Pathology Flashcards
Pathologic findings of apoptosis
Deeply eosinophilc cytoplasm Cell and nuclear shrinkage Basophilia Membrane blebbing and nuclear karyorrhexis Apoptotic bodies
DNA laddering
Sensitive indicators of apoptosis. Endonucleases cleave nucleosomes leaving 180bp multiples.
MOA of radiation therapy
Causes apoptosis of tumors and surrounding tissues by causing free radical formation and dsDNA breakage. Rapidly dividing cells most susceptible
Intrinsic vs extrinsic pathway of apoptosis
Intrinsic
- used in tissue remodeling in embryogenesis as well as after exposure to injrious stimuli
- inccreased pro/decreased anti apoptotic factors increases mitochondrial permeability and increases cytochrome c release
- BAX and BAK are proapoptotic; bcl-2 is antiapoptotic
Extrinsic
- occurs due to Fas-FasL interactions in thymic medulla negative selection
- also can occur by immune cell release of perforin and granzyme B
- defective Fas-FasL interactions a cause of autoimmune disease
Bcl-2
Anti-apoptotic factor that prevents cytochrome c release. Bcl-2 overexpression leads to decreased caspase activation and tumorigenesis
Coagulative necrosis
- seen in ischemia/infarcts in most tissues
- proteins denature, enzymatic degradation
- cell outlines preserved
- increased cytoplasmic binding of acidophilic dyes
Liquefactive necrosis
- seen in bacterial abscesses and brain infarcts
- neutrophils release lysosomal enzymes that digest tissue
- early findings are cellular debris and macrophages
- late findings are cystic spaces and cavitation
Caseous necrosis
- seen in TB, systemic fungi infection, Novardia
- macrophages wal off organism resulting in granular debris
- pathology: fragmented cells and debris surrounded by lymphocytes and macrophage
Fat necrosis
- seen in acute panreatitis (enzymatic) and breast trauma (non-enzymatic)
- damaged cells release lipase which breaks down fatty acids of membranes
- pathology: outline of dead fat cells, saponification of fat is dark blue on H%E
Fibrinoid necrosis
- caused by immune reactions in vessels when immune complexes combine with fibrin, causing vessel wall damage
- vessel walls thick and pink
Irreversible forms of cell damage
- nuclear changes of apoptosis
- plasma membrane damage
- lysosomal rupture
- mitochondrial permeability/vacuolization
Ischemic-prone area of kidney
Straight segment of proximal tubule
Thick ascending limb
Rep vs white infarct
Red
- occurs in venous occlusion in tissues with multiple blood supplies (liver, lung, intestine)
- reperfusion injury
White
- occurs in solid organs with single end-arterial blood supply
- heart, kidney, spleen
Chromatolysis
- seen in neuronal cell body following axonal injury
- increased protein synthesis to repair damaged axon
- round cellular swelling, displacement of nucleus to periphery, dispersion of Nissl substance
Dystrophic vs metastatic calcification
Dystrophic
- Ca++ deposition in abnormal tissues secondary to injury or necrosis
- seen in TB, liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis
Metastatic
- widespread deposition in normal tissue secondary to hypercalcemia
- deposits predoinantly in interstitial tissues of kidney, lung, gastric mucosa
