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MOD-E1 > Chapter 2: Cell responses to stress and toxic insults > Flashcards

Chapter 2: Cell responses to stress and toxic insults Flashcards

1
Q

what are four aspects of a disease process that form the core of pathology

A

cause (etiology)
pathogenesis
morphologic changes
clinical manifestations

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2
Q

what are the two principal pathways of cell death

A

apoptosis

necrosis

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3
Q

physiologic hyperplasia vs pathologic hyperplasia

A

physiologic - due to action of hormones of GFs

pathologic - excessive or inappropriate actions of hormones of growth acting on target cells

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4
Q

what are some circumstances in which physiologic hyperplasia can occur

A

when there is a need to increase functional capacity of hormone sensitive organs

when there is a need for compensatory increase after damage or resection

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5
Q

atrophy definition

A

decrease in both size and number of cells –> reduction of size of organ or tissue

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6
Q

common causes of pathologic atrophy

A 
decreased workload (disuse)
loss of innervation
diminished blood supply 
inadequate nutrition
loss of endocrine stimulation
pressure
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7
Q

what is senile atrophy

A

brain atrophy caused by diminished blood supply as a result of atherosclerosis

in late adult life

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8
Q

marasmus

A

profound protein-calorie malnutrition

utilizing skeletal muscle proteins as a source of energy after all else is depleted

results in cachexia (marked muscle wasting)

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9
Q

in chronic inflammatory diseases what could cause cachexia

A

TNF thought to be responsible for decreasing appetite and lipid depletion –> muscle atrophy

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10
Q

characteristics of cells in atrophic muscles

A

fewer mito
fewer myofilaments
fewer RER

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11
Q

in mechanism of atrophy, what is main degradation pathway of cellular proteins

A

ubiquitin-proteasome pathway

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12
Q

most common epithelial metaplasia

what could induce it

A

columnar to squamous metaplasia in the respiratory tract in response to chronic irritation

can also be induced by vitamin A deficiency

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13
Q

Barrett esophagus

A

esophageal squamous epithelium –> intestinal-like columnar type bc of GERD

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14
Q

hallmarks of reversible cell injury

A

reduced oxphos –> decreased ATP and cellular swelling (caused by changes in ion concentrations and water influx)

intracellular organelles (mito and cell skeleton) may show alterations

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15
Q

morphological features of apoptosis

A

reduced cell size
fragmentation of nucleus into nucleosome size
intact; altered PM especially arrangement of lipids
intact cellular contents; may be in apoptotic bodies
no inlammation
often physiologic

chromatin condensation most characteristic
formation of cytoplasmic blebs and apoptotic bodies
phagocytosis of apoptotic cells or cell bodies usually
by macros

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16
Q

morphological features of necrosis

A

enlarged cell size
pyknosis–>karyorrhexis–>karyolysis (nucleus)
disrupted PM
enzymatic digestion of cell contents; may leak out
frequent inflammation
pathologic

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17
Q

two features of reversible cell injury that can be seen on light microscopy

A

cell swelling

fatty change

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18
Q

coagulative necrosis morphology

A

architecture of dead cells is preserved for a span of at least some days

injury denatures not only structural proteins but enzymes as well

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19
Q

liquefactive necrosis morphology

A

digestion of the dead cells

“means brain necrosis” - dobson

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20
Q

caseous necrosis morphology

A

“cheese necrosis”

indicative of mycrobacterial tuberculosis (MTB)

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21
Q

fibrinoid necrosis morphology

A

usually seen in immune reactions involving blood vessels

immune complexes deposit on walls of arteries
bright pink and amorphous appearance in H&E stains

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22
Q

what can cause dystrophic calcification

A

if necrotic cells and cellular debris are not promptly destroyed and reabsorbed, can cause calcium salts and other minerals to deposit and become calcified

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23
Q

what is a fundamental cause of necrotic cell death

A

reduction in ATP levels

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24
Q

major causes of ATP depletion

A

reduced supply of oxygen and nutrients
mito damage
some toxins

25
Q

results of depletion of ATP to 5 to 10% of normal

A

NaK ATPase activity reduced –> cell swelling bc of [ion] and water gain

cellular energy metabolism is altered – in ischemic events switches to anaerobic glycolysis –> glycogen stores are rapidly depleted and accumulation of lactic acid

failure of Ca pump –> influx Ca

decreased protein synth

unfolded protein response

necrosis

26
Q

major consequences of mito damage (3)

A

mitochondrial permeability transition pore
ROS (from abnormal oxphos due to pore)
caspases (apop)

27
Q

what does the mitochondrial permeability transition pore do to the mito

A

disperses membrane potential –> failure of oxphos and decreases ATP

can also be opened by accumulation of Ca in mito

28
Q

cyclophilin D

A

protein component in mito permeability transition pore

target of cyclosporin (immunosuppresive) –> closes pore
reduces injury

29
Q

what can increased intracell Ca cause

A

opening of mito permeability transition pore

activation of phospholipases, proteases, endonucleases, and ATPases

induction of apop –> caspases and pore opening

30
Q

mechanisms to remove free radicals

A

antioxidants (vit E, A, ascorbic acid, glutathione)

binding iron and copper (catalyze formation of ROS) to their storage and transport proteins

enzymes (catalase, SODs, glutathione peroxidase)

31
Q

effects of ROS relevent to cell injury (3)

A

lipid peroxidation – causes membrane damage

oxidative modification of proteins

lesions in DNA

32
Q

two phenomena that characterize irreversibility

A

inability to reverse mito dysfxn

profound disturbances in membrane f(x)

33
Q

what is the most common type of cell injury in clinical medicine and what is it a result of

A

ischemia

results from hypoxia induced by reduced blood flow commonly due to a mechanical arterial obstruction

34
Q

how long does it take for heart muscle to stop contracting in a coronary artery occlusion

A

(stops within) 60 seconds

loss of contractility does not mean cell death

35
Q

hypoxia-inducible factor-1

A

mammalian cell protective response to hypoxic stress

promotes new blood vessel formation

36
Q

two mechanisms chemicals induce injury

A

direct toxicity

conversion to toxic metabolites

37
Q

two pathways of activating caspases

A

intrinsic (mito) pathway –> caspase-9

(extrinsic) death receptor pathway –> caspase-8,10

38
Q

anti-apoptotic proteins

A

BCL2, BCL-XL, MCL1, IAPs

in outer membrane and cytosol and ER membranes
prevent leakage of cyt c and other pro-apop proteins into cytosol

39
Q

pro-apoptotic proteins

A

BAX, BAK

promote mito permeability

40
Q 
sensor proteins
(intrinsic pathway apop)
A

BH3-only proteins

BAD, BID, BIM, puma, nox

41
Q

what protein can inhibit the extrinsic apop pathway

A

FLIP

binds pro-caspase-8 but can’t cleave
lacks protease domain

42
Q

executioner caspases

A

3 and 6

43
Q

kinases involved with necroptosis

A

receptor associated kinase 1 and 3 (RIP1 & 3)

44
Q

three types of autophagy

A

chaperone-mediated - direct translocation across
lysosomal membrane by chaperone proteins
microautophagy - invag of lysosome
macroautophagy - major form

45
Q

useful marker for indication of autophagy

A

LC3

46
Q

pathways of abnormal intracellular accumulations (4)

A

inadequate removal –> fatty liver

defect in protein folding, transport

lack of enzyme –> lysosomal storage diseases (accumulation of endogenous materials

ingestion of indigestible materials –> accumulation of exogenous materials

47
Q

atherosclerosis

A

smooth m cells and macrophages within intimal layer of the aorta and large arteries are filled with lipid vacuoles, most of which are made up of cholesterol and cholesterol esters

foam cells

48
Q

Xanthomas

A

intracellular accumulation of cholesterol within macrophages

49
Q

cholesterolosis

A

focal accumulation of cholesterol-laden

50
Q

nieman-pick disease, type c

A

lysosomal storage disease

mutations affecting an enzyme involved in cholesterol trafficking –> cholesterol accumulation in multiple organs

51
Q

what pigment is a telltale sign of free radical injury and lipid peroxidation

A

lipofuscin (brown lipid)

52
Q

two forms of pathologic calcification

A

dystrophic

metastatic – almost always hypercalcemia 2nd to some disturbance in Ca metabolism

53
Q

4 principle causes of hypercalcemia

A

increased PTH
resorption of bone tissue
vitamin-D related disorders
renal failure

54
Q

cellular aging is the result of

A

a progressive decline in cellular function and viability

55
Q

two mechanisms that underlie senescence

A

telomere attrition

activation of tumor suppressor genes

56
Q

how do cancer cells overcome senescence

A

reactivate telomerase to lengthen telomeres

57
Q

rapamycin

A

inhibits mTOR pathway – increased lifespan of middle aged mice

promotion of autophagy

58
Q

how does restricting caloric intake increase longevity

A

reducing signaling intensity of IGF-1

increasing sirtuins

59
Q

sirtuins f(x)

A

promote expression of proteins that inhibit metabolic activity, reduce apop, stim protein folding, and inhibit harmful effects of O2 free radicals

contribute to metabolic adaptations to caloric restriction
promote genomic integrity by activating DNA repair enzymes through deacylation

MOD-E1 (3 decks)

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