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physiology 2 > salt and water balance > Flashcards

salt and water balance Flashcards

1
Q

aldosterone site of action

A

collecting tubule and duct

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2
Q

angiotensin 2 site of action

A

proximal tubule, thick ascending loop of henle/disal tubule, collecting tubule

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3
Q

ADH

A

anti diuretic hormone
water loss r regulated by sodium osmolarity
an increase in extra cellular fluid osmolarity causes osmoreceptor cells to shrink, triggering an action potential causing posterior pituitary to release ADH
ADH goes to kidneys to increase water permeability of the DCT/CT.CDs
increased reabsorption of water
H2O is conserved which Na+ solutes continue to be excreted - dilution of ECF solutes

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4
Q

ADH is synthesised in

A

produced in the supraoptic and paraventricular nuclei in the hypothalamus
stored in the posterior pituitary

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5
Q

ADH is released when

A

release is triggered by increase in plasma osmolarity

stimulates exocytosis of ADH into the blood stream

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6
Q

what does ADH do

A

increased water permeability of DCT/CT.CD
retains water
increases aquaporinb activity

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7
Q

aquaporin 2

A

has two states

  • can be endocytose into a vesicle so it is not active
  • can be expocytosed and presented to the membrane where it can be open
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8
Q

how does ADH increase aquaporinb activity

A
  • binds V2 receptors > cAMP > kinases > translocation of aquaporin 2 to the luminal membrane where it is active
  • aquaporin 2 cluster together, form water channels that permit rapid H2O diffusion
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9
Q

aquaporin 3 and 4

A

in the basolateral membrane provide a path for water to rapidly exit the cells - not ADH regulated

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10
Q

chronic ADH

A

alo stimulates aquaporinb 2 transcription

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11
Q

decrease in ADH concentration affect on aquaporinb 2

A

causes aquaporinb 2 to be endocytosed

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12
Q

renin-angiotensin-aldosterone system

A
  • decrease in renal perfusion - tubuloglomerular feedback - renin is released which converted angiotensinogen to angiotensin 1
  • angiotensin 1 has low activity, ACE activates it to angiotensin 2 - high activity, short half life - acts in the systemic circulation and is degraded before it reaches the pulmonary circulation
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13
Q

angiotensin 2 affect on the kidney

A
  • increasing activity of sodium potassium pumps which causes more sodium to be retained
  • stimulates release and production of aldosterone
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14
Q

aldosterone affect on the kidney

A
  • increase sodium potassium pump activity and therefore sodium retention
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15
Q

angiotensin 2

A

high activity, short half life
activated version of angiotensin 1
acts on the systemic circulation and is deactivated before it reaches the pulmonary circulation

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16
Q

renin is secreted by

A

granular cells of the JGA

17
Q

renin is secreted due to

A

catalysed by tubuloglomerular feedback
when there is a decrease in the amount of sodium in the distal collecting tubules
triggers the release of renin into the plasma

18
Q

renin causes

A

turns angiotensin 1 to angiotensin2

19
Q

aldosterone

A
  • secreted by adrenal cortex zona glomerulosa

- secretion is mediated by angiotensin 2 and increased local potassium concentration

20
Q

aldosterone action in kidney

A

steroid
diffuses across plasma membrane and binds mineralocorticoid receptor and becomes a transcription factor when activated
changes transcription in cells o produce more sodium potassium pump and sodium channels

21
Q

ANP

A

atrial natriuretic peptide

  • decreases Na+ and H2o reabsorption
  • antagonist of aldosterone and angiotensin
  • produced in response to atrial stretch
  • inhibits sodium retention mechanism - slows sodium potassium pumps
  • increases GFR
22
Q

ANP affect on GFR

A

increases

23
Q

ANP affect on sodium potassium pumps

A

slows

24
Q

ANP secreted in response to

A

atrial stretch - too much venous blood volume

25
Q

when the atria are stretched

A

ANP releases

  • increases GFR
  • decreases renin and aldosterone
  • increased sodium and H2O excretion
26
Q

potassium regulation

A

lethal - must be controlled/sequestered inside cells

- intracellular fluid is high in potassium

27
Q

factor that shift K into cells

A
  • insulin
  • aldosterone
  • beta adrenergic stimulation
  • alkalosis
28
Q

factors that shift K out of cells

A
  • insulin deficiency - diabetes
  • aldosterone deficiency - Addison’s disease
  • beta adrenergic blockade
  • acidosis
  • cell lysis
  • strenuous exercise
  • increased extracellular fluid osmolarity
29
Q

insulin and adrenaline on potassium

A

ECF > ICF

30
Q

cell lysis and muscle damage on potassium

A

ICF > ECF

31
Q

potassium secretion

A

balance of secretion and resorption
regulated section - principle cells (late DCT/CT)
by retaining more sodium, more potassium is lost

32
Q

secretion rate of potassium is determined by

A
  • Na/K ATPase activity
  • K electrochemical gradient
  • K permeability
    minimally resorbed
33
Q

K feedback control

A

local potassium levels are a trigger for aldosterone release - elevated potassium increases aldosterone to stop potassium from being toxic

34
Q

3 mechanisms of K feedback control

A
  • increase in K stimulates NA K ATPase
  • increase in K stimulates increase in K gradient to drive diffusion
  • increase in K stimulates aldosterone secretion
35
Q

drinking threshold is regulated by

A

sodium

increase in extracellular sodium ECF triggers thirst mechanism

36
Q

thirst stimuli

A
  • hypertonicity - hypothalamic osmoreceptors which inactivated thirst mechanisms
  • hypovolaemia
  • hypotension
  • angiotensin 2 - potent dipsinogen

all feed into the hypothalamus

37
Q

osmoreceptors are located in

A

AV3V region
receive information for medullary blood pressure centres
project to supraoptic and paraventricular nuclei - ADH synthesis

38
Q

2 primary stimuli for salt appetite

A
  • decrease of ECF sodium - decreases thirst/more hunger for salt
  • decrease of blood pressure increases thirst and salt appetite
39
Q

region that governs salt appetite

A

AV3V region

physiology 2 (21 decks)

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