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18 Cards in this Set
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- 3rd side (hint)
Necrosis defn |
Necrosis is defined as localized area of cell death followed by degradation of tissue by hydrolytic enzymes liberated from dead cells. invariably accompanied by inflammatory reaction . ( diff it from apoptosis) |
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Types of necrosis name them and give examples. |
Coagulative necrosis: heart, lidney, spleen. Due to iireversible focal injury brought about by ischemia. Agents could be chemical, bacterial. Liquefactive necrosis: brain & abscess cavity. Due to action of hydrolytic enzymes. Agents: bacterial/ fungal/ chemical agents Causing hypoxic injury Caseous necrosis: found in tuberculosis foci. Combines 1&2 fat necrosis: two types-pancreatic &traumatic fat necrosis. pancreatic trauma releases lipases which cause necrosis of pancreas & fat depots, adipose. Traumatic fat necrosis is injury to adipose which converts neutral fat into glycerol &fatty acids. Fibrinoid necrosis : deposition of fibrin like material which has staining properties of fibrin. Eg : immunologic tissue injury. Like autoimmune, vasculitis etc |
Pancreas suicide :p ? |
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Pathology of necrosis |
Coagulative type : Gross- three opposites hint Microscopy: tombstone, nuclear changes, cytoplasmic changes ( more eosinophilic) no cell digestion. Instead engulfed... Granular debris |
Tombstones; granular debris, inflammation |
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Liquefactive necrosis |
Grossly: liquefactive center contains liquified cell debris and surrounded by cyst wall. Soft & yellow
Microscopy: an area of necrosis: cell debris+ macrophages containing cell debris. Surrounded by granulation tissue & gliosis( brain) & fibrosis ( abscess cavity) |
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Caseous necrosis |
Gross: foci looks granular, dry cheese, yellowish Microscopy: centre: eosinophilic & granular surrounded by characteristic granulomatois reaction with giant cells and a peripheral mantle of lymphocytes |
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Fat necrosis |
Gross: yellowish white, firm deposits. Chalk white appearance die to calcium salts Microscopically: necrosed fat tissue have cloudy appearance. Calcium salts have amorphous, granular & basophilic material |
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Fibrinoid necrosis |
Gross: brightly eosinophilic, hyaline like deposits in vessel wall Surrounded by nuclear debris of neutrophils |
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Dystrophic calcification defn |
Calcification in dead tissues & degenerated tissue Pathogensis: cause---> denaturation of proteins---> bind phosphate. This complex binds free calcium ions to form calcium phosphate crystals. Two steps: initiation & propagation. Iniation is deposition of salts intracellulary in mitochondria & vesicles. Propagation is continuation to form crystals |
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Sites of dystrophic calcification |
Dead tissue: hint: 3 types of necrosis; one CVC (gg bodies), two parasites. Infarcts, breast cancer Degenerated tissue: what does HP have?, atheromas, mockenbergs, uterine fibroids, senile degenerative changes, psammoma bodies in uterine cyst a democrat con on a, meningioma |
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Metastatic calcification defn |
Occurs in normal living tissues due to case 1: 1) hyperparathyroidism 2) bony destructive lesions like MM/ metastatis( think why) 3) Prolonged immobilisation-->disuse atrophy-->hyoercalcemia Case 2: Excessive calcium abs from gut 1) hypervitamisnos d 2)milk alkali syndrome 3) infancy hypercalcemia
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Two cases of metastatic calcification : excessive secretion & excessive absorption |
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Sites of metastatic calcification |
Kidneys: BM. Lungs: alveolar walls Stomach : fundal glands Blood vessels: internal elastic lamina Cornea Synovium ( beans breathe, blood, :P) |
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HYPERPLASIA |
Hyperplasia is increase in number of pafenchymal cells resulting in enlargement of the organ or tissue More cells from g0 are stimulated for recruitment into mitosis. Labile cells- epithelial cells of skin & mucous membranes)/ stable cells( parenchymal cells of liver, adrenal, kidney, thyroid) can undergo this while permanent cells( neurons, skeletal & cardiac muscle) cannot Persists only as long as stimulus persists ( unlike neoplasms) |
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Metaplasia |
Metaplasia is defined as change of one type of epithelial or mesenchymal cell into another type of epithelial m or e cell usually due to abnormal stimuli but reverts back after removal of stimulus |
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Dysplasia |
"Disordered cellular development" 1) increased layers of epithelial cells 2) nuclear hyperchromatism 3) increased mitotic activity 4) n/c ratio increase 5)pleomorphism 6) basal polarity lost Seen in uterine cervix and resp tract wlithelim. Dysplasia progresses into ca in situ |
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Read |
Read |
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Lipofuschin |
Yellowish brown, intracellular lipid pigment, atrophied cells in old age, Locations: myocardial fibers, leydig cells of testis, neurons in senile dementia. That's why called wear & tear ligament Light microscopy: coarse, golden brown, granular, central part of cells around nuclei accumulates. Heart: associated with brown atrophy( muscle watsing) EM: intralysosomal elsectron dense granules in perinuclear location. Granules are lipid-protein complexes. |
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Why is lipofuschin a residual body |
Because it represents the collection of indigestable material in lysosomes after lipid peroxidation. |
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Endogenous pigments exogenous |
Melanin, bilirubin, hemosiderin, porphyrins, lipofuschin Exogenous: inhaled: coal & iron oxide: anthracosis Ingested: carotenemia, chronic lead poisoning- blue lines on teeth Injected: tattooing. Dyes taken up by macrophages so perm |
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