Patholgy Slides : Cell Injury and Adaptation
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Fatty change liver steatosis
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)
Cholesterolosis of the gallbladder
Cholesterolosis of the gallbladder. (HE, ob x4)
Cholesterolosis of the gallbladder (detail of an enlarged mucosal fold). (HE, ob x10)
Cholesterolosis is an intracellular accumulation of lipids (cholesterol). When cholesterol is in
excess in the bile, it passes into the lamina propria where is phagocitated by macrophages. These macrophages become larger and polygonal, with foamy cytoplasm and small, hyperchromatic, central nucleus (xantic cells). Aggregation of xantic cells may enlarge the mucosal folds, producing a polypoid appearance of the mucosal surface. At gross examination, these yellow micropolyps (1-2 mm) contrasts with the red aspect of the surrounding mucosa, hence the term "strawberry gallbladder".
Sometimes, cholesterolosis is associated with inflammation of the gallbladder (cholecystitis) or with gallstones (cholelithiasis)
Amyloid (an abnormal protein) accumulates as extra-cellular deposits, nodular or diffuse, as pink, amorphous material. Initially, the deposits appear in the glomeruli: within the mesangial matrix and along the basement membranes of the capillary loops. Continuous accumulation of the amyloid will compress and obliterate the capillary tuft. With progression, amyloid deposits appear also peritubular and within the arteriolar wall, narrowing them. Congo red is a special staining, elective for amyloid. (Congo Red, ob. x20)
Hyaline arteriolosclerosis (Benign nephrosclerosis)
In benign hypertension, hyaline (pink, amorphous, homogeneous material) accumulates in the wall of small arteries and arterioles, producing the thickening of their walls and the narrowing of the lumens. Consequent ischemia will produce tubular atrophy, interstitial fibrosis, glomerular alterations (smaller glomeruli with different degrees of hyalinization - from mild to sclerosis of glomeruli) and periglomerular fibrosis. (Hematoxylin-eosine, ob. x10)
Cellular swelling (liver)
Cellular swelling (synonyms : hydropic change, vacuolar degeneration, cellular edema) is an acute reversible change resulting as a response to nonlethal injuries. It is an intracytoplasmic accumulation of water due to incapacity of the cells to maintain the ionic and fluid homeostasis. It is easy to be observed in parenchymal organs : liver (hepatitis, hypoxia), kidney (shock), myocardium (hypoxia, phosphates intoxication). It may be local or diffuse, affecting the whole organ.
atlas of pathology