Chap 2- cell response to stress Flashcards

1
Q

adaptation

A
  • stress induced change in a cell

- can happen under normal or disease state

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2
Q

types of adaptation

A
  • hypertrophy
  • hyperplasia
  • atrophy
  • metaplasia
  • dysplasia
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3
Q

Hypertrophy

A
  • increase in cell size, no new cells added
  • due to synthesis of proteins and other cellular organelles required
  • happens in organs not capable of division
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4
Q

Hyperplasia

A
  • addition of new cells
  • organ cells can multiply
  • in response to GF
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5
Q

Atrophy

A
  • decrease in cell size and number
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6
Q

Metaplasia

A
  • change from one cell type to another, reversible

- protective mechanism

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7
Q

Dysplasia

A
  • cells become abnormal or more primitive
  • severity ranges
  • due to chronic irritation or inflammation
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8
Q

Causes of cell injury

A
  • hypoxia
  • immune reactions
  • ROS
  • infection
  • physical/ chemical agents
  • genetics
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9
Q

hypoxia

A
  • limited oxygen carrying capacity

- does not limit bloods ability to carry other nutrients or waste

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10
Q

ischemia

A
  • reduced blood flow
  • stops all nutrients/waste removal
  • causes more rapid response and severe tissue damage compared to hypoxia
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11
Q

mechanism of cell injury

A

Stress -> decreased ATP -> Loss of function of ion pumps -> cell swells

  • in irreversible damage cell swells then bursts
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12
Q

ischemia- reperfusion injury

A
  • organ is damaged when blood supply is reestablished because cell function was weakened
  • cannot reduce oxygen to water properly during oxidative phosphorylation -> ROS
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13
Q

mechanism of reperfusion injury

A
  • increased generation of ROS
  • Intracellular Ca overload
  • increased local inflammatory infiltrate
  • complement activation
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14
Q

ROS

A
  • cause aging, necrosis, apoptosis
  • generated in mitochondria
  • too much damage leads to lipid peroxidation in p. membrane- unstable and reactive p. membrane
  • can lead to protein modifications and DNA damage
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15
Q

manifestation of cell injury

A
  • accumulation of abnormal/toxic substance
  • inadequate removal of normal substance
  • abnormal endogenous substance accumulation
  • substance accumulation due to enzyme deficiency
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16
Q

steatosis

A

fatty change due to abnormal accumulation of TG

17
Q

intracellular protein accumulation can be due to

A
  • excessive synthesis
  • excessive reabsorption
  • defects in cellular transport
  • aggregation of abnormal proteins
18
Q

accumulation of pigments

A
  • can cause cell damage

- can be due to exogenous or endogenous substances that we cannot metabolize

19
Q

dystrophic calcification

A
  • abnormal deposition of Ca salts
  • occurs in cells that are dying
  • Ca levels in blood are normal
20
Q

metastatic calcification

A
  • abnormal deposition of Ca salts

- happens in normal tissues under conditions of hypercalcemia

21
Q

where is calcium normally found

A

mitochondria and e.r.

22
Q

what is the hormone that maintains Ca levels?

A

parathyroid hormone

23
Q

principle causes of metastatic calcification

A
  • elevated parathyroid hormone
  • bone destruction
  • vitamin- d disorders
  • renal failure causing secondary hyperparathyroidism
24
Q

what is the role of vitamin d and ca?

A

vitamin d absorbs Ca, if excess in vitamin d then excess Ca is absorbed and leads to high levels of Ca in blood

25
Q

necrosis

A
  • always pathological
  • due to external agents
  • ATP depleted -> membrane pumps fail -> ion imbalance -> water moves into cell -> swelling -> cell bursts
26
Q

types of necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • fatty
27
Q

coagulative necrosis

A
  • loss of blood supply
  • tissue appears firm and opaque
  • happens in all organs except brain/neurons
28
Q

liquefactive necrosis

A
  • loss of blood supply in the brains/neurons
  • fluid created by enzymes leaking outside of cell
  • fluid is so corrosive they digest other cells around them
29
Q

caseous necrosis

A
  • looks like cheese

- occurs with mycobacterium tuberculosis and some fungal infections

30
Q

fatty necrosis

A
  • occurs in issues that have a lot of fat
  • fat cells attacked by lipase, destroys fat cells
  • lipids combine with Ca to form Ca salts -> soapy/chalky look
31
Q

gangrene

A

necrosis + infection

32
Q

apoptosis

A
  • programmed cell death
  • apoptotic cells break up into fragments called apoptotic bodies which are targets for phagocytes
  • normal or disease states
  • results from activation of enzyme caspases
  • minimal to no inflammation
33
Q

pathological causes of apoptosis

A
  • DNA damage
  • accumulation of misfolded proteins
  • cell death in certain viral infections
  • cytotoxic t cells
  • pathologic atrophy
34
Q

autophagy

A
  • cell eats its own contents, self cleansing process
  • delivery of cytoplasmic material to lysosome for degradation
  • normal and disease states
35
Q

when does autophagy occur?

A
  • starvation
  • maintenance
  • aging
  • exercise
  • can be non-selective- cell eats anything and everything to survive