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Body systems 2 > management of electrolyte and water balance > Flashcards

management of electrolyte and water balance Flashcards

1
Q

salt intake and excretion

A

intake = 10g
sweat - 0.25g
urine - 9.5 g
faeces - 0.25g

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2
Q

what hormone controls the amount of sodium lost in urine or reabsorbed into the plasma

A

aldosterone

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3
Q

what is aldosterone

A

a steroid hormone produced in the adrenal cortex from cholesterol
- plasma conc 0.1-0.15

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4
Q

what is aldosterone produced in response to

A

in response to a fall in NaCl intake or an increase in the potassium concentration in the interstitial fluid

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5
Q

what is aldosterone stimulated and inhibited by

A

stimulated by angiotensin 2 and inhibited by ANP

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6
Q

what stimulates aldosterone release if Na+ loss is less severe

A

ACTH - corticotrophin

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7
Q

main functions of aldosterone

A

sodium retention
potassium excretion
secondary retention of water - increased ECF

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8
Q

Stretch receptors

A

We have specialized cells that sit around the afferent arteriole that can detect changes in pressure
- they are stretch receptors.

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9
Q

macula densa

A

Macula densa - this has a sensing capability so it can detect changes in sodium levels
and also osmolality

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10
Q

what does aldosterone work with

A

renin - angiotensin system
- detects changes in BP and blood volume
a fall: in BP in afferent arteriole or in Na+ conc in the filtrate
Triggers the renin angiotensin system

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11
Q

renin angiotensin system

A
  • decreased plasma volume
  • decreased arterial BP - detected by macula densa cells
  • renin granular cells
  • renin will active the angiotensinogen by chopping it into bits and it becomes angiotensin 1
  • ACE converts angiotensin 1 to 2
  • angiotensin 2 is a powerful vasoconstrictor
  • adrenal cortex secrete aldosterone
  • renal tubule increase sodium reabsorption and decrease sodium excretion
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12
Q

another hormone affecting sodium reabsorption

A

atrial natriuretic peptide (ANP)

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13
Q

how does aldosterone increase sodium and decrease potassium

A
  • main site of action DCT and CD
  • insertion of sodium channels (ENaC)
  • activate Na+/H+ - more sodium pumped out of the cell by active transport - increasing conc gradeint for sodium to go back in
  • activation of Na+/H+
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14
Q

ANP

A
  • produced in heart - stored in atrial cells
  • trigger - stretching of atrium (high ECV) from increased blood volume
  • ANP release into circulation and goes to kidneys
  • increased NaCl and water excretion
  • blood volume will decrease
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15
Q

actions of ANP

A
  • inhibit NaCl reabsorption in medullary CD
  • inhibits ADH stimulated water reabsorption in collecting duct
  • inhibits ADH secretion from posterior pituitary
  • inhibit angiotensin 2 and aldosterone
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16
Q

BNP

A

b type
- lower BP, relax BV, reduce workload on the heart
- BNP effective in diagnosing congestive heart failure
- B type found in the brain and also highly concentrated in the ventricles

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17
Q

how can congestive heart failure happen

A

Congestive heart failure can happen if you have a problem with Your ventricles- they can’t push the blood out as they should do.
- So if you’ve got any issues with contractile apparatus in the heart or if you’ve got a problem with the valves - can get increased pressure in the Atria which can then back up into the pulmonary system.
- Eventually We’ll get a backup in the pulmonary system and that can then further lead to a backup within the systemic circulation and begin increasing pressure in the systemic circulation from the pulmonary circulation, which can then lead to right side failing

18
Q

other factors affecting sodium reabsorption/ secretion - urodilatin

A
  • same gene as ANP
  • similar AA sequence
  • secreted by DCT and CD cells
  • inhibits sodium reabsorption
  • much more potent than ANP
19
Q

other factors affecting sodium reabsorption/ secretion - sympathetic nerves

A
  • secrete catecholamines - Adr/ NAdr
  • stimulate sodium, water reabsorption in PCT, LOH, DCT, CD
20
Q

other factors affecting sodium reabsorption/ secretion - DOPAMINE

A

dopamine synthesised by PCT cells has opposite effects to Adr/NAdr
- acts in PCT

21
Q

other factors affecting sodium reabsorption/ secretion - uroguanylin

A

produced in small intestine
also inhibit sodium and water reabsorption

22
Q

total body water

A

32 - 40 litres - 70% body weight

23
Q

by what mechanism does the body tell us that we need more/ less water

A

thirst and sweating

24
Q

control of ECV by thirst/ sweating

A

Na+/H20 intake = Na+/H20 excretion

sweat :
- hypo-osmotic fluid
- causes decreased ECV
- increases body fluid osmolality

25
Q

what happens when prolonged/ severe sweating

A

decreased plasma volume:
decreased GFR
- increased plasma aldosterone (salt reabsorb in CD)
- decreased sodium excretion

also an increase in plasma osmolality at the same time:
- increased ADH - water absorption
- decreased water excretion

26
Q

thirst- blood volume and plasma osmolality

A

decreased blood volume - detected by baroreceptors
increased plasma osmolality - detected by osmoreceptors
causes angiotensin 2 release - stimulates thirst centre in hypothalamus - DRINK
angiotensin 2 also causes release of aldosterone - helps to rebalance with increase in sodium reabsorption and water

27
Q

diuretics

A

substances that cause enhanced excretion of water and solutes

28
Q

uses of diuretics

A

hypertension
pulmonary oedema
oedema
chronic heart failure

29
Q

common mechanism of diuretics

A

inhibition of sodium reabsorption in the nephron

30
Q

non clinical diuretics
- pressure diuresis

A

-increased ECV and BP
Autoregulation in cortex but not in the medulla
- washout of sodium/ solutes decrease osmotic gradient and decrease max urine osmolality
- less reabsorption - more diuresis - EVC returns to normal

31
Q

non clinical diuretics
H20 diuresis

A

increased water intake thus inhibiting ADH excretion of water - more diuresis

32
Q

clinical diuretics
- osmotic diuretics

A

e.g. mannitol
act on PCT
- enters tubule fluid by filtration
- exerts osmotic pressure in the tubule as it cannot be reabsorbed
- inhibits reabsorption of solute and water by altering osmotic drivign forces
- doesn’t act on specific membrane proteins
- alters water reabsorption in PCT and descending LOH

33
Q

carbonic anhydrase inhibitors

A

e.g. acetazolamide
- act primarily on PCT where enzyme carbonic anhydrase is most abundant
- also acts on principal and intercalating cells in the collecting duct
- carbonic anhydrase causes carbon dioxide and water to combine to form carbonic acid which dissociates in protons and bicarbonate ions
- bicarbonate reabsorbed with sodium
- inhibition of carbonic anhydrase means less formation of bicarbonate, which is driven by Na+, therefore less Na+ reabsorbed

34
Q

loop diuretics

A

e.g. furosemide and bumetanide
- act on the loop of Henle
- enter tubule lumen by secretion
- block Na+-K+-2Cl- symport on apical membrane ascending limb
- prevent sodium reabsorption
- disrupt countercurrent multiplier as ascending limb impermeable to water
- impair kidneys role of diluting and concentrating urine

35
Q

when are loop diuretics used

A

they are the most potent diuretics
- used for decreasing ECV
- used in treatment of high BP and pulmonary oedema - chronic heart failure

36
Q

problems with loop diuretics

A

hypokalaemia (low potassium in plasma)
- postural hypotension

37
Q

thiazide diuretics

A

e.g. bendroflumethiazide
- enters tubule fluid by filtration/ secretion
- inhibit sodium reabsoprion
- blocks Na+/Cl- symport on distal tubule cell apical membrane
- thus inhibits water reabsorption

38
Q

problems with diuretics

A

if overused can lead to dehydration
- can cause electrolyte imbalances

39
Q

amiloride drug

A

sodium channel blockers (ENaC)
- less water reabsorption
potassium-sparing diuretic

40
Q

spironolactone drug

A

blocks aldosterone receptors in cytoplasm

potassium sparing diuretic

41
Q

fluid rebound with diuretics

A
  • important that patients continue taking fluids with diuretics
  • if not they will produce small amounts of concentrated urine
  • this will be sensed by the nephrons to activate the renin -angiotensis system
  • the rise in plasma osmolality also stimulates a release of ASH which will also act to retain water

Body systems 2 (19 decks)

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