ChemPath: Potassium Flashcards
What is the normal range for serum potassium?
3.5-5.0 mmol/L
K+ = most abundant intracelllular
Na+ = most abundant extracellular
What are the two main hormones involved in the regulation of potassium?
- Angiotensin II
- Aldosterone
Outline how the renin-angiotensin-aldosterone system works.
- Reduced perfusion or low sodium will stimulate the production of renin from the juxta-glomerular cells
- This cleaves angiotensinogen to angiotensin I
- This is then converted by ACE in the lungs to angiotensin II → stimulates aldosterone release from the adrenals
- Aldosterone stimulates sodium reabsorption and potassium excretion in the principal cells of the cortical collecting tubule
NOTE: water will also be drawn in with the sodium so aldosterone should not greatly affect sodium concentration
Outline the mechanisms of action of aldosterone.
- Aldosterone binds to MR on principal cells in cortical collecting duct
- Insertion of epithelial Na+ channels –> increases Na+ reabsorption
- As you reabsorb more sodium, the lumen becomes more negative
- K+ will move down (secreted) the electrochemical gradient into the lumen via K+ channels
Aldosterone –> Na+ in, K+ out
What are the main stimuli for aldosterone release?
- Angiotensin II
- High potassium
List some causes of hyperkalaemia.
- Reduced GFR (renal failure)
- Reduced renin activity (renal tubular acidosis type 4 - diabetic nephropathy, NSAIDs)
- Drugs - ACE inhibitors/ARBs, aldosterone antagonists (spironolcatone)
- Addison’s disease
- Potassium release from cells (rhabdomyolysis, acidosis)
ECG change for hyperkalaemia
peaked T waves
Explain how acidosis leads to hyperkalaemia.
- When plasma H+ concentration is high, the cells try to take in more H+ from the plasma
- To maintain electrochemical neutrality, K+ must leave the cell when H+ enters
- This leads to hyperkalaemia
Outline the management of hyperkalaemia.
- **30 ml 10% calcium gluconate **- stabilizes myocardium
- 50 ml 50% dextrose + 10 Units insulin - insulin drives K+ into cells, glucose to prevent hypoglycaemia
- Nebulised salbutamol - drives K+ into cells
- Treat the cause
NOTE - salbutamol can cause hypokalemia
List some causes of hypokalaemia.
- GI loss
- Renal loss
- Hyperaldosteronism, Cushing’s syndrome (excess cortisol binds to MR)
- Increased Na+ delivery to distal nephron
- Osmotic diuresis
- Redistribution into cells
- Insulin
- Beta-agonists (e.g. Salbutamol)
- Alkalosis
- Rare causes
- Renal tubular acidosis (type 1 and 2)
- Hypomagnesaemia
Name two conditions that can block the triple transporter.
- Loop diuretics
- Bartter syndrome (mutation in triple transporter)
In loop of henle
more Na+ delivered distally
Name two conditions that can block the Na+/Cl- cotransporter.
- Thiazide diuretics
- Gitelman syndrome (mutation in Na+/Cl- cotransporter)
In collecting duct
More Na+ delivery distally
Explain how increased delivery of sodium to the distal nephron can cause hypokalaemia.
- Increased delivery of Na+ to the distal nephron (e.g. because of blocking/ineffective triple transporter or Na+/Cl- cotransporter) leadas to increased reabsorption of Na+ in the distal nephron
- This leads to the lumen of the distal nephron becoming more negative
- This results in the movement of K+ down the electrochemical gradient through into the lumen
What are the clinical features of hypokalaemia?
- Muscle weakness
- Arrythmia
- Polyuria and polydipsia (hypokalaemia leads to nephrogenic DI / AVP resistance)
What screening test should be done in a patient with hypokalaemia and hypertension?
Aldosterone: renin ratio
(primary hyperaldosteronism will show high aldosterone and low renin)
