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Physiology I Block 4 > Blood Flow > Flashcards

Blood Flow Flashcards

1
Q

each tissue control its own

A

blood flow in proportion to its needs

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2
Q

tissues blood flow is closely related to its

A

metabolic rate

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3
Q

as metabolic rate increases,

A

tissue blood flow increases

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4
Q

skeletal muscle blood flow

A

don’t get much even though make up a lot of body weight

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5
Q

every day exercise will do what to skeletal muscle

A

increase the blood flow to the skeletal muscles

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6
Q

why not just give all the blood flw all they might ever need?

A

heart can’t keep up with that, so it jsut gives tissues what they need

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7
Q

what is acute control

A

local control within tissues: rapid, seconds to minutes

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8
Q

vasoconstriction and vasodilation is acute or long term control?

A

acute

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9
Q

what is long term control

A

increases/derease in size and number of blood vessels

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10
Q

how long does long term control take

A

ours, days, weeks -takes awhile

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11
Q

how long does acute control take

A

not long - imediate

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12
Q

for us students, where should a lot of blood flow be going right now?

A

brain

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13
Q

what factor is most important for blood flow control

A

oxygen

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14
Q

as oxygen saturation decreases, blood flow

A

increases

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15
Q

locally in interstitial fluid, the cells are eating up oxygen which is what causes

A

blood flow to increase

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16
Q

physiological examples where blood flow increases

A

high altitudes
pneumonia
carbon monoxide poisoning
cyanide poisoning

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17
Q 
high altitudes
pneumonia
carbon monoxide poisoning
cyanide poisoning
the common theme in all of these, that cause blood flow to increase is:
A

lower oxygen throughout body

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18
Q

cyanide poisoning

A

doesn’t allow oxygen to bind in body

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19
Q

vasodilator theory

A

when the cell is using up oxygen it releases substances like adenosine, CO2, lactic acid ,postassium ions, histamine, and the local substances diffuse back to the arterioles and dilate them, the dilation causes increase in blood flow to the tissue that is releasing the chemicals

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20
Q

adenosine is biproduct of

A

ATP

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21
Q

why is adenosine high when cells are using oxygen

A

adenosine is biproduct of ATP

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22
Q

adenosine in heart

A

dilator

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23
Q

when heart is oorking hard puping oxygen, what is a local dilator that causes blodo vessels going to heart to dilate

A

adenosine

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24
Q

oxygen demand theory, how do we know its a thing

A

you can block all of the mediators from going out and you still have local control, so will still have increased blod flow

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25
Q

describe oxygen demand theory

A

when oxygen is high precapillary sphincters contract and blood won’t go through where there is high oxygen. if oxygen is low the precapilary sphincter sense low oxygen and open up and blood goes through the area and brings oxygen to it

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26
Q

reality, what theory is it?

A

combination of both theories

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27
Q

the way we increase blood flow the two theories: oxygen demand & vasodilator theory are independent of

A

nerves

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28
Q

all the capilaries arent always

A

open

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29
Q

the oxygen demand and vasodilatory theory are more powerful than

A

nerve control

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30
Q

active hyperemia

A

increased blood flow, occurs when tissue metabolic rate increases

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31
Q

reactive hyperemia

A

Occurs after the Tissue Blood Supply Is Blocked for a Short Time

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32
Q

look at graphs on pg 11

A

11

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33
Q

if you occlude artery going to muscle, then you release occulsion, describe what happens to blood flow

A

blood flwo goes higher than normal to resupply and then iwill come back down

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34
Q

the longer you occlude an artery the higher the

A

reactive hyperemia is

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35
Q

autoregulation, what is it

A

if you increase the pressure gradient to a tissue the flow goes up to that tissue but then blood flow will go back down, so the tissue is autoregulating its own blood flow

maintainign a constant bloodf low to a tissue regardless of arterial pressure

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36
Q

all tissues have

A

autoregulation

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37
Q

what two mechanisms are involved in autoregulation

A

metabolic & myogenic mechanism

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38
Q

metabolic theory

A

when you increase blood flow it will wash away the stuff (like adenosine) that caused the increase in blood flow, causing it gto go back down

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39
Q

myogenic theory

A

just property f blood vessels
Based on fact that sudden stretch of small blood vessels and arterioles will cause smooth muscle cells of vessel to contract (they don’t really understand why)

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40
Q

review graph pg 13

A

13

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41
Q

factors released from endothelial cells of blood vessels help control

A

blood flow

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42
Q

two important things released from endothelial cells in blodo vessels

A

nitric oxide

endothelin

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43
Q

nitric oxide synthase does what

A

converts arginine into gas: nitric oxide

44
Q

nitric oxide is a gas and is diffusible, it can do what

A

go wherever, can go into smooth muscles

45
Q

NO does what

A

stimulates guanylate cyclase which converts cGTP to cGMP which causes relaxation

46
Q

NO is a (generally)

A

vasodilator

47
Q

what is one thing that causes blood to release NO

A

shear stress

48
Q

when is endothelin released frm blood cells

A

when there is damaged endothelium

49
Q

endothelin causes

A

vasoconstriction

50
Q

long term control changes what about blood vessels

A

number r size

51
Q

angiogenesis:

A

growth of new blood vessels

52
Q

angiogenesis occurs in respnse to angiogenic factors released from:

A

ischemic tissue
rapidly growing tissue
tissue with high metabolic rate (like cancer)

53
Q

when heart hypertrophies, what long term effects happen

A

angigenesis - more blood vessels occur but they don’t increase in size

54
Q

Collateral Circulation:

A

development of small channels around some particular block

55
Q

how long dos Collateral Circulation take

A

a long time

56
Q

if a blood vessel is blocked, what will grow to help

A

Collateral Circulation

57
Q

BY THE TIME SOMEONE IS 60 OR 70 have a lot of

A

microchannels in heart

58
Q

whahow does Collateral Circulation work

A

Dilation of vascular loops that already connect a vessel above and below the block.

59
Q

why wuld it cause more damage for young person to have MI than an old

A

b/c old ppl have more collateral circulation, young people haven’t had the time the develop the collateral circulation

60
Q

if you plant vein into arterial system what happens

A

it will hypertrophy to be able to withstand the new high pressure

61
Q

blood vessels themselves can change depending on

A

what situation they are in

62
Q

AV fistula

A

connect artery and vein, like pts undergoing dilaysis with renal failure

63
Q

what happens to artery in AV fistula

A

gets bigger b/c its not in as much pressure

64
Q

what happens to vein in AV fistula

A

vein gets bigger also

65
Q

name three humora vasoconstrictors

A

Norepinephrine
Angiotensin II
Vasopressin

66
Q

name two vasodilator humroal

A

Histamine

Nitric oxide

67
Q

NE activate what in blood vessels

A

alpha 2 and alpha 2 reeptors and beta 1 in heart

68
Q

NE activates alpha 1 and alpha2 and causes

A

vasoconstriction

69
Q

EPI activates

A

alpha 1, alpha 2, beta 1, beta 2

70
Q

EPI in blood vessels activates alpha 1 and alpha 2 and causes

A

vasoconstriction

71
Q

EPI acting on Beta 2 causes

A

vasodilation

72
Q

in kidney blood vessels only have what receptors

A

alpha1 and alpha 2

73
Q

epi and NE in kidney what do you see

A

constriction

74
Q

blood vessels in skeletal muscle have what receptors

A

alpha 1, alpha 2, beta2 receptors

75
Q

infuse NE into skeletal muscle what happens

A

vasoconstriction

76
Q

infuse EPI into sekeletal muscle what happens

A

vasodilation, because of the beta 2 receptor

77
Q

dog infused with EPI vs NE which will have highest blood rpessure

A

the one with NE

78
Q

Angiotensin II is pathway what inhibitors work on

A

ACE

79
Q

Angiotensin is released in response to what enzyme

A

REnin

80
Q

anytime there is fall in BP kidneys release

A

renin

81
Q

draw angiotensin II pathway

A

pg 22

82
Q

what does Angiotensin II do

A

constricts arterioles in body

83
Q

what does Angiotensin II do to kidney

A

releases aldosterone and increases sodium reabosption

84
Q

if you gave ACE inhibitor what would it do

A

blocks angiotensin II from being prduced, so high levels of angiotensin I, less constriction of bloodv essels, decreased sodium reabsorption

85
Q

when might renin be released in kidney

A

hemorrhage

86
Q

vasopressin is also known as

A

antidiuretic hormone

87
Q

vasopressin is peptide produced where

A

hypothalamus

88
Q

where is vasopressin released from

A

posterior pituitary

89
Q

vasopressin is released in response to:

A
  1. Decrease in arterial pressure

2. Increase in plasma osmolarity

90
Q

alcohol inhibits the release of

A

vasopressin

91
Q

what does vasopresin do

A

Potent vasoconstrictor
Increases renal reabsorption of water
- Concentrated urine

92
Q

histamine is a vaso:

A

dilator

93
Q

histmaine is released from what cells

A

mast cells

94
Q

histamine does what to capillary

A

increases its permeability

95
Q

histamine is very powerful

A

vasodilator

96
Q

histimen increasing capillary permeability, what is example he used

A

bee sting, it gets red and swolen

97
Q

antihistamine is taken to block the effects of

A

histamine

98
Q

Bradykinin is an _____ mediator

A

inflammatory

99
Q

when is Bradykinin released

A

tissue damage

100
Q

Bradykinin is very similar to

A

histamine

101
Q

Bradykinin causes arterial

A

dilation

102
Q

bradykinin does what to capillary

A

increases its permeability

103
Q

what breaks Bradykinin to inactive fragments

A

kininase II or angiotensin converting enzyme

104
Q

inhibition of angiotensin converting enzyme decreases production of angiotensin II but allows what to stay around longer

A

bradykinin

105
Q

look at pg 26

A

26

Physiology I Block 4 (13 decks)

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