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 causes renin to cleave 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

Where aldosterone acts

A

Principal cortical cells

in the collecting duct

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5
Q

Outline the mechanisms of action of aldosterone.

A
  • Aldosterone binds to MR and stimulates the transcription of ENaC channels (Epithelial Sodium 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, and get dumped into the lumen
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6
Q

How Na affects K excretion

A

Sodium resorbed - making the lumen more negative

K then excreted along the electrochemical gradient

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7
Q

What are the main stimuli for aldosterone release?

A
  • Angiotensin II
  • High serum potassium (most potent stimulator)
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8
Q

What are the causes of hyperkalaemia

A
  1. Renal failure (low GFR, reduced excretion)
  2. Drugs (ACEi / ARBs / Aldosterone antagonists)
  3. Low Aldosterone
    1. Addisons
    2. Type 4 renal tubular acidosis (low renin, low aldosterone)
  4. Release from cells (Rhabdomyolysis, acidosis)
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9
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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10
Q

Outline the management of hyperkalaemia.

A
  • 10 ml 10% calcium gluconate
  • 50 ml 50% dextrose + 10 U insulin
    • In reality - 100ml 20% dextrose
  • Nebulised salbutamol - beta agonists drive K into cell
  • Treat the cause
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11
Q

List some causes of hypokalaemia.

A
  • GI loss (diarrhoea)
  • Renal loss
    • Hyperaldosteronism (Conn’s), Cushing’s syndrome (binding to MR)
    • 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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12
Q

Describe Renal K handling, and how renal Na+ affects K+ excretion

A

More Na to distal tubules causes increased exchange of K into the lumen, causing hypokalaemia

Block of Na/CL channels by Thiazides and Gitelman’s syndrome, increase the Na arriving at the distal tubule causing increased K excretion

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13
Q

Blocking what two transporters in the kidney, causes hypokalaemia (via increased K+ excretion)

A
  1. Na/K/Cl- Triple transporter (in the loop of Henle)
  2. Na+/Cl- cotransporter in the DCT (in the distal nephron)
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14
Q

Name two conditions that can block the Na/K/Cl- triple transporter.

A
  • Loop diuretics
  • Bartter syndrome (mutation in triple transporter)
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15
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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16
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) leads 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
17
Q

Why Distal Na resorption causes reduced K

A

Increased Na resorption in distal tubule
Increased Electronegative gradient

Increased K loss

18
Q

What are the clinical features of hypokalaemia?

A
  • Muscle weakness
  • Arrythmia
  • Polyuria and polydipsia (hypokalaemia leads to nephrogenic DI)
19
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)

20
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, needs to be given centrally
    • TREAT THE CAUSE