Chemical Pathology 13 - Potassium & electrolytes Flashcards

1
Q

What is the serum concentration of potassium?

A

3.5 - 5

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2
Q

What are the hormones involved in renal potassium regulation?

A

Angiotensin II

Aldosterone

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3
Q

Where is renin released from?

A

Juxtaglomerular apparatus

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4
Q

Where is angiotensinogen released from?

A

Liver

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5
Q

Where is angiotensin I converted to angiotensin II?

A

Lung

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6
Q

What is the action of angiotensin II

A

Secretion of aldosterone from adrenals

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7
Q

What are the two stimuli for aldosterone release?

A

Angiotensin II

Hyperkalaemia

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8
Q

How does aldosterone work?

A

Acts on cortical collecting tubule (distal tubule) of nephron

Causes sodium retention and potassium excretion:
Aldosterone –> synthesis of sodium channels –> lumen becomes negative –> potassium moves down electrochemical gradient into lumen

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9
Q

What are the main causes of hyperkalaemia?

A

First go thorough RAAS:

  1. Renal failure (as reduced GFR –> less renin –> less aldosterone)
  2. Reduced renin (rare)
  3. ACE inhibitor (less ACE –> less angiotensin II –> less aldosterone)
  4. AgII receptor blocker (–> less aldosterone)
  5. Addison’s disease (less aldosterone)
  6. MR receptor blockers = aldosterone antagonists

Then:

  1. Rhabdomyolysis (damaged cells leak out potassium)
  2. Acidosis (H+ enters cell, K+ moves into lumen following electrochemical gradient)
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10
Q

Which 3 drug classes are associated with hyperkalaemia?

A

ACE inhibitors
ARBs
Spironolactone

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11
Q

How can diabetic nephropathy cause hyperkalaemia?

A

Type 4 renal tubular acidosis - causes reduced renin which in turn reduces aldosterone –> less K+ excretion

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12
Q

What ECG change is associated with hyperkalaemia?

A

Peaked T waves

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13
Q

Why is hyperkalaemia not seen until late renal failure?

A

Initially reduced GFR –> increased aldosterone to compensate –> hyperkalaemia only occurs when compensatory mechanism falls

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14
Q

How do you manage a patient with hyperkalaemia?

A

10mls 10% calcium gluconate (ONLY when potassium is over 6.5 or there are ECG changes)

20% dextrose + 10 units insulin (give dextrose alongside insulin to prevent hypoglycaemia)

Nebulised salbutamol (if hyperkalaemia is severe, it puts potassium into cells)

Treat the underlying cause

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15
Q

What are the 3 broad causes of hypokalaemia?

A

GI loss
Renal loss
Redistribution into the cells

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16
Q

Why is calcium gluconate used in hyperkalaemia?

A

It stabilises the membrane of cells in the myocardium (doesn’t actually reduce potassium)

17
Q

Why is insulin given in hyperkalaemia?

A

Drives potassium into cells

18
Q

When would you give fluids in a hyperkalaemic patient, as well as calcium gluconate + insulin?

A

If their hyperkalaemia is secondary to renal failure that is caused by hypovolaemia

19
Q

How does heart failure cause hyponatraemia?

A

Reduced CO –> reduced BP –> detected by baroreceptors –> Excess ADH –> sodium loss
ALSO
Lower BP –> lower GFR –> ADH –> sodium wasting

20
Q

What is reabsorbed in the ascending limb of the loop of henle?

A

Na
K
Cl

21
Q

What is reabsorbed in the DCT of the loop of henle?

A

Na

Cl

22
Q

Give 2 causes of impaired sodium resorption in the ascending limb of the loop of henle

A

Loop diuretics

Barter syndrome

23
Q

Give 2 causes of impaired sodium resorption in the DCT of the loop of henle

A

Thiazide diuretic

Gitelman syndrome

24
Q

What is the effect on potassium of impaired sodium resorption in the nephron?

A

More sodium delivered to distal nephron –> sodium goes from urine into cell, making urine more negative –> potassium drawn out into urine

25
Q

How does excess aldosterone affect potassium?

A

Causes increased sodium in cells –> exchanged with potassium –> hypokalaemia

26
Q

What are the 3 mechanisms of renal loss of potassium?

A

Hyperaldosteronism

Increased sodium delivery to distal nephron

Osmotic diuresis

27
Q

How does alkalosis affect potassium?

A

Hypokalaemia

28
Q

What are the top 3 methods of potassium loss?

A
GI loss (vomiting)
Renal loss
Redistribution into cells (insulin/ beta agonists/ alkalosis - treatments for hyperkalaemia!)
29
Q

What are the clinical features of hypokalaemia?

A

Muscle weakness
Cardiac weakness (arrhythmia)
Polyuria and polydipsia (somehow potassium affects ADH, causing nephrogenic DI)

30
Q

What screening test would you order in a patient with hypokaleamia and hypertension?

A

Aldosterone: renin ratio

31
Q

How does Cushing’s affect potassium?

A

Excess cortisol acts like excess aldosterone –> hypokalaemia

32
Q

Where is hyperkalaemia detected?

A

Adrenal cortex

33
Q

How does osmotic diuresis affect potassium?

A

Drags potassium out with water loss –> hypokalaemia

34
Q

How would you manage a patient with hypokalaemia?

A

Potassium between 3-3.5: oral KCl

Potassium <3: IV KCl, max rate = 10mmol/hour

Treat the underlying cause

35
Q

How does cirrhosis cause hyponatraemia?

A

Cirrhosis causes vasodilators to be released (nitric oxide)

BP reduced

ADH released

36
Q

How come SIADH doesn’t cause hypervolaemia?

A

Initial hypervolaemia is followed by NP release –> natiuresis –> euvolaemia –> euvolaemic hyponatraemia