Chemical Pathology 13 - Potassium & electrolytes Flashcards

1
Q

What is the normal serum concentration of potassium?

A

3.5 - 5

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

What are the hormones involved in renal potassium regulation?

A

Angiotensin II

Aldosterone

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

Where is renin released from?

A

Juxtaglomerular apparatus

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

Where is angiotensinogen released from?

A

Liver

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

Where is angiotensin I converted to angiotensin II?

A

Lung

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

What is the action of angiotensin II

A

Secretion of aldosterone from adrenals

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

What are the two stimuli for aldosterone release?

A

Angiotensin II

Hyperkalaemia

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

How does aldosterone work?

A

Acts on principal cells of DCT and collecting duct

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

Aldosterone binds to MR receptor - leads to upregulation of Sgk-1 -> phosphorylates and inactivates Nedd4-3 which usually degrades sodium channels -> more sodium channels and more reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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, type 4 renal tubular acidosis - may be caused by diabetic nephropathy or NSAIDs)
  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 there’s potassium release from cells:

  1. Rhabdomyolysis (damaged cells leak out potassium)
  2. Acidosis (H+ enters cell, K+ moves into lumen following electrochemical gradient)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which 3 drug classes are associated with hyperkalaemia?

A

ACE inhibitors
ARBs
Spironolactone

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

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

What ECG change is associated with hyperkalaemia?

A

Peaked/tall tented T waves

Generalised across the leads

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

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

100mls of 20% dextrose + 10 units insulin (give dextrose alongside insulin to prevent hypoglycaemia)
Textbooks will say 50ml 50% dextrose but this isn’t really seen in clinical practice due to risk of extravasation

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

Treat the underlying cause

KNOW THESE DOSES BECAUSE HYPERKALAEMIA IS A MATTER OF LIFE AND DEATH

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

What are the 3 broad causes of hypokalaemia?

A

GI loss
Renal loss
Redistribution into the cells

Rare causes like renal tubular acidosis type 1 and 2, hypomagnesaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
ALSO
Lower BP –> lower GFR –> ADH

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?

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

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 reabsorbed from lumen into cell, making lumen more negative –> potassium drawn out into urine

25
Q

How does excess aldosterone affect potassium?

A

Causes increased sodium reabsorption –> lumen more negative -> potassium excreted –> 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

Protons released from cells in exchange for K+ absorption into cells =
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 low potassium affects ADH resistance, causing nephrogenic DI)

30
Q

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

A

Aldosterone: renin ratio

Suspecting Conn’s

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

What is the best order for thinking about the main causes of hyperkalaemia?

A

Renal impairment - reduced renal excretion

Drugs: ACE inhibitors, ARBs, spironolactone

Low aldosterone: Addison’s, type 4 renal tubular acidosis

Release from cells: rhabdomyolysis, acidosis