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Pathology test 1 w/ pics

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Coagulative necrosis (I) in kidney cells
Liquefactive necrosis. An infarct in the brain, showing dissolution of the tissue
Caseous necrosis. Tuberculosis of the lung, with a large area of caseous necrosis containing yellow-white and cheesy debris.
Fat necrosis. The areas of white chalky deposits represent foci of fat necrosis with calcium soap formation (saponification) at sites of lipid breakdown in the mesentery
Fibrinoid necrosis in an artery. The wall of the artery shows a circumferential bright pink area of necrosis with inflammation (neutrophils with dark nuclei).
Morphologic changes in reversible cell injury and necrosis. A, Normal kidney tubules with viable epithelial cells. B, Early (reversible) ischemic injury showing surface blebs, increased eosinophilia of cytoplasm, and swelling of occasional cells. C, Necrosis (irreversible injury) of epithelial cells, with loss of nuclei, fragmentation of cells, and leakage of contents.
Ultrastructural features of reversible and irreversible cell injury (necrosis) in a rabbit kidney. A, Electron micrograph of a normal epithelial cell of the proximal kidney tubule. Note abundant microvilli (mv) lining the luminal surface (L). B, Epithelial cell of the proximal tubule showing early cell injury resulting from reperfusion following ischemia. The microvilli are lost and have been incorporated in apical cytoplasm; blebs have formed and are extruded in the lumen. Mitochondria would have been swollen during ischemia; with reperfusion, they rapidly undergo condensation and become electron-dense. C, Proximal tubular cell showing late injury, expected to be irreversible. Note the markedly swollen mitochondria containing electron-dense deposits, expected to contain precipitated calcium and proteins. Higher magnification micrographs of the cell would show disrupted plasma membrane and swelling and fragmentation of organelles.
FIGURE 1-22 Morphologic features of apoptosis. A, Apoptosis of an epidermal cell in an immune reaction. The cell is reduced in size and contains brightly eosinophilic cytoplasm and a condensed nucleus. B, This electron micrograph of cultured cells undergoing apoptosis shows some nuclei with peripheral crescents of compacted chromatin, and others that are uniformly dense or fragmented. C, These images of cultured cells undergoing apoptosis show blebbing and formation of apoptotic bodies (left panel, phase contrast micrograph), a stain for DNA showing nuclear fragmentation (middle panel), and activation of caspase-3 (right panel, immunofluorescence stain with an antibody specific for the active form of caspase-3, revealed as red color).
The intrinsic (mitochondrial) pathway of apoptosis. A, Cell viability is maintained by the induction of anti-apoptotic proteins such as Bcl-2 by survival signals. These proteins maintain the integrity of mitochondrial membranes and prevent leakage of mitochondrial proteins. B, Loss of survival signals, DNA damage, and other insults activate sensors that antagonize the anti-apoptotic proteins and activate the pro-apoptotic proteins Bax and Bak, which form channels in the mitochondrial membrane. The subsequent leakage of cytochrome c (and other proteins, not shown) leads to caspase activation and apoptosis.
The extrinsic (death receptor-initiated) pathway of apoptosis, illustrated by the events following Fas engagement. FAAD, Fas-associated death domain; FasL, Fas ligand
Autophagy. Cellular stresses, such as nutrient deprivation, activate autophagy genes that create vacuoles in which cellular organelles are sequestered and then degraded following fusion of the vesicles with lysosomes. The digested materials are recycled to provide nutrients for the cell
Fatty liver. A, Schematic diagram of the possible mechanisms leading to accumulation of triglycerides in fatty liver. Defects in any of the steps of uptake, catabolism, or secretion can result in lipid accumulation. B, High-power detail of fatty change of the liver. In most cells the well-preserved nucleus is squeezed into the displaced rim of cytoplasm about the fat vacuole.
Cholesterolosis. Cholesterol-laden macrophages (foam cells, arrow) in a focus of gallbladder cholesterolosis.
Protein reabsorption droplets in the renal tubular epithelium.
Lipofuscin granules in a cardiac myocyte shown by (A) light microscopy (deposits indicated by arrows), and (B) electron microscopy (note the perinuclear, intralysosomal location).
Hemosiderin granules in liver cells. A, H+E stain showing golden-brown, finely granular pigment. B, Prussian blue stain, specific for iron (seen as blue granules).
Dystrophic calcification of the aortic valve. View looking down onto the unopened aortic valve in a heart with calcific aortic stenosis. It is markedly narrowed (stenosis). The semilunar cusps are thickened and fibrotic, and behind each cusp are irregular masses of piled-up dystrophic calcification.
Punctate petechial hemorrhages of the colonic mucosa, a consequence of thrombocytopenia. B, Fatal intracerebral bleed.
Liver with chronic passive congestion and hemorrhagic necrosis. A, Central areas are red and slightly depressed compared with the surrounding tan viable parenchyma, forming a "nutmeg liver" pattern (so-called because it resembles the cut surface of a nutmeg. B, Centrilobular necrosis with degenerating hepatocytes and hemorrhage.