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21 Cards in this Set
- Front
- Back
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what causes fat necroses?
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enzymatic (pancreatic enzymes), trauma (pelvic fat, skin, etc), abdominal fat necrosis in cattle (unknown cause)
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what is the pathogenesis of enzymatic fat necrosis?
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lipases release fatty acids from triglyderides, free fatty acids combine with Ca++ to form soaps, Soaps stimulate inflammatory reaction
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what is the gross morphology of fat necrosis?
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chalky white to yellow foci in peripancreatic fat
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what is the microscopic morphology of fat necrosis?
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indistince cellular outlines, granular cytoplasm (eosinophilic or basophilic), soaps, infiltration of neutrophils
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what is liquefaction necrosis?
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a form of necrosis in which dead tissue is converted to a liquefied mass
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what are the two manifestations of liquefaction necrosis?
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pyogenic abscess and malacia
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what is pyogenic abscess?
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a localized bacterial infection which attracts large numbers of neutrophils (any tissue)
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what is malacia?
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an area of softeining in the brain (encephalomalacia) or spinal cord (myelomalacia); limited to CNS
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what is gangrenous necrosis?
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modification of necrotic tissue following invasion and putrefaction by saprophytic bacteria
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what are the two presentations of gangrenous necrosis?
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dry gangrene (coagulation over liquafaction) and wet gangrene (liquafaction over coagulation)
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what are necrosis and apoptosis two forms of?
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cell death
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what is apoptosis?
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a unique form of cell death (programmed cell death) that occurs normally in many situations (the deletion of unneeded cells) but may also be a pathologic event in cells damaged beyond repair, esp when cell's DNA is damaged)
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what are some examples of apoptosis in physiologic situations?
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programmed destruction of cells during embryogenesis (tadpole tail), hormone-dependent involution in adult (mammary tissue after weaning), cell deletion in proliferating cell populations (intestinal epithelial cells, skin cells), deletion of autoreactive T cells in thymus, or of cells no longer needed (neutrophils after responding to antigen), cell death induced by cytotoxic T cells (granzyme B-mediated)
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what are some examples of apoptosis in pathologic conditions?
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pathologic atrophy of hormone-dependent tissues (prostate after castration, T cells after glucocorticoid administration), pathologic atrophy of parenchymal organs after duct obstruction (pancreas), cell death in tumors (inadequate blood supply), cell death by viruses, many other stimuli not severe enough to cause necrosis (radiation, chemotherapy, other causes of DNA damage)
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what are the biochemical features of apoptosis?
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protein cleavage by caspases > DNA breakdown (internucleosomal cleavage into oligonucleosomes, 180-200 base pairs, by enconucleases) > phagocytic recognition (apoptotic cells express phosphatidylserine in outer plasma membrane = flipped out, gobbled up by neighboring cells and/or macrophages > inflammation is absent)
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briefly describe what occurs to a cell during necrosis?
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enzymatic digestion and leakage of cellular contents
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briefly describe what occurs to a cell during apoptosis?
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cell breaks up into apoptotic body that is phagocytized
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what are the mechanisms that initiate apoptosis?
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injury, intrinsic (mitochondrial) pathway, extrinsic (death receptor-initiated) pathway, cytotoxic T lymphocytes
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in detail, describe what occurs to a cell during necrosis?
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cell swelling > disruption of organelles > random diffuse DNA breakdown > elicits inflammation
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in detail, describe what occurs to a cell during apoptosis?
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cell shrinkage > chromatin condensation > formation of apoptotic bodies with intact membranes > endonuclease internucleosomal cleavage of DNA to 180-200bp segments > protein cleavage by caspases > elicits NO inflammatory response > formation of cytoplasmic blebs >phagocytosis of apoptotic bodies by adjacent healthy cells (apoptotic cells express phosphatidylserine on outer membrane = flipped out)
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what are the mechanisms of apoptosis?
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internucleosomal DNA fragmentation into 180-200bp lengths = mediated by Ca++ sensitive endonuclease (constitutive or induced), induction of transglutaminase activity > excessive cross-linking of cytoplasmic proteins > altered cell volume/shape, phagocytosis of apoptotic bodies by MPs/others (receptor mediated ie vitronectin receptor on MPs = B3 integrin that binds apoptotic neutrophils for phagocytosis), or gene activation (induced by p53, c-mync oncogene, Fas-Fas ligand, TNF-induced and inhibited by bcl-2 known as survival signal for cell growth)
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