Gastrointestinal & Hepatobiliary Disorders – Comprehensive Review

A collection of high-yield question-and-answer flashcards covering GI reflux, bleeding, hernias, ulcers, peritonitis, inflammatory bowel disease, intestinal obstructions, hepatic disorders, pancreatitis, and related dermatologic manifestations to aid exam preparation.

What primary dysfunction causes Gastroesophageal Reflux Disease (GERD)?

Decreased tone or dysfunction of the lower esophageal sphincter (LES) allowing acid to reflux into the esophagus.

List at least four common lifestyle or dietary GERD triggers.

Alcohol, chocolate, coffee, fatty foods, nicotine; also obesity and pregnancy increase risk.

Which drug classes can precipitate GERD symptoms?

Anticholinergics, beta-agonists, calcium channel blockers.

What is the long-term cellular change in Barrett’s esophagus and why is it worrisome?

Squamous epithelium is replaced by columnar cells, increasing the risk of esophageal adenocarcinoma.

Classic triad of GERD symptoms?

Heartburn, epigastric pain, and regurgitation with a bitter taste.

First-line pharmacologic therapy for frequent GERD?

Proton-pump inhibitors (PPIs) such as omeprazole.

What surgical procedure wraps the gastric fundus around the LES to treat refractory GERD?

Nissen fundoplication.

Define an Upper GI Bleed (UGIB).

Bleeding originating from the esophagus, stomach, or duodenum.

Most common cause of UGIB worldwide?

Peptic ulcer disease, often related to H. pylori infection.

Initial management steps for a hemodynamically unstable UGIB patient?

IV fluids (large-bore), blood transfusion if needed, and urgent endoscopy.

What are esophageal varices and their usual underlying condition?

Dilated submucosal veins in the esophagus due to portal hypertension, typically from cirrhosis.

Name two pharmacologic or procedural treatments to prevent variceal rebleeding.

Non-selective beta-blockers (e.g., propranolol) and endoscopic band ligation.

Differentiate sliding vs paraesophageal hiatal hernia.

Sliding: GE junction and stomach slide upward, causing reflux; Paraesophageal: stomach herniates beside the esophagus, risk of strangulation.

Main bacterial cause of peptic ulcer disease (PUD)?

Helicobacter pylori infection.

How do NSAIDs contribute to PUD formation?

They inhibit prostaglandin synthesis, reducing mucosal protection and increasing acid injury.

Best diagnostic test for suspected PUD needing biopsy?

Upper endoscopy (esophagogastroduodenoscopy).

Standard triple therapy for H. pylori–positive ulcers?

PPI + clarithromycin + amoxicillin (or metronidazole if PCN-allergic).

Classic presentation triad of acute peritonitis?

Severe abdominal pain worsened by movement, abdominal rigidity, and rebound tenderness.

Define Crohn’s disease in terms of location and depth.

A transmural inflammatory disease that can affect any GI segment, commonly terminal ileum and colon, with skip lesions.

Two hallmark endoscopic findings in Crohn’s disease.

Cobblestoning of mucosa and skip lesions.

First-line medication class for mild Crohn’s flares.

5-Aminosalicylic acid (5-ASA) agents such as mesalamine.

Ulcerative colitis always begins in which intestinal segment?

The rectum, then spreads proximally in a continuous fashion.

Which long-standing IBD carries higher colorectal cancer risk and requires surveillance colonoscopy?

Ulcerative colitis, especially >8–10 years duration.

What is toxic megacolon and why is it dangerous?

Massive colonic dilation with systemic toxicity; risk of perforation and sepsis.

Most common cause of small-bowel obstruction (SBO) in adults?

Postsurgical adhesions.

Key radiographic sign of SBO on abdominal X-ray.

Multiple air-fluid levels with dilated loops of small bowel.

First management steps for partial SBO.

NPO, nasogastric decompression, IV fluids, electrolyte correction, and close monitoring.

Classic migratory pain pattern in appendicitis.

Begins as diffuse periumbilical pain then localizes to the right lower quadrant (McBurney’s point).

Two physical signs supporting appendicitis diagnosis.

Psoas sign (pain on hip flexion) and Rovsing’s sign (LLQ pressure causing RLQ pain).

Mainstay treatment for acute uncomplicated appendicitis.

Prompt surgical removal—appendectomy.

Describe irritable bowel syndrome (IBS) in one sentence.

A functional GI disorder characterized by chronic abdominal pain and altered bowel habits without structural cause.

Dietary approach often recommended for IBS symptom control.

Low FODMAP diet to reduce fermentable carbohydrates.

Differentiate diverticulosis and diverticulitis.

Diverticulosis: asymptomatic outpouchings; Diverticulitis: inflammation/infection of diverticula causing pain and fever.

Typical pain location in acute diverticulitis.

Left lower quadrant abdominal pain.

First-line outpatient treatment for mild diverticulitis.

Bowel rest plus 7–10 days of oral broad-spectrum antibiotics (e.g., ciprofloxacin + metronidazole).

Mode of transmission for hepatitis A.

Fecal–oral route via contaminated food or water.

Best prevention strategy for hepatitis A.

Two-dose HAV vaccination series.

Laboratory marker indicating acute hepatitis B infection.

Positive HBsAg with anti-HBc IgM antibodies.

First-line antiviral agents for chronic HBV with high viral load.

Pegylated interferon-α, tenofovir, or entecavir (lamivudine no longer preferred due to resistance).

Define non-alcoholic fatty liver disease (NAFLD).

Hepatic fat accumulation (>5–10% liver weight) unrelated to significant alcohol use, often linked to metabolic syndrome.

Two cornerstone lifestyle interventions for NAFLD management.

Gradual weight loss (1–2 lb/week) and low-carbohydrate/low-fructose diet.

Classic AST/ALT ratio suggesting alcoholic hepatitis.

AST:ALT > 2:1.

Name three major clinical manifestations of cirrhosis-induced portal hypertension.

Esophageal varices, ascites, and splenomegaly.

Why does cirrhosis cause hepatic encephalopathy?

Impaired ammonia detoxification leads to neurotoxic accumulation crossing the blood–brain barrier.

Most common precipitating factors for acute pancreatitis.

Gallstones and chronic heavy alcohol consumption.

Characteristic abdominal pain of acute pancreatitis.

Sudden severe epigastric pain radiating to the back, worsened by eating or lying supine.

Two bedside ecchymosis signs suggesting severe pancreatitis.

Cullen’s sign (periumbilical) and Grey-Turner sign (flanks).

Key initial treatment priorities for acute pancreatitis.

Aggressive IV crystalloid hydration, opioid pain control, and early enteral nutrition.

Pathophysiologic change in chronic pancreatitis.

Repeated inflammation causes fibrosis and calcification leading to exocrine and endocrine insufficiency.

Classic stool change in chronic pancreatitis and its cause.

Steatorrhea due to pancreatic exocrine enzyme deficiency.

Most common histologic type of pancreatic cancer.

Ductal adenocarcinoma (>90%).

Why do pancreatic head tumors often present with painless jaundice?

Obstruction of the common bile duct without pain fibers in the pancreas itself.

Curative surgical procedure for localized pancreatic head cancer.

Pancreaticoduodenectomy (Whipple procedure).

ABCDE mnemonic for malignant melanoma detection.

Asymmetry, Border irregularity, Color variegation, Diameter >6 mm, Evolution of lesion.

Typical appearance of basal cell carcinoma.

Pearly, flesh-colored papule with telangiectasias; rarely metastasizes.

Characteristic rash distribution of pityriasis rosea.

‘Christmas-tree’ pattern on the trunk preceded by a herald patch.

Define acute vs chronic urticaria.

Acute <6 weeks; chronic ≥6 weeks of recurrent pruritic wheals.

Primary transmission route for hepatitis C in developed nations.

Blood exposure, especially intravenous drug use.

Why is there no vaccine for hepatitis C?

HCV has a high mutation rate producing multiple genotypes, preventing stable immunity.

Current standard therapy capable of curing >95 % of HCV infections.

Direct-acting antiviral (DAA) combinations targeting viral protease, NS5A, or polymerase proteins.