Inflammatory Bowel Disease & Hepatitis Lecture Notes

Inflammatory Bowel Disease (IBD)

• Chronic inflammatory processes that can occur anywhere along the gastrointestinal tract (mouth → anus)
• Two major sub-types with distinct but overlapping characteristics:
  • Crohn Disease (CD)
  • Ulcerative Colitis (UC)
• Shared themes
  • Autoimmune contribution & genetic predisposition
  • Cycles of exacerbation and remission
  • Risk for malabsorption, obstruction, perforation, bleeding, fistula formation, and systemic manifestations (weight loss, fatigue, anemia)

Crohn Disease (CD)

• Pathophysiology
  • Chronic, granulomatous inflammatory process
  • Most common sites: terminal ileum, ascending colon, but "skip lesions" can appear anywhere along GI tract
  • Inflammation begins in mucosa/submucosa → ↑ vascular permeability → edema → fibrosis → bowel‐wall thickening
  • Consequences
  • Luminal narrowing → potential obstruction
  • Deep linear ulcerations may penetrate full thickness → fistulae between bowel segments or adjacent organs/skin
  • Greatest complication: perforation → massive infection → septic shock
• Local clinical manifestations
  • Rapid stool transit time (hyper-motility)
  • Intestinal edema & fibrosis
  • Crampy abdominal pain (often RLQ)
  • Diarrhea (may be steatorrhea)
  • Malnutrition & weight loss (↓ absorptive surface)
  • Occult or frank blood in stool → iron-deficiency anemia
• Systemic manifestations
  • Fever, fatigue, anorexia
  • Extra-intestinal: arthritis, skin lesions, ocular inflammation (noted in broader CD literature)

Ulcerative Colitis (UC)

• Pathophysiology
  • Chronic inflammation limited to large intestine (colon + rectum)
  • Begins in distal rectum, progresses proximally in a continuous pattern (no skip lesions)
  • Primarily affects mucosal layer → superficial, diffuse ulcerations; mucosa becomes erythematous, granular, friable (bleeds easily)
  • Risk for perforation, toxic megacolon, massive hemorrhage
• Clinical manifestations
  • Large-bowel irritability → frequent, urgent stools
  • Bloody diarrhea with mucus (hallmark)
  • Rectal bleeding
  • Crampy lower-abdominal pain relieved by defecation
  • Impaired water & electrolyte absorption → dehydration, electrolyte imbalance
  • Systemic: fever, weakness, fatigue, weight loss, iron-deficiency anemia

Hepatitis (General)

• Definition: inflammation of the liver parenchyma
• Etiologies
  • Viral infections (HAV, HBV, HCV, HDV, HEV; focus on A–D in transcript)
  • Alcohol abuse
  • Drug or toxin exposure (e.g., acetaminophen, industrial solvents)
• Routes of viral transmission
  • Fecal–oral (acute) → HAV, HEV
  • Blood & body fluids (often chronic) → HBV, HCV, HDV
• Pathophysiology
  • Viral entry → hepatocyte infection → immune-mediated cytolysis → hepatic necrosis
  • Possible progression to fibrosis & \text{cirrhosis} (end-stage liver disease)
• Clinical course (three classical phases)
  1. Prodromal/Pre-icteric (≈ 2 weeks)
  • Fatigue, anorexia, malaise, headache, low-grade fever, nausea
  1. Icteric (≈ 2–6 weeks)
  • Onset of jaundice, dark urine, clay-colored stools
  • Pruritus (from bile salt deposition), right-upper-quadrant pain
  • Hepatomegaly (enlarged, tender liver)
  1. Recovery/Convalescent
  • Jaundice resolves ≈ 8 weeks after exposure
  • Symptoms improve, but hepatomegaly/tenderness may persist 1–4 additional weeks

Types of Viral Hepatitis

• Hepatitis A (HAV)
  • Transmission: fecal–oral (contaminated food/water)
  • Incubation: 1–2 months
  • Course: acute, self-limiting; no chronic/carrier state
  • Prevention: effective vaccine; post-exposure immune globulin
  • Diagnosis: serum anti-HAV IgM antibodies
• Hepatitis B (HBV)
  • Transmission: blood, sexual fluids, perinatal (mother → baby)
  • Incubation: 2–3 months
  • May become chronic; carrier state possible
  • Prevention: recombinant vaccine; needle safety; perinatal prophylaxis
  • Diagnosis: presence of HBV surface antigen (HBsAg) ± DNA viral load
• Hepatitis C (HCV)
  • Transmission: infected blood (IV drug use, transfusion pre-1992, needlesticks)
  • Incubation: 2–3 months
  • High rate of chronicity ≈ 75–85\%; leading indication for liver transplantation
  • No vaccine; direct-acting antivirals now curative in >95\% of cases
  • Diagnosis: anti-HCV antibodies → confirm with HCV RNA
• Hepatitis D (HDV)
  • Defective RNA virus; requires HBsAg (hepatitis B surface antigen) to replicate
  • Transmission identical to HBV (blood/body fluids)
  • Incubation: 2–3 months
  • Co-infection (simultaneous HBV + HDV) or super-infection (HDV added to chronic HBV) → more severe disease, fulminant hepatitis risk
  • No dedicated vaccine; prevention via HBV vaccination
  • Diagnosis: serum anti-HDV antibodies or HDV RNA

Key Integrations & Clinical Implications

• IBD vs. Acute Viral Hepatitis
  • Though both involve immune-mediated tissue injury, IBD targets gut mucosa whereas viral hepatitis targets hepatocytes.
  • Systemic signs (fever, fatigue, anemia) overlap; careful history & labs distinguish etiologies.
• Nutritional/Metabolic Considerations
  • Crohn’s malabsorption of B12, fat-soluble vitamins; liver disease alters vitamin K-dependent clotting factors → combined bleeding risk.
• Pharmacotherapeutics
  • IBD: aminosalicylates, corticosteroids, biologics (anti-TNF, anti-integrin)
  • Viral hepatitis: antivirals (tenofovir for HBV; sofosbuvir combinations for HCV)
• Complications & Monitoring
  • Crohn’s fistulae → require surgical or biologic therapy; screen for sepsis.
  • Ulcerative colitis → colonoscopy surveillance after 8–10 years for colorectal cancer.
  • Chronic HBV/HCV → ultrasound + AFP every 6 months for hepatocellular carcinoma.
• Ethical/Population Health
  • Vaccination campaigns (HAV, HBV) drastically reduce incidence; inequities persist in low-resource areas.
  • Harm-reduction (needle-exchange, safe injection sites) critical for HCV control.
  • Access to biologics & antivirals: high cost vs. long-term societal savings by preventing complications.