lecture 10: guyton ch 19 Flashcards

1
Q

the rapidly acting arterial pressure control mechansms come from para or sympathetic nervous symtpoc

A

sympatethic

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2
Q

what does the sympathetic nervous system have an effect on for arterial pressure control

A

effect on total peripheral vascular resistance and capacitance as well as cardiac pump

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3
Q

what are some examples of rapidly acting arterial pressure control mechanisms

A

metabolic controls
myogenic controls
shift of fluid thorugh cap walls

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4
Q

things like metabolic controls, myogenic controls etc are acute or long term control

A

acute

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5
Q

metabolic controls depend on

A

the tissues metabolic needs

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6
Q

myogenic cotnrols depeond on

A

pressure stretching

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7
Q

what is the cocnept taht explaisn how the body maintainns flow despite increase in BP

A

autoregulation

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8
Q

when you think of long term control mechanisms for arterial BP what organ is important

A

kidneys

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9
Q

what organ is important for long term BP regulationn

A

kidney

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10
Q

long term mechanisms for BP regulation are related to what

A

maintaining homeostatis of body fluid volume

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11
Q

long term mechanisms for BP regulation is based on what

A

on maintaining a balance between intake and output of body fluid
(overall regulation of kidney excretion of h20 and na+)

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12
Q

what is the simple concept behind long term regulation

A

Increase in extracellular fluid results in increased blood volume and arterial pressure

Normal body response: kidneys excrete excess extracellular fluid and returns the pressure to normal

Mechanism reverses if reduced blood volume

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13
Q

the simple concept of long term conctrol is based on what mechanism

A

starling

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14
Q

an increase in extracellular fluid reslts in an inxreased or decreased blood volume and pressure

A

increase

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15
Q

what is the bodyies normal response if there is an increased bp and fluid

A

kidneys excrete excess extracellular fluid and returns the pressure to normal

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16
Q

explain why exrta fluid inn extracellular space will cause increse BP and stim the kidneys

A

increase fluid from extracellular space will go into plasma, travel trhough circulation innto the kidneys

=kidneys will excrete extra fluid to return the bp to normal

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17
Q

what are some reasons that extracellular fluid would inxrease

A

dysfunctional lymph, increae water intake

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18
Q

what are renal corpuscles\glomular bodies

A

they enclose bundles of capillariies, make them pressure together and have a high pressure

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19
Q

is the hydrostatic capilary pressure in the kidneys high? and why

A

yes very high because of corpuscles

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20
Q

what is the mainn pressure that drives fluid from cap to inerstricum

A

hydrostatic cap pressure

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21
Q

In kidneys blood flows from capillary to regular intersticium

A

false from capillaries to glomular bodies

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22
Q

what are the determinants of net fluid movement across the kidney capilaries

A

the high pressures

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23
Q

what is the Amount of filtrate produced in the kidneys each minute.

A

125mL/min = 180L/day (because of high BP)

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24
Q

what are the factors that alter filtration pressure change GFR

A
Increased renal blood flow
       Increased GFR
Decreased plasma protein 
       Increased GFR. Causes edema.
Hemorrhage 
      Decreased capillary BP 
      Decreased GFR
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25
Q

what is GFR

A

glomerular filtration rate

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26
Q

explain how incnreased renal blood flow leads to an increased GFR

A

there will be more blood to glomerular bodies, increase hydrostatic pressure, increase filtration, increase GFR

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27
Q

explain how decreased plasma leads to an icnreased GFR

A

if there is not a lot of plasma protein in blood, there will be an icnreased filtration (removing fluid from blood) to maintain plasma concentration
increase GFR filtration (edema)

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28
Q

explain how hemmorage will lead to a decreased GFR

A

you are losing blood volume (which decreases stroke and cardiac output therefore decreaes BP)
=decrease GFR to maintain fluid within our plasma to maitnain plasma volume

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29
Q

GFR is important for controllinng/reduces changes in bp how

A

by adjusting blood flow

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30
Q

Glomerular filtration rate is regulated using three mechanisms which are

A
  1. Renal autoregulation
  2. Neural regulation
  3. Hormonal regulation
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31
Q

all three mechanisms of GFR adjust what

A

adjust renal blood pressure and resulting blood flow

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32
Q

the renal body fluid system plays a dominant role in what

A

in long term pressure control

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33
Q

as extracellular fluid volume increases, what happens to arterial pressure and why

A

it increases because CO will increase, increase stroke volume etc)

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34
Q

an increase in arterial pressure causes the kidneys to do what

A

to lose NA and water to retrun exrtacellular fluid volume to normal (icnrease urinary)

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35
Q

over long term, water and salt inntake must equal water

A

the output

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36
Q

explain how over long term, water and salt intake must equal output

A

ex: eating something salty means you need to drink a lot of water )

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37
Q

what are the two determinantns of long term arternal pressure

A

Location of renal output curve (shift?)

Level of intake line

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38
Q

where is the equilibrium point on the renal body fluid mechansm

A

where intake=output

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39
Q

renal body fluid feeback ssystem has infinite or finite gain

A

infine

40
Q

long term mechanisms control BP (renal regulation) by doing what

A

alterinng blood volume

41
Q

increased BP stimulates the kidneys to do what to water

A

eliminate watera nd reduce bp_

42
Q

decreased BP stimulates the kidneys to do what to blood volume

A

increase blood volume and BP

43
Q

true or false: long term kidneys will be able to return the BP back to normal due to increased filtration

A

true

44
Q

true or false: kidneys act directly or inndirectly to maintain long term pressure

A

both

45
Q

what mechanism alters blood volume directly

A

direct renal mechanism

=thru starling

46
Q

indirect renal mechanisms involves what

A

renin angiotensin mecahnisms (hormones)

47
Q

what happens if we end up witih an increased TPR

A

Get acute rise in arterial pressure
However, normal kidney function will respond by returning arterial pressure to the pressure level of the equilibrium point – How?

48
Q

epxlain how an icnrease TPR can be regulated by kidneys

A

1) increased TPR w/o icnrease in vascular resistance
2) increase arterial pressure
3) increase sodium and water extretionn
4) to re maintain the arterial pressure there will be reasborption of extracellular bluid volume from other tissues 0

49
Q

true or false: Changes in TPR does not affect long-term arterial pressure level

A

true

50
Q

how do you get long term changes in artterial pressure

A

One must alter the renal function curve in order to have long-term changes in arterial pressure.

ex: changing renal vascular resistance does lead to long-term changes in arterial pressure.

51
Q

what are some ways to change renal vasculat resistance

A

plaque formation

diabtes (increase glucose)

52
Q

what does an increase NA intake stimulate

A

increases dirnking/thirst

53
Q

changes in Na intake leads to changse in what bolume

A

interstitial fluid volume

if theres more Na in interstiium, wyou will take fluid from other cells to dilute it making u thirst

54
Q

what is interstial fluid volume determined by

A

determined by the balance of Na intake and output

55
Q

a low effective circulation volume triggers what

A

triggers 4 parallel effector pathways that act on the kidney

56
Q

the 4 parallel effector patways act on the kidneys how

A

Either changes haemodynamics or changes Na+ transport by renal tubule cells.

57
Q

explain atrial and pulmonary artery reflexes

A

Low pressure receptors (ANP) in atria and pulmonary arteries minimize arterial pressure changes in response to changes in blood volume.

58
Q

what does ANP stand for

A

atrial natriuretic peptide

59
Q

inrcases in blood volume in the atrial and pulmonary activates what

A

activates low pressure receptors which in turn lower arterial pressure.

60
Q

how does activation of low pressure receptors enhances NA and water by what methods

A

Decreasing rate of antidiuretic hormone
- Increasing glomerular filtration rate
Decreasing Na reabsorption

61
Q

what does ANP promote

A

natriuresis (loss of sodium)

62
Q

what do atrial myocytes do in terms of ANP

A

Atrial myocytes synthesise, store and release ANP in response to stretch (low pressure / volume sensor).

63
Q

what is the major effect of ANP release

A

renal vasodilation, icnrased blood flow and increased GFR

=more Na+ reaches macula densa cells and more na is excreted

64
Q

what is ADH

A

antidiuretic hormone

65
Q

what is AVP

A

arginine vaspressine

66
Q

what is the main goal of ADH

A

concetrate urine

67
Q

what is the function of ADH

A

Increases permeability of collecting ducts to H2O by inserting H2O channels (Aquaporins).

Helps make small amounts of concentrated urine.

68
Q

ADH allows blank of urine concentration

A

allows rapid graded control of urinne concentration

very sensitve

69
Q

ADH released is response to waht

A

ADH released in response to plasma osmolality and interstitial fluid volume – osmoreceptors and baroreceptors.

70
Q

what is the proble mwith volume loding hypertension

A

overtime, without fully funcntional kidneys, even as fluid, CO and BV goes down, TPR will icnreae and pressure will nerve actually decrease

71
Q

where is renin synthesized and stored

A

is synthesized and stored in modified smooth muscle cells in afferent arterioles of the kidney

72
Q

renin is released is response to

A

fall in pressure

73
Q

what does renin act on

A

acts on a substance called angiotensinogen to form a peptide called angiotensin I (AI).

74
Q

what is AI converted to

A

AII

75
Q

how is AI converted to AII

A

by a converting enzyme located in the endothelial cells in the pulmonary circulation.

76
Q

what does angiotension II do

A

vasoconstric (decrease vessel diamter and affects resistance and BP)

77
Q

what is the principal factor controllingn ANG II levels

A

renin release

78
Q

what stimulates renin release

A

decrease circualting volume

79
Q

Decreased circulating volume stimulates renin release via what

A

Decreased BP (symp effects on JGA).
Decreased [NaCl] at macula densa (“NaCl sensor”)
Decreased renal perfusion pressure (“renal” baroreceptor)

80
Q

what does aldosterone stimulate

A

stimulates Na+ reabsorption and K+ excretion by the renal tubule.

81
Q

was is RAS

A

renin angiotension system

82
Q

aldosterone exerts what type of feedback on RAS

A

negative

83
Q

how does Aldosterone exerts indirect negative feedback on RAS by

A

increasing interstitial volume and by lowering plasma [K+].

84
Q

what is imporatnt in conserving Na+ and water

A

aldosterone

85
Q

aldosteronne is imporatnt for consevring Na+ and water but also good at …

A

preventing massive swings in K+ levels.

86
Q

what are the 3 main action of reninn angiotensinn system

A

Causes vasoconstriction (direct effect)

Causes Na retention by direct and indirect actions on the kidney (increased secretion of aldosterone by the adrenal cortex)

Causes shift in renal function curve to right (acts on brain to increase thirst)

87
Q

RAS is imporant in mainting what during changes in NA intake

A

normal arterial pressure

88
Q

as Na intake is increased, renin levels fall or rise to near what

A

fall near 0

89
Q

as Na intake is decreased renin levels BLANK

A

icnrease signifcantly

90
Q

RAS causes the Na loading renal funcnntion curve to be steep or not

A

steep

91
Q

essential hypertension or seconndary is more common

A

essential

92
Q

what is the incidence of essential hypertensionn

A

90%

93
Q

what is the cause of essential hypertension

A

not exactly known but hereditaty component

94
Q

what is the incidence of secodnary hypertension

A

less than 10%

95
Q

what are the common causes of secondaary hypertension

A

common causes: chronic kidney disease, renovascular disease

Prescription drugs, street drugs, natural products, food, industrial chemicals

96
Q

severe BP does water to blood flow

A

doesnt allow good flow by breaking up vessels