ChemPath: Potassium Flashcards

1
Q

What is the normal range for serum potassium?

A

3.5-5.0 mmol/L

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2
Q

What are the two main hormones involved in the regulation of potassium?

A
  • Angiotensin II
  • Aldosterone
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3
Q

Outline how the renin-angiotensin-aldosterone system works.

A
  • 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

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4
Q

Outline the mechanisms of action of aldosterone.

A
  • 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
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5
Q

What are the main stimuli for aldosterone release?

A
  • Angiotensin II
  • High potassium
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6
Q

List some causes of hyperkalaemia.

A
  • 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)
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7
Q

Explain how acidosis leads to hyperkalaemia.

A
  • 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
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8
Q

Outline the management of hyperkalaemia.

A
  • 10 ml 10% calcium gluconate
  • 50 ml 50% dextrose + 10 U insulin
  • Nebulised salbutamol
  • Treat the cause
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9
Q

List some causes of hypokalaemia.

A
  • 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
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10
Q

Name two conditions that can block the triple transporter.

A
  • Loop diuretics
  • Bartter syndrome (mutation in triple transporter)
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11
Q

Name two conditions that can block the Na+/Cl- cotransporter.

A
  • Thiazide diuretics
  • Gitelman syndrome (mutation in Na+/Cl- cotransporter)
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12
Q

Explain how increased delivery of sodium to the distal nephron can cause hypokalaemia.

A
  • 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
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13
Q

What are the clinical features of hypokalaemia?

A
  • Muscle weakness
  • Arrythmia
  • Polyuria and polydipsia (hypokalaemia leads to nephrogenic DI)
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14
Q

What screening test should be done in a patient with hypokalaemia and hypertension?

A

Aldosterone: renin ratio (primary hyperaldosteronism will show high aldosterone and low renin)

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15
Q

Outline the management of hypokalaemia:

  1. 3-3.5 mmol/L
  2. <3 mmol/L
A
  1. 3-3.5 mmol/L
    • Oral potassium chloride (2x SandoK TDS for 48 hours)
    • Re-check serum K+ concentration
  2. < 3 mmol/L
    • IV potassium chloride infusion
    • Maximum rate: 10 mmol/hr
    • NOTE: rates > 20 mmol/hr irritate the superficial veins
    • TREAT THE CAUSE
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