Pages

Thursday, September 1, 2011

Histology and Explanation of Fatty change or Steatosis In Liver

Fatty change or Steatosis represents the intracytoplasmic accumulation of triglyceride (neutral fats) of parenchimal organs, such as: liver, myocardium and kidney.



Mechanisms : increase of free fatty acids (starvation, diabetes and chronic ethylism/alcoholism), reduction of free fatty acids oxidation (hypoxia, toxins, chronic ethylism/alcoholism), increase of esterification of free fatty acids into triglycerides (due to increased free fatty acids or reduction of their oxidation, chronic ethylism/alcoholism) and reduced export of tryglicerides due to deficiency of lipid binding apoprotein (starvation/malnutrition, toxins). Initially, fatty change does not impair the cells function, being reversible.

At the beginning, the hepatocytes present small fat vacuoles in the vicinity of the endoplasmic reticulum (liposomes) - microvesicular fatty change (photo). In the late stages, the size of the vacuoles increases pushing the nucleus to the periphery of the cell - macrovesicular fatty change. These vesicles are well delineated and optically "empty" because fat solves during tissue processing (paraffin embedding). Large vacuoles may coalesce, producing fatty cysts - which are irreversible lesions. (HE, ob. x20)

No comments:

Post a Comment