GI Disorders & Assessment: GERD, PUD, IBS, IBD, Appendicitis

Lower esophageal sphincter (LES) function?

Prevents gastric reflux; relaxes during swallowing.

Achalasia?

Impaired esophageal motility and failure of LES relaxation, causing dysphagia.

GERD: mechanism and presentation?

Incompetent LES → acid reflux; heartburn, regurgitation, worse after meals/lying down.

GERD risk factors?

Obesity, smoking, hiatal hernia, and dietary triggers.

Sliding vs. paraesophageal hiatal hernia?

Sliding: GE junction moves above diaphragm; paraesophageal: stomach protrudes beside esophagus.

Barrett esophagus?

Chronic reflux causes squamous-to-columnar metaplasia; increases adenocarcinoma risk.

GERD diagnosis and treatment?

Symptoms, PPI trial, endoscopy/pH monitoring; lifestyle changes and acid suppression.

Parietal vs. chief vs. G cells?

Parietal: HCl/intrinsic factor; chief: pepsinogen/lipase; G cells: gastrin.

Gastric mucous cells?

Produce protective mucus against acid and pepsin.

Intrinsic factor deficiency?

Decreased B12 absorption → pernicious anemia and possible neurologic dysfunction.

Small intestine: primary functions?

Duodenum: digestion; jejunum: nutrient absorption; ileum: bile salt/B12 absorption.

Intestinal villi and microvilli?

Increase absorptive surface area.

Paneth vs. goblet vs. enteroendocrine cells?

Paneth: antimicrobial enzymes; goblet: mucus; enteroendocrine: digestive hormones.

Colon function?

Absorbs water/electrolytes and forms stool.

Slow vs. rapid colonic transit?

Slow → constipation; rapid → diarrhea.

Prolonged vomiting/diarrhea complications?

Dehydration, electrolyte loss, and acid-base disturbances.

Hematemesis vs. melena vs. hematochezia?

Vomiting blood vs. black tarry stool vs. red/maroon stool.

Epigastric pain: major differentials?

GERD, PUD, pancreatitis.

RUQ vs. RLQ pain?

RUQ: gallbladder/liver disease; RLQ: appendicitis or Crohn disease.

LUQ vs. LLQ pain?

LUQ: gastric/pancreatic/splenic disease; LLQ: diverticulitis.

CBC vs. CMP in GI assessment?

CBC: anemia/infection; CMP: electrolytes, metabolism, organ function.

Endoscopy with biopsy?

Visualizes mucosa and obtains tissue for diagnosis.

Age-related GI changes?

Reduced motility, digestive secretions, B12 absorption, and hepatic drug metabolism.

Peptic ulcer disease (PUD)?

Deep gastric/duodenal mucosal injury from acid and pepsin.

Major PUD causes?

H. pylori and NSAID/aspirin use.

PUD presentation?

Burning epigastric pain; may have nausea, bleeding, or anemia.

PUD complications?

Bleeding, perforation, obstruction, and penetration.

Perforated ulcer presentation?

Sudden severe abdominal pain, rigidity, guarding, and peritonitis.

PUD diagnosis and management?

H. pylori testing/endoscopy; PPIs, antibiotics if H. pylori, avoid NSAIDs.

IBS: mechanism and presentation?

Functional gut-brain disorder causing abdominal pain and altered bowel habits.

IBS vs. IBD?

IBS lacks destructive inflammation; IBD causes chronic inflammatory tissue injury.

IBS alarm findings?

GI bleeding, unexplained weight loss, or concerning history.

IBS management?

Dietary modification, stress reduction, fiber, and symptom-directed medication.

IBD: underlying mechanism?

Chronic immune-mediated intestinal inflammation.

Crohn vs. UC: distribution?

Crohn: mouth to anus, skip lesions; UC: continuous colon inflammation starting at rectum.

Crohn vs. UC: inflammation depth?

Crohn: transmural; UC: mucosa/submucosa.

Crohn vs. UC: characteristic findings?

Crohn: cobblestoning/granulomas; UC: ulceration/pseudopolyps.

Crohn hallmark complications?

Fistulas, strictures, bowel obstruction, malabsorption.

UC hallmark complications?

Bloody diarrhea, toxic megacolon, colorectal cancer risk.

IBD extraintestinal manifestations?

Arthritis and inflammatory skin conditions.

IBD diagnosis?

Endoscopy with biopsy to assess distribution and inflammatory changes.

IBD management?

Nutrition, corticosteroids for flares, 5-ASA/immunomodulators, surgery when indicated.

Toxic megacolon?

Severe acute colonic dilation with systemic toxicity; risk of perforation/sepsis.

Appendicitis mechanism?

Appendiceal obstruction → pressure → ischemia/infection → possible rupture.

Classic appendicitis presentation?

Periumbilical pain migrating to RLQ, anorexia, nausea, fever.

McBurney point tenderness?

Localized RLQ tenderness over appendix.

Rovsing sign?

RLQ pain elicited by LLQ palpation.

Psoas sign?

RLQ pain with passive right hip extension.

Obturator sign?

RLQ pain with right hip flexion/internal rotation.

Rebound tenderness?

Pain upon release of abdominal pressure; suggests peritoneal irritation.

Appendicitis diagnosis and management?

Exam, inflammatory markers, imaging; appendectomy/antibiotics as indicated.

Peritonitis?

Peritoneal inflammation causing severe pain, rigidity, guarding; often from perforation.

Gastritis?

Superficial gastric mucosal inflammation, commonly H. pylori or autoimmune.

Diverticulosis vs. diverticulitis?

Diverticulosis: colonic pouches; diverticulitis: inflamed pouches with LLQ pain.

Diverticulitis complications?

Abscess, perforation, obstruction, or bleeding.

Celiac disease?

Immune reaction to gluten damages small intestine → malabsorption.

Hemorrhoids?

Dilated perianal veins causing bleeding, irritation, or pain.

Abdominal hernia complications?

Incarceration or strangulation with compromised bowel blood supply.

Hepatic lobule organization?

Hepatocytes around central vein; sinusoids carry blood toward center.

Portal triad components?

Portal vein branch, hepatic artery branch, bile duct.

Blood vs. bile flow in liver?

Blood → central vein; bile → portal triads.

Hepatocytes: major functions?

Metabolism, detoxification, albumin/clotting factor synthesis, bile production.

Kupffer vs. stellate cells?

Kupffer: liver macrophages; stellate: vitamin A storage/fibrosis.

Liver carbohydrate metabolism?

Glycogenesis, glycogenolysis, gluconeogenesis regulate glucose.

Liver protein synthesis?

Produces albumin and most clotting factors.

Liver ammonia metabolism?

Converts toxic ammonia to urea for renal excretion.

Bile function?

Emulsifies fats and facilitates vitamins A, D, E, K absorption.

Bile components?

Bile salts, bilirubin, cholesterol, phospholipids, bicarbonate/water.

Unconjugated vs. conjugated bilirubin?

Indirect: albumin-bound, pre-liver processing; direct: water-soluble, liver-conjugated.

Bilirubin pathway?

Heme → indirect bilirubin → liver conjugation → bile → intestine.

Stercobilin vs. urobilin?

Stercobilin colors stool; urobilin colors urine.

Enterohepatic circulation?

Terminal ileum reabsorbs bile salts, returning them to liver.

Gallbladder function?

Stores/concentrates bile and releases it during digestion.

CCK vs. secretin?

CCK: gallbladder contraction and pancreatic enzymes; secretin: pancreatic bicarbonate.

Pancreatic acinar vs. ductal cells?

Acinar: digestive enzymes; ductal: bicarbonate-rich fluid.

Pancreatic alpha vs. beta vs. delta cells?

Alpha: glucagon; beta: insulin; delta: somatostatin.

Pancreatic digestive enzymes?

Amylase: carbs; lipase: fats; proteases: proteins; nucleases: nucleic acids.

Why are pancreatic proteases initially inactive?

Prevents pancreatic autodigestion.

Bile duct pathway?

Hepatic ducts → common hepatic duct → common bile duct → duodenum.

Cystic duct function?

Connects gallbladder with common hepatic duct.

Sphincter of Oddi?

Regulates bile and pancreatic juice entry into duodenum.

ALT vs. AST?

Both indicate hepatocyte injury; ALT more liver-specific.

ALP vs. GGT?

ALP suggests cholestasis or bone disease; GGT supports hepatobiliary source.

Albumin vs. PT/INR in liver disease?

Albumin and clotting factor synthesis reflect hepatic function; prolonged INR suggests impairment.

Indirect bilirubin elevation?

Hemolysis or impaired conjugation.

Direct bilirubin elevation?

Impaired bile excretion or obstruction.

Jaundice?

Yellow skin/sclera from bilirubin accumulation.

Prehepatic vs. hepatic vs. posthepatic jaundice?

Hemolysis vs. hepatocyte dysfunction vs. biliary obstruction.

Obstructive jaundice presentation?

Dark urine, pale stools, pruritus, elevated direct bilirubin.

Spider angiomas in liver disease?

Superficial dilated vessels associated with impaired estrogen metabolism.

Cirrhosis mechanism?

Chronic liver injury → stellate activation → fibrosis/regenerative nodules.

Portal hypertension?

Elevated portal pressure from increased vascular resistance, commonly cirrhosis.

Portal hypertension complications?

Ascites, varices, splenomegaly, GI bleeding.

Ascites mechanism?

Portal hypertension + sodium/water retention; low albumin contributes.

Hepatic encephalopathy mechanism?

Ammonia accumulation/portosystemic shunting impairs brain function.

Hepatic encephalopathy presentation?

Confusion, altered sleep, asterixis, possible coma.

Hepatic encephalopathy treatment?

Lactulose, rifaximin, correct precipitating causes.

Liver failure complications?

Bleeding, hypoglycemia, toxin buildup, edema/ascites, fat malabsorption.

Ascites management?

Sodium restriction, diuretics, paracentesis when indicated.

Variceal bleeding prevention?

Nonselective beta-blockers or endoscopic band ligation.