Pathology Cheat Sheet
Read Decompensated Liver Disease
Liver failure and portal hypertension for NEET-PG: acinar zones, Mallory-Denk hyaline, cirrhosis, stellate cells, varices, ascites, and hepatic encephalopathy.
MedNext Academy | 3 min read
Read Decompensated Liver Disease
Liver failure and portal hypertension for NEET-PG: acinar zones, Mallory-Denk hyaline, cirrhosis, stellate cells, varices, ascites, and hepatic encephalopathy.
Hepatic failure, alcoholic liver disease and cirrhosis, and the consequences of portal hypertension.
High-yield lines
- The hepatic acinus zone 3 is least oxygenated, richest in cytochrome P450, and most vulnerable to ischaemic and toxic injury.
- Alcoholic liver disease progresses from fatty liver to alcoholic hepatitis and finally cirrhosis.
- Alcoholic hepatitis shows Mallory-Denk hyaline, neutrophilic infiltration, and hepatocyte ballooning.
- Cirrhosis is diffuse fibrosis with regenerative nodules that disrupt the normal liver architecture.
- Hepatic stellate cells activate to myofibroblasts and drive the fibrosis of cirrhosis.
- Portal hypertension results from increased resistance to portal flow, most often from cirrhosis.
- Portal hypertension causes oesophageal varices, splenomegaly, ascites, and caput medusae.
- Bleeding oesophageal varices are a life-threatening complication of portal hypertension.
- Ascites in cirrhosis results from portal hypertension and hypoalbuminaemia and shows a high serum-ascites albumin gradient.
- Hepatic encephalopathy results from failure to clear ammonia and other toxins.
- Fulminant hepatic failure causes coagulopathy, encephalopathy, and jaundice within weeks of onset.
- Non-alcoholic fatty liver disease is associated with obesity and insulin resistance and can progress to steatohepatitis and cirrhosis.
Mapped competency codes
- PA25.2
- PA25.4
- PA25.5
Continue into the full chapter
This summary maps to PA25-hepatobiliary-system.
Frequently Asked Questions
What is the histological hallmark of alcoholic hepatitis?
Mallory-Denk hyaline within ballooned hepatocytes, accompanied by a neutrophilic infiltrate and pericellular fibrosis.
What causes cirrhosis at the cellular level?
Activation of hepatic stellate cells into collagen-producing myofibroblasts, driven by transforming growth factor beta, producing diffuse fibrosis with regenerative nodules.
What are the main consequences of portal hypertension?
Oesophageal varices, splenomegaly, ascites, and caput medusae, with variceal bleeding being the most dangerous.
Why does zone 3 suffer toxic injury preferentially?
Because it is the least oxygenated and richest in cytochrome P450 enzymes that generate reactive metabolites from toxins such as paracetamol.
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