Hepatobiliary System

Liver

Gross Anatomy · Microscopic Anatomy · Function · Embryology · Clinical
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Gross Anatomy

The liver is the largest internal organ (~1500 g) located in the right upper quadrant under the diaphragm. It has four lobes: right (largest), left, caudate, and quadrate.

Lobar Anatomy

  • Falciform ligament — separates right and left lobes on anterior surface; contains ligamentum teres (remnant of umbilical vein)
  • Porta hepatis — hilum containing portal vein, hepatic artery, and bile duct (portal triad)
  • Bare area — peritoneum-free area on posterior surface in direct contact with the diaphragm

Blood Supply

Vessel% O₂ Supply% Blood FlowNotes
Portal vein50-60%~75%Nutrient-rich blood from GI tract and spleen
Hepatic artery40-50%~25%Branch of celiac trunk; O₂-rich
🩺 Clinical

The liver has dual blood supply — portal hypertension results when portal venous pressure rises, causing varices, splenomegaly, and ascites.

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Microscopic Anatomy

Hepatic Lobule

Classic hexagonal lobule with central vein and portal triads at each corner. Hepatocytes radiate from the central vein in cords/plates.

Acinar Zones (Rappaport)

ZoneLocationO₂ LevelVulnerable To
Zone 1Near portal triadHighestToxic injury (phosphorus, beryllium)
Zone 2IntermediateIntermediateYellow fever necrosis
Zone 3Near central veinLowestIschemic necrosis; acetaminophen; alcohol
⭐ Boards Pearl

Zone 3 (centrilobular) = acetaminophen toxicity, alcoholic liver disease, ischemic hepatitis. Zone 1 = toxic damage from phosphorus, beryllium, salicylates.

Key Cell Types

  • Hepatocytes — main metabolic/synthetic cells; 80% of liver mass
  • Kupffer cells — resident macrophages in sinusoids
  • Stellate (Ito) cells — store vitamin A; activated → collagen → fibrosis
  • Space of Disse — perisinusoidal space between hepatocytes and endothelium
🧠 Mnemonic

"Ito = Italian sculptor" — stellate cells sculpt/scar the liver. Store fat+vitamin A normally; when activated produce collagen causing fibrosis.

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Function

  • Carbohydrate metabolism — glycogenesis, glycogenolysis, gluconeogenesis
  • Protein synthesis — albumin, clotting factors (I, II, V, VII, IX, X, XI), complement, transport proteins
  • Lipid metabolism — FA oxidation, ketogenesis, VLDL synthesis, cholesterol synthesis
  • Detoxification — CYP450 system; first-pass metabolism; ammonia → urea
  • Bile production — ~600-1000 mL/day; bile salts emulsify dietary fats
  • Storage — glycogen, TG, vitamins A, D, E, K, B12, iron (ferritin)

Bilirubin Pathway

StepLocationFormTransport
Heme breakdownSpleen/macrophagesUnconjugated (indirect)Bound to albumin
ConjugationHepatocytes (UGT1A1)Conjugated (direct)Water-soluble
ExcretionBile → gut → urobilinogenStercobilin/urobilinStool/urine
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Ethanol Metabolism

  • Alcohol dehydrogenase (ADH) — Ethanol → Acetaldehyde → Acetate (ALDH)
  • Microsomal ethanol-oxidizing system (MEOS) — CYP2E1; produces free radicals; inducible
⭐ Boards Pearl

Alcohol ↑ NADH/NAD+ ratio → inhibits gluconeogenesis (hypoglycemia) + FA oxidation → fatty liver. Acetaldehyde is directly hepatotoxic. Progression: Steatosis → Alcoholic hepatitis (AST:ALT >2:1) → Cirrhosis → HCC.

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Embryology

Liver develops from the hepatic diverticulum of foregut endoderm at ~week 4.

  • Hepatic bud → hepatocytes + intrahepatic bile ducts
  • Septum transversum mesoderm → Kupffer cells, stellate cells, connective tissue
  • Ligamentum teres — remnant of umbilical vein
  • Ligamentum venosum — remnant of ductus venosus
🧠 Mnemonic

"Liver = Foregut" — hepatic diverticulum grows from foregut at week 4. Liver and pancreas both bud off the foregut simultaneously.

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Clinical Pearls

ConditionKey FeaturesLab Clue
Hepatitis AFecal-oral; self-limited; no chronic formAnti-HAV IgM (acute)
Hepatitis BBlood/sexual; can be chronic; HBsAg+HBsAg, HBeAg, anti-HBc
Hepatitis CMostly chronic; leads to cirrhosis/HCCAnti-HCV Ab; RNA PCR
Alcoholic hepatitisFatty change, neutrophils, Mallory bodiesAST:ALT >2:1; ↑GGT
Wilson diseaseCopper; Kayser-Fleischer rings↓ceruloplasmin; ↑urine Cu
HemochromatosisIron overload; bronze diabetes↑ferritin, ↑transferrin sat.
🩺 Clinical

Child-Pugh (Bilirubin, Albumin, PT/INR, Ascites, Encephalopathy) assesses cirrhosis severity. MELD score predicts 90-day mortality and is used for transplant prioritization.