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MDTI > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

hypoxia

A

oxygen deprivation due to inadequate oxygenation of the blood (cardiorespiratory failure, CO poisoning)

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2
Q

Ischemia

A

loss of blood supply. more rapidly injurious than hypoxia bc of loss of both oxygen and nutrients. No glycolytic energy production can occur (as in hypoxia)

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3
Q

cellular adaptations

A

physiologic and morphologic cellular changes leading to a new but altered steady state. caused by excessive stress or pathologic stimuli. REVERSIBLE

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4
Q

four types of cellular adaptations

A

hyperplasia, hypertrophy, atrophy, metaplasia

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5
Q

hyperplasia

A

an increase in the number of cells in an organ or tissue due to an increased demand for function

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6
Q

types of hyperplasia

A

normal hormonal (uterus during pregnancy), compensatory (regeneration), pathologic (excessive hormonal stimulation to divide)

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7
Q

hypertrophy

A

an increase in cell size due to increased protein synthesis (not due to cell swelling). caused by in increased demand for function, mechanically or hormonally.

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8
Q

types of hypertrophy

A

skeletal muscle (exercise, steroids), cardiac (hypertension, valvular stenosis)

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9
Q

atrophy

A

decrease in cell size. caused by decreased workload, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, denervation

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10
Q

metaplasia

A

a reversible change in the differentiation program of tissue stem cells to a different mature cell type

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11
Q

classic example of metaplasia

A

protective change from psuedostratified to squamous metaplasia of the respiratory tract due to smoking. loss of mucus production/cilia. also metaplasic changes may predispose to neoplastic formation and cancer

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12
Q

which cells are most susceptible to ischemic injury?

A

neurons>myocardium, hepatocytes, renal epithelia>fibroblast, epidermis, skeletal muscle

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13
Q

consequences of ischemia

A

decreased oxphos=decreased ATP=decreased Na pump (swelling), increased glycolysis (acidosis), decreased protein synthesis (lipid deposition)

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14
Q

what is generally indicative of irreversible cell injury

A

large increase in intracellular Ca2+ (after damage to membrane. activates proteases and leads to lysosomal lysis which damages membranes)

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15
Q

how does mitochondrial dysfunction lead to cell injury?

A

via formation of free radicals

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16
Q

defenses against free radicals

A

antioxidants, superoxide dismutase, catalase, glutathione peroxidase, ferritin

17
Q

ferritin

A

an iron is an iron storage and detoxifying protein. limits toxicity due to iron donating electrons to H2O2–> OH*

18
Q

which nucleic bases do free radicals react with?

A

A & T, cause single chain breaks

19
Q

lipid peroxidation

A

free radicals interact with the double bonds in poly-unsaturated fatty acids resulting in lipid peroxides, which react with O2 which ultimately produces lipid hydroperoxides. (chain rxn of radical formation)

20
Q

carbon tetrachloride

A

dry cleaning solvent. converted by cytochrome P-450 to highly reactive free radical. Causes lipid peroxidation (a chain rxn). ER in liver is affected=decreased protein synthesis and fat export (hepatocyte fat accumulation=cell death)

21
Q

necrosis

A

morphological changes that follow cell death due to the degradative actions of enzymes and protein denaturation

22
Q

three types of necrosis

A

coagulative, caseous, liquefactive

23
Q

coagulative necrosis

A

most common type of necrosis, proteins denature & coagulate, cytoplasm becomes eosinophilic, cellular architecture is preserved. characteristic pattern of irreversible ischemic injury to solid organs.

24
Q

why is coagulative necrosis surrounded by red border?

A

RBCs pile up since their entry into the necrotic area is impaired

25
Q

liquefactive necrosis

A

hydrolytic enzymes predominate over protein denaturation. rapid softening with loss of cell outlines. characteristic of brain tissue and inflammatory rxns.

26
Q

caseous necrosis

A

combination of coagulative and liquefactive. principally associated with TB. cells aren’t totally liquefied, but outlines are not preserved and necrotic areas is surrounded by granulomatous inflammatory wall.

27
Q

apoptosis

A

morphological manifestation of programmed cell death, which is designed to eliminate unwanted cells through the activation of a coordinated set of regulatory and effector proteins

28
Q

morphological changes associated with apoptosis

A

cell shrinks, chromatin condenses, cytoplasmic blebs break off, macrophages phagocytose blebs, membrane remains in tact, doesn’t elicit inflammation

29
Q

p53

A

normally delays cell cycle allowing for DNA damage repair, but stimulates apoptosis when repair fails. mutated in tumors

30
Q

extrinsic pathway of apoptosis (death receptor pathway)

A

initiated by binding of FasL from CTLs to Fas death receptor. multimerization in induced and activates FADD protein, which activates pro-caspase 8, the executioner proteins.

31
Q

Bcl-2 protein family function

A

regulates outer membrane permeability. consist of BH genes

32
Q

apoptotic mitochondrial pathway

A

outer mitochondrial membrane becomes permeable and pro-apoptotic proteins (cytochrome c) are released, which neutralize apoptotic inhibitors in cytosol. Forms apoptosome, which activates caspases

33
Q

caspase

A

the executioner proteins of apoptosis that process substrates leading to DNA degradation, chromatin condensation, and membrane blebbing

34
Q

what is required for the apoptosome formation?

A

ATP

35
Q

multi domain, anti apoptotic protein in Bcl-2 family

A

Bcl-2 (inhibits permeability)

36
Q

which Bcl-2 gene on its own is pro-apoptotic?

A

BH3 (enhances permeability)

37
Q

multi-domain, pro apoptotic protein in Bcl-2 family

A

Bak, Bax (enhances permeability)

38
Q

what sets the threshold of susceptibility to apoptosis for the mitochondrial/intrinsic pathway?

A

ratio of anti to pro apoptotic proteins in the membrane

MDTI (42 decks)

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