ChemPath: Potassium Flashcards
What is the normal range for serum potassium?
3.5-5.0 mmol/L
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 and stimulates the transcription of ENaC channels
- Aldosterone binding to MR also leads to increased Sgk1 which inhibits Nedd4
- Nedd4 usually ubiquitinates sodium channels and degrades them
- Inhibition of Nedd4 leads to preservation of sodium channels thereby increasing sodium reabsorption
- As you reabsorb more sodium, the lumen becomes more negative and K+ will move down the electrochemical gradient into the lumen via ROMK channels
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, NSAIDs)
- ACE inhibitors/ARBs
- Addison’s disease
- Aldosterone antagonists
- Potassium release from cells (rhabdomyolysis, acidosis)
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.
- 10 ml 10% calcium gluconate
- 50 ml 50% dextrose + 10 U insulin
- Nebulised salbutamol
- Treat the cause
List some causes of hypokalaemia.
- GI loss
- Renal loss
- Hyperaldosteronism, Cushing’s syndrome
- Increased sodium delivery to distal nephron
- Osmotic diuresis
- Redistribution into cells
- Insulins
- Beta-agonists
- 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)
Name two conditions that can block the Na+/Cl- cotransporter.
- Thiazide diuretics
- Gitelman syndrome (mutation in Na+/Cl- cotransporter)
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 ROMK channels into the lumen
What are the clinical features of hypokalaemia?
- Muscle weakness
- Arrythmia
- Polyuria and polydipsia (hypokalaemia leads to nephrogenic DI)
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)
Outline the management of hypokalaemia:
- 3-3.5 mmol/L
- <3 mmol/L
-
3-3.5 mmol/L
- Oral potassium chloride (2x SandoK TDS for 48 hours)
- Re-check serum K+ concentration
-
< 3 mmol/L
- IV potassium chloride infusion
- Maximum rate: 10 mmol/hr
- NOTE: rates > 20 mmol/hr irritate the superficial veins
- TREAT THE CAUSE
