INTRODUCTION:

Fatty change, steatosis or fatty metamorphosis is the intracellular accumulation of neutral fat within parenchymal cells.
The liver is the commonest site for the accumulation of fat because it plays a central role in fat metabolism. It may also occur in other non-fatty tissue like heart, kidney and skeleton muscle and other organs.

Etiology:

Fatty change in the liver may result due to-

  1. Conditions with excess fat (HYPERLIPIDEMIA). 
  2. Liver cell damage:- When fat can't be metabolized in it. 


Causes:


1. Conditions with excess fat- 
  • Obesity.
  • Diabetes mellitus.
  • Congenital hyperlipidemia.

2. Liver cell damage:
  • Alcoholic liver disease. (Most common cause)
  • Starvation.
  • Protein calories malnutrition.
  • Chronic illness.
  • Acute fatty liver in late pregnancy.
  • Hypoxia.
  • Hepatotoxin.
  • Drug-induced liver cell injury.
  • Reye’s syndrome.

Pathogenesis:

Mechanism of fatty liver depends upon the state at which the etiologic agent acts in normal fat transport and metabolism.
Normally lipid as free acids enter the liver cell from either the following two sources-

1. From diet:- as chylomicrons and free fatty acids.
2. From adipose tissue as free fatty acids.



In fatty liver, intracellular accumulation of triglycerides occur due to - defect in one or more steps in the normal fat metabolism.
  1. Increased entry of fatty acid into the liver.
  2. Increased synthesis of fatty acids by the liver.
  3. The decreased conversion of fatty acid to ketone bodies resulting in the increased esterification of fatty acids to triglycerides.
  4. Deceased synthesis of lipids acceptors protein resulting in the formation of lipoprotein.
  5. Increased alpha-glycerophosphate causing increased esterification of fatty acid to triglycerides.
  6. Block in the secretion of lipoprotein from the liver into plasma.

Alcoholic Steatosis:

  • In the case of liver cell injury by chronic alcoholism many factors are implicated which includes-
  • Increased lipolysis.
  • Increased free fatty acid synthesis.
  • Decreased triglyceride utilization.
  • Decreased fatty acid oxidation to ketone bodies.
  • Block in lipoprotein excretion.

Morphologically Features:

Grossly:

  • The liver is in enlarge (wt- 4 to 6kg) with a tense glistening capsule and round margins.
  • It is pale yellow and greasy to touch.

Microscopically:

  • The characteristic feature is the presence of numerous lipid vacuole in the cytoplasm of hepatocytes.
  • The vacuoles are initially small and are present around the nucleus (microvesicular).
  • with the progression of the process, the vacuole becomes larger pushing the nucleus to the peripheral of cells (macrovesicular).
  • The hepatocytes laden with large lipid vacuole may rupture and liquid vacuole coalesces to form fatty cysts. 
  • Infrequently lipogranulomas may appear consisting of a collection of lymphocytes, macrophages and some multiple giant cell.
  • Fat can be demonstrated in fresh unfixed tissue by frozen section following by  fat stains such as Sudan dyes &oil red.