management of electrolyte and water balance Flashcards
salt intake and excretion
intake = 10g
sweat - 0.25g
urine - 9.5 g
faeces - 0.25g
what hormone controls the amount of sodium lost in urine or reabsorbed into the plasma
aldosterone
what is aldosterone
a steroid hormone produced in the adrenal cortex from cholesterol
- plasma conc 0.1-0.15
what is aldosterone produced in response to
in response to a fall in NaCl intake or an increase in the potassium concentration in the interstitial fluid
what is aldosterone stimulated and inhibited by
stimulated by angiotensin 2 and inhibited by ANP
what stimulates aldosterone release if Na+ loss is less severe
ACTH - corticotrophin
main functions of aldosterone
sodium retention
potassium excretion
secondary retention of water - increased ECF
Stretch receptors
We have specialized cells that sit around the afferent arteriole that can detect changes in pressure
- they are stretch receptors.
macula densa
Macula densa - this has a sensing capability so it can detect changes in sodium levels
and also osmolality
what does aldosterone work with
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
renin angiotensin system
- 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
another hormone affecting sodium reabsorption
atrial natriuretic peptide (ANP)
how does aldosterone increase sodium and decrease potassium
- 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+
ANP
- 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
actions of ANP
- 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
BNP
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
how can congestive heart failure happen
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
other factors affecting sodium reabsorption/ secretion - urodilatin
- same gene as ANP
- similar AA sequence
- secreted by DCT and CD cells
- inhibits sodium reabsorption
- much more potent than ANP
other factors affecting sodium reabsorption/ secretion - sympathetic nerves
- secrete catecholamines - Adr/ NAdr
- stimulate sodium, water reabsorption in PCT, LOH, DCT, CD
other factors affecting sodium reabsorption/ secretion - DOPAMINE
dopamine synthesised by PCT cells has opposite effects to Adr/NAdr
- acts in PCT
other factors affecting sodium reabsorption/ secretion - uroguanylin
produced in small intestine
also inhibit sodium and water reabsorption
total body water
32 - 40 litres - 70% body weight
by what mechanism does the body tell us that we need more/ less water
thirst and sweating
control of ECV by thirst/ sweating
Na+/H20 intake = Na+/H20 excretion
sweat :
- hypo-osmotic fluid
- causes decreased ECV
- increases body fluid osmolality
what happens when prolonged/ severe sweating
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
thirst- blood volume and plasma osmolality
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
diuretics
substances that cause enhanced excretion of water and solutes
uses of diuretics
hypertension
pulmonary oedema
oedema
chronic heart failure
common mechanism of diuretics
inhibition of sodium reabsorption in the nephron
non clinical diuretics
- pressure diuresis
-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
non clinical diuretics
H20 diuresis
increased water intake thus inhibiting ADH excretion of water - more diuresis
clinical diuretics
- osmotic diuretics
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
carbonic anhydrase inhibitors
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
loop diuretics
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
when are loop diuretics used
they are the most potent diuretics
- used for decreasing ECV
- used in treatment of high BP and pulmonary oedema - chronic heart failure
problems with loop diuretics
hypokalaemia (low potassium in plasma)
- postural hypotension
thiazide diuretics
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
problems with diuretics
if overused can lead to dehydration
- can cause electrolyte imbalances
amiloride drug
sodium channel blockers (ENaC)
- less water reabsorption
potassium-sparing diuretic
spironolactone drug
blocks aldosterone receptors in cytoplasm
potassium sparing diuretic
fluid rebound with diuretics
- 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
