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

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

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

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

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

A

midlest form and ussually reverisible regressive chnages besides amyloidosis

25
Q

protein dystrophies: types

A

albuminoid(parenchymatous), vacuolar = intracellular

hyaline and mucinous= both intracell and interstitial

fibrinoid and amyloid=interstitial

26
Q

albuminoid/ parenchymal dystrophy

A
  • mildest
  • EX: kidney: pathological noxa–>mitochondria becomes enlarged–>granules
  • cloudy swelling, by chabge of color of cytoplasm of cells,
    -functional overload, hypoxia, ischmia
27
Q

vacoluar dystrophy

A
  • videre av alubminoid
  • întake of water–>droplets/vacuoles=hydropic degenration
  • tubular epo broken, see only fragments of cytoplasm
28
Q

hyaline- intracellualr

A
  • 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
Q

epithelial hyaline

A

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
Q

hyalin dyrstrophy: interstitial

A
  • 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
Q

mucin dystrophies: intarceulluar

A
  • 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
Q

mucinous - interstitial

A
  • mucopolysaccharides
  • myxedema: hypofunction of TG-error of metabolism
  • ganglion: near joints and tendons
  • adenocardinomas
    • signet cell apperance
    • mucin stained with PAS
33
Q

fibrinoid

A

mixture of fibrin, fibrinogen, circulating immunocomplexes and complement

34
Q

fibrinoid sytrophies

A
  • autoimmune and immunopathological disorder
  • arterial hypertension: leaking of eaosinophilic, proteinaceous material to interstitum around vv
35
Q

amyloidosis is always

A

irreverisble

36
Q

what is amylodosis

A

disease caused by accumulation of pathological extracellular (interstitial) glycoprotein called amyloid(heterogenous group of proteins)

37
Q

each type of amyloid has 2 components

A

Component P: identical for all types (5%)
- protein of blood plasma

Component F-fibrbillar: different -95
- amyloidogenic protein
-b pleated sheat

38
Q

classification of amyloidosis

A

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
Q

how does amyloid look like

A

eosinophilic, homogenous, amorphous material within interstitum

USE CONGO RED-

40
Q

where can amyloid feposit

A

muscles, haert, kidney, git, liver, spkeen

41
Q

lipid dyrstrophies- intracellular

A

steatosis:
- accuulation of lipids-TAG, in cytoplasm of cells of parenchymatous organs
- liver
- see multiple lipid droplets in hepatocytes

42
Q

lipid dystrophies- interstitial

A

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
Q

mechanism of steatosis development

A

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
Q

types of steatosis

A
  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
Q

carbohydrate dystrophies

A

glycogen dystrophies
- metabolism
- only glycogen can be accumulated, not glucoseee

46
Q

primary and secondary glycogen dystiophies

A

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
Q

Atrophia fusca is what and what does it affect

A

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
Q

Amyotrophia is caused by

A

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 inpoliomyelitis, when the alpha motoneurons of the anterior horns of the spinal cord disappear (so-called amyotrophy = muscle denervation atrophy)
49
Q

dysplastic changes include

A

increased number of mitoses, loss of cell polarity, nuclear pleomirphism

50
Q

what grades are dysplaisa divided into

A
  • 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
Q

what may we see in dysplasia

A
  • 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
Q

what is gallmark of coagulative necrosis

A

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
Q
A

PATHOANA (13 decks)

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