Pathophysiology
P-II-8. Liver disease, Case 5
肝疾患 症例5
A 47-year-old man arrived at the internal medicine ward because his skin turned yellow. Additionally, his bulging, distended abdomen has recently become larger, which made him difficult to move and also caused him a kind of “pulling” sensation in his spine. The patient’s relatives noticed that he was confused and restless lately. He is unaware of general illnesses or drug intolerance, and he does not take any medication but drinks alcohol regularly.
Physical examination:
- height: 178 cm
- weight: 97 kg
- Characterized by sparse hair, large protruding abdomen, gynecomastia.
Laboratory test — Blood:
- ASAT: 85 U/l
- ALAT: 76 U/l
- prothrombin time: INR = 2.7, unchanged after vitamin K administration
- albumin: 28 g/l
- K+: 3.3 mmol/l
- Ht: 0.36
Key Quotes & What They Tell Us
| Quote / Value | Interpretation |
|---|---|
| “drinks alcohol regularly”; sparse hair, gynecomastia | Chronic alcohol use with signs of hyperoestrogenism → chronic liver disease/cirrhosis |
| “bulging, distended abdomen … became larger”; large protruding abdomen | Ascites from portal hypertension and hypoalbuminaemia |
| “confused and restless lately” | Hepatic encephalopathy from impaired ammonia clearance |
| Albumin 28 g/L (low) | Reduced hepatic synthetic function → low oncotic pressure (contributes to ascites) |
| INR 2.7, “unchanged after vitamin K administration” | Coagulopathy due to hepatocellular synthetic failure, not vitamin K deficiency |
| ASAT 85 > ALAT 76 (AST/ALT > 1) | Ratio favouring AST is typical of alcoholic liver disease |
| K⁺ 3.3 (low); Ht 0.36 (low) | Hypokalaemia (can worsen encephalopathy) and anaemia of chronic liver disease |
Key Points
- Diagnosis: Decompensated (alcoholic) liver cirrhosis.
- Decompensation features: Jaundice, ascites, hepatic encephalopathy, and coagulopathy.
- Synthetic failure: Low albumin and a vitamin K–resistant high INR show the liver can no longer make proteins/clotting factors.
- Portal hypertension: Drives ascites; hyperoestrogenism causes gynaecomastia and sparse body hair.
- Pathophysiology: Chronic alcohol injury → fibrosis/cirrhosis → portal hypertension + loss of hepatocyte function → multi-system decompensation.
- Watch-outs: Hypokalaemia and constipation can precipitate or worsen encephalopathy.
一問一答
▶What is the diagnosis in a 47-year-old regular drinker with jaundice, ascites, confusion, and vitamin K–resistant coagulopathy?
Decompensated (alcoholic) liver cirrhosis.
▶What are the four hallmark features of hepatic decompensation in this case?
Jaundice, ascites, hepatic encephalopathy, and coagulopathy.
▶Why does this patient develop ascites?
Portal hypertension plus hypoalbuminaemia (low oncotic pressure) drive fluid into the peritoneal cavity.
▶Why is the patient confused and restless (hepatic encephalopathy)?
The failing liver cannot clear ammonia and other toxins, which accumulate and affect the brain.
▶Why does the INR stay high (2.7) even after vitamin K administration?
The coagulopathy is due to hepatocellular synthetic failure, not vitamin K deficiency, so vitamin K cannot correct it.
▶What does a low albumin (28 g/L) indicate in cirrhosis?
Reduced hepatic synthetic function, lowering plasma oncotic pressure and contributing to ascites/oedema.
▶What does an AST/ALT ratio greater than 1 suggest about the cause of liver disease?
It is typical of alcoholic liver disease.
▶Why does this patient have gynaecomastia and sparse body hair?
Hyperoestrogenism from impaired hepatic metabolism of oestrogens in cirrhosis.
▶What causes portal hypertension in cirrhosis?
Fibrosis and regenerative nodules distort hepatic architecture, increasing resistance to portal blood flow.
▶What are the major consequences of portal hypertension?
Oesophageal/gastric varices, splenomegaly, ascites, and caput medusae.
▶Why can hypokalaemia worsen hepatic encephalopathy?
Low potassium increases renal ammonia production and shifts ammonia into cells/brain, aggravating encephalopathy.
▶Why is this patient anaemic (low haematocrit)?
Anaemia of chronic liver disease (hypersplenism, GI blood loss, marrow suppression, nutritional deficiency).
▶What is the main mediator of hepatic encephalopathy?
Ammonia, which is normally cleared by the liver via the urea cycle.
▶What are common precipitants of hepatic encephalopathy?
GI bleeding, infection, constipation, electrolyte disturbances (e.g. hypokalaemia), and dehydration.
▶Why are the transaminases only modestly elevated despite severe liver disease?
In end-stage cirrhosis much functional liver tissue is already lost ('burnt-out'), so enzyme leakage is limited.
▶What is the basic management of cirrhotic ascites?
Sodium restriction and diuretics (spironolactone +/- furosemide), with paracentesis for tense ascites.
▶How can ascitic fluid be characterised to confirm portal hypertension?
A high serum-ascites albumin gradient (SAAG, 1.1 g/dL or more) indicates portal-hypertensive ascites.
▶How is hepatic encephalopathy treated?
Lactulose (to reduce ammonia absorption) and rifaximin, plus correcting precipitating factors.
▶Why does jaundice occur in decompensated cirrhosis?
Failing hepatocytes cannot adequately conjugate and excrete bilirubin, so it accumulates in blood.
▶What is the overall pathophysiology of alcoholic cirrhosis?
Chronic alcohol injury causes fibrosis/cirrhosis, leading to portal hypertension plus loss of hepatocyte function and multi-system decompensation.