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
necrosis
- always pathological - due to external agents - ATP depleted -> membrane pumps fail -> ion imbalance -> water moves into cell -> swelling -> cell bursts
26
types of necrosis
- coagulative - liquefactive - caseous - fatty
27
coagulative necrosis
- loss of blood supply - tissue appears firm and opaque - happens in all organs except brain/neurons
28
liquefactive necrosis
- 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
caseous necrosis
- looks like cheese | - occurs with mycobacterium tuberculosis and some fungal infections
30
fatty necrosis
- 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
gangrene
necrosis + infection
32
apoptosis
- 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
pathological causes of apoptosis
- DNA damage - accumulation of misfolded proteins - cell death in certain viral infections - cytotoxic t cells - pathologic atrophy
34
autophagy
- cell eats its own contents, self cleansing process - delivery of cytoplasmic material to lysosome for degradation - normal and disease states
35
when does autophagy occur?
- starvation - maintenance - aging - exercise - can be non-selective- cell eats anything and everything to survive