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Pathoma > Growth Adaptations, Cell Injury, Cell Death > Flashcards

Growth Adaptations, Cell Injury, Cell Death Flashcards

1
Q

hypertrophy

A

gene activation, protein synthesis and production of organelles

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2
Q

hyperplasia

A

new cells from stem cells

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3
Q

decrease in cell number

A

apoptosis

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4
Q

decrease in cell size

A

ubiquitin-proteosome degradation

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5
Q

metaplasia

A

reprogramming of stem cells

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6
Q

dysplasia

A

disordered cell growth

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7
Q

aplasia

A

failure of cell production during embryogenesis

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8
Q

hypoplasia

A

decrease in cell production

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9
Q

high altitude

A

decreased PAO2

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10
Q

hypoventilation

A

decreased PAO2

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11
Q

diffusion defect

A

decreased PaO2

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12
Q

CO poisoning

A

PaO2 normal, SaO2 decreased

cherry red skin

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13
Q

anemia

A

PaO2 normal, SaO2 normal

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14
Q

methemoglobinemia

A

PaO2 normal, SaO2 decreased

cyanosis

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15
Q

the hallmark of reversible injury

A

swelling

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16
Q

the hallmark of irreversible injury

A

plasma (Ca), mitochondrial (cytochrome c), lysosomal (hydrolytic enzymes) membrane damage

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17
Q

low ATP causes

A

1) Na and H2O build up in cell
2) Ca build up in cytosol
3) lactic acid –> low pH –> denatured protein/DNA

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18
Q

the hallmark of cell death is

A

loss of nucleus

1) pyknosis
2) karyorrhexis
3) karyolysis

19
Q

coagulative necrosis

A

tissue firm; cell shape and organ structure preserved – no nucleus

ie ischemic infarction

20
Q

liquefactive necrosis

A

tissue liquefied; enzymatic lysis of cells

ie brain infact, abscess, pancreatitis

21
Q

gangrenous necrosis

A

mummified tissue

ie ischemia of lower limb & GI tract

22
Q

caseous necrosis

A

soft; friable tissue; “cottage cheese-like”
coagulative + liquefactive

ie granulomatous inflammation

23
Q

fat necrosis

A

necrotic adipose tissue w/ chalky-white apperance from Ca

ie fat trauma

24
Q

fibrinois necrosis

A

necrosis in blood vessel wall

25
Q

apoptosis is mediated by

A

caspases that activate

1) proteases breakdown cytoskeleton
2) endonucleases breakdown DNA

26
Q

intrinsic mitochondrial pathway

A

inactivation of Bcl2 –> leak of cytochrome c from innter mitochondria into cytoplasm –> caspases activated

27
Q

extrinsic receptor-ligand pathway

A

FAS ligand binds to CD95 –> caspases activated

TNF binds to TNF receptor –> caspases activated

28
Q

cytotoxin CD8+ T-cell mediated pathway

A

1) perforins create pores in membrane

2) granzymes activated caspase

29
Q

free radicals

A

O2 –> O2- –> H2O2 –> OH

30
Q

superoxide dismutase

A

O2- –> H2O2

31
Q

glutathione peroidase

A

2GSH + free radical –> GS-SG + H2O

32
Q

catalase

A

H2O2 –> O2 + H2O

33
Q

generation of free radicals

A

ionizing radiation
inflammation
metals
drugs/chemicals

34
Q

elimination of free radicals

A

antioxidants
enzymes
metal carrier proteins

35
Q

free radicals cause cell damage by

A

peroxidation of lipids
oxidation of DNA/proteins

ie CCl4, reperfusion injury

36
Q

carbon tetrachloride

A

dry cleaning chemical
p450 of hepatocytes
swelling of RER –> ribosomes detach –> impaired protein synthesis –> decreased apolipoproteins –> fatty change in liver

37
Q

primary amyloidosis

A

systemic deposition of AL amyloid

ie plasma cell dyscrasia

38
Q

secondary amyloidosis

A

systemic deposition of AA amyloid

ie chronic inflammation, malignancy, and Familial Mediterranean fever

39
Q

DMT2

A

amylin deposits in pancreas

40
Q

Alzheimer dz

A

AB amyloid deposits in brain (gene 21)

41
Q

dialysis-associated

A

B2 microglobulin in joints

42
Q

medullary carcinoma

A

calcitonin amyloid

43
Q

senile cardiac amyloidosis

A

non-mutated serum transthyretin deposits in heart

44
Q

familial amyloid cardiomyopathy

A

mutated serum transthyretin deposits in heart –> restrictive cardiomyopathy

Pathoma (3 decks)

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