Cirrhosis Pathology
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Direct answer
Diffuse fibrosis dissecting the liver into regenerative nodules, with bridging septa linking portal tracts to each other and to central veins, defines cirrhosis — anatomically distorting the vascular bed so that resistance rises (portal hypertension) and blood bypasses hepatocytes through portosystemic shunts. Alcohol classically gives a micronodular (under 3 mm) liver, chronic viral hepatitis and metabolic disease a macronodular one, though the patterns evolve into each other. Indian aetiology is shifting: alcohol, hepatitis B and hepatitis C now share the stage with metabolic dysfunction-associated steatotic liver disease, rising fastest in urban India alongside the obesity and diabetes epidemic. The complications — variceal bleeding, ascites, encephalopathy, hepatorenal syndrome and hepatocellular carcinoma — are all vascular or synthetic consequences of the distorted architecture.
What you must remember
- Definition triad: diffuse involvement of the whole liver, fibrous septa bridging portal-portal and portal-central, and regenerative nodules of surviving hepatocytes — all three required.
- Nodular patterns: micronodular (under 3 mm, alcohol, biliary obstruction) and macronodular (over 3 mm, chronic viral hepatitis, haemochromatosis, Wilson disease); a micronodular liver frequently converts to macronodular over years.
- Portal hypertension consequences: oesophageal and gastric varices via the left gastric vein, caput medusae through the recanalised umbilical vein, splenomegaly with hypersplenism, and ascites (portal pressure plus sodium retention and hypoalbuminaemia; serum-ascites albumin gradient above 1.1 g/dL).
- Portosystemic shunting: encephalopathy from ammonia-laden blood skipping the liver, with Alzheimer type II astrocytosis in the brain; lactulose acidifies the colon and rifaximin reduces ammonia-producing flora.
- Synthetic failure markers: falling albumin and clotting factors with a rising prothrombin time-INR — the measurable half of the Child-Pugh score alongside bilirubin, ascites and encephalopathy (grades A 5-6, B 7-9, C 10-15).
- Hyperoestrogenism: spider naevi, palmar erythema, gynaecomastia and testicular atrophy from reduced hepatic metabolism and increased sex hormone-binding globulin.
- Hepatorenal syndrome: functional renal vasoconstriction with avid sodium retention (urine sodium low) in the absence of structural kidney disease, precipitated by infections and gastrointestinal bleeding; hepatocellular carcinoma risk accumulates yearly in viral and alcoholic cirrhosis.
When a compensated cirrhotic decompensates
A 54-year-old with hepatitis B cirrhosis, stable for two years, arrives with increasing abdominal girth, confusion and a fluttering asterixis. The instinct to reach for diuretics comes second; the hunt for a precipitant comes first, because decompensation is usually an event, not a drift. Spontaneous bacterial peritonitis leads the list — hence diagnostic paracentesis on admission, a polymorph count of 250 per microlitre or more mandating cefotaxime. Gastrointestinal bleeding delivers a protein load that tips encephalopathy; constipation, hyponatraemia, diuretic excess, sedatives and urinary sepsis complete the set. Two management details separate the trained from the rote: dietary protein is no longer restricted (sarcopenia worsens outcomes), and lactulose is titrated to two or three soft stools daily with rifaximin added for recurrence. The Child-Pugh score computed at admission, more than any single laboratory value, predicts survival and brackets the transplant conversation.
What the Child-Pugh score rewards
Five inputs — bilirubin, albumin, INR, ascites and encephalopathy — with no place for transaminases, because aminotransferases measure injury while the score measures function. Two related exam facts: ascites and encephalopathy are graded clinically (absent, slight, moderate), making the score partly subjective, and the MELD score (bilirubin, INR, creatinine) has displaced Child-Pugh for transplant prioritisation while Child-Pugh still predicts variceal bleeding and surgical mortality — a distinction between scoring systems that vivas probe.
Frequently asked questions
What three features define cirrhosis histologically?
Diffuse fibrosis with bridging septa connecting portal tracts and central veins, and regenerative nodules of hepatocytes throughout the entire liver.
How do micronodular and macronodular cirrhosis differ?
Nodules under 3 mm (micronodular, typical of alcohol and biliary disease) versus over 3 mm (macronodular, chronic viral and metabolic disease); patterns interconvert with time.
Why does cirrhosis cause portosystemic encephalopathy?
Fibrosis and shunting divert ammonia-rich portal blood away from hepatocytes; ammonia crosses into the brain, producing astrocytic swelling and Alzheimer type II change, with asterixis and fluctuating consciousness.
What are the components of the Child-Pugh score?
Bilirubin, albumin, prothrombin time-INR, ascites and encephalopathy, graded into classes A (5-6), B (7-9) and C (10-15).
What precipitates spontaneous bacterial peritonitis work-up in ascites?
Every admission with cirrhotic ascites: diagnostic paracentesis with a polymorphonuclear count of 250 or more per microlitre triggers third-generation cephalosporin therapy and albumin.