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18 Cards in this Set

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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)

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 ?

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

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)

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

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

Fibrinoid necrosis

Gross: brightly eosinophilic, hyaline like deposits in vessel wall


Surrounded by nuclear debris of neutrophils

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

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

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


Two cases of metastatic calcification : excessive secretion & excessive absorption

Sites of metastatic calcification

Kidneys: BM.


Lungs: alveolar walls


Stomach : fundal glands


Blood vessels: internal elastic lamina


Cornea


Synovium


( beans breathe, blood, :P)

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)

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

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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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.

Why is lipofuschin a residual body

Because it represents the collection of indigestable material in lysosomes after lipid peroxidation.

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