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understanding human disease > chapter 4 > Flashcards

chapter 4 Flashcards

1
Q

hypoxia

A

less oxygen then normal

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2
Q

anoxia

A

no oxygen

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3
Q

how can cells become injured

A

hypoxia, anoxia, trauma, radiation, inflammation, immune responses, genetic defects, nutritional imbalance, trauma, aging, dehydration

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4
Q

most common cell injury

A

hypoxia

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5
Q

hypoxia most often occurs due to?

A

ischemia

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6
Q

ischemia

A

insufficient blood supply, not enough blood flow, the blood is carrying the oxygen throughout the body

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7
Q

failure of Na+/K+ pump

A

maintains the balance between sodium and potassium inside and outside of the cell
- water follows salt
sodium should be pumped out and potassium in

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8
Q

steatosis

A

accumulation of fat

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9
Q

hydropic changes

A

cell swelling

  • loss of atp
  • sodium remains in cell
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10
Q

cell response to injury

A

not an all or nothing phenomenon

  • response to a given stress depends on the type, status and genetic make up of the inured cell
  • cells are complex interconnected systems, and single local injuries can result in multiple secondary and tertiary effects
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11
Q

adaptations of cells

A

altered growth, atrophy, hypertrophy, metaplasia, dysplasia

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12
Q

atrophy

A

shrinkage, decrease in cell size

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13
Q

physiological atrophy

A

aging

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14
Q

pathological atrophy

A

decreased blood supply, decreased nutrtiion, lack of neural or hormone support

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15
Q

hypertrophy

A

increase in cell size

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16
Q

hypertrophy due to

A

hormonal stimulation

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17
Q

hypertrophy results in

A

increased protein synthesis within cell, decrease protein breakdown

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18
Q

hyperplasia

A

increase in cell number

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19
Q

hyperplasia due to

A

hormonal stimulation, increased functional demand, chornic stress

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20
Q

hypereplasia results in

A

increased cell division, if the cell can divide

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21
Q

metaplasia

A

replacement of one cell type with another
- most common is epithelium
reversible

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22
Q

dysplasia

A

change in cell resulting in abnormal cell size, shape or organization

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23
Q

apoptosis

A 
programmed cell death 
- not always an indication of injury
- removes cells that are "worn out" 
- removes unwanted tissue 
physiological or pathological
24
Q

necrosis

A

unregulated death

cells swell and rupture - damage nearby cells and inflammation results

25
Q

different types of necrosis

A

coagulation, liqufication, caseousm and gangrenous

26
Q

inflammation

A 
a nonspecific response to any agent that causes cell injury 
function - limit extent of injury, remove necrotic debris, prepare for healing process
27
Q

acute inflammation

A

good, limits and contains, and repairs itself

28
Q

chronic inflammation

A

can be bad, a number of diseases that are associated with chronic inflammation, weeks to years, mediator of chronic disease

29
Q

acute inflammation - vascular

A

increase of blood flow to injured area, increase in vascular permeability,

30
Q

vascular permeability

A

the blood vessels become more leaky during inflammation, white blood cells are able to enter in through the spaces

31
Q

exudate

A

fluid that is accumulating in the interstitial space which causes edema and swelling

32
Q

mast cells stimulated to

A

release histamine

33
Q

acute inflammation - cellular

A

leukocytes move from blood into tissue at injury site, leukocytes move to injury site and activate, phagocytosis

34
Q

prostaglandins

A

promote inflammation, vasodilation, chemotaxis, can be reduced by NSAIDs

35
Q

steps of cellular phase of acute inflammation

A

leukocytes enter the injured area

  • margination
  • emigration/diapedesis
  • chemotaxis
  • phagocytosis
36
Q

diapedesis

A

across, the endothelial cells are leaky, white blood cells enter through the leaks

37
Q

chemotaxis

A

moving in the direction of the bacteria

38
Q

chemical mediators of inflammation

A

some are released by bacteria at infection site, others are produced by cells at injury site during and in response to inflammatory activation

39
Q

cytokines

A

molecules that help the immune system to communicate

40
Q

cardinal signs of inflammation

A

redness, swelling, heat, and pain

41
Q

chronic inflammation may result from

A

acute inflammation that persists because the cause is not completely eliminated, non-acute cause present at low level for long time

42
Q

characteristics of chronic inflammation

A

typically low grade, edema and hyperemia less pronounced, few or no neutrophils present, fibrosis is common

43
Q

transudate

A

low protein content

44
Q

abscess

A

collection of pus

45
Q

cellulits

A

deep skin infection of the dermis

46
Q

ulcer

A

lesion in an organ

47
Q

mineral accumulation during inflammation

A

calcium

48
Q

accumulation of insoluble protein

A

amyloid

49
Q

amyloid

A

insoluble deposit that never goes away, organ function decreases

50
Q

repair

A

inflammation has to end for this to begin

51
Q

regenration

A

nearly complete restoration

52
Q

scarring

A

fibrous connective tissue repair

  • does not restore original function
  • not the same cell type as vefore
53
Q

stages of regeneration

A

1) inflammation
2) proliferative
3) remodeling

54
Q

proliferative

A

a cell proliferates to make new cells
- epithelialization by regenerating basal cells
granulation - filling in the wound with new capillaries, epithelial cells, filling in the gap temporarily until the correct cells can be formed, red because of new capillaries

55
Q

remodeling

A

maturation and reorganization
- reorganization of collagen - so its much more uniform in direction, lose blood vessels, you would want to remove blood vessels because blood vessels aren’t as strong as collagen

56
Q

factors that may detract from the body’s ability to repair

A

continuation of inflammation, advancing age, poor nutrition, diabetes, steroid therapy

57
Q

continuation of inflammation

A

this is the first step of repair, so it needs to be completed before the body can start to heal

understanding human disease (25 decks)

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