Potassium and Electrolytes

Question 1

which is the most abundant intracellular cation

Answer 1

Potassium

Question 2

normal range of Potassium

Answer 2

3.5-5.0mmol/L

Question 3

main source of K+

Answer 3

dietary intake: fruit and vegetables mainly

Question 4

hormones involved with renal regulation of K+

Answer 4

• Angiotensin II
• Aldosterone

Question 5

where is renin released from

Answer 5

juxtaglomerular apparatus in kidney

Question 6

what stimulates renin release

Answer 6

reduced perfusion pressure

low Na

Question 7

what does renin do

Answer 7

causes angiotensinogen to be cleaved to form angiotensin I in the liver

Question 8

how is Angiotensin II formed

Answer 8

Angiotensin I is converted to Angiotensin II via angiotensin converting enzyme (ACE) in the lung

Question 9

role of Angiotensin II

Answer 9

AT II acts on the adrenal gland to stimulate the production of aldosterone

Question 10

role of aldosterone

Answer 10

Aldosterone causes excretion of K+ and reabsorption of Na+.

acts on principle cells of collecting duct to reabsorb Na + water and excrete K+.

It also increases Na reabsorption via reduced degradation of Na channels

Question 11

what happens if If K+ levels are too high

Answer 11

stimulate increased aldosterone release so K+ excreted in urine

net effect will be loss of K+ and retaining Na and water to maintain BP.

Question 12

relationship between aldosterone and potassium and sodium (plasma)

Answer 12

high aldosterone–>high sodium (directly proportional)

high aldosterone–>low potassium (inversely proportional)

Question 13

Causes of HyperK+

Answer 13

1. renal impairment (reduced GFR) - AMIR SAM- THINK OF THIS FIRST

2. Reduced renin: NSAIDS + Type 4 renal tubular acidosis

3. ACEi (i.e, ramipril, lisinopril)
4. ARBs (i.e. losartan, candesartan)
5. Addison’s disease
6. Aldosterone antagonists (e.g. spironolactone, eplerenone

• *7. Potassium release from cells:**
• biggest intracellular cation = any cell injury and cell death can cause a big release of K+ (rhabdomyololysis)
• acidotic states acidotic state (an abundance of H+ and low pH),

Question 14

Main causes of HyperK+

Answer 14

• Renal impairment- reduced renal excretion
• Drugs- ACEi, ARBs, spironolactone
• Low aldosterone
  o Addison’s disease
  o Type 4 renal tubular acidosis (low renin, low aldosterone)
• Release from cells: rhabdomyolysis, acidosis

((See picture- Nidhish’s pathsoc lecture))

Question 15

Main ECG changes associated with hyperK+ and other findings:

Answer 15

main: Peaked T waves
other findings:
- Bradycardia
- Widened QRS
- Prolonged PR interval
- Late change= sine wave

Question 16

Management of Hyperkalaemia

Answer 16

• 10ml 10% calcium gluconate: note: does not reduce K+ but stabilises cardiac membrane
• 50ml 50% dextrose (Amir sam: 100 ml of 20% dextrose…) + 10 units of insulin
• Nebulised salbutamol
• Treating the underlying cause

Question 17

Causes of HYPOkalaemia (3)

Answer 17

- GI loss- D&V, Diarrhoea > vomiting

**- Renal loss:** Anything that increases renal aldosterone will increase K+ loss:
o Hyperaldosteronism (Conn's syndrome), Excess cortisol (has promiscuity for MRs)
o Increased Na delivery to distal nephron (Drugs- Loop diuretics, Thiazides; conditions- barter's and gilteman's)
o Osmotic diuresis

• Redistribution into cells:
• Insulin
• BETA agonist (salbutamol)
• Alkalosis

______________________

Barters: LOH

Gitleman’s: DCT

Question 18

ECG finding in hypoK+

Answer 18

NOTE: in HypoK+, get U waves

**INCREASED RISK OF VT AND TORSADES DE POINTES

Question 19

Loop diuretics + potassium

Answer 19

Diuretics increase the loss of K+

Loop diuretics act on the triple transporter. and block the reabsorption of Na+ so more Na+ in distal nephron.

This will stimulate renin release and eventually aldosterone release

Question 20

Thiazide diuretics + potassium

Answer 20

Diuretics increase the loss of K+

These work in the DCT- block Na reabsorption via the NaCl transporter. so more more Na delivered to the distal nephron.

So more Na is crossing through the epithelial Na channels >>>> MORE K+ is LOST by maintaining the electrochemical gradient

Question 21

Clinical Features of HypoK+

Answer 21

• Muscle weakness
• Cardiac arrhythmia: Increased risk of VT and Torsades de pointes
• Polyuria and polydipsia (nephrogenic DI)

Question 22

Management of Hypokalaemia if Serum K+ 3.0-3.5mmol/L

Answer 22

o PO potassium chloride (two SandoK tablets TDS for 48 hours)
o Recheck serum K+

Question 23

Management of Hypokalaemia if Serum K+ < 3.0mmol/L

Answer 23

o IV potassium chloride + Maximum rate 10mmol per hour

Question 24

Screening Test for Hypokalaemia with Hypertension

Answer 24

• Aldosterone: renin ratio: Primary hyperaldosteronism- High aldosterone: renin ratio (as high aldosterone will suppress renin)

Rmb: in conn’s syndorme, you get HYPERTENSION and HYPOKALAEMIA (may not necessarily have hypernatraemia)

Question 25

Conn’s syndrome can be due to

Answer 25

• bilateral adrenal hyperplasia
• Aldosterone producing adenomas (autonomous production of aldosterone is produced)

Question 26

What is the cause of the electrolyte abnormaities here?

Answer 26

Not ramipril because creatinine is also high

therefore it’s because of REDUCED GFR

Question 27

What happens in barter syndrome?

Answer 27

autosomla recessive

hypokalaemia

hypotension

metabolic alkalosis

hypercalciuria

**affects the ascending limb of loop of henle

Question 28

what effect does spurious blood sampling have on potassium?

Answer 28

can lead to hyperkalaemia because the needle you use can lead to haemolysis–>potassium leaks out

Question 29

when to suspect renal tubilar acidosis?

Answer 29

if you have hypokalaemia and acidosis

**rmb usually you get hypokalaemia with alkalosis, so when you see hypolalaemia with acidosis think renal tubular acidosos*

mechanism: failure to excrete H+ into the kidneys, so you excrete K+ instead to enable Na+ reabsorption

*NB: type 4 causes hyperkalaemia so ignore that