W6 - K+ & electrolytes Flashcards
What is the most abundant intracellular cation?
Potassium
What is the range for potassium serum concentration?
3.5-5.0 mmol/L
Which hormones are involved in renal regulation of potassium?
- Angiotensin II
- Aldosterone
Describe the renin-angiotensin-aldosterone system (RAAS)
Renin is released from the juxtaglomerular apparatus => angiotensinogen (from liver) becomes angiotensin I => Ag I is converted to Ag II in the lungs by ACE => Ag II stimulates the release of aldosterone from the adrenal glands => aldosterone causes Na+ and H2O retention, K+ excretion into urine = hence BP and BV go up
What are the stimulants for the production of aldosterone?
- Angiotensin II (via RAAS)
- High potassium
Where in the kidney does aldosterone act?
On principal cells in the cortical collecting tubule
Describe the normal physiology of potassium excretion in collecting tubule?
Na reabsorption through ENac (epithelial sodium channels) leads to tubular lumen negative electrical potential => potassium moved down the electrical gradient into the negatively charged lumen (urine) => K+ Excretion
How does aldosterone induce K+ excretion in the collecting tubule?
Aldosterone binds the MR (mineralocorticoid receptor) => increased sodium channels => increased Na+ reabsorption from lumen => lumen negatively charged => K+ moves down its electrical gradient to lumen, and out into urine
What are the main causes (4 categories) of hyperkalaemia?
- Renal impairment – i.e., renal failure
- Drugs – i.e., ACEi (ramipril), ARBs (losartan), aldosterone antagonist (spironolactone)
- Low aldosterone – Addison’s disease, type 4 renal tubular acidosis (diabetic nephropathy; low renin => low aldosterone)
- Release from cells – i.e., rhabdomyolysis, acidosis (maintain electroneutrality)
What is the main ECG change associated with hyperkalaemia?
Peaked T waves
How would you manage a patient with hyperkalaemia?
1) 10 ml 10% calcium gluconate
2) 100 ml 20% dextrose + 10 units of insulin*
3) Nebulised salbutamol
+ Treat the underlying cause
*dextrose given with insulin to ensure the insulin alone does not make patient hypoglycaemic
What are the causes (4 main categories + more specific ones) of hypokalaemia?
- GI loss
- Renal loss
- Hyperaldosteronism (excess cortisol)
- increased sodium delivery to distal nephron
- Osmotic diuresis (thiazide diuretics, loop diuretics) - Redistribution into the cells
- insulin, beta-agonists, alkalosis - Rare causes:
- renal tubular acidosis type 1 & 2, hypomagnesaemia
Explain the MOA of renal potassium loss
Reabsorption of sodium can be blocked anywhere along the nephron:
Loop of Henle blockage => loop diuretics, Barter syndrome (deficiency of Na+/K+/Cl- channel)
Distal tubule => thiazide diuretics, Gitelman syndrome
Increased sodium delivery to collecting tubule => potentiates electrical gradient => K+ loss
What are the clinical features (3) of hypokalaemia?
- Muscle weakness
- Cardiac arrhythmia
- Polyuria & polydipsia (nephrogenic DI)
Why does hypokalaemia cause polyuria and polydipsia?
Hypokalemia leads to resistance to ADH => will NOT reabsorb water => polyuria + polydipsia (nephrogenic DI)