control of blood volume Flashcards

1
Q

Where is blood volume controlled on the long term?

A

controlled in the kidneys. the renal body fluid feedback system

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2
Q

What effect does increased arterial pressure have on urine production?

A

increases urine production

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3
Q

What does an increase in hydrostatic pressure in the kidneys mean?

A

increase across the kidneys and the glomeruli will push out more fluid into the bladder

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4
Q

what effect does increase in blood pressure have on sodium ions? What effect do sodium ions have on water?

A
  • more sodium ions are pushed out

- water follows sodium hence more water will be pushed out

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5
Q

what happens to renal output when salt and water intake is increased?

A

kidney function takes on a more chronic regulation to keep blood pressure low

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6
Q

what happens to renal output if blood pressure increases?

A

increases renal output of water and salt causing blood pressure to go back down again by reducing blood volume

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7
Q

what are the meanings of volume and osmolarity?

A

volume- total amount of blood in the system

osmolarity- right concentration of blood

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8
Q

how is blood osmolarity sensed?

A

osmotic receptors in the hypothalamus

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9
Q

what hormone is released by the hypothalamus?

A

antidiuretic hormone ADH

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10
Q

what stimulates ADH to be released?

A

released in response to increased osmotic pressure detected in the hypothalamus

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11
Q

what effect does hypovolemia have on ADH release? Explain the mechanism

A
  • arterial baroreceptors normally inhibit ADH release however the decrease in volume therefore decreases the firing rate and hence
  • increases ADH release
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12
Q

How does ADH reduce urine output?

A

increases water permeability in renal collecting ducts by increasing the tuber of aquoporins there hence decreasing urine production

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13
Q

Which system is involved in the long term control of blood volume and plasma salt composition?

A

renin angiotensin aldosterone system

RAAS

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14
Q

how is decreased blood volume controlled by the long term control RAAS?

A
  • decrease in blood volume decreases mean arterial blood pressure sensed by baroreceptors
  • baroreceptors feed the info to the MCVCC
  • increase in renal sympathetic nerves increases kidney renin output decreasing urine formation
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15
Q

What are the component parts of the RAAS?

A

-renin (an enzyme)

angiotensin 2

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16
Q

what does Angiotensin 2 act on? what 2 things does it do?

A
  • directly on the kidney
  • constricts arteries in the kidneys decreasing blood flow to kidneys and stimulates the release of aldosterone from adrenal glands which increases sodium and therefore water reabsorption
17
Q

how and where is angiotensin 2 formed?

A
  • angiotensin 1 is pumped through the system to heart and then when it arrives in the pulmonary circulation it meets an enzyme
  • enzyme converts 1 into 2
18
Q

what are the 4 functions of angiotensin 2?

A
  • vasoconstriction
  • renal retention of sodium and therefore water
  • increased arterial pressure
  • increase release of ADH
19
Q

what is produced by atrial cells when the atrial wall is stretched?

A

atrial natriuretic peptide ANP

20
Q

what is the structure of ANP? Where is it stored? what is its function?

A
  • 28 amino acid peptide
  • stored in muscle cells of the atria
  • released in response to the stretch of the atria and helps oppose effects of RAAS
21
Q

what effect does haemorrhage have on the blood volume?

A

decrease blood volume, decreased venous return, decreased arterial pressure, decreased end diastolic volume

22
Q

what features are involved in the baroreceptor reflex response to haemorrhage?

A

Stroke volume, hear rate, cardiac output, total peripheral resistance, mean arterial blood pressure

23
Q

What happens to SV during haemorrhage?

A
  • decreases at the point of haemorrhage

- then is increased since veins are squeezed in response however it does not increase to the same level it was at

24
Q

what happens to heart rate during haemorrhage?

A

remains constant at time of haemorrhage then increases with sympathetic nerve stimulation to increase CO

25
Q

what happens to total peripheral resistance as a result of haemorrhage?

A

increases because veins constrict to decrease capacity in order to push blood back to the heart in response to sympathetic innervation

26
Q

What other conditions cause hypovolemia?

A
  • decreased plasma as a result of burns
  • decreased sodium form vomiting
  • decreased blood pressure
27
Q

what is the later response to hypovolemia since nerve innervation reflex mechanisms are short term?

A
  • arteriole constriction to decrease hydrostatic pressure in capillaries favouring fluid reabsorption
  • temporary redistribution of blood flow
  • decreased renal blood flow, decreased urine output
28
Q

what happens in severe hypovolemia?

A

if fluid lost can’t be compensated fro damage to tissue and organs may occur
-can lead to heart failure

29
Q

how is severe hypovolemia treated?

A

-fluid replacement is required: resuscitation fluids, colloid, blood

30
Q

what factors input into the medullary cardiovascular control centre?

A

cortex, blood hormone levels, posture and movements, hypothalamus and thalamus