Internal Medicine EOR: Gastrointestinal (2026) (Smarty PANCE)

What is Cholangitis?

An ascending bacterial infection of the biliary tree, usually caused by obstruction (most often a stone) leading to stasis and infection.

What is the classic Charcot triad of cholangitis?

RUQ pain, fever, and jaundice.

What is Reynolds pentad and what does it indicate?

Charcot triad (RUQ pain, fever, jaundice) PLUS hypotension and altered mental status; indicates suppurative cholangitis and impending sepsis.

What is the most common organism causing cholangitis?

E. coli (other enterics: Klebsiella, Enterococcus, Enterobacter).

What is the diagnostic and therapeutic procedure of choice for cholangitis?

ERCP for biliary decompression/stone removal; US is first-line imaging to detect duct dilation.

What is the management of acute cholangitis?

IV fluids, broad-spectrum antibiotics, and urgent biliary decompression (ERCP); emergent if Reynolds pentad present.

What is Cholecystitis?

Inflammation of the gallbladder, most commonly caused by cystic duct obstruction by a gallstone (calculous cholecystitis).

What is the classic physical exam finding in acute cholecystitis?

Positive Murphy sign — inspiratory arrest with deep RUQ palpation.

What is the first-line imaging for acute cholecystitis?

RUQ ultrasound (shows gallbladder wall thickening >3 mm, pericholecystic fluid, stones, sonographic Murphy sign).

What is the gold standard imaging if ultrasound is equivocal for cholecystitis?

HIDA scan (cholescintigraphy) — nonvisualization of the gallbladder confirms cystic duct obstruction.

What is acalculous cholecystitis and who gets it?

Cholecystitis without stones, seen in critically ill, TPN-dependent, or post-surgical patients; higher morbidity.

What is the definitive treatment for acute cholecystitis?

Cholecystectomy (preferably laparoscopic), typically within 72 hours; plus IV fluids and antibiotics.

What is Cholelithiasis?

The presence of gallstones in the gallbladder, often asymptomatic but a leading cause of biliary colic.

What are the classic risk factors for cholelithiasis (the 4 F's)?

Female, Fat (obesity), Forty, Fertile (multiparous); also rapid weight loss and estrogen use.

What are the two main types of gallstones?

Cholesterol stones (most common, ~80%) and pigment stones (black = hemolysis; brown = infection).

What is the classic presentation of biliary colic?

Episodic RUQ/epigastric pain after fatty meals, lasting

What is the first-line diagnostic test for cholelithiasis?

RUQ ultrasound.

What is the management of symptomatic cholelithiasis?

Elective laparoscopic cholecystectomy; asymptomatic stones generally do not require treatment.

What is an Esophageal Stricture?

A pathologic narrowing of the esophageal lumen, most commonly from chronic acid reflux (peptic stricture).

What is the hallmark symptom of an esophageal stricture?

Progressive dysphagia to solids (typically without weight loss in benign strictures).

What are common causes of esophageal strictures?

Chronic GERD (most common), caustic ingestion, radiation, pill esophagitis, and eosinophilic esophagitis.

How are esophageal strictures diagnosed?

Barium swallow and/or upper endoscopy (EGD); EGD allows biopsy to exclude malignancy.

What is the treatment for a benign esophageal stricture?

Endoscopic dilation plus PPI therapy to address underlying reflux.

What are Esophageal Varices?

Dilated submucosal veins in the distal esophagus that develop as a consequence of portal hypertension, usually from cirrhosis.

What is the classic presentation of bleeding esophageal varices?

Painless, large-volume hematemesis, often with signs of chronic liver disease; a medical emergency.

What is the acute medical management of bleeding esophageal varices?

IV octreotide (splanchnic vasoconstrictor), IV antibiotics (ceftriaxone) for prophylaxis, and urgent endoscopic band ligation.

What is used for primary prophylaxis against variceal bleeding?

Nonselective beta-blockers (propranolol, nadolol) and/or endoscopic variceal band ligation.

What is the rescue procedure for refractory variceal bleeding?

TIPS (transjugular intrahepatic portosystemic shunt); balloon tamponade as a temporizing measure.

What is Esophagitis?

Inflammation of the esophageal mucosa, which may be reflux-related, infectious, pill-induced, or eosinophilic.

What are the major infectious causes of esophagitis and their hallmark findings?

Candida (white plaques, seen in immunocompromised/HIV), HSV (small punched-out ulcers), CMV (large linear ulcers).

What is eosinophilic esophagitis and who is affected?

An allergic/immune-mediated esophagitis in atopic patients; presents with dysphagia and food impaction; EGD shows stacked circular rings ("trachealization").

What is the diagnostic criterion for eosinophilic esophagitis?

Esophageal biopsy showing ≥15 eosinophils per high-power field.

What causes pill-induced esophagitis and how is it prevented?

Common culprits include doxycycline, bisphosphonates, NSAIDs, and potassium chloride; prevent by taking pills with plenty of water and remaining upright.

What is the treatment for eosinophilic esophagitis?

Dietary elimination, topical/swallowed corticosteroids (fluticasone or budesonide), and PPIs.

What is Gastroesophageal Reflux Disease (GERD)?

A condition in which retrograde flow of gastric contents into the esophagus causes symptoms or mucosal injury, often due to a dysfunctional lower esophageal sphincter.

What are the classic symptoms of GERD?

Heartburn (pyrosis), regurgitation, often worse after meals and when supine.

What are the alarm ("red flag") symptoms in GERD that warrant endoscopy?

Dysphagia, odynophagia, weight loss, GI bleeding/anemia, persistent vomiting, or age >50–60 with new symptoms.

What is the most serious complication of chronic GERD?

Barrett esophagus (metaplasia of squamous to columnar epithelium), a premalignant lesion for esophageal adenocarcinoma.

What is the first-line pharmacologic treatment for GERD?

Proton pump inhibitors (PPIs), along with lifestyle modifications (weight loss, head-of-bed elevation, avoiding late meals).

What is the surgical option for refractory GERD?

Nissen fundoplication.

What is a Mallory-Weiss Tear?

A non-penetrating mucosal laceration at the gastroesophageal junction, classically caused by forceful retching or vomiting.

What is the classic presentation of a Mallory-Weiss tear?

Hematemesis following an episode of repeated vomiting or retching, often in alcoholics or bulimics.

How is a Mallory-Weiss tear diagnosed?

Upper endoscopy (EGD).

What is the typical clinical course and treatment of a Mallory-Weiss tear?

Most bleeding stops spontaneously; supportive care with PPIs; endoscopic therapy (clipping, epinephrine) if bleeding persists.

How does a Mallory-Weiss tear differ from Boerhaave syndrome?

Mallory-Weiss is a partial-thickness mucosal tear (bleeding); Boerhaave is a full-thickness transmural rupture (mediastinitis).

What is Achalasia?

An esophageal motility disorder characterized by failure of LES relaxation and loss of peristalsis due to degeneration of the myenteric (Auerbach) plexus.

What is the classic presentation of achalasia?

Progressive dysphagia to BOTH solids and liquids, with regurgitation of undigested food.

What is the classic barium swallow finding in achalasia?

"Bird's beak" tapering of the distal esophagus with proximal dilation.

What is the gold standard diagnostic test for achalasia?

Esophageal manometry (shows incomplete LES relaxation and absent peristalsis).

What malignancy must be excluded in suspected achalasia (pseudoachalasia)?

Esophageal or gastric cancer at the GE junction; EGD is performed to rule this out.

What are the treatment options for achalasia?

Pneumatic dilation, surgical (Heller) myotomy or POEM, and botulinum toxin injection for poor surgical candidates.

What is Diffuse Esophageal Spasm?

An esophageal motility disorder featuring uncoordinated, simultaneous contractions of the esophageal body with normal LES function.

What is the classic presentation of diffuse esophageal spasm?

Intermittent chest pain (can mimic cardiac pain) and dysphagia, sometimes triggered by hot or cold liquids.

What is the classic barium swallow finding in diffuse esophageal spasm?

"Corkscrew" or "rosary bead" esophagus.

How is diffuse esophageal spasm confirmed?

Esophageal manometry showing intermittent, simultaneous, non-peristaltic contractions.

What is the treatment for diffuse esophageal spasm?

Calcium channel blockers (diltiazem), nitrates, and tricyclic antidepressants; treat coexisting reflux.

What is a Zenker Diverticulum?

A false (pulsion) diverticulum that herniates through Killian triangle in the posterior hypopharynx, due to upper esophageal sphincter dysfunction.

What is the classic presentation of a Zenker diverticulum?

Dysphagia, regurgitation of undigested food, halitosis, and a gurgling sensation in the neck.

What is the diagnostic test of choice for Zenker diverticulum?

Barium swallow (esophagram); nasogastric tube and blind endoscopy are avoided due to perforation risk.

What is the treatment for a symptomatic Zenker diverticulum?

Surgical or endoscopic cricopharyngeal myotomy with diverticulectomy.

What is Boerhaave Syndrome?

A spontaneous full-thickness (transmural) rupture of the esophagus, usually caused by forceful vomiting against a closed glottis.

What is the Mackler triad of Boerhaave syndrome?

Vomiting, severe chest pain, and subcutaneous emphysema.

What is Hamman sign/crunch?

A crunching sound synchronous with the heartbeat heard on auscultation, due to mediastinal emphysema in esophageal rupture.

What is the diagnostic study of choice for Boerhaave syndrome?

Contrast esophagram with water-soluble contrast (Gastrografin), or CT; CXR may show pneumomediastinum/pleural effusion.

What is the treatment for Boerhaave syndrome?

Emergent surgical repair, NPO, broad-spectrum antibiotics, and IV fluids; it is a surgical emergency with high mortality.

What is Gastritis?

Inflammation of the gastric mucosa, which may be erosive or non-erosive and acute or chronic.

What are the most common causes of gastritis?

H. pylori infection (most common), NSAIDs, alcohol, and stress (critically ill patients).

What are the two types of chronic gastritis?

Type A (autoimmune, fundus/body, associated with pernicious anemia) and Type B (H. pylori, antrum, most common).

How is H. pylori gastritis diagnosed?

Urea breath test, stool antigen test, or endoscopic biopsy; serology is less useful for confirming active infection.

What is the treatment for H. pylori gastritis?

Quadruple therapy (PPI + bismuth + tetracycline + metronidazole) or triple therapy (PPI + clarithromycin + amoxicillin).

What complication is autoimmune (Type A) gastritis associated with?

Pernicious anemia (B12 deficiency) and increased risk of gastric adenocarcinoma.

What is Peptic Ulcer Disease (PUD)?

A defect in the gastric or duodenal mucosa extending through the muscularis mucosa, most commonly caused by H. pylori or NSAID use.

How do duodenal and gastric ulcers differ in their relationship to food?

Duodenal ulcer pain improves with food (and recurs 2–3 hrs later); gastric ulcer pain worsens with food, often causing weight loss.

Which type of peptic ulcer is more concerning for malignancy?

Gastric ulcers (require biopsy to exclude cancer); duodenal ulcers are almost always benign.

What are the two main causes of PUD?

H. pylori infection and NSAID use.

What is the most common complication of PUD and how does perforation present?

Bleeding is most common; perforation presents with sudden severe pain, rigid abdomen, and free air under the diaphragm on upright CXR.

What is Zollinger-Ellison syndrome?

A gastrin-secreting tumor (gastrinoma) causing refractory, multiple, or distal duodenal ulcers; diagnosed with elevated fasting gastrin.

What is the treatment for PUD?

PPIs, H. pylori eradication if positive, and stopping NSAIDs.

What is Gastrointestinal (GI) Bleeding?

Hemorrhage anywhere from the mouth to the anus, classified as upper (proximal to ligament of Treitz) or lower GI bleeding.

How do you distinguish upper from lower GI bleeding by presentation?

Upper GI bleed: hematemesis, coffee-ground emesis, melena; Lower GI bleed: hematochezia (bright red blood per rectum).

What is the most common cause of upper GI bleeding?

Peptic ulcer disease.

What is the most common cause of lower GI bleeding in adults?

Diverticulosis (also angiodysplasia and hemorrhoids); in adults overall, consider malignancy.

What lab finding suggests an upper GI source in GI bleeding?

An elevated BUN:creatinine ratio (>20–30:1) due to absorption of digested blood.

What is the initial management of significant GI bleeding?

Two large-bore IVs, fluid/blood resuscitation, type and crossmatch, PPI for upper bleeds, and urgent endoscopy.

What is Cirrhosis?

Irreversible hepatic fibrosis with regenerative nodules that distort liver architecture, representing the end stage of chronic liver disease.

What are the most common causes of cirrhosis?

Chronic alcohol use, chronic hepatitis C and B, and MASLD/MASH (fatty liver disease).

What are the major complications of cirrhosis?

Portal hypertension, varices, ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, hepatorenal syndrome, and hepatocellular carcinoma.

What physical exam findings suggest cirrhosis?

Jaundice, spider angiomata, palmar erythema, gynecomastia, caput medusae, ascites, and asterixis.

What scoring systems are used to assess cirrhosis severity?

Child-Pugh score and MELD score (the latter for transplant prioritization).

What is the diagnostic test for spontaneous bacterial peritonitis (SBP)?

Paracentesis with ascitic fluid PMN count ≥250 cells/mm³; treat with cefotaxime.

What is the treatment of hepatic encephalopathy?

Lactulose (lowers ammonia) and rifaximin.

What is Hepatitis?

Inflammation of the liver, which may be caused by viruses, alcohol, drugs/toxins, autoimmune disease, or metabolic conditions.

How are hepatitis A, B, C, D, and E transmitted?

A and E: fecal-oral; B, C, D: blood/body fluids (parenteral, sexual, perinatal); D requires coexisting B.

Which hepatitis viruses cause chronic infection?

Hepatitis B, C, and D; A and E are typically acute and self-limited.

What does a positive HBsAg indicate, and what does anti-HBs indicate?

HBsAg = active infection (acute or chronic); anti-HBs = immunity (recovery or vaccination).

What does isolated anti-HBc IgM indicate in Hepatitis B?

Acute or recent infection, including the "window period."

What is the treatment approach for hepatitis C?

Direct-acting antivirals (DAAs), which are curative in most patients.

Which hepatitis is most dangerous in pregnancy?

Hepatitis E (high mortality in pregnant women).

What is MASLD/MASH (Fatty Liver Disease)?

Metabolic dysfunction-associated steatotic liver disease (MASLD) is hepatic fat accumulation without significant alcohol use; MASH is the inflammatory form with hepatocyte injury that can progress to fibrosis.

What are the major risk factors for MASLD/MASH?

Obesity, type 2 diabetes, metabolic syndrome, dyslipidemia, and insulin resistance.