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
different types of necrosis
coagulation, liqufication, caseousm and gangrenous
26
inflammation
``` a nonspecific response to any agent that causes cell injury function - limit extent of injury, remove necrotic debris, prepare for healing process ```
27
acute inflammation
good, limits and contains, and repairs itself
28
chronic inflammation
can be bad, a number of diseases that are associated with chronic inflammation, weeks to years, mediator of chronic disease
29
acute inflammation - vascular
increase of blood flow to injured area, increase in vascular permeability,
30
vascular permeability
the blood vessels become more leaky during inflammation, white blood cells are able to enter in through the spaces
31
exudate
fluid that is accumulating in the interstitial space which causes edema and swelling
32
mast cells stimulated to
release histamine
33
acute inflammation - cellular
leukocytes move from blood into tissue at injury site, leukocytes move to injury site and activate, phagocytosis
34
prostaglandins
promote inflammation, vasodilation, chemotaxis, can be reduced by NSAIDs
35
steps of cellular phase of acute inflammation
leukocytes enter the injured area - margination - emigration/diapedesis - chemotaxis - phagocytosis
36
diapedesis
across, the endothelial cells are leaky, white blood cells enter through the leaks
37
chemotaxis
moving in the direction of the bacteria
38
chemical mediators of inflammation
some are released by bacteria at infection site, others are produced by cells at injury site during and in response to inflammatory activation
39
cytokines
molecules that help the immune system to communicate
40
cardinal signs of inflammation
redness, swelling, heat, and pain
41
chronic inflammation may result from
acute inflammation that persists because the cause is not completely eliminated, non-acute cause present at low level for long time
42
characteristics of chronic inflammation
typically low grade, edema and hyperemia less pronounced, few or no neutrophils present, fibrosis is common
43
transudate
low protein content
44
abscess
collection of pus
45
cellulits
deep skin infection of the dermis
46
ulcer
lesion in an organ
47
mineral accumulation during inflammation
calcium
48
accumulation of insoluble protein
amyloid
49
amyloid
insoluble deposit that never goes away, organ function decreases
50
repair
inflammation has to end for this to begin
51
regenration
nearly complete restoration
52
scarring
fibrous connective tissue repair - does not restore original function - not the same cell type as vefore
53
stages of regeneration
1) inflammation 2) proliferative 3) remodeling
54
proliferative
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
remodeling
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
factors that may detract from the body's ability to repair
continuation of inflammation, advancing age, poor nutrition, diabetes, steroid therapy
57
continuation of inflammation
this is the first step of repair, so it needs to be completed before the body can start to heal