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PH-GI09

Cirrhosis and portal hypertension

How years of liver injury turn healthy liver into scar and regenerating nodules, why that raises pressure in the portal vein so blood bypasses the liver through fragile varices, and how loss of liver function causes jaundice, bleeding, ascites and confusion.

By the end, you can

  • Describe the liver’s dual blood supply, its sinusoids and its main functions.
  • Explain how chronic injury activates stellate cells and leads to fibrosis, nodules and cirrhosis.
  • Explain how cirrhosis raises portal pressure and why portosystemic collaterals and splenomegaly follow.
  • Explain the mechanisms of ascites.
  • Relate jaundice, bruising, encephalopathy and other signs to loss of liver function.
  • Recognise micronodular and macronodular cirrhosis, regenerative nodules, varices and caput medusae, the Child–Pugh and MELD scores and the key tests, and explain how beta-blockers, vasoactive drugs, diuretics, albumin, lactulose and transplantation act on the mechanism.

What it is

Cirrhosis is the late stage of chronic liver injury, in which the normal architecture is replaced by bands of fibrous scar surrounding regenerative nodules. It causes portal hypertension (raised pressure in the portal venous system) and, as it advances, liver failure. Common causes are alcohol, fatty liver disease linked to metabolic dysfunction, and chronic hepatitis B and C.

2 types to tell apart
Compensated cirrhosis
No major complications yet; often silent and found by chance.
Decompensated cirrhosis
Ascites, variceal bleeding, encephalopathy or jaundice; the outlook is much worse.

Normal function

A liver fed by two blood supplies

The receives about three quarters of its blood from the , formed by the and , carrying nutrient-rich blood from the gut and spleen at low pressure. The rest comes from the hepatic artery.

Both flow into wide, leaky capillaries, the sinusoids, lined by fenestrated endothelium, past plates of hepatocytes, and drain to the central veins. Between sinusoid and hepatocyte, in the space of Disse, quiescent stellate cells store vitamin A.

Hepatocytes make albumin and clotting factors, process and excrete bilirubin, store glucose, detoxify ammonia into urea, and break down hormones and drugs.

Point to it on the model