Potassium Flashcards

1
Q

What is the normal reference range (NR) for potassium and its primary role? (2)

A

Potassium is the main intracellular cation.

NR = 3.5–5.5 mmol/L.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does hypokalaemia always cause, and why? (2)

A

Always causes metabolic alkalosis.

When potassium is low in the blood, cells compensate by moving potassium out of cells and into the bloodstream.
To maintain electrical neutrality, hydrogen ions (H⁺) move into cells.
This reduces the number of free hydrogen ions in the blood, increasing pH and causing alkalosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What categories can causes of hypokalaemia be split into? (4)

A

GI loss
Renal loss
Redistribution
Rare causes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the GI causes of hypokalaemia? (3

A

Diarrhoea
Vomiting
Fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the renal causes of hypokalaemia? (6)

A

Conn’s syndrome

Cushing’s syndrome

Loop diuretics

Thiazide diuretics

Osmotic diuresis

Bartter or Gitelman syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does Cushing’s syndrome cause renal hypokalaemia? (1)

A

Ectopic ACTH stimulates mineralocorticoid receptors (MRs), leading to severe hypokalaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do loop and thiazide diuretics cause hypokalaemia? (2)

A

Loop diuretics: Block the triple transporter in the ascending loop of Henle (Bartter syndrome mutation).

Thiazide diuretics: Block the Na+-Cl− transporter in the distal convoluted tubule (Gitelman syndrome mutation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the redistribution causes of hypokalaemia? (3)

A

Insulin
Alkalosis
Beta-agonists (e.g., Salbutamol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the rare causes of hypokalaemia? (2)

A

Renal tubular acidosis (RTA) Types 1 & 2

Hypomagnesaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is paradoxical aciduria in hypokalaemia? (1)

A

H+ is lost in urine as a physiological response where the kidney retains K+ in exchange for H+.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does hypokalaemia present clinically? (2)

A

Muscle weakness

Arrhythmias (e.g., ventricular fibrillation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the ECG changes in hypokalaemia? (3)

A

Flattened T waves

U waves

ST depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the management of hypokalaemia based on potassium levels? (2)

A

K+ 3–3.5 mmol/L:
Oral potassium chloride for 48 hours and recheck levels.

K+ <3 mmol/L:
IV potassium chloride.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the types of renal tubular acidosis (RTA), and their key features?

A

Type 1 (distal RTA):
Most severe.
Distal failure of H+ excretion.
Associated with acidosis and hypokalaemia.

Type 2 (proximal RTA):
Milder.
Proximal failure to reabsorb HCO3−.
Associated with acidosis and hypokalaemia.

Type 4 RTA:
Aldosterone deficiency/resistance.
Associated with acidosis and hyperkalaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens in type 1 renal tubular acidosis?

A

Type 1 (distal RTA):

Most severe.
Distal failure of H+ excretion.
Associated with acidosis and hypokalaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens in type 2 renal tubular acidosis?

A

Type 2 (proximal RTA):

Milder.
Proximal failure to reabsorb HCO3−.
Associated with acidosis and hypokalaemia.

17
Q

What happens in type 4 renal tubular acidosis?

A

Type 4 RTA:

Aldosterone deficiency/resistance.
Associated with acidosis and hyperkalaemia.

18
Q

What are the 4 main causes of hyperkalaemia?

A

Renal impairment (CKD) – Main cause

Decreased renin – Type 4 renal tubular acidosis (RTA), NSAIDs

Drugs – ACE inhibitors (ACEis), ARBs, K+ sparing diuretics (e.g., Spironolactone)

K+ release from cells – Rhabdomyolysis, acidosis

19
Q

How does renal impairment (CKD) cause hyperkalaemia?

A

Reduced glomerular filtration rate (GFR) leads to decreased potassium excretion.

20
Q

What drugs can cause hyperkalaemia? (3)

A

ACE inhibitors (ACEis)

Angiotensin receptor blockers (ARBs)

Potassium-sparing diuretics (e.g., Spironolactone)

21
Q

How does rhabdomyolysis or acidosis cause hyperkalaemia?

A

Rhabdomyolysis releases intracellular K+ from damaged muscle cells.

Acidosis drives K+ out of cells in exchange for H+ ions.

22
Q

What are the key ECG changes seen in hyperkalaemia? (6)

A

Peaked/tented T waves
Bradycardia (progressing to asystole)
Prolonged PR interval
Flattened P waves
Widened QRS
Sine waves (indicate impending cardiac arrest)

23
Q

How is hyperkalaemia managed?

A

If K+ >6.5 mmol/L or ECG changes present:

  1. IV 10mL 10% Calcium Gluconate – protects the myocardium by reducing excitability.
  2. 10U Insulin + 50mL 50% Dextrose – drives K+ into cells.
  3. Alternative: Nebulised Salbutamol (beta-agonist).

-> If K+ <6.5 mmol/L: Treat the underlying cause.

-> If K+ >7 mmol/L: Recheck the sample to ensure no haemolysis.

24
Q

How is hyperkalaemia managed when K+ is >6.5 mmol/L or ECG changes are present? (3 steps)

A

IV 10mL 10% Calcium Gluconate – Protects the myocardium by reducing excitability.

10U Insulin + 50mL 50% Dextrose – Drives potassium into cells.

Alternative: Nebulised Salbutamol (beta-agonist).

25
What is the role of IV Calcium Gluconate in hyperkalaemia?
It protects the myocardium by stabilizing cardiac membranes and reducing excitability, preventing arrhythmias.
26
How does insulin with dextrose help in hyperkalaemia?
Insulin promotes the uptake of potassium into cells, and dextrose prevents hypoglycaemia caused by insulin administration.
27
How does nebulised salbutamol help in hyperkalaemia?
Salbutamol (a beta-agonist) drives potassium into cells via beta-adrenergic stimulation.
28