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sodium and potassium balance Flashcards

1
Q

what is osmolarity

A

measure of solute concentration in solution (osmoles/litre)

*depends on number of dissolved particles

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2
Q

what is our normal plasma osmolarity

A

285-295 mosmol/L

sum of all particles

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3
Q

what is the most prevalent and important solute in ecf

A

sodium

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4
Q

how does increased dietary sodium lead to increased bp and vol

A

increased total body sodium
increased osmolarity
increased water intake and retention
increased ecf vol

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5
Q

what happens to sodium during euvolemia

A

supress na+ intake via lateral parabrachial nucleus

supressed by serotonin and glutamate

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6
Q

what happens during na+ deprivation

A

increased appetite for sodium driven by gaba and opioids

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7
Q

what is the peripheral mechanism for sodium reg

A

taste

salt is appetitive at low conc

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8
Q

how do macula densa cells respond to high tubular sodium

A

increased sodium and chloride uptake via triple transporter
adenosine is released from macula densa
this is detected by extraglomerular mesangial cells
reduces renin production
promotes afferent smc contraction
reduces perfusion pressure and so gfr

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9
Q

what happens if you need to retain/reabsorb sodium or water

A

reduce filtration rate
increase sympathetic activity which constricts efferent arteriole and sodium uptake by cells or pct
slso stimulates jca to secrete renin which leads to production of angiotensin 2 which further stimulates cells of pct to take up sodium
ag2 anlso stimulates production of aldosterone which stimulates uotake of na+ in dct and cd

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10
Q

what mechanisms take place to decrease sodium reabsorption

A

atrial naturietic peptide acts as vasodilator
reduces na+ uptake in pct,dct and ct
suppresses prod of renin by jca

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11
Q

what happens in cases of low sodium

A

low bp
decreased fluid vol
simulation of b1 sympathetic pathway which causes constriction of afferent arteriole and reduce pressure
increased production of renin (raas) stimulates zona glomerulosa producing aldosterone
angiotensin 2 also causes vasoconstriction
and increases nacl/h2o reabsorption

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12
Q

what happens in case of high sodium

A

higher blood pressure
increased fluid vol
decreased b1 sympathetic activity and decreased anp
reduces renin - downreg of raas, decreased aldosterone
decreased nacl/h20 reabsorption
decreased vasoconstriction/promote vasodilation

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13
Q

what is aldosterone

A

steroid hormone
synthesised and released from adrenal cortex
released in response to angioten2
stimulated by decrease in bp via baroreceptors

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14
Q

what is role of angiotensin 2

A

causes production of aldosterone synthase which is required in last 2 steps of aldosterone syn

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15
Q

what is the function of aldosterone

A

increased sodium reabsorption
controls at 35gna/day
increased potassium secretion
increased h+ secretion

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16
Q

what can aldosterone excess lead to

A

hypokalaemic alkalosis

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17
Q

how does aldosterone work

A

is a steroid hormone so lipid soluble
binds to mineralcorticoid receptor which is bound to hsp90
once aldosterone binds mineralocorticoid receptor dimerises and translocates into nucleus binds to dna
increased active sodium channels

18
Q

what happens in hypoaldosteronism

A

reabsorption of sodium in distal nephron is reduced
increased urinary loss of sodium
ecf vol falls - causes diziness, low bp, salt cravings and palpitations
increased renin,ang2 and adh

19
Q

what happens in hyperaldosteronism

A

reabsorption of sodium in distal nephron is increased
reduced urinary loss of sodium
ecf vol increases - causes high bp, muscle weakness,polyuria and thirst
reduced renin,ang2 and adh
increased anp and bnp

20
Q

what is liddles syndrome

A

inherited disease of high bp
mutation in aldosterone activated sodium channel
channel is always on/activated
results in sodium retention, leads to hypertension
(low/normal aldosterone)

21
Q

on the low pressure side where do we find baroreceptors

A

atria
right ventricle
pulmonary vasculature

22
Q

on the high pressure side where do we find baroreceptors

A

carotid sinus
aortic arch
juxtaglomerular apparatus

23
Q

on the low pressure side what happens when low pressure

A

reduced baroreceptor firing

signal through afferent fibres to brainstem increased sympathetic activity and adh release

24
Q

what happens on the low pressure side when there is high pressure

A

atrial stretch

anp and bnp released

25
Q

what happens on high pressure side when there is low pressure

A

reduced baroreceptor firing

  1. signal through afferent fibres to brainstem causes increased sympathetic activity and adh released
  2. renin released from jca cells
26
Q

what is atrial natriuretic peptide

A

small peptide made in atria

released in response to atrial stretch(ie high bp)

27
Q

what are the actions of anp

A

binds to guanylyl cyclase receptor which causes conversion of gtp to cyclic gmp and protein kinase g is activated
Causing:
- vasodilation of renal + other blood vessels
- inhibition of sodium reabsorption in pct and ct
- inhibits release of renin and aldosterone
- reduces bp

28
Q

what does volume expansion cause

A

reduced sympathetic activity
reduced renin and angiotensin
increased anp and bnp
increased na+h2o excretion

29
Q

what is the role of ace inhibitors

A

reduce production of ang2
also causes vasodilation which increases vasc vol will lead to low bp
direct renal effects: reduces na+ reuptake in pct
increased na+ in distal nephron
indirect effects: reduced na+ uptake in cct
increased na+ in distal nephron
reduces water reabsorption

30
Q

where do other diuretics work

A 
osmotic diuretics - less water reabsorp in pct
carbonic anhydrase inhibitors - pct
loop diuretics - thin ascending limb
thiazide diuretics - dct
k+ sparing diuretics - cd
31
Q

how to carbonic anhydrase inhibitors work

A

block carbonic anhydrase
reduced na+ reuptake in pct
increased na+ in distal nephron
reduced water reabsorption

32
Q

how do loop diuretics work

furosemide

A

triple transporter (na,cl,k) inhibitors
reduced na+ reuptake in loh
increased na+ in distal nephron (lose less water)
reduced water reabsorption

33
Q

what is the role of thiazides

A

reduce na+ reuptake in dct
increased na+ in distal nephron
reduced water reabsorption
increased calcium reabsorption

34
Q

what are potassium sparing diuretics

A

inhibitors of aldosterone function

e.g spironolactone

35
Q

what is the main intracellular ion

A

potassium

36
Q

what does high potassium cause

A

depolarises membranes
action potentials
heart arrhythmias

37
Q

what does low potassium cause

A

heart arrhythmias

asystole

38
Q

what is increased k+secretion in collecting duct stimulated by

A

increase in plasma k+
increase in aldosterone
increase in tubular flow rate
increase plasma ph

39
Q

what can cause hypokalaemia

A 
inadequate dietary intake
diuretics
diarrhoea
surreptitious vomiting
genetics e.g gitelmans syndrome
40
Q

what can cause hyperkalaemia

A 
seen in response to k+ sparing diuretics
ace inhibitors
elderly
severe diabetes
kidney disease

brs2 (65 decks)

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