cellular injury and adaptation ii

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Cellular Adaptation & Injury II 5. Cloudy Swelling of Kidney Low mag. Note that the slide looks grossly normal.

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Page 1: Cellular Injury and Adaptation II

Cellular Adaptation & Injury II

5. Cloudy Swelling of Kidney

Low mag. Note that the slide looks grossly normal.

Page 2: Cellular Injury and Adaptation II

Higher mag of cortex. Normal architecture is present, including glomeruli and defined tubules, with areas of pale foaminess.

Higher mag. Notice some normal, pink tubule cells, others swollen and pale. Example of CLOUDY SWELLING.

Page 3: Cellular Injury and Adaptation II

Same as above. Cloudy swelling cells are swollen and foamy (granular looking), but still viable. There are many normal cells still present. If the cells were to start breaking apart, that would be vacuolar degeneration.

6a. Coagulation Necrosis of Liver

Low mag. Even here you can see pallor in areas throughout.

Page 4: Cellular Injury and Adaptation II

Higher mag. You can see normal hepatic architecture with triad at lower left and viable hepatocytes at bottom. Top shows area of COAGULATIVE NECROSIS. Cells are pale and have no nuclei.

Higher mag. Cell shape and general architecture IS PRESERVED to a large extent, characteristic of coagulative necrosis.

Page 5: Cellular Injury and Adaptation II

Close up. Note pallor, lack of nuclei.

6b. Coagulation Necrosis of Spleen

Low mag. Necrosis is visible as pallor.

Page 6: Cellular Injury and Adaptation II

Higher mag. Note flat, pink quality of cells, lack of nuclei. Again, notice that general architecture is preserved.

Here’s a close up. This is splenic coagulative necrosis!

Page 7: Cellular Injury and Adaptation II

6C. Coagulation Necrosis of Kidney

Low mag. Again, note broad areas of pallor, representing necrosis.

Again, note presence of normal architecture. There is also hyperemia (increased blood flow) and many RBCs, representing unsuccessful blood flow.

Page 8: Cellular Injury and Adaptation II

Close up showing area with remaining viable cells (star) and coagulation necrosis. As before, necrosis exemplified by lost nuclei, pallor, and mummified quality of tissue.

7. Liquefaction Necrosis, Cerebral Infarct

Low mag. Note gyrus and sulcus, some integrity on left hand side. On the left, it looks like everything has fallen apart!

Page 9: Cellular Injury and Adaptation II

Higher mag. Note normal tissue on the right. There is no tissue on the left! The liquid state of the dead tissue is a result of rapid hydrolysis. This is called LIQUEFACTIVE NECROSIS.

Close up. Microglial cells that phagocytose debris are foamy and have granular cytoplasm. These are called Gitter cells. Some astrocytes are also present.

Page 10: Cellular Injury and Adaptation II

8. Fat Necrosis, Acute Pancreatitis

Low mag. Notice areas of pallor (necrosis) and pale emptiness (normal fat).

Compare normal fat (round, white) to necrotic tissue, which is pink, washed out looking and blurry.

Page 11: Cellular Injury and Adaptation II

Again, digested fat is translucent pink, vs. the normal fat to the right. Note the presence of inflammatory cells. Explanation from Robbins: The released lipases split the triglyceride esters contained within fat cells. The fatty acids, so derived, combine with calcium to produce grossly visible chalky-white areas (fat saponification). One should see shadowy outlines of necrotic fat cells, with basophilic calcium deposits, surrounded by an inflammatory reaction.

Page 12: Cellular Injury and Adaptation II

At higher mag you can see some fine granules (star) which represent Ca2+ as explained above.

9. Caseation Necrosis, Spleen

Low Mag. Note areas of pallor and darker, relatively contained, immune-infiltrated areas.

Page 13: Cellular Injury and Adaptation II

The center of a caseating lesion contains amorphous, granular debris. This is NOT liquefied (liquefactive)! There is no remaining architecture either (coagulative)! There is immune infiltration in surrounding tissue.

Higher mag of caseous material. Note granularity and acellularity.

Page 14: Cellular Injury and Adaptation II

At higest mag, you can see the presence of some immune cells and some fibroblasts maybe.

10. Fibrinoid Necrosis, Liver

Low mag. Note vessels have marked eosinophilic color.

Page 15: Cellular Injury and Adaptation II

Fibrinoid necrosis is classified by a deeply eosinophilic, smudged, fibrin-like appearance. This type of necrosis is usually seen in immune reactions, i.e. vasculitis, involving blood vessels. Notice the diffuse immune infiltration. From Robbins: This type of necrosis typically occurs when complexes of antigens and antibodies are deposited in the walls of arteries. Deposits of these “immune complexes,” together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like).

Page 16: Cellular Injury and Adaptation II

Notice how cells have lost definition and are truly necrotic, vs. hyaline change.

Here is another image from Robbins:

Page 17: Cellular Injury and Adaptation II