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USMLE Step 2 (Subject) / Gastroenterology (Lesson)

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• Ischemic colitis Epidemiology:- Most common form of intestinal ischemia- Mainly occurs in adults > 60 years- In ∼ 80–85% mild, non-gangrenous form Etiology:- Usually caused by transient hypoperfusion- Thromboembolism- Hypotension, hypovolemia (e.g., sepsis, dehydration, hemorrhage)- Cardiovascular surgery (especially aortic repairs or cardiac bypass)- Vasoconstrictive drugs- Thrombophilias (e.g., anticardiolipin syndrome)- Colonic obstruction from tumors, adhesions, etc. Pathophysiology:- Intestinal blood flow of the superior mesenteric artery (SMA) and/or inferior mesenteric artery (IMA) is suddenly compromised → intestinal hypoxia → intestinal wall damage → mucosal inflammation + possibly bleeding → may progress to infarction and necrosis (gangrenous type) → disruption of mucosal barrier and perforation → release of bacteria, toxins, vasoactive substances → life-threatening sepsis Clinical features:1. Hyperactive phase- Sudden onset of crampy abdominal pain (usually left lower quadrant)- Bloody, loose stools- > 80% of patients recover and do not progress beyond this phase2. Paralytic phase- Pain more diffuse- Bowel sounds become absent. - Bloating- Bloody stools cease3. Shock phase- Acute abdomen with abdominal guarding and rebound tenderness- Signs of septic shockA classic case of ischemic colitis is a patient who presents with bloody diarrhea and severe abdominal pain after an abdominal aortic aneurysm repair! Diagnostics:- ↑ Lactate, ↑ LDH, ↑ creatine kinase, leukocytosis, metabolic acidosis- Colonoscopy Treatment:- Supportive care (IV fluids, bowel rest, nasogastric tube in case of an ileus)- Antiplatelet drugs- Reduce risk of atherosclerosis- Severe forms (signs of peritonitis, sepsis): surgical intervention (laparotomy and bowel resection)
• Hepatitis B - Treatment Acute hepatitis B: Supportive care Chronic hepatitis B:- Nucleoside/nucleotide analogs→ Tenofovir is commonly the drug of choice→ Entecavir- Pegylated interferon alfa (PEG-IFN-α)
• Hepatitis C - Treatment Acute hepatitis C: peginterferon-α (PEG-INF) for 6 months Chronic hepatitis C:- Combination of two direct-acting antivirals (DAAs)→ Ledipasvir + sofosbuvir for 12 weeks (genotypes 1, 4, 5, 6)→ Sofosbuvir + velpatasvir for 12 weeks (all 6 genotypes)- Interferon + ribavirin (genotypes 2 and 3)- In addition to any treatment regimen, give vaccinations for hepatitis A and B
• Scurvy (vitamin C deficiency) Epidemiology:- Due to insufficient dietary intake (lack of citrus fruits/vegetables)- Most common in alcoholics, drug abusers & severely malnourished Manifestations:- Cutanous: petechia, follicular hemorrhage, bruising, coiled hairs- Gingival: bleeding/receding gums & dental carries- Constitutional: arthralgias, weakness, malaise, depression- Impaired wound healing- Vasomotor instability Treatment:- Oral/injectable vitamin C resolves most symptoms within days- Toxicity (e.g., abdominal pain, diarrhea, nausea) can occur with excessive supplementation
• Hemorrhoids Hemorrhoids, also called piles, arise from a cushion of dilated arteriovenous blood vessels and connective tissue in the anal canal that may abnormally enlarge or protrude. Etiology: - Excessive straining (e.g., from chronic constipation, frequent bowel movements, chronic cough, heavy lifting, benign prostatic hyperplasia)- Extended periods of sitting (e.g., due to occupation or sedentary lifestyle)- Pregnancy Classification:I – Hemorrhoids do not prolapse (only project into the anal canal); above the dentate (pectinate) line; reversible; often bleedII – Prolapse when straining, but spontaneously reduce at restIII – Prolapse when straining; only reducible manuallyIV – Irreducible prolapse; may be strangulated and thrombosed with possible ulceration Internal hemorrhoids:- Often painless, bright red bleeding at the end of defecation (potentially dull, aching pain with severe sphincter spasm)- Perianal mass in the event of prolapse- Pruritus- Discharge (containing mucus or fecal debris)- Ulceration (in grade IV) External hemorrhoids:- Painful perianal mass- Pruritus Diagnostics:- Anoscopy Treatment:- Grade I-II internal hemorrhoids and external hemorrhoids→ Lifestyle modifications: weight loss, exercise, high fiber diet, avoid fatty and spicy foods, increase water intake→ Alter stool habits (e.g., avoid excessive straining or > 5 min periods on the toilet)→ Sitz baths→ Stool softeners (e.g., docusate)→ Topical analgesia (e.g., lidocaine), anti‑inflammatory (e.g., hydrocortisone, especially with pruritus, but no longer than 1 week), antispasmodic agents (e.g., nitroglycerin)- All internal hemorrhoids with symptoms persisting despite conservative treatment and grade III internal hemorrhoids→ Rubber band ligation (RBL) → Sclerotherapy→ Infrared coagulation
• Rotavirus infection Epidemiology:- Infants and young children are most often affected, although all age groups are susceptible to infection. - A leading cause of severe (> 10 loose, watery stools within 24 hours) diarrhea in infants and children Clinical features:- Incubation period: 1-3 days- Vomiting and watery diarrhea lasting 3-7 days- Fever- Malaise Diagnostics:- Antigen detection in stool via enzyme immunoassay (EIA) Treatment:- Oral rehydration- IV fluids in cases of severe dehydration Prevention:- Rotavirus vaccination (a live attenuated vaccine) is recommended unless there is a contraindication. These may include:→ A history of severe allergic reaction after exposure to a previous rotavirus vaccine or to any of its components→ Infants with severe combined immunodeficiency (SCID)→ Infants with a history of intussusception
• Norovirus infection Epidemiology:- Peak incidence: November-March (winter months) - Community outbreaks (in nursing homes, hospitals, preschools, cruise ships, etc.) are common- Elderly and immunocompromised patients are commonly affected.- Most common cause of→ Adult gastroenteritis→ Severe acute gastroenteritis in children younger than 5 years of age → Foodborne illness Clinical features:- Incubation period: 12-48 hours- Nausea and acute-onset vomiting- Watery, non-bloody diarrhea- Abdominal cramps- Symptoms resolve after 48-72 hours (DD: Rotavirus lasts 3-7 days) Diagnostics:- Norovirus should be suspected in potentially exposed individuals if vomiting and/or diarrhea consisting ≥ 2 loose stools occur within a 24‑hour period.- Clinical suspicion of norovirus infection should be confirmed with reverse transcription PCR (RT-PCR). Treatment:- Rehydration, if necessary with IV fluids (especially in the elderly and children)- If myalgia and/or headache are present: NSAIDs or acetaminophen Prevention: Obligation to report
• Acute purulent sialadenitis Acute inflammation of the salivary glands Pathogens: usually bacterial (commonly Staphylococcus aureus) Risk factors:- Cachexia in intensive care patients- Postoperatively (due to dehydration, intubation)- Intensive teeth cleaning- Decreased salivation (due to fasting, special diet)- Immunodeficiency- Salivary stones- Advanced age- Anticholinergic drug use- Oral neoplasia- Malnutrition Location: most often the parotid gland Clinical features:- Acute onset- Unilateral painful swelling and erythema overlying the salivary gland- Usually with purulent discharge expressed from duct orifice- Systemic toxicity: fever, chills Diagnostics:- Mostly a clinical diagnosis- ↑ Serum amylase indicates parotid involvement- Gram stain and culture of discharge- Ultrasound or CT if abscess is suspected Treatment:- Hydration- Stimulation of salivation (chewing gum, lemon drops)- Intravenous antibiotics: nafcillin + metronidazole OR clindamycin→ Poor response to 48 hours of antibiotics or an abscess: surgical drainage and decompression- Recurrent infections: parotidectomy
• Anal cancer Risk factors:- Immunodeficiency (e.g., HIV)- Receptive anal intercourse- Smoking- HPV infection Clinical features:- Rectal bleeding (most important initial symptom)- A lump or tumor around the anus- Pruritus ani- Tenderness, pain in the anal area- Fecal incontinence- History of anorectal condyloma Diagnostics:- Digital rectal exam- Anoscopy- Biopsy for histology (small tumors are fully excised) Treatment:- Anal canal cancer: radiochemotherapy- Anal margin cancer:→ If possible, local excision with safety margin→ Advanced tumor: (Neoadjuvant) radiochemotherapy with subsequent resection
• Abdominal compartment syndrome Etiology:- Penetrating abdominal trauma- Pelvic trauma- Rupture of abdominal aortic aneurysm- Massive volume resuscitation (e.g., postoperative patients, treatment of hypovolemic shock, severe burns)- Severe ascites- Abdominal surgery- Sepsis Pathophysiology: ↑ intra-abdominal pressure → organ dysfunction Clinical features: - May develop within hours or over days- Critically ill patient- Cardiovascular: signs of increased central venous pressure (e.g., distended jugular veins), hypotension, tachycardia- Renal: oliguria, progressive renal failure- Gastrointestinal: tight, distended abdomen, nausea, vomiting- Pulmonary: tachypnea, wheezing Diagnostics:- Best initial test: indirect measurement of intra-abdominal pressure (Can be indirectly measured by measuring the pressure in the bladder via an intravesical catheter)- CT imaging: increased abdominal diameter, compression of the inferior vena cava, intestinal wall thickening, bilateral inguinal herniation Treatment:- Laparotomy for decompression- Temporary abdominal closure (e.g., patch technique, vacuum-assisted closure)- Definitive closure
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• Rectus abdominis diastasis Weaking of the linea alba, the fascia that lies between the rectus abdominis muscles and keeps them in close proximity. Risk factors:- Chronic abdominal stretching (e.g., pregnancy, multiparity)- Surgical weakening (e.g., prior cesarean deliveries)- Increased intraabdominal pressure (e.g., constipation) Clinical features:- Nontender midline mass- No associated fascial defect (not a true hernia)- No associated pain, acute GI symptoms, or risk of bowel strangulation or incarceration Treatment: Conservative- Observation and reassurance
• Microscopic colitis Epidemiology:- Older women > 60 years- Associated with other autoimmune conditions Clinical features:- Watery, nonbloody diarrhea; fecal urgency & incontinence- Abdominal pain, fatigue, weight loss, arthralgias Triggers:- Smoking, medications (e.g., NSAIDs, PPIs, SSRIs, ranitidine) Diagnostics:- Colonoscopic biopsy with lymphocytic infiltration of lamina propria→ Collagenous: thickened subepithelial collagen band→ Lymphocytic: high levels of intraepithelial lymphocytes Management:- Remove possible triggers- Antidiarrheal medications & budesonide
• Postcholecystectomy syndrome Persistent abdominal pain or new symptoms following gallbladder removal Frequency: 10–15% of patients Etiology: - Biliary (e.g., biliary injury, retained cystic duct, sphincter of Oddi dysfunction) - Extrabiliary (e.g., irritable bowel syndrome, pancreatitis)  Clinical features: abdominal pain and upper GI tract (e.g., dyspepsia) or lower GI tract (e.g., diarrhea) symptoms Diagnosis: ultrasound or CT scan followed by ERCP (preferred test if intervention is planned) or MRCP Treatment: treat the underlying cause (e.g., sphincterotomy if there is evidence of sphincter dysfunction)
• Irritable bowel syndrome Rome IV diagnostic criteria:Recurrent abdominal pain/discomfort ≥ 1 day/week for past 3 months & ≥ 2 of the following:- Related to defecation (improves or worsens)- Change in stool frequency- Change in stool form Alarm features:- Older age of onset (≥ 50)- Gastrointestinal bleeding- Nocturnal diarrhea- Worsening pain- Unintended weight loss- Iron deficiency anemia- Elevated CRP- Positive fecal lactoferrin or calprotectin- Family history of early colon cancer or IBD Treatment:- Dietary adjustments: Plenty of fluid, high‑fiber foods- Physical activity- Stress management- Diarrhea → Antidiarrheals (loperamide)- Constipation → Soluble fibers/bulk‑forming laxatives (psyllium), osmotic laxatives (polyethylene glycol)- Cramping/pain: Antispasmodics (dicyclomine, hyoscyamine), TCAs (e.g., amitriptyline, nortriptyline)
• Gilbert's syndrome Epidemiology:- Most common inherited hyperbilirubinemia: The prevalence is 3-7% in the US. - ♂ > ♀- Age of onset: adolescence Etiology: Mutation in the promoter region of UGT1A1 gene → ↓ activity of UDP-glucuronosyltransferase→ decreased conjugation of bilirubin → ↑ indirect bilirubin Clinical features:- Asymptomatic or unspecific symptoms such as fatigue and loss of appetite- Transient jaundice (varying from mild scleral jaundice to general jaundice)- Trigger factors of transient jaundice→ Physical stress (trauma, disease, exhaustion)→ Fasting periods→ Alcohol consumption Diagnosis:- ↑ Indirect bilirubin but < 3 mg/dL (higher levels are possible during episodes of increased bilirubin breakdown) - Normal liver function- No evidence of hemolysis- Detection of mutation using PCR Treatment: no management required
• Peutz-Jeghers syndrome Inheritance: Autosomal dominantNew mutations: 20% of cases Clinical features: 95% of patients have mucocutaneous hyperpigmentation that typically affects the lips (perioral lentigines), buccal mucosa, palms, and soles Enteroscopy: multiple hamartomatous polyps throughout the gastrointestinal tract Prognosis:- The lifetime risk of colorectal cancer is ∼40%. - Increased risk of ovarian, breast, and pancreatic cancer    
• Gardner syndrome FAP + extracolonic bony and/or soft tissue tumors (e.g., osteomas, desmoid tumors, sebaceous cysts, lipomas, fibromas) APC gene mutation with autosomal dominant inheritance The lifetime risk of developing colorectal cancer is 100%.

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