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sodium homeostasis disorders Flashcards

1
Q

why is sodium homeostasis important

A

key regulator of fluid volume
determines excitability of cells (muscle, cardiac, neuronal)
controls arterial BP

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2
Q

how does the osmotic pressure of filtrate change along nephron?

A

isoosmotic at Bowmans capsule and PCT as equal sodium and water reabsorb

down into medulla, filtrate osmolarity increases (hypertonic) as impermeable to ions so only only water reabsorbed (600 to 1400 mOsm)

towards DCT and CD to 90mOsm (hypotonic filtrate) as impermeable to water so only ions are actively pumped out

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3
Q

where is most of sodium reabsorbed along nephron?

A

pCT 60-70
loH/ TAL 25%
CD and DCT 5% each

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4
Q

why does the osmolarity around loop of henle change so much? what is the advantage?

A

different permeabilities of the ascend and descend limb which create different concentration gradients

allows control of water (and ion) reabsorption

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5
Q

how does ADH influence water reabsorp?

A

introduced Aquaporins to increase water reabsorption

creates CONCENTRATED urine

acts to conserve water

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6
Q

why is the basolateral Na/K atpase important in the PCT for sodium transport?

A

active transport removes sodium from intracellular space

this provides an electrochemical gradient for the apical transporters to passively transport sodium into cell

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7
Q

what is special about sodium reabsoprtion at the PCT?

A

sodium reabsorp is coupled to chlorine transport too!

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8
Q

what are the 2 types of CD cells? what is their functions

A

primary CD cells transport sodium / influence fluid volum

intercalated CD cells transport H+/ influence pH

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8
Q

how can NKCC2 be regulated?

A

channel present in the TAL
regulated by aldosterone

which activates SPAK1 kinase -> phosphroylate and activates NKCC2

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9
Q

what is the difference between type A + B intercalated duct cells?

A

type A transport H+

type B transport BICarbonate ions

very important to regulate pH balancw

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10
Q

describe strucutre of ENaC channel. Where is it found?

A

found at principle CD cells but can be found in other organs too

in kidney it is a heterotrimeric structure with alpha,beta and gamma subunits

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11
Q

what are some electrophysiological features of ENaC?

A

voltage and ligand independent channel
it is constiuitively open!

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12
Q

how is ENaC regulated?

A

by Nedd4-2 protein which ubiquinates and marks for internalisation + degradation

by SGK1 that phosphorylates and activates and increases OPEN PROBABILITY of channel! And increases ROMK channel activity and can inhibit Nedd4-2

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13
Q

how does ADH/AVP regulate activity of ENaC?

A

binds to receptor activating signalling cascade involving PKA

phosphorylates AQ2 and ENaC increasing their activity and ROMK secretion

reabsopb increases, concentrated urine produced

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13
Q

how does aldosterone influence ENaC activity?

A

expression of SGK1 increases so open probability of channel increases

conformation of inhibitory Nedd4-2 changes

promotes sodium reabsorp

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14
Q

what is CAP1?

A

Cap1 is a extracellular protein which can proteolytically cleave gamma subunit of ENaC

increase its open probability

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15
Q

where and why is aldosterone produced?

A

mineralcorticoid produced in zona glomerulosa of adrenal cortex in response to increased Angll (RAAS) or increased plasma K+

acts to increase sodium reabsorp/ increase BP and fluid volume

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16
Q

where and why is ANP produced?

A

small peptide secretred from atria muscle in response to stretch/increased fluid volume

aims to reduce BP/ reduce sodium reabsorb by inhibiting the ENaC, inhibit RAAS

17
Q

what is the end aim of RAAS?

A

increases ADH and aldosterone secretion amongst other actions (vasocontrict, SNS activity)

to increase the BP

18
Q

where is cortisol produced? what is the rate limiting enzyme?

A

cortisol, a glucocorticoid is produced in zona fasciulata

11-beta hydroxylase is rate limiting enzyme

18
Q

what is the mutation in Liddle’s syndrome

A

GoF of ENaC as the PY motif on beta and gamma subunit is mutated

so Nedd4-2 unable to recognise, internalise and degrade ENaC

so ENac persists on apical CD membrane and continues to reabsorb sodium

19
Q

is the genetic cause of all Liddle’s syndrome the same?

A

No!

some novel mutations have been uncovered but same end result which is GoF of ENaC

20
Q

how would one treat Liddle’s syndrome

A

use ENaC pore blockers like Amirolide

this would reduce BP and blood volume

21
Q

what is the cause of glucocorticoid remediable Aldosteronism?

A

chimeric gene affecting biosynthesis of cortisol and results in excess aldosterone production

due to ACTH signalling

22
Q

how would one treat glucocorticoid remediable Aldosteronism

A

use corticosteroids to correct the HPA axis and stop signalling of ACTH

e.g dexamethosome, a synthetic glucocorticoid

23
Q

what are symptoms of increases aldosterone

A

over activity of ENaC channel so hypertension,
overactivity of ROMK channel so hypokalcemia

hyporeninemia from the RAAS system

24
Q

what happens in apparent mineralcorticoid excess?

A

there is a deficit in 11-beta dehydrogenase activity so cortisol isn’t converted to cortisone

this overstimulates the mineralcorticoid receptro

25
Q

what are the consequences of overactive mineral corticoid receptor:

A

activates same signalling pathways as aldosterones

so increased sodium and water reabsorb, increased pottassium wasting

26
Q

how does liquorice consumption affect sodium homeostasis?

A

liquorice contains compounds which stimulate the Mcorticoid Receptor

so can lead to hypotensive disorder

27
Q

how to treat Apparrent mineral corticoid excess?

A

block ENaC with pore blocker like Amirolide or Benzamil

28
Q

how do diuretics work? / what is their aim

A

aim to create concentrated urine

so increase water reabsorption

29
Q

how do diuretics work

A

the severity/ potentcy of each diuretic depends on which area of the nephron they target

target different proteins involved in sodium (and hence water) transport and block their activity

30
Q

which of the diuretics are most potent?
thiazide
potassium sparing
loop
acetazoliimde

A

loop diureitc most potent

targets the NKCC tri-cotransporter and blocks it (mimics Bartters syndrome)

31
Q

what causes Bartters syndrome?

A

mutation of NKCC2 in the TAL so has reduced function

this has downstream affects on the NCX1 transporter and works against conc. grad. So calcium reabsorb decreases

32
Q

what is the key differences in Bartters and Gitelmans

A

B - mutation at TAL but affects transport at DCT decreasing NCX1 function. So results in hypocalcemia

G - mutation at the DCT, NCX1 function increases,
hypercalcemia

32
Q

how to treat Bartters syndrome?

A

can give potassium sparing diuretics to increase water + sodium excretion

33
Q

what causes Gitelmans syndrome

A

NCC in the DCT mutated and has LoF

34
Q

how to treat Gitelmans

A

use NaCL and KCL supplements and Mg

NSAIDs to block COX activity

potassium sparing diruretics can be used to prevent any futhur secretion of K+

35
Q

what is the relationship between sodium and potassium?

A

because of the Na/K atpase, they move in opposite directions

so if hypotension, then hypokalemia also ??????

36
Q

what does COX enzyme do?

A

wasting of NaCL activates the COX enzyme
so there is elevated prostaglandin synthesis

prostaglandins are pro -inflame so patiens can feel vomit, nausea

37
Q

what casues pseudohypoaldosteronism

A

LoF of ENaC or the McorticodiR in collecting duct

38
Q

why is it called pseudohypoaldoseronism?

A

actually patients have high aldosterone levels to try and correct the the hypotension

but as ENaC or receptor is faulty, the collecting duct cells are unresponsive to the aldosterone signalling

so symptoms of hypoaldosterone remain, despite actual plama aldo is high

39
Q

how would one treat pseudohypoaldosteronism?

A

use NaCl supplements,

ion exhcnage resins too

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