Family Medicine EOR (Gastrointestinal): New for 2026 Topic List (Smarty PANCE)

What is Cholecystitis/Cholelithiasis?

Cholelithiasis is the presence of gallstones in the gallbladder; cholecystitis is inflammation of the gallbladder, most commonly due to obstruction of the cystic duct by a gallstone.

What is the classic presentation of acute cholecystitis?

RUQ pain (often postprandial, radiating to right shoulder/scapula), fever, nausea/vomiting, and a positive Murphy sign (inspiratory arrest with RUQ palpation).

What are the 5 F's risk factors for cholelithiasis?

Female, Fat (obesity), Forty, Fertile (multiparous), Family history.

What is the first-line imaging study for suspected cholecystitis?

RUQ ultrasound — findings include gallbladder wall thickening (>3mm), pericholecystic fluid, gallstones, and sonographic Murphy sign.

What is the next test if ultrasound is non-diagnostic for cholecystitis?

HIDA scan (cholescintigraphy) — non-visualization of the gallbladder at 4 hours confirms cystic duct obstruction.

What is Charcot's triad and what does it indicate?

RUQ pain, fever, and jaundice — indicates ascending cholangitis (infection of the biliary tree).

What is Reynolds pentad?

Charcot's triad (RUQ pain, fever, jaundice) PLUS hypotension and altered mental status — indicates suppurative cholangitis requiring emergent biliary decompression.

What is the definitive treatment for acute cholecystitis?

Laparoscopic cholecystectomy within 72 hours, plus IV antibiotics (ceftriaxone + metronidazole) and supportive care.

What is porcelain gallbladder and why is it concerning?

Calcification of the gallbladder wall from chronic inflammation; increases risk of gallbladder carcinoma and warrants prophylactic cholecystectomy.

What is Neonatal Hyperbilirubinemia?

Elevated total serum bilirubin in a newborn, presenting as jaundice; can be physiologic (benign) or pathologic (requiring evaluation and treatment).

What distinguishes physiologic from pathologic neonatal jaundice?

Physiologic: appears after 24 hours, peaks at days 3-5, resolves by 1-2 weeks; Pathologic: jaundice within first 24 hours, bilirubin rise >5 mg/dL/day, or persists >2 weeks.

What is the most feared complication of severe neonatal hyperbilirubinemia?

Kernicterus — bilirubin-induced neurologic dysfunction with deposition in basal ganglia, causing cerebral palsy, hearing loss, and developmental delay.

What is the difference between breastfeeding jaundice and breast milk jaundice?

Breastfeeding jaundice: occurs in first week from inadequate intake/dehydration; Breast milk jaundice: occurs after first week from substances in breast milk inhibiting bilirubin conjugation, can persist weeks.

What is the first-line treatment for significant neonatal hyperbilirubinemia?

Phototherapy — converts unconjugated bilirubin to water-soluble isomers for excretion; thresholds based on Bhutani nomogram (age in hours + risk factors).

What is the treatment for severe neonatal hyperbilirubinemia unresponsive to phototherapy?

Exchange transfusion — indicated when bilirubin approaches neurotoxic levels or signs of acute bilirubin encephalopathy appear.

What is Esophagitis?

Inflammation of the esophageal mucosa, with common causes including reflux (most common), infections, pills, eosinophils, and radiation.

What organisms cause infectious esophagitis and in what populations?

Candida (white plaques, most common in HIV/immunocompromised), HSV (small vesicles/ulcers), CMV (large linear ulcers, AIDS with CD4 <50).

What characterizes eosinophilic esophagitis (EoE)?

Dysphagia and food impaction in young adults with atopic history; endoscopy shows ringed/trachealized esophagus with linear furrows; biopsy ≥15 eosinophils/HPF.

What is the treatment for eosinophilic esophagitis?

PPI trial first, then swallowed topical corticosteroids (fluticasone or budesonide), dietary elimination (6-food elimination diet), and dilation for strictures.

What medications most commonly cause pill esophagitis?

Bisphosphonates, doxycycline/tetracycline, potassium chloride, NSAIDs, and iron — prevent by taking with full glass of water, remaining upright 30 minutes.

What is GERD?

Gastroesophageal reflux disease — chronic symptoms or mucosal damage caused by abnormal reflux of stomach contents into the esophagus due to LES dysfunction.

What are the classic symptoms of GERD?

Heartburn (pyrosis), regurgitation, and dysphagia; atypical symptoms include chronic cough, hoarseness, asthma, and dental erosions.

What are the alarm symptoms in GERD requiring endoscopy?

Dysphagia, odynophagia, weight loss, GI bleeding, anemia, persistent vomiting, age >60 with new symptoms, or family history of GI malignancy.

What is the first-line treatment for GERD?

Lifestyle modifications (weight loss, head of bed elevation, avoiding triggers/late meals) plus PPI therapy (omeprazole, pantoprazole) for 8 weeks.

What is Barrett's esophagus and why is it concerning?

Metaplasia of distal esophageal squamous epithelium to columnar (intestinal) epithelium from chronic GERD; precursor to esophageal adenocarcinoma — requires surveillance endoscopy.

What is the surgical treatment for refractory GERD?

Nissen fundoplication — wrapping gastric fundus around distal esophagus to reinforce LES.

What are Food Allergies and Food Sensitivities?

Food allergies are IgE-mediated immune reactions causing systemic symptoms; food sensitivities/intolerances are non-immune reactions (enzymatic, pharmacologic) with primarily GI symptoms.

What are the most common food allergens (Big 9)?

Milk, eggs, peanuts, tree nuts, soy, wheat, fish, shellfish, sesame.

What is the gold standard test for food allergy diagnosis?

Oral food challenge (double-blind, placebo-controlled); supported by skin prick testing and specific IgE testing.

What is the immediate treatment for anaphylaxis from food allergy?

Intramuscular epinephrine (0.3 mg adult, 0.15 mg child) into anterolateral thigh; adjuncts include antihistamines, corticosteroids, and beta-agonists.

What characterizes lactose intolerance?

Lactase deficiency causing bloating, diarrhea, flatulence after dairy; diagnosed by hydrogen breath test; treated with lactase supplementation or lactose avoidance.

What is Foodborne Illness/Acute Infectious Gastroenteritis?

Inflammation of the GI tract from ingestion of contaminated food/water with pathogens or toxins, causing diarrhea, vomiting, and abdominal pain.

What pathogen causes rapid-onset (1-6 hours) vomiting after food ingestion?

Staphylococcus aureus or Bacillus cereus (preformed toxins); classic sources include mayonnaise, dairy, and reheated rice.

What is the most common cause of traveler's diarrhea?

Enterotoxigenic E. coli (ETEC) — treat with fluid replacement and azithromycin or ciprofloxacin if severe.

What pathogen is associated with raw poultry and triggers Guillain-Barré syndrome?

Campylobacter jejuni — most common bacterial gastroenteritis in the US.

What pathogen causes bloody diarrhea from undercooked beef and can lead to HUS?

E. coli O157:H7 (EHEC) — Shiga toxin-producing; avoid antibiotics as they increase risk of hemolytic uremic syndrome.

What is Gastritis?

Inflammation of the gastric mucosa, most commonly caused by H. pylori, NSAIDs, alcohol, or stress (critical illness).

What is the most common cause of chronic gastritis worldwide?

Helicobacter pylori infection (gram-negative urease-producing spiral bacterium).

What is the diagnostic test of choice for H. pylori in patients not undergoing endoscopy?

Urea breath test or stool antigen test (both highly sensitive/specific); avoid serology as it doesn't distinguish active from past infection.

What is the first-line treatment for H. pylori?

Quadruple therapy: PPI + bismuth + tetracycline + metronidazole for 10-14 days (preferred); or PPI + clarithromycin + amoxicillin if local resistance <15%.

What is Gastroparesis?

Delayed gastric emptying without mechanical obstruction, presenting with nausea, vomiting, early satiety, bloating, and postprandial fullness.

What is the most common cause of gastroparesis?

Diabetes mellitus (autonomic neuropathy); other causes include idiopathic, post-surgical (vagus nerve injury), and medications (opioids, GLP-1 agonists).

What is the gold standard test for diagnosing gastroparesis?

Gastric emptying scintigraphy (4-hour solid meal study) showing >10% retention at 4 hours or >60% at 2 hours.

What is the first-line treatment for gastroparesis?

Dietary modification (small frequent low-fat low-fiber meals) plus metoclopramide (limited to 12 weeks due to tardive dyskinesia risk) or erythromycin.

What is Peptic Ulcer Disease?

Mucosal break ≥5mm in the stomach (gastric ulcer) or duodenum (duodenal ulcer), most commonly caused by H. pylori or NSAIDs.

How do gastric and duodenal ulcers differ in pain pattern?

Duodenal ulcer: pain RELIEVED by food, occurs 2-3 hours after meals or nocturnally; Gastric ulcer: pain WORSENED by food, weight loss common.

What are the two most common causes of PUD?

H. pylori infection (most common worldwide) and NSAID use (most common in US); other causes include Zollinger-Ellison syndrome and stress ulcers.

What is the most serious complication of PUD?

Perforation — sudden severe abdominal pain with rigid abdomen, free air under diaphragm on upright CXR; surgical emergency.

Why must all gastric ulcers be biopsied?

To rule out gastric malignancy (adenocarcinoma); duodenal ulcers do not require biopsy as they are rarely malignant.

What is Zollinger-Ellison syndrome?

Gastrinoma (gastrin-secreting tumor) causing severe recurrent PUD, multiple ulcers in unusual locations, and diarrhea; associated with MEN1; diagnose with fasting gastrin >1000.

What is GI Bleeding?

Hemorrhage from anywhere along the GI tract; classified as upper (proximal to ligament of Treitz) or lower (distal to ligament of Treitz).

What distinguishes upper from lower GI bleeding clinically?

Upper: hematemesis, coffee-ground emesis, melena (black tarry stools), elevated BUN/Cr ratio >30; Lower: hematochezia (bright red blood per rectum), typically normal BUN.

What are the most common causes of upper GI bleeding?

Peptic ulcer disease (most common), esophageal/gastric varices, Mallory-Weiss tear, esophagitis, gastritis, and Dieulafoy lesion.

What are the most common causes of lower GI bleeding?

Diverticulosis (most common), angiodysplasia, hemorrhoids, colorectal cancer, IBD, and ischemic colitis.

What is the initial management of acute GI bleeding?

ABCs, 2 large-bore IVs, fluid resuscitation, type and crossmatch, transfuse if Hgb <7 (or <8 if cardiac disease), IV PPI for upper GI bleed, urgent endoscopy.

What is the treatment for variceal bleeding?

IV octreotide (vasoconstrictor), prophylactic antibiotics (ceftriaxone), urgent endoscopic band ligation; TIPS if refractory.

What is Cirrhosis?

End-stage fibrosis of the liver with regenerative nodules causing portal hypertension and hepatic dysfunction; irreversible architectural distortion.

What are the most common causes of cirrhosis in the US?

Alcohol-related liver disease, chronic hepatitis C, MASH/MAFLD; less common: hemochromatosis, Wilson disease, autoimmune hepatitis, PBC.

What are the major complications of cirrhosis?

Portal hypertension (varices, ascites, splenomegaly), hepatic encephalopathy, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome, hepatocellular carcinoma.

What scoring systems are used in cirrhosis?

Child-Pugh score (A/B/C based on bilirubin, albumin, INR, ascites, encephalopathy); MELD score (bilirubin, INR, creatinine, sodium) for transplant prioritization.

What is the diagnosis and treatment of spontaneous bacterial peritonitis (SBP)?

Ascitic fluid PMN ≥250/mm³; treat with IV cefotaxime or ceftriaxone; give albumin to prevent hepatorenal syndrome; lifelong prophylaxis with norfloxacin/ciprofloxacin after episode.

What is hepatic encephalopathy and how is it treated?

Neuropsychiatric dysfunction (asterixis, confusion, coma) from ammonia accumulation; treat with lactulose (titrate to 3 stools/day) and rifaximin.

What is the treatment for ascites in cirrhosis?

Sodium restriction (<2g/day), spironolactone + furosemide (100:40 ratio), large-volume paracentesis with albumin replacement for tense ascites.

What is Hepatitis?

Inflammation of the liver, most commonly viral (A-E), but also caused by alcohol, drugs (acetaminophen), autoimmune disease, and metabolic conditions.

How are hepatitis A, B, and C transmitted?

Hep A: fecal-oral (contaminated food/water); Hep B: blood, sexual, perinatal; Hep C: blood (IV drug use most common).

What serology indicates acute hepatitis B infection?

HBsAg positive, anti-HBc IgM positive, HBeAg positive (high infectivity); HBsAg persists >6 months indicates chronic infection.

What serology indicates immunity to hepatitis B?

Anti-HBs positive alone = vaccination immunity; Anti-HBs + Anti-HBc = recovered from natural infection.

What is the treatment for chronic hepatitis C?

Direct-acting antivirals (DAAs) such as sofosbuvir/velpatasvir or glecaprevir/pibrentasvir for 8-12 weeks; cure rates >95%.

Which hepatitis virus is most dangerous in pregnancy?

Hepatitis E — high mortality (up to 25%) from fulminant hepatic failure in pregnant women.

What is MASH/MAFLD?

Metabolic dysfunction-Associated Steatohepatitis (formerly NASH) / Metabolic dysfunction-Associated Fatty Liver Disease (formerly NAFLD) — hepatic steatosis with inflammation and fibrosis in absence of significant alcohol use.

What are the risk factors for MASH/MAFLD?

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

How is MASH/MAFLD diagnosed?

Hepatic steatosis on imaging (ultrasound, MRI) or biopsy with metabolic risk factors; liver biopsy distinguishes simple steatosis from steatohepatitis (inflammation + ballooning).

What is the cornerstone of MASH/MAFLD treatment?

Weight loss (7-10% body weight), management of metabolic syndrome (diabetes, lipids, BP), exercise; resmetirom (Rezdiffra) FDA-approved for MASH with fibrosis.

What is Jaundice?

Yellow discoloration of skin, sclera, and mucous membranes from bilirubin deposition when serum bilirubin exceeds 2.5-3 mg/dL.

What distinguishes pre-hepatic, hepatic, and post-hepatic jaundice?

Pre-hepatic: unconjugated bilirubin elevated (hemolysis); Hepatic: both elevated with AST/ALT rise (hepatitis); Post-hepatic: conjugated elevated with ALP/GGT rise (obstruction).

What is Courvoisier's sign?

Palpable, non-tender gallbladder with painless jaundice — suggests malignant obstruction (pancreatic head cancer or cholangiocarcinoma) rather than gallstones.

What is Gilbert syndrome?

Benign inherited UGT1A1 deficiency causing mild unconjugated hyperbilirubinemia with stress, fasting, or illness; no treatment needed.

What are Ingestion of Harmful Substances/Toxidromes?

Recognizable clinical syndromes from toxic exposures that help identify the offending agent and guide treatment.

What characterizes anticholinergic toxidrome?

"Hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter" — hyperthermia, dry skin, flushing, mydriasis, delirium, urinary retention, tachycardia.

What characterizes cholinergic toxidrome?

SLUDGE/BBB: Salivation, Lacrimation, Urination, Defecation, GI cramping, Emesis + Bradycardia, Bronchorrhea, Bronchospasm; caused by organophosphates — treat with atropine + pralidoxime.

What characterizes sympathomimetic toxidrome?

Hypertension, tachycardia, hyperthermia, mydriasis, DIAPHORESIS (distinguishes from anticholinergic), agitation; caused by cocaine, amphetamines, MDMA.

What characterizes opioid toxidrome?

Triad: CNS depression, respiratory depression, miosis (pinpoint pupils); treat with naloxone.

What is the treatment for acetaminophen overdose?

N-acetylcysteine (NAC) within 8-10 hours; use Rumack-Matthew nomogram to guide treatment based on 4-hour level.

What is the treatment for ethylene glycol or methanol poisoning?

Fomepizole (alcohol dehydrogenase inhibitor), sodium bicarbonate for acidosis, and hemodialysis if severe.

What is Acute Infectious Gastroenteritis (Viral, Bacterial)?

Acute inflammation of the stomach and intestines from viral or bacterial pathogens causing diarrhea, vomiting, abdominal cramps, and sometimes fever.

What is the most common cause of viral gastroenteritis in adults?

Norovirus — outbreaks on cruise ships, daycares, nursing homes; self-limited 24-48 hour course.

What is the most common cause of severe viral gastroenteritis in young children?

Rotavirus — significant cause of childhood mortality worldwide; preventable with oral live attenuated vaccine.

When should antibiotics be used in bacterial gastroenteritis?

Severe illness (sepsis, dehydration), immunocompromised, extremes of age, bloody diarrhea (except suspected EHEC), Shigella, Vibrio cholerae, or systemic symptoms.

What pathogen is associated with pseudoappendicitis presentation?

Yersinia enterocolitica — mesenteric adenitis mimicking appendicitis; transmitted by undercooked pork or contaminated water.

What is the management of C. difficile colitis?

Stop offending antibiotic; first-line: oral vancomycin or fidaxomicin; recurrent: fecal microbiota transplant; severe/fulminant: add IV metronidazole.

What is an Anal Fissure/Fistula?

Anal fissure: linear tear in anoderm distal to dentate line; Anal fistula: abnormal tract connecting anal canal to perianal skin, usually from prior abscess.

What is the classic presentation of an anal fissure?

Severe sharp pain with bowel movements, scant bright red blood on toilet paper; fissure most commonly in posterior midline.

What is the treatment for an anal fissure?

Sitz baths, fiber, stool softeners, topical nitroglycerin or nifedipine ointment, lidocaine; refractory cases need lateral internal sphincterotomy or botulinum toxin.

What is Goodsall's rule for anal fistulas?

Anterior external openings track in a straight line to the dentate line; posterior external openings curve to the posterior midline internal opening.

What is the treatment of an anal fistula?

Surgical: fistulotomy for simple low fistulas; setons, advancement flaps, or LIFT procedure for complex/high fistulas to preserve continence.

What is Appendicitis?

Acute inflammation of the vermiform appendix, usually from luminal obstruction (fecalith, lymphoid hyperplasia, tumor), requiring surgical removal.

What is the classic clinical presentation of appendicitis?

Periumbilical pain migrating to RLQ (McBurney point) over 12-24 hours, anorexia, nausea, vomiting, low-grade fever.

What are the classic physical exam signs of appendicitis?

McBurney point tenderness, Rovsing sign (RLQ pain with LLQ palpation), Psoas sign (pain with right hip extension), Obturator sign (pain with internal hip rotation).

What is the imaging test of choice for appendicitis in adults?

CT abdomen/pelvis with contrast — appendix >6mm, wall thickening, periappendiceal fat stranding, fluid; ultrasound preferred in children and pregnant women.

What is the treatment for acute appendicitis?

Laparoscopic appendectomy with perioperative antibiotics (cefoxitin or ceftriaxone + metronidazole); IV antibiotics alone may be considered for uncomplicated cases.