Chemical Pathology 13 - Potassium & electrolytes Flashcards
What is the normal serum concentration of potassium?
3.5 - 5
What are the hormones involved in renal potassium regulation?
Angiotensin II
Aldosterone
Where is renin released from?
Juxtaglomerular apparatus
Where is angiotensinogen released from?
Liver
Where is angiotensin I converted to angiotensin II?
Lung
What is the action of angiotensin II
Secretion of aldosterone from adrenals
What are the two stimuli for aldosterone release?
Angiotensin II
Hyperkalaemia
How does aldosterone work?
Acts on principal cells of DCT and collecting duct
Causes sodium retention and potassium excretion:
Aldosterone –> synthesis of sodium channels –> more sodium reabsorbed from lumen and so the lumen becomes negative –> potassium moves down electrochemical gradient into lumen
Aldosterone binds to MR receptor - leads to upregulation of Sgk-1 -> phosphorylates and inactivates Nedd4-3 which usually degrades sodium channels -> more sodium channels and more reabsorption
What are the main causes of hyperkalaemia?
First go thorough RAAS:
- Renal failure (as reduced GFR –> less renin –> less aldosterone)
- Reduced renin (rare, type 4 renal tubular acidosis - may be caused by diabetic nephropathy or NSAIDs)
- ACE inhibitor (less ACE –> less angiotensin II –> less aldosterone)
- AgII receptor blocker (–> less aldosterone)
- Addison’s disease (less aldosterone)
- MR receptor blockers = aldosterone antagonists
Then there’s potassium release from cells:
- Rhabdomyolysis (damaged cells leak out potassium)
- Acidosis (H+ enters cell, K+ moves into lumen following electrochemical gradient)
Which 3 drug classes are associated with hyperkalaemia?
ACE inhibitors
ARBs
Spironolactone
How can diabetic nephropathy cause hyperkalaemia?
Type 4 renal tubular acidosis - causes reduced renin which in turn reduces aldosterone –> less K+ excretion
What ECG change is associated with hyperkalaemia?
Peaked/tall tented T waves
Generalised across the leads
Why is hyperkalaemia not seen until late renal failure?
Initially reduced GFR –> increased aldosterone to compensate –> hyperkalaemia only occurs when compensatory mechanism falls
How do you manage a patient with hyperkalaemia?
10mls 10% calcium gluconate (ONLY when potassium is over 6.5 or there are ECG changes)
100mls of 20% dextrose + 10 units insulin (give dextrose alongside insulin to prevent hypoglycaemia)
Textbooks will say 50ml 50% dextrose but this isn’t really seen in clinical practice due to risk of extravasation
Nebulised salbutamol (if hyperkalaemia is severe, it puts potassium into cells)
Treat the underlying cause
KNOW THESE DOSES BECAUSE HYPERKALAEMIA IS A MATTER OF LIFE AND DEATH
What are the 3 broad causes of hypokalaemia?
GI loss
Renal loss
Redistribution into the cells
Rare causes like renal tubular acidosis type 1 and 2, hypomagnesaemia
Why is calcium gluconate used in hyperkalaemia?
It stabilises the membrane of cells in the myocardium (doesn’t actually reduce potassium)
Why is insulin given in hyperkalaemia?
Drives potassium into cells
When would you give fluids in a hyperkalaemic patient, as well as calcium gluconate + insulin?
If their hyperkalaemia is secondary to renal failure that is caused by hypovolaemia
How does heart failure cause hyponatraemia?
Reduced CO –> reduced BP –> detected by baroreceptors –> Excess ADH
ALSO
Lower BP –> lower GFR –> ADH
What is reabsorbed in the ascending limb of the loop of henle?
Na
K
Cl
What is reabsorbed in the DCT?
Na
Cl
Give 2 causes of impaired sodium resorption in the ascending limb of the loop of henle
Loop diuretics
Barter syndrome
Give 2 causes of impaired sodium resorption in the DCT
Thiazide diuretic
Gitelman syndrome
What is the effect on potassium of impaired sodium resorption in the nephron?
More sodium delivered to distal nephron –> sodium reabsorbed from lumen into cell, making lumen more negative –> potassium drawn out into urine
