Diagnosis:- Serum creatinine > 1.5 mg/dL- Elevated BUN:creatinine ratio (> 20:1)- Protein excretion < 500 mg/d- Hyponatremia with relative sodium deficiency- Low sodium excretion in urine (< 10 mmol/L) Therapy:- General measures: improvement of liver function if possible (e.g., cessation of alcohol use)- Pharmacotherapy: combination of midodrine, octreotide, and albumin- Placement of a transjugular intrahepatic portosystemic shunt (TIPS)- A liver transplant is the only curative option in advanced liver disease
  • Small intestinal bacterial overgrowth (SIBO) Etiology:- Anatomic abnormalities: (e.g., surgery causing blind intestinal loops – blind loop syndrome), strictures- Motility disorders (e.g., uncontrolled diabetes mellitus, chronic opiate use) Pathophysiology: bacterial overgrowth → bacteria deconjugate bile acids, increase vitamin B12 turnover, and produce increased amounts of vitamin K and folic acid Clinical features: - Abdominal pain, bloating, flatulence - Diarrhea- Steatorrhea- Weight loss- Malabsorption (e.g., deficiency of vitamin B12, A, E, D, zinc, and iron) Diagnostics:- Jejunal aspirate cultures collected during endoscopy showing >105 organisms/mL- Positive lactulose breath test Treatment: - Antibiotics (e.g., rifaximin, amoxicillin-clavulanate)- Parenteral supplementation of vitamins and proteins, possibly surgical treatment
  • Clinical manifestations of trace mineral deficiencies Chromium: Impaired glucose control in diabetics Copper:- Brittle hair- Skin depigmentation- Neurologic dysfunction (eg, ataxia, peripheral neuropathy)- Sideroblastic anemia- Osteoporosis Iron: Microcytic anemia Selenium:- Thyroid dysfunction- Cardiomyopathy- Immune dysfunction Zinc:- Alopecia- Pustular skin rash (perioral region & extremities)- Hypogonadism- Impaired wound healing- Impaired taste- Immune dysfunction
  • Anorectal fistula Etiology:- Perianal abscess- Crohn disease- Malignancy, radiation proctitis- Infection (eg, lymphogranuloma venereum) Clinical presentation:- Perirectal pain, discharge- Inflammatory papule/pustule- Palpable fistula tract Treatment:- Assess extent of fistula→ Gentle probe→ Imaging (endosonography, fistulogram, MRI)- Surgery (eg, fistulotomy)
  • Toxic megacolon Etiology:- Infectious colitis: C difficile, Salmonella, Shigella, Campylobacter, Trypanosoma cruzi (Chagas disease), E histolytica- Inflammatory bowel disease Clinical features:- Systemic toxicity: Fever, tachycardia, hypotension- Bloody diarrhea- Abdominal distension/peritonitis Diagnostics:- Lab findings: neutrophilic leukocytosis, ↑ ESR/CRP, hypokalemia (due to diarrhea)- Abdominal x-ray: Dilation of the colon, loss of haustration, multiple air-fluid levels- Contrast-enhanced CT scan (oral and IV contrast) Treatment:- NPO, nasogastric tube insertion, IV fluids, correction of electrolyte imbalances- Antibiotics: Oral metronidazole for C difficile- IBD: IV steroids- Surgery if no response to medical treatment within 24-72 hours → subtotal colectomy
  • Esophageal perforation Etiology:- Spontaneous rupture (Boerhaave syndrome)- Instrumentataion (eg, endoscopy)- Esophagitis (infectious/pills/caustic)- Esophageal ulcer Clinical features:- Chest & abdominal pain, systemic findings (eg, fever)- Subcutaneous emphysema in the neck- Hamman sign (crunching sound on chest auscultation)- Pleural effusion with atypical (eg, green) fluid Diagnosis:- CXR or CT scan: Wide mediastinum, pneumomediastinum, pneumothorax, air around paraspinal muscles, pleural effusion (late)- CT scan: Esophageal wall thickening, mediastinal air fluid level- Water-soluble contrast esophagogram: Leak at perforation site Management:- NPO, IV antibiotics & PPIs- Surgical repair for significant leakage with systemic inflammatory response
  • Psoas abscess Clinical features:- Subacute fever, abdominal/flank pain radiating to groin- Anorexia, weight loss- Abdominal pain with hip extensors (psoas sign) Diagnosis:- CT scan of the abdomen & pelvis- Leukocytosis, elevated inflammatory markers- Blood & abscess cultures Treatment:- Drainage- Broad-spectrum antibiotics
  • Dumping syndrome Rapid gastric empyting due to either defective gastric reservoir or pyloric emptying mechanism, or anomalous postsurgery gastic motor function. Clinical features:- Abdominal pain, diarrhea, nausea- Hypotension/tachycardia- Dizziness/confusion, fatigue, diaphoresis Timing:- 15-30 minutes after meals Initial management:- Small/frequent meals- Replace simple sugars with complex carbohydrates- Incorporate high-fiber & protein-rich foods
  • Recommended vaccines for chronic liver disease Tdap/Td: Tdap once as substitute for Td booster, then Td every 10 years Influenza: Annually Pneumococcal vaccines: PPSV23 once, then revaccination with sequential PCV13 & PPSV23 at age 65 Hepatitis A: 2 doses 6 months apart  Hepatitis B: 3 doses at 0 months, 1 month & at least 4 months 
  • Gastroparesis Diabetic autonomic neuropathy of the gastrointestinal tract.  Clinical features:- Anorexia, nausea, vomiting- Abdominal bloating- Loss of appetite- Early satiety- Diarrhea, constipation, incontinence- Postprandial hypoglycemia Diagnostics:- EGD: To rule out malignancy or gastric outlet obstruction- Gastric emptying study Treatment:- Optimize diabetes control- Dietary modifications with increased fiber intake and small, frequent meals- Prokinetic agents:→ Metoclopramide→ Erythromycin (more useful when used intravenously for acute exacerbations)
  • Hepatic encephalopathy Triggers:- Deterioration of liver function- Infections (e.g., SBP)- Gastrointestinal bleeding- Constipation- Portal vein thrombosis- Hypovolemia and electrolyte disturbances (hypokalemia, hyponatremia)- Renal failure- Excessive protein consumption Clinical features:- Disturbances of consciousness, ranging from mild confusion to coma- Multiple neurological and psychiatric disturbances like:→ Asterixis→ Fatigue, lethargy, apathy→ Memory loss→ Impaired sleeping patterns→ Irritability→ Disoriented, socially aberrant behavior (e.g., defecating/urinating in public, shouting at strangers, etc)→ Slurred speech→ Muscle rigidity Diagnostics:- Elevated ammonia levels- Assessment of mental status: Number connection test; psychometry-based diagnostic method Treatment:- Avoidance of trigger substanes (eg, hepatotoxic mediation, alcohol)- Treatment of "triggers"- Lactulose: Improves HE by decreasing absorption of ammonia in the bowel: lactulose is converted to lactic acid by intestinal flora → acidification in the gut leads to conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration- Rifaximin: Non‑absorbable antibiotic→ May be added to lactulose to prevent recurrent episodes of HE after the second episode
  • Specialized nutrition support Indications:- Dysphagia (eg, post-stroke state, multiple sclerosis, esophageal carcinoma)- Patients with a low GCS who cannot be fed- Difficulty with oral intake in the postoperative state- Severe anorexia  Enteral feeding- Administration of nutrients directly into the stomach, duodenum, or jejunum- Intestinal motility is stimulated, preventing mucosal atrophy, lower risk of blood stream infection- Contraindications: Mechanical ileus, bowel obstruction, acute abdomen, upper GI bleeding- Complications: Blockage of the feeding tube, iatrogenic trauma Parenteral feeing- Intravenous administration of nutrients that bypasses the GI tract- Contraindications: Enteral nutrition is feasible, serum hyperosmolality, severe hyperglycemia, severe electrolyte abnormalities, volume overload- Complications: Catheter displacement, thrombosis/embolism, catheter-related blood stream infection Metabolic complications:- Severe electrolyte imbalances (eg, hypocalcemia, hypomagnesemia, hypophosphatemia)- Hyperglycemia- Refeeding syndrome- Hyperlipidemia- Gallstone disease (> 2 weeks)- NASH
  • Complications of Roux-en-Y gastric bypass surgery Early:- Anastomosis leak (sepsis)- Bowel ischemia (diffuse abdominal pain) Late:- Anastomotic stricture (dysphagia, bowel obstruction)- Marginal ulcer (abdominal pain, bleeding, peri-anastomotic perforation)- Cholecystitis (right upper quadrant pain) - due to resulting rapid weight loss- Dumping syndrome (diarrhea, crampy abdominal pain, vasomotor)
  • Acute liver failure Etiology:- Viral hepatitis (eg, HSV, CMV, hepatitis A, B, D, E)- Drug toxicity (eg, acetaminophen overdose, idiosyncratic)- Ischemia (eg, shock liver, Budd-Chiari syndrome)- Autoimmune hepatitis- Wilson disease- Malignant infiltration Clinical presentation:- Generalized symptoms (eg, fatigue, lethargy, anorexia, nausea)- Right upper quadrant abdominal pain- Pruritus & jaundice due to hyperbilirubinemia- Renal insufficiency- Thrombocytopenia- Hypoglycemia Diagnostic requirements:- Severe acute liver injury (ALT & AST often > 1000 U/L)- Signs of hepatic encephalopathy (eg, confusion, lethargy)- Synthetic liver dysfunction (INR ≥ 1.5) Treatment:- Early transfer to a liver transplant center- Intravenous N-acetylcysteine- Address/prevent complications: e.g., cerebral edema, encephalopathy, coagulopathy, renal failure, and infection - Address underlying cause: e.g., antiviral treatment for hepatitis B, steroids for autoimmune hepatitis, or delivery for HELLP syndrome- Liver transplantation is the only therapeutic option for patients without sufficient regeneration of hepatocytes
  • Ascites fluid characteristics Color:- Bloody: Trauma, malignancy, TB (rarely)- Milky: Chylous, pancreatic- Turbid: Possible infection- Straw color: Likely more benign causes Neutrophils:- < 250/mm3: No peritonitis- ≥ 250/mm3: Peritonitis (secondary or sponteanous bacterial) Total protein:- ≥ 2.5 g/dL (high-protein ascites): CHF, constrictive pericarditis, peritoneal carcinomatosis, TB, Budd-Chiari syndrome, fungal (eg, coccidioidomycosis)- < 2.5 g/dL (low-protein ascites): Cirrhosis, nephrotic syndrome SAAG:- ≥ 1.1 g/dL (indicates portal hypertension): Cardiac ascites, cirrhosis, Budd-Chiari syndrome- < 1.1 g/dL (absence of portal hypertension): TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome
  • Glucagonoma Clinical features:- Necrolytic migratory erythema→ Erythematous papules/plaques on face, perineum, extremities→ Lesions enlarge & coalesce over next 7-14 days with central clearing & blistering, crusting & scaling at borders- Diabetes mellitus→ Mild hyperglycemia easily controlled with oral agents & diet→ Usually does not require insulin- GI symptoms→ Diarrhea, anorexia, abdominal pain, or occasional constipation- Weight loss- Neuropsychiatric (eg, ataxia, dementia, proximal muscle weakness)- Association with venous thrombosis Diagnosis:- Hyperglycemia with elevated glucagon > 500 pg/mL- Normocytic, normochromic anemia due to likely anemia of chronic disease or glucagon directly affecting erythropoiesis- Abdominal imaging (CT or MRI) to localize tumor &/or metastases
  • Emphysematous cholecystitis Risk factors:- Diabetes mellitus- Vascular compromise- Immunosuppression Clinical features:- Fever, right upper quadrant pain, nausea/vomiting- Crepitus in abdominal wall adjacent to gallbladder Diagnostics:- Air-fluid levels in gallbladder, gas in gallbladder wall- Cultures with gas-forming Clostridium, E coli- Unconjugated hyperbilirubinemia, mildly elevated aminotransferases Treatment:- Emergency cholecystectomy- Broad-spectrum antibiotics with Clostridium coverage (eg, piperacillin-tazobactam)
  • VIPoma Pathophysiology:- Excess VIP → increases relaxation of gastric and intestinal smooth muscles and adenylate cyclase (cAMP) activity (similar to cholera toxin) → secretory diarrhea and inhibition of gastric acid production- Associated with MEN1 syndrome (5% of cases) Tumor location: The primary tumor is most frequently found in the pancreas. Clinical features:- WDHA syndrome (Watery Diarrhea, Hypokalemia, Achlorhydria)→ Tea-colored watery diarrhea (> 700 mL/day) → dehydration- Weight loss- Abdominal pain, nausea, vomiting- Achlorhydria → ↓ iron and B12 absorption → anemia Diagnostics:- ↑ Serum VIP concentration (> 75 pg/mL)- Hypokalemia (↑ intestinal potassium secretion)- Hypercalcemia (increased bone resorption)- Hyperglycemia due to increased glycogenolysis- Secretory diarrhea with ↑ sodium & osmolol gap < 50 mOsm/kg- Abdominal CT or MRI to localize tumor in pancreas (usually in pancreatic tail) Treatment: Resection or ocreotide
  • Biliary cysts Epidemiology:- Asian descent Pathogenesis: Type I cysts (most common): extrahepatic, single cystic dilatation of the bile duct Clinical features:- Classic triad of pain, jaundice & palpable mass- Majority of cysts present at age < 10 years Diagnosis:- Visualization on ultrasonography- ERCP Treatment: Surgical resection to relieve obstruction & prevent malignant transformation
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  • Eosinophilic esophagitis Epidemiology:- Young men (age 20-30)  Pathogenesis: Chronic, immune-mediated esophageal inflammation Clinical features:- Dysphagia- Chest/epigastric pain- Reflux/vomiting- Food impaction- Associated atopy (eg, asthma, aczema) Diagnosis:- Endoscopy & esophageal biopsy (≥ 15 eosinophils per high-power field) Treatment:- Dietary modification- Even if there are eosinophils on the biopsy, treat it like GERD with PPI. - If PPI fails, then use swallowed aerosolized steroids
  • Atraumatic splenic rupture Risk factors:- Hematologic malignancy (eg, leukemia, lymphoma)- Infection (eg, CMV, EBV, malaria)- Inflammatory disease (eg, SLE, pancreatitis)- Splenic congestion (eg, cirrhosis, pregnancy)- Medications (eg, anticoagulation, G-CSF) Clinical presentation:- Diffuse or LUQ abdominal pain, peritonitis- Referred left shoulder pain (Kehr sign)- Hemodynamic instability Diagnosis:- Acute anemia- Intraperitoneal free fluid on imaging Treatment:- Catheter-based angioembolization (stable patients)- Emergency splenectomy (unstable patients)
  • Diverticulitis Etiology:- Increasing age- Diet (low-fiber, rich in red meat and fat)- Obesity, low physical activity- Cigarette consumption Classification: Hinchey Clinical features:- Low-grade fever- Sigmoid colon most commonly affected → left lower quadrant pain- Possibly tender, palpable mass (pericolonic inflammation)- Change in bowel habits (~ 50% constipation, 25-35% diarrhea)- Nausea and vomiting- ↑ Urinary urgency and frequency (~ 15%) Diagnostics:- Lab: Leukocytosis, ↓ hemoglobin, ↑ CRP- 1st line: CT with oral and IV contrast- Colonoscopy performed once inflammation has subsided (after 6 weeks) Treatment:- Uncomplicated: Broad-spectrum oral antibiotics for 7-10 days→ Ciprofloxacin + metronidazole→ TMP-SMX + metronidazole- Complicated: Broad-spectrum IV antibiotics→ Piperacillin/tazobactam→ Ampillin/sulbactam+ CT-guided percutaneous abscess drainage if > 3 cm/surgery
  • Colon cancer screening Family history of adenomatous polyps or CRC:- 1 first-degree relative age < 60- ≥ 2 first-degree relatives at any age→ Age 40 or 10 years before the age of diagnosis in affected relative→ Repeat every 5 years Inflammatory bowel disease→ 8-10 years postdiagnosis (12-15 years if disease only in left colon)→ Repeat every 1-3 years Classic familial adenomatous polyposis→ Age 10-12→ Repeat annually HNPCC (Lynch syndrome)→ Age 20-25→ Repeat every 1-2 years Normal population:- All asymptomatic women and men ≥ 50 years- Complete colonoscopy (gold standard): Repeat every 10 years OR- Sigmoidoscopy every 5 years and FOBT every 3 years OR- Annual fecal immunochemical testing (FIT)
  • Ascites Etiology:- The etiology can be determined using the serum-ascites albumin gradient (SAAG) based on Starling's law. - Calculation: SAAG = (albumin levels in serum) - (albumin levels in ascitic fluid)- High SAAG: ≥ 1.1 g/dL → Portal hypertension- Low SAAG: < 1.1. g/dL→ Hypoalbuminemia → Malignancy→ Infections→ Pancreatitis Clinical features:- Progressive abdominal distension- Fluid wave test- Shifting dullness- Abdominal wall hernias- Peripheral or generalized edema- Signs of underlying disease Diagnostics:- Dilutional hyponatremia, hypoalbuminemia- Ultrasound (best initial test)- Ultrasound-guided diagnostic paracentesis→ Indication: First diagnosed ascites, worsening ascites, or suspected complication Treatment:- Fluid restriction- Diuretic therapy with spironolactone
  • Drug-induced esophagitis Some medications may cause esophageal mucosal irritation, leading to erosions and ulcers. Causes:- Antibiotics (e.g., tetracycline, doxycycline, and clindamycin)- Anti-inflammatory drugs (e.g., NSAIDs, aspirin)- Bisphosphonates (e.g., Alendronate)- Anti-retrovirals- Others (e.g., potassium chloride, quinidine, and iron compounds) Endoscopic findings: punched-out ulcers with mild inflammatory changes of the surrounding mucosa Treatment:- Take pills with 4 oz of water and while erect and upright- Endoscopy can reveal and allow removal of tablet or pill
  • Infectious esophagitis Generally in immunocompromised patients.- Organ transplant- Leukemia or lymphoma- Steroids- HIV/AIDS Esophageal candidiasis: Endoscopy shows white or yellowish adherent plaques. Herpes esophagitis: Endoscopy shows ulcers in the upper or mid esophagus in the absence of plaques.- CD4 counts < 100/mm3- Round, superficial, friable mucosa CMV esophagitis: Endoscopy shows distal mucosal erosions and ulcers; viral inclusion bodies in cell nuclei on biopsy.- CD4 counts < 50/mm3- Deep linear or longitudinal ulcers Treatment:- Candida: Nystatin and fluconazole- Herpes: (Val)acyclovir or foscarnet- CMV: (Val)acyclovir or foscarnet- HIV: HAART
  • Caustic esophagitis Clinical features:- Chest pain- Odynophagia- Drooling- Burning of the larynx → stridor, wheezing Diagnosis:- Endoscopy within 24 hours Treatment:- Low severity (edema, erythema, shallow ulcers) → move from liquid to solid diet in the first 24-48 hours- High severits (deep ulcers, circumferential burns, black necrosis) → remain NPO for 72 hours due to risk of perforation, bleeding, strictures, and fistulas Prognosis:- 70% develop strictures- 2-3% develop cancer (surveillance required 15-20 years later)
  • Scleroderma Collagen in the esophagus → LES cannot contract Clinical features: Relentless GERD Diagnosis:- Manometry: Relaxed esophagus and ↓ pressure in the LES Treatment: PPI
  • Esophageal stricture Most common sequela of reflux esophagitis Clinical features: - Solid food dysphagia Diagnostics:- Barium esophagram (best initial test): narrowing of the esophagus at the gastroesophageal junction- Endoscopy with biopsies: to rule out malignancy and eosinophilic esophagitis Treatment:- First-line treatment: dilation with bougie dilator/balloon dilator + proton pump inhibitors in patients with reflux - In refractory cases (multiple recurrences): steroid injection prior to dilation, endoscopic electrosurgical incision Recurrence occurs in the majority of patients; often multiple treatment attempts necessary
  • Barrett esophagus Pathophysiology: Reflux esophagitis → stomach acid damages squamous epithelium → squamous epithelium becomes replaced by columnar epithelium and goblet cells (intestinal metaplasia, Barrett's metaplasia) - The physiological transformation zone ("Z-line") between squamous and columnar epithelium is shifted upwards Complications: precancerous condition for adenocarcinoma  Management and surveillance:- Medical treatment with high-dose PPIs- Endoscopy with four-quadrant biopsies at every 2 cm of the suspicious area (salmon colored mucosa)→ If no dysplasia: repeat endoscopy every 3-5 years→ If indefinite for dysplasia: repeat endoscopy with biopsies after 3-6 months of optimized PPI therapy→ If low-grade dysplasia: Endoscopic therapy of mucosal irregularities or surveillance every 1 year→ If high-grade dysplasia: Endoscopic therapy of mucosal irregularities
  • Gastrinoma (Zollinger-Ellison syndrome) A gastrin-secreting neuroendocrine tumor that is most often localized to the duodenum and pancreas. Epidemiology: - Sex: ♂ > ♀ (2:1)- Age of onset: 30-50 years Pathophysiology:- Hypergastrinemia → stimulation of parietal cells → gastric acid hypersecretion, which leads to peptic ulcer disease- Inactivation of pancreatic enzymes → diarrhea, steatorrhea → malabsorption Clinical features:- Recurrent, therapy-resistant peptic ulcer disease- Abdominal pain- Diarrhea and steatorrhea- Dyspeptic symptoms (e.g., heartburn)- Upper gastrointestinal bleeding- Weight loss- Possible symptoms of other endocrine neoplasias (see MEN 1) Diagnostics:- Best initial test: esophagogastroduodenoscopy: Important to rule out H. pylori infection and malignant ulcers→ Typically reveals multiple ulcers and thick gastric folds→ ↓ Gastric pH- A gastrin level > 1000 pg/mL is conclusive evidence of a gastrinoma.- If serum gastrin levels increase (> 100 pg/mL) but are not more than 1000 pg/mL, a secretin stimulation test should be performed.→ Secretin stimulation test: A two-fold increase in gastrin above the basal level is indicative of a gastrinoma.- CT/MRI scan, somatostatin receptor scintigraphy (octreotide scan) and/or endoscopic ultrasonographyThe presence of multiple, large (> 2 cm) ulcers in atypical locations (e.g., the jejunum) should raise suspicion of gastrinoma! Treatment:- PPIs (e.g., omeprazole), H2 antagonists (e.g., ranitidine) - Octreotide (a somatostatin analog) may be used in refractory cases- Nonmetastatic disease: surgical resection of the gastrinoma- Metastatic disease: chemotherapy
  • Gastric outlet obstruction Mechanical obstruction of the pyloric channel or duodenum Etiology:- Malignancy (most common)- Acute PUD → inflammation and edema- Chronic PUD → scarring and fibrosis- Gastric volvulus Clinical presentation:- Postprandial, nonbilious vomiting- Succussion splash: A stethoscope is placed over the upper abdomen while the patient lies supine, then the patient is rocked back and forth at the hips. If a “splash” is heard, it suggests retained gastric content due to obstructed passage into the duodenum. - Early satiety- Progressive gastric dilation- Weight loss Diagnosis:- Barium swallow: enlarged stomach and string sign- Upper endoscopy (confirmatory test): identification of the gastric pathology- Laboratory tests: hypokalemic hypochloremic metabolic alkalosis- Saline load test: Inject 750 mL of saline into the patient's nasogastric tube on an empty stomach. If the aspirate after 30 min is > 400 mL, gastric outlet obstruction is present. Management:- Symptomatic: nasogastric suction, electrolyte and fluid replacement, and parental nutrition- Definitive: surgery or endoscopic dilation
  • Malabsorption Maldigestion = Impaired breakdown of food in the intestinal lumen- Exocrine pancreatic insufficiency → reduced hydrolysis of carbohydrates, proteins, and lipids- Following gastric resection → lack of gastric acid → impaired breakdown of nutrients- Bile acid deficiency (e.g., cholestasis, bile acid malabsorption) → incomplete emulsification of fats- Medications: Orlistat (reversibly inhibits gastric and pancreatic lipase) Malabsorption = Impaired absorption of digested food caused by alterations of the intestinal mucosa- Inflammatory bowel disease (e.g., Crohn's disease) - Celiac disease (gluten-sensitive enteropathy) - Infections (e.g., tropical sprue, giardiasis, traveler's diarrhea, Whipple's disease)- Lactose intolerance- Small intestine resection (short bowel syndrome)- Small intestinal bacterial overgrowth (SIBO; blind loop syndrome) - HIV enteropathy Diagnostics:1. Fecal fat test: Give 100 g fat/day + analysis of fecal fat over 72 hours- < 14 g/24 hours → Not malabsorption- > 14 g/24 hours → Malabsorption2. D-xylose absorption test: assesses the absorptive function of the upper small intestine- Overnight fast → collection of urine for 5 hours following oral administration of 25 g xylose → if urine xylose levels < 4 g/5 h, diagnostic for malabsorptive disorders with damage to the intestinal mucosa (e.g., celiac disease, Whipple's disease)- Collection of a venous blood sample after one hour → levels < 20 mg/dL of serum D-xylose are pathological- Absorbed → Pancreas deficiency
  • Diverticular spasm Epidemiology: Elderly patients Clinical features:- LLQ post-prandial pain - Relieved by a bowel movement Treatment: high fiber diet  "IBD of the elderly"
  • Diverticular bleeding Frequency: occurs in around 5% of cases of patients with diverticulosis Etiology: Erosions around the edge of diverticula- Diverticuli bleed from the right colon more than the left Clinical features:- Brisk, painless bleeding per rectum- Severe or ongoing bleeding: significant drop in hemoglobin, hemodynamic instability (hypotension, tachycardia, dizziness, reduced level of consciousness) Diagnostics:1. Rule out upper gastrointestinal bleed with NG tube + EGD2. Colonoscopy (ø bleeding), tagged RBC scan (slow bleeding), angiogram (brisk bleeding) - Therapy: → Endoscopic hemostasis during colonoscopy (epinephrine injection, thermal coagulation, ligation)→ Angiography with vessel embolization
  • Colonoscopy - Follow-up None → q10 years Low → q5-10 years- 1-2 polyps- < 1 cm- Tubular- Low-grade High → q1-3 years- ≥ 3 polyps- ≥ 1 cm- Villous- High-grade Mega → q2-6 months
  • Alpha-1 antitrypsin deficiency A congenital disorder characterized by the accumulation of defective alpha-1 antitrypsin enzyme. Epidemiology: more common in individuals of European descent  Etiology: mutations in SERPINA1 gene- M is the normal allele.- S mutation causes a moderate decrease in AAT production.- Z mutation causes a significant decrease in AAT production.- Order of severity of genotypic expression: PiMS < PiSS < PiMZ < PiSZ < PiZZ Inheritance: autosomal codominant Pathophysiology:- Alpha-1 antitrypsin: a protease inhibitor that is synthesized in the liver and protects cells from breakdown by neutrophil elastase- Effect on the liver: impaired secretion of AAT by hepatocytes → accumulation of AAT in hepatocellular ER → hepatocyte destruction → hepatitis and liver cirrhosis- Effect on the lungs: lack of functional AAT → uninhibited neutrophil elastase activity in the lungs → destruction of the pulmonary architecture → panacinar emphysema Clinical features:- Severe form: prolonged neonatal jaundice, hepatitis, cirrhosis, and panacinar emphysema- Mild form: manifests in adolescence, primarily with pulmonary disease; hepatic symptoms may also be present- Increased risk of hepatocellular carcinoma (HCC) Diagnostics:- Chest x-ray: panacinar emphysema (in contrast to centriacinar emphysema in smoking-related emphysema) - Serum: decreased antitrypsin protein levels- Electrophoresis: decreased alpha-1 peak- Liver biopsy: PAS-positive, spherical inclusion bodies in periportal hepatocytes Treatment:- Avoid active and passive exposure to cigarette smoke.- Symptomatic treatment: bronchodilators, pulmonary rehabilitation, preventive vaccination, nutritional support if necessary- Antitrypsin replacement: patients with severe AAT deficiency (e.g., ATT < 57 mg/dL) and evidence of decreased airflow- Liver transplantation: results in correction of AAT deficiency; considered for end-stage liver disease
  • Autoimmune hepatitis Epidemiology: - Bimodal distribution: 10-20 years and 45-70 years- Sex: ♀ > ♂ (∼ 4:1) Clinical features:- Fatigue- Abdominal pain- Weight loss- Signs of acute liver failure (∼ ⅓ of patients): Jaundice, RUQ pain, fever Diagnsotics:- ↑ ALT and ↑ AST- Autoantibodies: antinuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA)- Hypergammaglobulinemia (↑ IgG)- Liver biopsy: Biopsy should be performed following the detection of AIH antibodies to confirm the diagnosis. Treatment:- Initial therapy: combination of prednisone and azathioprine- Maintenance therapy: azathioprine or prednisolone
  • Dieulafoy's lesion In this rare disease, minor mucosal trauma can lead to major bleeding. It is caused by an abnormal submucosal artery. Location: proximal stomach Clinical presentation: signs of acute upper GI bleeding Treatment: endoscopic hemostasis (injection therapy, hemoclips, etc.), excision of the susceptible mucosa

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