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PATHOANA 1 > Regressive chnages: necrosis, apooptosis, involution, atropphy, dysplasia, autolysis > Flashcards

Regressive chnages: necrosis, apooptosis, involution, atropphy, dysplasia, autolysis Flashcards

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1
Q

rversible chnages

A

atrophy and dystrophy(lipid, proteins and saccharides)

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2
Q

irreversibel

A

necrosis

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3
Q

differece btw autolysis and necrosis=celldeaths

A

autoysis(lysososmes–>hydrolytic enzymes–>intracell material–>selfdigestion). IN DEAD BODY=POST MORETM CHNAGE AND NO INFLAMMATORY

necrosis: LIVING BODY, SURRONDED BY INFLAMMATORY CELLS

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4
Q

How does cell deth looks like

A

cytoplasm: homogenous, ^eosiniphilic(loss of rna and coagulation of proteins)
nucelar changes:
- pyknonsis: nucleus shrinkage–>darker and smaller
- karyorrhexis: frgamentation on nucleus
- karyolysis: diminishin of nucleus(loss of staining)
cellular details: lost but debris remains

ER:
- rER lose ribosmes
- may ubergo lyssi and drisupt

mitochondria:
- sweeling and leading to microgranular apperance of cytoplasm of cells

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5
Q

necrosis

A

intravital detah of cell, aka surroinding tissue is still alive

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6
Q

necrosis is the result of

A

liberation of intracellular enzymes following upon disruption of cytoplasmic organelles, disintegration of the nucelus and changes in the plasma membrane.

^conc of enzyems in blood

passage of ca2+ and na+ into cell, and K+ and enzymes out

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7
Q

liquefactive necrosis

A
  • semiliquid (dissolution by hydrolytic enxymes)
  • ^LIPID rich
  • Only brain-arterial occlusion, bacterial ifnection
  • cystic spaces
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8
Q

coagulative necrosis: divided into

A

caseous
fibrinoid
fat
haemorrhagic
gummatous

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9
Q

coagulation

A
  • ^protein rich
  • firm and pale
  • still can see som archtectural
  • caused by arterial occlusion
  • HEART AND KIDNEY

COMES FORM PROTEIN DENATURATION

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10
Q

caseous necrosis

A
  • cheese like, soft and white
  • no architerctural (maybe some debris can be seen-like dusty)
  • TUBERCULOSIS
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11
Q

gummatous

A
  • 3rd stage of syphilis- spirochete bacteria(treponema pallidum)
  • firm, rubbery, wollen, tender or painful
    no architerture only pink with few nuclei
  • ## LIVER, SKIN, HEART, BRAIN, BONE , GENITALS
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12
Q

heamorrhagic necrosis

A
  • dark and red
    due to blackage of venous drainage of tissue–>congestion of blood (infarction of jejunum) or arterial failure of perfusion (lung infarcts)
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13
Q

fat necrosis

A
  • fat by digestive enzymes: lipase releas FA from TAG–>FA + ca2+–>soaps–<white chalky deposits
  • ACUTE PANCREATITIS (balzeri necrosis) OR TRAUMA TO PANCREAS, also brast, salivary glands neonates after traumatic delic\very
  • foci of hard, yellow material
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14
Q

fibrinoid necrosis

A
  • artieris in vasuculitis and hypertension
  • deposition of fibrin like material
  • acc of amorphous, basic proteinaceous material in tissue matrix
  • pathologic immune complexe and autoimmune
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15
Q

what is gangrene

A

encrosis with superadded putrefication
- form coagualtive necrosso bc ischemia
- characterized primarly inflammation provoked by virulent bacterial
- is secondary form of necrosis

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16
Q

types of gangrene

A

dry: ischemia-distal part of limbs(toes)-buergers disease

wet:moist tissue like motuh, bowel, lung, cervic, vulva
gas: form of wet by gas forming clostridia

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17
Q

special forms of gangrnee

A

internal gangrene: affect multiple organs like intestines, gallbaldder, appendic
- blocked BF-liek twisting
- fever and pain

fourniers gangrene:
- genital organs
- men more
- in genital are or urinary tarct–>genitla pain, tenderness, redness, swellign

progressive bacterial synergistic gangerene(meleneys grangrene
- after operation–>skin lesions

noma: face
necrotzing fascitis: deep layers of skin

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18
Q

what is atrophy

A

simple decrease in cell size and number–>shrinkage of organs or tisse

pathologic but reversible

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19
Q

involution

A

atrphy of old age

  • natural like thymus, uterus after gravidity, ovarian tissue
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20
Q

simple atrophy

A

decreae of cellualr size like hrart

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21
Q

numeric atrophy

A

decrease of cellular number like BM

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22
Q

causes of atrophy

Study These Flashcards
A

gradual diminution of blood supply=low o2 and nutrients–>fall of cell activity and shrinkage

lipofusinc: undigestied lipid material

23
Q

atrophy leads to

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A

reduced functional activity(diffuse)
- atropgy of cells
- obstruction of galnd duct–>gland atorphy

interrupted nerve supply
- SM in poliomyelitis

endocrine deficiency
- loss of regualtiing mechnaism
- reduced metabolic act
- pituitary deficince–>thyroid, adrenal, gonads, genital organs atrophy

pressure
- interruption of blood supply and interference of funciton
- neoplasm pressing of surrounding tissyes

24
Q

dystrophy is the

Study These Flashcards
A

midlest form and ussually reverisible regressive chnages besides amyloidosis

25
protein dystrophies: types
albuminoid(parenchymatous), vacuolar = intracellular hyaline and mucinous= both intracell and interstitial fibrinoid and amyloid=interstitial
26
albuminoid/ parenchymal dystrophy
- mildest - EX: kidney: pathological noxa-->mitochondria becomes enlarged-->granules - cloudy swelling, by chabge of color of cytoplasm of cells, -functional overload, hypoxia, ischmia
27
vacoluar dystrophy
- videre av alubminoid - întake of water-->droplets/vacuoles=hydropic degenration - tubular epo broken, see only fragments of cytoplasm
28
hyaline- intracellualr
- proteinaceous droplets within cells - not true hyaline - ex: - russels bodies in plasma cells: acc immmunoglobulin - mallory hyalin in hepatocytes: alcholism - cells of procimal tubules in kidney - cooks cells in adenohypofysis: cushings syndrome - intracellular inclusions in viral infections (cytomegalovirus) - hyaline dropletes in tumour cells (pheochromocytomatous) -
29
epithelial hyaline
of prostate and cropora amylacea in prostate glands: COMMON FINDINF IN NODULAR PROSTATIC HYPERPLASIA kidney: within tubules are accumulating proteins and this develops proteins cusps
30
hyalin dyrstrophy: interstitial
- degenerated collagen - chronic inflammation: leads to fibrotisation , healing and scarring - regressive chnges in tumours hyaline: homogenoys apperanse, no cell elemets or vessels, eosinophilic amorphous apperance, similar to cartilage
31
mucin dystrophies: intarceulluar
- aka epithelial mucin, produces by goblet and mucinous glands - quantitative and qualitative disorders in mucin production( hyper or hypocrinia), or qualitiy(dyscrinia) - signet ring morphology: acc in cytoplasm - extracellular accumulaiton of mucin in tumors - cystic fibrosis (mucoviscoidosis)-dyscrinia -
32
mucinous - interstitial
- mucopolysaccharides - myxedema: hypofunction of TG-error of metabolism - ganglion: near joints and tendons - adenocardinomas - signet cell apperance - mucin stained with PAS
33
fibrinoid
mixture of fibrin, fibrinogen, circulating immunocomplexes and complement
34
fibrinoid sytrophies
- autoimmune and immunopathological disorder - arterial hypertension: leaking of eaosinophilic, proteinaceous material to interstitum around vv
35
amyloidosis is always
irreverisble
36
what is amylodosis
disease caused by accumulation of pathological extracellular (interstitial) glycoprotein called amyloid(heterogenous group of proteins)
37
each type of amyloid has 2 components
Component P: identical for all types (5%) - protein of blood plasma Component F-fibrbillar: different -95 - amyloidogenic protein -b pleated sheat
38
classification of amyloidosis
primary: AL type - overproduction of immunoglobulin light chains -b-cell lymphoma-->multiple myeloma secondary: AA type - produced after overproduction of protein of acute phase inflammation, aka serum amyloid protein - long lasting chronic inflammation or some tumours
39
how does amyloid look like
eosinophilic, homogenous, amorphous material within interstitum USE CONGO RED-
40
where can amyloid feposit
muscles, haert, kidney, git, liver, spkeen
41
lipid dyrstrophies- intracellular
steatosis: - accuulation of lipids-TAG, in cytoplasm of cells of parenchymatous organs - liver - see multiple lipid droplets in hepatocytes
42
lipid dystrophies- interstitial
Free lipids in interstitium - not extraceullar steaotis - atherosclerosis Lipomatosis: - PROLIFERATION OF LIPOMATOUS TISSUE - Find in adipocytes-->proliferating in interstitum - in organs-->atrophy and volume of lost tissue replaced by lipomatous tissue=lipomatous atrophy psudohyperthrophy: when we have enlarged organ but functional parenchyme is atrophic
43
mechanism of steatosis development
1) increased intake of lipid - brain infarct: gligal cells pahgocytose necrotic tissue-->intake of tissue rich of lipif-->accumualiton-->foamy cells/lipophages 2) disroders of mobilization of lipids form cells - poisings, drugs - liver enzyme fucntion 3) disorders of intracellualr degradation of lipids - lipidosis: disorders whrre we have inhertided defects in fucntion of enzymes - GAUCHERS disease: acc in cells of mononuclear phagocyting systems - affect apleen, liver, kidney, lungs, brain 4) increased synthesis of lipids
44
types of steatosis
1. stetosis of sagnativa: îalimentary intake of lipids 2. steatosis resoptive-brain infarction, cholesterolosis 3. steatosis transportive-intoxification 4- statosis retentive-due to hypoxia(heart, liveR) - due to venostasis
45
carbohydrate dystrophies
glycogen dystrophies - metabolism - only glycogen can be accumulated, not glucoseee
46
primary and secondary glycogen dystiophies
secondary: acc of gly in non-neoplastic and neoplastic tissues primary: glycogenosis 1: von gierke (glu-6-phos) 2: pompe (lysosomal a1-6, a1-4 glucosidase 3: cori (a1-6 glucosidase 4: andersen (glycosyltransferase 5: mc ardle (muscular phosphorylase 6: hers (hepatal phosphoylase 7: thomson(muscular phosphofructokinase
47
Atrophia fusca is what and what does it affect
brown atrophy - lipofuscin is stored in cells -tissues are darker - common IN LIVER AND MYOCARDIUM - similar in accumulaiton of lipochrome in atrophic adipose tissue
48
Amyotrophia is caused by
Atrophy due from lack of usage, may be due to denervation atrophy. - The basis is also in inactivity in peripheral nerve palsy - Significant muscle atrophy occurs in poliomyelitis , when the alpha motoneurons of the anterior horns of the spinal cord disappear (so-called amyotrophy = muscle denervation atrophy)
49
dysplastic changes include
increased number of mitoses, loss of cell polarity, nuclear pleomirphism
50
what grades are dysplaisa divided into
- Grade I - Mild / low: atypia involves < one - third - Grade II - Moderate / intermediate: atypia involves one to two - thirds of the epithelial thickness - Grade III - Severe / high: atypia involves > two - thirds of the epithelial thickness
51
what may we see in dysplasia
- **Hyperkeratosis** is the increased thickening of stratum corneum, - **Parakeratosis** is Hyperkeratosis with retention of the nuclei in corneum, - **Acanthosis** is Epidermal hyperplasia of the Stratum spinosum
52
what is gallmark of coagulative necrosis
hallmark of coagulative necrosis is conversion of normal cells into tombstones - outlines of the cells are retained so that the cell type can still be recognised but their cytoplasmic and nuclear details are lost.
53

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