Gastrointestinal System

Acute Appendicitis

  • Inflammation of the vestigial vermiform appendix; one of the most common causes of acute abdomen and a frequent reason for emergent abdominal surgery.
  • Typical presentation in a young adult: acute onset periumbilical pain that steadily worsens over 12\text{ to }24\text{ hours} and localizes at McBurney's point.
  • Associated symptoms: anorexia (loss of appetite).
  • Classic exam findings: low-grade fever and right lower quadrant (RLQ) pain with rebound tenderness and guarding.
  • Special signs often positive: psoas sign and obturator sign.
  • If the appendix ruptures: signs of acute abdomen with involuntary guarding, rebound, and a board-like abdomen; refer to ED.
  • Key management cue: consider ED referral for suspected perforation/complication.

Acute Cholecystitis

  • Inflammation of the gallbladder; often a complication of gallstone disease.
  • Typical presentation: overweight patient with severe RUQ or epigastric pain within 1\text{ hour} (or more) after a fatty meal; pain may radiate to the right shoulder.
  • Associated symptoms: nausea, vomiting, anorexia.
  • Complications if untreated: gangrene of the gallbladder; may require hospitalization.

Acute Diverticulitis

  • Inflammation of diverticula (sac-like protrusions of the colonic wall), often due to perforation.
  • Typical patient: elderly with acute high fever, anorexia, nausea/vomiting, LLQ abdominal pain.
  • Risk factors: increased age; constipation; low dietary fiber with high fat/red meat; obesity; lack of exercise; frequent NSAID use.
  • Physical findings: rebound tenderness, Rovsing’s sign, board-like abdomen (acute abdomen).
  • Laboratory: CBC with leukocytosis and neutrophilia; left shift; bands indicate severe bacterial infection.
  • Complications: abscess, sepsis, ileus, small-bowel obstruction, hemorrhage, perforation, fistula, phlegmon/stricture; can be life-threatening.
  • Note on diagnosis: presence of band forms signals severe infection.

Acute Pancreatitis

  • Acute inflammatory process of the pancreas.
  • Typical presentation: acute onset fever, nausea, vomiting with abdominal pain in epigastric region radiating to LUQ/back.
  • Common etiologies: \approx \frac{2}{3} of cases due to gallstones or chronic alcohol use disorder.
  • Exam: guarding and epigastric tenderness; may radiate to back; Cullen’s sign (blue periumbilical discoloration) and Grey Turner’s sign (bluish flank discoloration).
  • Complications: ileus; signs of shock.
  • Management: refer to ED.

Clostridium Difficile Colitis

  • Spore-forming, toxin-producing, gram-positive anaerobic bacterium causing colitis.
  • Severity: non-severe, severe, fulminant, or recurrent.
  • Classic presentation: severe watery diarrhea (10\text{ to }15\text{ stools/day}) with lower abdominal cramping and fever; symptoms typically appear 5\text{ to }10\text{ days} after antibiotic initiation.
  • Common offending antibiotics: clindamycin, fluoroquinolones, cephalosporins, penicillins.
  • Risk factors: age >65 years; recent hospitalizations.
  • Diagnosis: NAAT (nucleic acid amplification test) on stool; stool toxin assay; CBC; BUN/electrolytes.
  • Treatment (initial): discontinue inciting antibiotic; fidaxomicin 200\,\text{mg PO BID for }10\text{ days} or vancomycin 125\,\text{mg PO QID for }10\text{ days}; alternative metronidazole 500\,\text{mg PO TID for }10\text{–}14\text{ days}.
  • Recurrent cases: fidaxomicin or vancomycin in tapered/pulsed regimen; adjunctive bezlotoxumab.
  • Third or subsequent recurrence: fecal microbiota transplant (FMT).
  • Other supportive measures: antimotility agents (loperamide) with caution; limited evidence for probiotics; hydration and electrolyte management; early oral refeeding; avoid BRAT as routine.

Colon Cancer

  • Gradual progression with vague GI symptoms; possible intermittent GI bleeding leading to iron-deficiency anemia.
  • Symptoms: changes in bowel habits, stool color, or bloody stool; heme-positive stool or dark tarry stool; palpable abdominal mass possible.
  • Risk factors for referral to GI: males; age >50; history of multiple polyps or IBD (Crohn’s disease or ulcerative colitis); postmenopausal women with iron-deficiency anemia.
  • Population data: African Americans have the highest US incidence.
  • Screening guidance: USPSTF recommends colon cancer screening between ages 45\text{ and }75.

Crohn’s Disease (CD)

  • Type of IBD that may affect any part of the GI tract from mouth to anus; transmural inflammation with skip lesions.
  • Ileal involvement: watery diarrhea without blood/Mucus.
  • Colonic involvement: bloody diarrhea with mucus.
  • Relapses: fever, anorexia, weight loss, dehydration, fatigue; periumbilical to RLQ pain with relapses.
  • Complications: fistula formation; anal disease (CD only, not UC); abdominal mass on palpation.
  • Course: remissions and relapses; higher risk of toxic megacolon and colon cancer.
  • Lymphoma risk increased with azathioprine treatment.

Ulcerative Colitis (UC)

  • Form of IBD limited to colon/rectum.
  • Symptoms: bloody diarrhea with mucus (hematochezia); left-sided cramping with bloating and gas aggravated by food.
  • Relapses: fever, anorexia, weight loss, fatigue; may have arthralgias/arthritis in large joints, sacrum, or ankylosing spondylitis.
  • Can have iron-deficiency anemia or anemia of chronic disease.
  • Course: remissions and relapses; increased risk of colon cancer and potential toxic megacolon.

Zollinger–Ellison Syndrome (Gastrinoma)

  • Gastrinoma located on pancreas or stomach; secretes gastrin causing high gastric acid output and multiple severe ulcers in stomach/duodenum.
  • Symptoms: epigastric to midabdominal pain; stools may be tarry (melena).
  • Diagnosis/Referral: screen with serum fasting gastrin level; refer to gastroenterologist.

Route of Food/Drink from the Mouth

  • Esophagus → stomach (HCl, intrinsic factor) → duodenum (bile, amylase, lipase) → jejunum → ileum → cecum → ascending colon → transverse colon → descending colon → sigmoid colon → rectum → anus.

Abdominal Regions

  • RUQ: Liver, gallbladder, ascending colon, kidney (right), pancreas (small portion). Right kidney is lower due to liver.
  • LUQ: Stomach, pancreas, descending colon, kidney (left).
  • RLQ: Appendix, ileum, cecum, ovary (right).
  • LLQ: Sigmoid colon, ovary (left).
  • Suprapubic: Bladder, uterus, rectum.

Abdominal Assessments (Signs and Maneuvers)

  • Psoas/Iliopsoas Sign: Supine; raise right leg with downward pressure; RLQ pain with passive hip extension indicates iliopsoas irritation; suggests retrocecal appendicitis.
  • Obturator Sign: Internal rotation of the hip causes RLQ pain; positive with pelvic appendix; low sensitivity; not frequently performed.
  • Rovsing’s Sign: LLQ deep palpation → referred RLQ pain; specificity for acute appendicitis; rule out acute/surgical abdomen.
  • McBurney’s Point: Maximal tenderness at 1.5–2 inches from ASIS on a line to the umbilicus (RLQ).
  • Markle Test (Heel Jar): Jump or sudden heel raise; positive if RLQ pain or patient refuses due to pain.
  • Involuntary Guarding: Abdominal muscles tense reflexively; suggests acute abdomen; refer to ED.
  • Rebound Tenderness: Pain worsens when hand is released after deep palpation; suspect acute/surgical abdomen; refer to ED.
  • Murphy’s Maneuver: Deep RUQ pressure during inspiration causes mid-inspiratory arrest and RUQ pain; positive for cholecystitis/gallbladder disease.
  • Carnett’s Sign: Supine with arms crossed; lift shoulders to tense abdominal muscles; increased pain suggests abdominal wall source; decreased pain suggests intra-abdominal source.
  • Cullen’s Sign: Periumbilical edema/bruising.
  • Grey Turner’s Sign: Flank bruising indicating retroperitoneal hemorrhage.

Hepatitis Serology and Liver Function Tests (LFTs)

  • Hepatitis A Virus (HAV)

    • IgM Anti-HAV: Acute infection; patient contagious.
    • IgG Anti-HAV: Lifelong immunity; no active virus; persists decades; history or vaccination.

  • Hepatitis B Virus (HBV)

    • HBsAg: Screen for current or past infection; positive with active infection or prior exposure.
    • Anti-HBs: Immunity marker; appears after clearance or vaccination.
    • HBeAg: Marker for actively replicating HBV; highly infectious.
    • Total HBcAg and Anti-HBc: Appears at onset of symptoms in acute HBV; IgM anti-HBc indicates acute infection; IgG anti-HBc persists with anti-HBs after recovery.
    • Serology tip: HBsAg-positive status means infection (new or chronic).

  • Hepatitis C Virus (HCV)

    • Anti-HCV: Screening test; a positive result does not always mean immunity; up to ~85\% become carriers.
    • HCV RNA (PCR): Needed to confirm active infection; if both negative, acute HCV unlikely.

  • Hepatitis D Virus (HDV)

    • Anti-HDV and HDV RNA tests; HDV infection requires HBV for virion assembly.
    • Co-infection with HBV and HDV increases risk of fulminant hepatitis, cirrhosis, and severe liver damage; transmission via sex, needles, vertical, etc.
    • Tip: HBsAg-positive status always indicates infection (new or chronic).

  • Hepatitis B and D relationship

    • HDV has no separate vaccine; HBV vaccination prevents HDV acquisition.

  • Hepatitis Serology Pitfalls

    • PCR tests detect viral RNA, not antibodies.

  • Hepatitis C Case Studies (brief)

    • Screen with anti-HCV; if positive, order HCV RNA; refer to GI for liver biopsy/treatment.

  • Hepatic Function Tests

    • AST (ASAT, SGOT): Normal 0\le \text{AST}\le 35\,\text{U/L}; elevations indicate liver disease, muscle injury, or other organ involvement.
    • ALT (ALAT, SGPT): Normal male 29\text{ to }33\,\text{U/L}; female 19\text{ to }25\,\text{U/L}; more specific for hepatocellular injury.
    • AST:ALT ratio: \text{AST:ALT} \ge 2:1 may indicate alcohol abuse.
    • GGT: Normal 0\text{ to }30\,\text{IU/L}; elevated with liver disease, biliary obstruction, alcohol use, or certain meds; helps differentiate liver vs bone disease when ALP is elevated.
    • ALP: Normal range varies with age; highest in bone/liver sources; elevated in biliary obstruction, cholestasis, bone disease, healing fractures; in pregnancy placenta contributes to ALP.
    • Tip: GGT elevation with ALP supports a liver/biliary etiology; lone GGT elevation suggests alcoholism risk.

Acute Diverticulitis (Expanded)

  • Diverticula: small pouch-like herniations on the colon.
  • Epidemiology: secondary to low fiber intake; higher incidence in Western societies; up to 50\% of Americans aged 60+ have diverticula.
  • Localization: in most Western cases, left colon (descending/sigmoid) is involved.
  • Pathophysiology: diverticulitis occurs when diverticula become infected; risk of rupture/bleeding; can be life-threatening.
  • Management (mild/uncomplicated): outpatient with liquid diet and oral analgesia; reassess in 2!- imes!3\,days; continue weekly until resolution; antibiotics not routinely required but may be used for high-risk patients.
  • Management (when to hospitalize): moderate-to-severe disease, dehydration, elderly, comorbidities, immunocompromise, or poor oral intake tolerance.
  • Inpatient criteria: abscess, obstruction, fistula, sepsis, perforation, age >70, significant comorbidities, immunosuppression, noncompliance, or failure of outpatient treatment.
  • Chronic/diverticulosis management: high-fiber diet, psyllium or methylcellulose; tobacco cessation; physical activity; reduced meat intake; probiotics limited evidence; colonoscopy after symptom resolution to rule out colon cancer.
  • Complications: perforation, peritonitis, abscess, obstruction, fistula.

Acute Hepatitis (General Concepts)

  • Acute liver inflammation with multiple etiologies: viral infections, hepatotoxic drugs, excessive alcohol, medications, toxins.
  • Classic presentation: fever, fatigue, anorexia, nausea, malaise, dark urine, scleral/icteric jaundice, RUQ pain; clay-colored stools possible.
  • Objective signs: jaundice; tender liver on exam.
  • Lab features: elevated ALT/AST; elevations >5\times ULN suggest extensive hepatocellular injury; bilirubin, ALP, GGT may be elevated; ammonia ↑, prolonged PT, ↓ albumin may occur.
  • Treatment: remove/avoid etiologic factors; supportive care; referral for advanced liver disease.
  • PCR note: PCR tests detect viral RNA, not antibodies.

Acute Pancreatitis (Detailed)

  • Reiterated etiologies: alcohol, gallstones, triglycerides >1000\,\text{mg/dL}, post-ERCP, genetics, drugs, and other rare factors.
  • Pathophysiology: pancreatic enzyme activation causes pancreatic damage, microcirculatory impairment, inflammatory mediators; possible necrosis.
  • Classification: mild, moderately severe, severe.
  • Classic case: nausea/vomiting with rapid onset of severe epigastric/LUQ pain radiating to the back in about half of patients; dyspnea, pleural effusions, ARDS may occur; guarding/tenderness; may have ileus and shock signs.
  • Signs: Cullen’s sign and Grey Turner’s sign; abdominal distention; hypoactive bowel sounds (ileus); scleral icterus/jaundice if choledocholithiasis.
  • Labs: elevated pancreatic enzymes (amylase, lipase, trypsin); elevated AST/ALT/GGT/bilirubin; leukocytosis.
  • Imaging: abdominal ultrasound and CT.
  • Complications: ileus, sepsis, shock, multiorgan failure, death.

Clostridium Difficile Associated Diarrhea (CDAD) and Colitis (Expanded)

  • Pathogen: C. difficile; spore-forming, toxin-producing gram-positive anaerobe.
  • Typical onset: after antibiotic use; watery diarrhea; anosmia? (not stated) – classic feature after antibiotics.
  • Risk factors: antibiotic exposure (especially clindamycin, fluoroquinolones, cephalosporins, penicillins); age >65; recent hospitalization.
  • Diagnostics: NAAT on stool; toxin assay; CBC; BMP; consider test of cure; avoid testing asymptomatic patients.
  • Treatment (initial episode): discontinue inciting antibiotic; fidaxomicin 200\,\text{mg PO BID for }10\,\text{days} or vancomycin 125\,\text{mg PO QID for }10\,\text{days}; metronidazole alternative 500\,\text{mg PO TID for }10!- 14\,\text{days}.
  • Recurrent episode: fidaxomicin or vancomycin in tapered/pulsed regimen; bezlotoxumab as adjunct.
  • Third or subsequent recurrence: fecal microbiota transplant (FMT).
  • Additional management: antimotility agents may be used with caution in high fluid losses; probiotics have limited evidence; supportive care with hydration and nutrition; early refeeding; avoid unnecessary restrictive diets.

Gastroenteritis (Overview)

  • Acute gastroenteritis: main symptom is diarrhea (loose, watery stools ≥3 times/day).
  • Durations: acute 1!- 2\,\text{days}; persistent 2!- 4\,\text{weeks}; chronic \ge 4\,\text{weeks}.
  • Pathogens: viruses (most common), bacteria, protozoa.
  • Viral gastroenteritis: abrupt onset of nausea/vomiting with watery, non-bloody diarrhea; self-limited, typically 1–3 days; noroviruses common in outbreaks (crowded settings); other viruses include rotavirus, enteric adenovirus, astrovirus.
  • Bacterial gastroenteritis: high fever with bloody diarrhea and severe abdominal pain; ≥6 stools/24h; incubation 1–6 hours for foodborne toxin; 1–3 days for bacterial infections; resolves 1–7 days; antibiotics can shorten duration but risk resistance.
  • Bacterial pathogens: E. coli, Salmonella, Shigella, Campylobacter, C. difficile, Listeria (pregnant patients higher risk).
  • Protozoal gastroenteritis: symptoms 7+ days; travel-related diarrhea lasts ~5 days; organisms include Giardia, Entamoeba histolytica, Cryptosporidium.
  • Risk factors: travel to developing countries; recent antibiotics; immunocompromised state; crowded settings (daycare, nursing homes).
  • Prevention: bottled water abroad; avoid ice; food/water precautions; handwashing; careful preparation; rotavirus vaccine for infants.

Gastroesophageal Reflux Disease (GERD)

  • Prevalence: ~40\% of U.S. adults.
  • Pathophysiology: regurgitation of acidic gastric contents due to inappropriate relaxation of the lower esophageal sphincter.
  • Complications of chronic GERD: Barrett’s esophagus (pre-cancer) with increased risk of esophageal adenocarcinoma; potential esophageal cancer; esophageal strictures.
  • Classic case: middle-aged/older adult with chronic heartburn for many years; symptoms worsen with large/fatty meals and when supine; long-term OTC antacid/H2 blocker use; risk factors include chronic NSAID, aspirin, or alcohol use.
  • Objective findings: acidic breath; regurgitation; enamel erosion on posterior teeth; chronic sore throat; chronic cough, hoarseness, wheezing.

GERD Treatment Plan

  • First-line for mild/intermittent GERD: lifestyle changes (avoid large/fatty meals, especially within 3–4 hours of bedtime); weight loss if BMI > 25; smoking cessation.
  • Pharmacologic steps (start with lifestyle; move up as needed):
    • Antacids: aluminum/mmagnesium/simethicone, calcium carbonate; caution with drug interactions (e.g., tetracycline, levothyroxine).
    • H2 receptor antagonists (H2RAs): first-line for mild-to-moderate symptoms or mild esophagitis; taken at bedtime (examples: Nizatidine 300 mg at bedtime; Famotidine 40 mg at bedtime).
    • Surfactants/alginate barriers: Sucralfate protects mucosa.
    • Proton pump inhibitors (PPIs): for erosive esophagitis; examples: Omeprazole 20\,\text{mg daily}; Esomeprazole 40\,\text{mg daily}; Lansoprazole 30\,\text{mg daily}; Pantoprazole 40\,\text{mg daily}; dosing 30–60 minutes before meals.
    • Long-term PPI considerations: increased risk of osteoporosis/fractures, acute interstitial nephritis, hypomagnesemia, C. difficile infection, reduced iron absorption; do not abruptly discontinue PPIs—taper.
  • When to refer to GI: poor response after 4!- 8\,\text{weeks} of therapy; high risk for Barrett’s; worsening symptoms; consider upper endoscopy/biopsy (gold standard) for persistent symptoms.
  • Complications prevention: Barrett’s esophagus, esophageal cancer, esophageal stricture.
  • Lifestyle/management tips:
    • Mild GERD: lifestyle with antacids/H2RAs.
    • Moderate-severe erosive esophagitis: start with PPIs and escalate as needed.
    • Red flags: odynophagia, dysphagia, early satiety, weight loss, iron-deficiency anemia; refer to ED/gastroenterologist.
  • Barrett’s esophagus considerations:
    • Increased cancer risk: up to about 30\text{ times} higher risk of esophageal adenocarcinoma.
    • Diagnosis via upper endoscopy with biopsy.
  • Nonpharmacologic lifestyle factors to teach patients: avoid smoking, alcohol, caffeine; reduce meal size; avoid trigger foods (see Box 11.1): peppermint, mint, chocolate, caffeine, alcohol, carbonated drinks, tomato sauce, citrus, fatty foods.
  • Medications that worsen GERD: calcium channel blockers, NSAIDs, nitrates, opioids, anticholinergics, iron supplements, bisphosphonates, TCAs, theophylline, barbiturates.

Irritable Bowel Syndrome (IBS)

  • Definition: chronic functional disorder of the colon with alternating exacerbations/remissions; often stress-related.
  • Classification: diarrhea-predominant, constipation-predominant, or alternating.
  • Classic case: young to middle-aged female with intermittent LLQ cramping, bloating, relief after defecation; stools range from diarrhea to constipation with increased frequency.
  • Evaluation: complete physical exam to exclude other causes; vital signs usually normal; abdominal and rectal exams may vary by flare.
  • Management (lifestyle first): increase dietary fiber (psyllium, methylcellulose, wheat dextrin); start low; avoid gas-producing foods (beans, onions, cabbage, high-fructose corn syrup); consider lactose/gluten-free trials; low FODMAP diet under dietician guidance.
  • Stress reduction; antispasmodics for pain (dicyclomine, hyoscyamine).
  • IBS with constipation: fiber; osmotic laxatives (polyethylene glycol).
  • Severe constipation: lubiprostone or linaclotide (caution in <6 years old).
  • IBS with diarrhea: loperamide prophylactically; bile acid sequestrants as second-line; severe diarrhea-predominant IBS in select women: alosetron (serotonin 3 receptor antagonist) with ischemic colitis warning.
  • Infections to rule out: ova/parasites, bacterial infections, inflammatory GI disease; stool cultures as indicated.
  • Important precaution: avoid antidiarrheals in acute bloody diarrhea or fever or pain worsened with defecation; ED referral if red-flag symptoms.

Nonalcoholic Fatty Liver Disease (NAFLD)

  • Pathophysiology: triglyceride deposition in hepatocytes; includes NAFL (steatosis without significant inflammation) and NASH (inflammation).
  • Epidemiology: common in Western industrialized countries; linked to central obesity, type 2 diabetes, metabolic syndrome, dyslipidemia.
  • Classic case: most patients asymptomatic; may have hepatomegaly.
  • Lab findings: mild-to-moderate elevations of ALT/AST; ALT/AST not always elevated in NAFLD.
  • Workup: LFTs (ALT/AST often up to 2–5x ULN); fasting lipids, glucose, A1C; hepatitis A/B/C serology.
  • Imaging: ultrasound first-line; CT/MRI can detect steatosis; liver biopsy gold standard; NAFLD fibrosis score to stage disease.
  • Management: weight loss, exercise, dietary modification; avoid alcohol; remove hepatotoxic drugs (e.g., acetaminophen, isoniazid, statins); vaccinate for hepatitis A and B; GI referral.
  • Patient education: all overweight/obese patients should be counseled on weight loss; daily aerobic exercise 30–45 minutes.

Peptic Ulcer Disease (PUD)

  • Definition: disruption of gastric or duodenal mucosa extending beyond the superficial layer; major risk factors include Helicobacter pylori infection and NSAID use; other factors: smoking, alcohol, genetics, diet; age-related incidence differences.
  • Etiology
    • H. pylori infection (gram-negative): major factor.
    • NSAID/aspirin use → decreased prostaglandins → reduced GI mucosal protection; COX-1/COX-2 inhibition leads to reduced mucus production and blood flow.
    • Other: cigarette smoking, alcohol; drug-induced ulcers (bisphosphonates, clopidogrel, anticoagulants, potassium supplements, corticosteroids, chemotherapeutic agents); hormonal/mediator-induced (gastrinoma); postsurgical/radiation; mechanical/obstructive causes; infiltrative disease (sarcoidosis, Crohn disease).
  • Classic case: recurrent epigastric pain with burning/gnawing; relieved by food/antacids in gastric ulcers; pain recurs 2–4 hours after meals in duodenal ulcers; may have melena, hematochezia, coffee-ground emesis, iron-deficiency anemia; signs of shock with board-like abdomen require ED.
  • Investigations: CBC (iron-deficiency anemia suggests bleeding); FOBT positive with active bleeding; H. pylori testing for all ulcers; urea breath test indicates active H. pylori; stool antigen (active infection/post-treatment); serology (IgG) indicates exposure but not active infection; endoscopy with biopsy is gold standard; fasting gastrin to rule out Zollinger–Ellison syndrome if multiple severe ulcers or unresponsive ulcers; gastric ulcers require endoscopy to rule out cancer and confirm healing.
  • Testing caveats: PPI use within 2 weeks can affect urea breath test results.
  • Treatment – H. pylori–negative ulcers: stop NSAIDs; smoking cessation; lifestyle changes; PPI/H2RA therapy for 4\text{ to }8\,\text{weeks}; avoid unnecessary antibiotic use.
    • H2RAs include nizatidine (Axid) 150\,\text{mg twice daily} or famotidine (Pepcid) 40\,\text{mg at bedtime}.
    • PPIs: Omeprazole 20\,\text{mg daily}; Esomeprazole 40\,\text{mg daily}; Lansoprazole 15!- 30\,\text{mg daily}; Pantoprazole 40\,\text{mg daily}; dosing 30–60 minutes before meals.
  • Treatment – H. pylori–positive ulcers (14-day regimens): triple therapy or quadruple therapy.
    • Triple therapy: Clarithromycin 500\,\text{mg twice daily} + Amoxicillin 1\,\text{g twice daily} OR Metronidazole 500\,\text{mg twice daily}; plus Standard-dose PPI twice daily for 14\,\text{days}.
    • Quadruple therapy: Bismuth subsalicylate 600\,\text{mg four times daily} + Metronidazole 250\,\text{mg four times daily} + Tetracycline 500\,\text{mg four times daily} + Standard-dose PPI twice daily for 14\,\text{days}.
    • Other regimens: sequential therapy, salvage therapy, and other regimens available but not required for exam.
  • Key pearls: about 5\%\text{ to }30\% ulcer recurrence in the first year. PPIs heal ulcers more effectively than H2RAs.

Viral Hepatitis: Hepatitis A, B, C, and D (Summary)

  • Hepatitis A (HAV)
    • Acute, self-limited infection; lifelong immunity after infection or vaccination.
    • Transmission: fecal-oral via contaminated food/drink; risky settings include travel to poor sanitation areas; household/sexual contact; daycare; IV drug use.
    • Symptoms: fever, headache, malaise, anorexia, nausea, vomiting, diarrhea, abdominal pain, dark urine, jaundice.
    • Serology: IgM anti-HAV detectable at symptom onset; IgG anti-HAV persists for decades.
    • Management: supportive; vaccination (HAV vaccine, Havrix) for at-risk individuals; HAV is reportable.
  • Hepatitis B (HBV)
    • Acute vs chronic infection; horizontal and vertical transmission; universal infant vaccination schedule; vaccination reduces HDV risk.
    • Vaccination schedule (infancy): birth, 1–2 months, and 6–18 months; adults at risk have various schedules.
    • Acute HBV management: supportive; antiviral therapy if indicated; preventive measures for household/contacts.
    • Chronic HBV management: referral to GI; antivirals (PEG-IFN-α and nucleos(t)ide analogs like entecavir, tenofovir).
    • Diagnostic markers: HBsAg, Anti-HBs, Anti-HBc (IgM vs IgG), HBeAg, HBcAb, etc.
  • Hepatitis C (HCV)
    • Can be acute or chronic; about 14\%\text{ to }50\% spontaneous clearance; chronic infection can lead to cirrhosis, hepatocellular carcinoma, liver transplant.
    • Transmission: IV drug use; blood transfusion (historically); perinatal; sexual contact; healthcare exposure.
    • Screening: USPSTF recommends one-time HCV screening for adults 18\text{ to }79.
    • Acute infection: HCV RNA detectable by PCR before antibodies appear (anti-HCV).
    • Treatment: highly effective antivirals (e.g., sofosbuvir/velpatasvir for 12\,\text{weeks} or glecaprevir/pibrentasvir for 8\,\text{weeks}).
    • Case management: similar antiviral treatment for acute and chronic infection; refer to GI for liver management.
  • Hepatitis D (HDV)
    • Requires HBV for virion assembly; HDV infection can worsen HBV disease.
    • Transmission similar to HBV; can be severe; HDV infection may be detected by anti-HDV or HDV RNA.
    • Vaccination against HBV provides protection against HDV.
  • Case studies (Viral Hepatitis)
    • Patient A: HBsAg negative, Anti-HBs positive, Anti-HBc positive → immune to HBV due to natural infection.
    • Patient B: HBsAg positive, IgM anti-HBc positive, Anti-HBs negative, Anti-HBc positive → acutely infected with HBV.
  • General tips for interpreting HBV/HCV serology
    • A positive HBsAg indicates infection status; anti-HBs indicates immunity; anti-HBc indicates exposure (IgM suggests recent infection; IgG persists).
    • For HCV, a positive anti-HCV requires HCV RNA testing to determine active infection.
    • HDV is associated with HBV coinfection; screen if severe HBV symptoms or acute exacerbations.

Acute Pancreatitis (Clinical Emphasis)

  • See above for signs, etiologies, labs, imaging, and complications under the Acute Pancreatitis section.

Hepatology: Tests and Interpretations (Additional Details)

  • Liver function test markers
    • AST/ALT: indicators of hepatocellular injury; AST also present in cardiac/skeletal muscle; ALT more specific to liver.
    • GGT: marker of biliary/hepatic disorders and alcohol use; elevates with liver disease or biliary obstruction; lone elevation suggests alcohol use risk.
    • ALP: bone and liver sources; pregnancy placenta contributes; elevated in biliary obstruction and bone disorders; ALP and GGT together help determine etiology.
  • Diagnostic workflow cautions
    • PCR vs antibody testing: PCR detects active viral genomes; antibodies reflect exposure or immune response.

Quick Reference: Key Numbers and Flags (Review)

  • Acute appendicitis progression: 12\text{ to }24\,\text{hours} before localization.
  • Colorectal cancer screening: 45\text{ to }75 years.
  • Gallstone/pancreatitis epidemiology: about \approx \frac{2}{3} of pancreatitis cases due to gallstones or alcohol.
  • Diverticulitis diverticula prevalence in older adults: up to 50\% for age 60+.
  • Diverticulitis inflammatory markers: WBC with neutrophilia; left shift; bands indicate severe infection.
  • C. difficile recurrence and treatment durations: most regimens span 10\,\text{days}; FMT for recurrent disease.
  • GERD therapy durations: trial periods of 4!- 8\,\text{weeks} for PPI; chronic management may require ongoing therapy.
  • H. pylori therapy duration: eradication regimens typically span 14\,\text{days} for both triple and quadruple therapies.
  • NAFLD evaluation: ALT/AST mildly elevated (often up to 2!- 5\times ULN); imaging with ultrasound; biopsy as gold standard.
  • H. pylori recurrence risk: ulcers recur in 5\%\text{ to }30\% in the first year.
  • Common stepwise therapy for GERD progression: lifestyle -> antacids/H2RAs -> PPIs.

Summary of Management Pathways (Exam-Focused Cues)

  • Suspect acute abdomen in appendicitis/diverticulitis with rebound, guarding, and Rovsing’s sign; refer to ED as indicated.
  • In suspected cholecystitis, Murphy’s maneuver positivity supports gallbladder disease; consider ED referral if signs of sepsis or perforation.
  • For suspected C. difficile, test stool with NAAT/toxin assay after antibiotic exposure; treat promptly; escalate to FMT for recurrent cases.
  • For GI cancers, screen appropriately (colorectal cancer); biopsy-based confirmation; follow GI guidance for surveillance.
  • In GERD, prioritize lifestyle modifications and stepwise pharmacotherapy (H2RAs, PPIs); monitor red flags that warrant endoscopy.
  • In PUD, distinguish H. pylori–positive from –negative ulcers; tailor therapy accordingly (antibiotics + PPI for H. pylori; PPI alone for negative ulcers); test for eradication after therapy.
  • In viral hepatitis, use appropriate serologies (IgM vs IgG, HBsAg, anti-HBs, anti-HBc, HBeAg, anti-HBc IgM/IgG, anti-HCV, HDV) and PCR as indicated; refer to GI for antiviral therapy where needed.
  • In IBS, emphasize lifestyle modification, dietary adjustments (fiber, low FODMAP), and symptom-specific pharmacotherapy with attention to red flags.

End of Transcript-Derived Notes

  • The above captures the major and minor points, diagnostic cues, management strategies, and key numbers from the transcript. Students should cross-reference with clinical guidelines for the most current recommendations and local protocols.