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 (distal nephron)
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 increases number of open Na+ channels (ENaC) in luminal membrane -> Na+ resorption
This makes the lumen electronegative and creates an electrical gradient -> K+ is secreted into the lumen -> excretion of potassium
*Meaning anything increasing delivery of sodium to DCT means more sodium in -> more potassium out
What are the main stimuli for aldosterone release?
- Angiotensin II
- High potassium
List some causes of hyperkalaemia.
Renal impairment – reduced renal excretion
Drugs – ACEi, ARBs, spironolactone
Low aldosterone - Addison’s disease, T4 renal tubular acidosis (low renin, low aldosterone)
Release from cells – rhabdomyolysis, acidosis
**If well patient but blood K+ is super high -> blood may have haemolysed. Take another sample
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.
- 30ml) 10% calcium gluconate
- 50 ml 50% dextrose
- 10 Units insulin
- Nebulised salbutamol
- Treat the cause
10 10, 50 50, 10 rule but now the first 10 is 30ml
List some causes of hypokalaemia.
- GI loss
- Renal loss
- Hyperaldosteronism (Conns), Cushing’s syndrome
- Increased sodium delivery to distal nephron (loop diuretics / Bartter syndrome, thiazides / gitelman syndrome)
- Osmotic diuresis (diabetes)
- Redistribution into cells
- Insulins (T2dm or insulinoma)
- Beta-agonists
- Alkalosis
- Rare causes
- Renal tubular acidosis (type 1 and 2)
- Hypomagnesaemia
Name two things that can block the triple transporter (Na+/K+/Cl- in LoH).
- 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 -> K+ gets peed out
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/conn’s 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
