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Advance Patho test #1 > Homeostasis and Disease > Flashcards

Homeostasis and Disease Flashcards

1
Q

Pathological process

A

disease process, loss of homeostasis, which really forms the basis of most of the disease processes

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2
Q

Pathologic stimuli can be

A

intrinsic or innate coming from the environment-external exposures, deprivations, nutritional

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3
Q

Cellular adaptation

A

Cells are able to compensate for challenges to homeostasis through a dynamic set of processes

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4
Q

Cellular injury

A

When cell doesn’t regain homeostatsis

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5
Q

regulated Variables

A

have a physical receptor Temp, BP, glucose keep are body wnl

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6
Q

stimulus or signal

A
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7
Q

Afferent

A

means towards, consists of nerves for neurological signals and blood for endrocrine

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8
Q

Integrating center

A

hypothalmus, cardiovascular and respiratory control,compares info to a range.

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9
Q

Efferent pathway

A

carries a response towards exit out, towards periphery.

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10
Q

Controlled variables

A

Heart rate, vaso const, vaso dilate also, known as effector response

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11
Q

Negative feedback

A

bringing things back to original signal

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12
Q

Receptors are

A

thermo, baro-bp, chemo, osomo,mechanoreceptors.

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13
Q

regulated variables are the…

A

Anchor

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14
Q

Patho

A

disease causing

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15
Q

Genetic causes

A

may be inherited

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16
Q

Mutations

A

genetic changes

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17
Q

Acquired mutation

A

environmental trauma, intoxication, or deficiency- nutritional or absence of a metabolite.

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18
Q

Diseases usually require both

A

genetic and environmental

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19
Q

Proteins are impacted in order to

A

cause a disease state

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20
Q

Disease process causes.

A

inflammation, aberrant immune response.

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21
Q

etiology

A

underlying cause of disease

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22
Q

Metobolic and Morphological

A

hallmarks of disease

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23
Q

Severity and Duration determine

A

outcome

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24
Q

trauma, deficiency are

A

external, intox, deficiency

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25
Q

Cell injury can be

A

hypoxic lack of o2, hypoxic injury. emia means bld

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26
Q

Ischemia

A

insufficient bld flow

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27
Q

oxygen most efficient

A

energy prod, o2 bound to hemoglobin

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28
Q

Aerobic metabolism releases

A

lactic acid

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29
Q

Acids are

A

denaturing causing cell injury and death.

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30
Q

oxidative damage

A

One of the things that can be produced during normal metabolism is what are called reactive oxygen species or ROS

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31
Q

ROS

A

unpaired oxygen molecules that produced superoxides

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32
Q

ROS are produced

A

clean up and inactive

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33
Q

Excessive ROS

A

leads to oxidative stress

34
Q

oxadative molecules come from

A

bursts, which are immature immune cells.

35
Q

Macrophages and neutrophils are considered

A

bursts

36
Q

Bursts are produced

A

from immature immune cells

37
Q

Macrophages and neutrophils

A

try to kill off microbes

38
Q

Superoxides have

A

unpaired electrons

39
Q

Unpaired electrons interact with

A

protein and lipids

40
Q

Unpaired electrons

A

damage protein and lipid cell membranes, causes cell damage under oxadative stress.

41
Q

A cell can

A

reverse it’s course

42
Q

Influx of CA+ =

A

cell death

43
Q

hypoxia

A

lack of oxygen

44
Q

Ischemia

A

reduction in bld flow

45
Q

hypoglycemic state

A

required for good energy production

46
Q

Aerobic - Anaerobic +

A

lactic acid

47
Q

Lactic acid is

A

denaturing

48
Q

Denaturing leads to

A

cell death

49
Q

In a lactic acid state we have

A

decrease ph, that causes damage to lipids and proteins that protect cell membrane.

50
Q

In anerobic conditions we

A

have decrease ph, and damages the cell.

51
Q

Limited ATP in anerobic state

A

contributes to impair cell function.

52
Q

Thrombus in a bld vessel is an example of

A

decrease oxidative phosphorylation and increase in our anaerobic process like glycolysis

53
Q

End of glycolysis

A

under anaerobic conditions produces lactic acid.,decrease ph hat leads to denaturing, which can be seen as clumping of nuclear material like the chromatin and eventually, can lead to the breakdown of lipids in the lysosomes, which are bags of basically degradative enzymes inside of cells. And that can lead to the autodigestion or autolysis, sometimes called autolysis of the cell itself.

54
Q

chromatin

A

clumping

55
Q

lipids break down into

A

lysomes

56
Q

lysomes

A

degradative enzyme inside cell, known as autolysis

57
Q

Autolysis

A

degeneration of the cell

58
Q

oxidative phosphorylation running at its full speed,

A

we will have a reduction in the amount of ATP that can be produced. And this is going to compromise a lot of the barriers at the membrane, such as our sodium-potassium ATPase.

59
Q

Water

A

causes cell to swell

60
Q

blebs

A

extension on the cell

61
Q

oranelles inside cell

A

swell

62
Q

Depending on

A

degree maybe reversible

63
Q

Lysosomal enzymes released

A

causes impairment to cell membrane, ca+ comes in now=irreversable cell injury=cell death.

64
Q

ROS is an ex of

A

superoxide

65
Q

Superoxides are

A

free radicals

66
Q

SOD converates to

A

superoxide and into hydrogen peroxide.

67
Q

Catalase

A

released from opening cells acting on hydrogen peroxide-water and oxygen seeing bubbles is an evidence of catalase reaction

68
Q

Refusion injury

A

plagues settings of transplant when we’re actually transplanting organs and tissues and that tissue is deprived for an extended period of time from blood, therefore for oxygen.

69
Q
A

What happens is we start to see an excessive amount of reactive oxygen species being produced by those cells. And over time, we’re going to have a depletion of our cleanup system. So our SOD and catalase protection system becomes depleted.

70
Q
A

reperfusion injury specialists that look at after transplant is that when we reperfuse that tissue, there’s an anticipation that we’re going to have additional cellular injury and potentially cell death. A

71
Q
A

And that’s because these reactive oxygen species are produced right away, but our cleanup systems are actually delayed in getting to their full speed. So that can lead to some cellular injury or damage, and that’s referred to as reperfusion injury.

72
Q

reprefusion injury is

A

combo of extra oxidative stress and oxidative damage

73
Q

Infusing antioxidants

A

like superoxide dismutase or catalase to reestablish our clean up system.

74
Q

Reprefusion injury occurs during

A

transplants and stroke

75
Q

Glucose 6-phospate dehdrogenese

A

is a genetic mutation causing reprefusion injury

76
Q

Fava beans

A

an example of extra oxidative stress

77
Q

Extra oxadative stress

A

can lead to cell injury and cell death

78
Q

death knell

A

influx of CA+

79
Q

Physical injury can compromise

A

the cell directly

80
Q

alteration in CA+ pump, altered electrolyte can

A

impair the pump and cause alteration in calcium homestatsis

Advance Patho test #1 (7 decks)

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