Page 451 - Concise Pathology for Exam Preparation ( PDFDrive )

436 SECTION II Diseases of Organ Systems

Clinical Features

• Haematemesis and melena (from variceal bleeding)
• Fetor hepaticus (a musty odour of breath, resulting from portal-systemic shunting
of blood, which allows mercaptans to pass directly to the lungs. Mercaptans are formed
by the action of GIT bacteria on methionine)
• Caput medusae (a number of prominent collateral vessels radiating from the
umbilicus)
• Splenomegaly (an important diagnostic sign of portal hypertension)
• Hypersplenism (manifests as thrombocytopenia and leucopenia)
• Small, contracted and fibrotic liver (usually seen associated with very high portal
venous pressure)
• Haemorrhoids (which occur from dilatation of rectal veins)
• Ascites (which occurs due to portal hypertension and hypoalbuminaemia due to liver
cell failure)

Q. Outline the salient features of hepatorenal failure.

Ans. Hepatorenal syndrome is defined as renal failure associated with chronic liver dis-
ease. Kidneys are histologically normal and their function reverts to normal after reversal
of hepatic failure. Renal failure is thought to result from diminished renal blood flow. In
cirrhosis, circulatory changes lead to increased peripheral blood flow and decreased vis-
ceral blood flow, especially to the kidneys (this clinically manifests as a drop in urine
output and rising blood urea and creatinine levels).

Q. Write briefly on alcoholic liver disease.

Ans. The spectrum of alcoholic liver disease varies from alcoholic steatosis to hepatitis, to
cirrhosis. The above do not necessarily occur sequentially and may occur independently
of each other. The short-term ingestion of 80 g of ethanol/day produces mild reversible
hepatic changes. Chronic intake of 50–60 g/day may cause severe injury.

Alcoholic Steatosis (Fatty Liver)
• The severity of fatty change is roughly proportional to the duration and degree of alcohol
intake.
• Patient presents with hepatomegaly and mildly increased serum bilirubin and alkaline
phosphatase.
Pathogenesis
Hepatocellular steatosis results from
• Impaired assembly and secretion of lipoproteins.
• Increased peripheral catabolism of fat to release free fatty acids (FFA) into the circulation
and increased delivery of FFA to liver.
• Generation of excess reduced NAD (NADH) by two major enzymes of alcohol me-
tabolism, namely, alcohol dehydrogenase and acetaldehyde dehydrogenase. Decreased
+
NAD inhibits catabolism (oxidation) of fatty acids and leads to increased lipid synthesis
and accumulation of fat in hepatocytes.
Pathology
• The liver is enlarged, soft, yellow and greasy.
• Micro- and macrovesicular fat droplets (clear vacuoles) are seen in the cytoplasm of
hepatocytes.
• Steatosis starts from the centrilobular region.
• There is minimal accompanying inflammation and absence of fibrosis.

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