Potassium and Electrolytes

Question 1

What is the most abundant intracellular cation?

Answer 1

Potassium

Question 2

What is the normal serum concentration of potassium?

Answer 2

3.5-5.0 mmol/L

Question 3

Which hormones are involved in renal regulation of potassium?

Answer 3

Angiotensin II

Aldosterone

Question 4

How does RAAS work?

Answer 4

Angiotensinogen (liver) gets converted to angiotensin I by Renin (from JGA)

Angiotensin I gets converted to angiotensin II from ACE (lung)

Angiotensin II stimulates aldosterone from the adrenals

Aldosterone causes Sodium and water retention from the urine which increases blood volume and pressure as well as potassium loss into urine

Question 5

Which cells does aldosterone work on?

Answer 5

Principal cells (in corticol collecting tubule)

Question 6

How is potassium secreted?

Answer 6

Na reabsorption through ENaC (stimulated by aldosterone) (epithelial sodium channels) leads to tubular lumen negative electrical potential, driving potassium secretion into lumen

Question 7

What are the stimuli for aldosterone secretion?

Answer 7

Angiotensin II

Potassium

Question 8

What are the main causes of hyperkalaemia?

Answer 8

1. Renal Impairment (low GFR)(Glomerulus)
2. Reduced renin (Type 4 renal tubular acidosis (diabetic nephropathy) or NSAIDs)
3. Drugs (ARBs (losartan), ACEi (ramipril), spironolactone (aldosterone antagonist))
4. Low aldosterone (Addison’s disease, Type 4 renal acidosis w/ low renin and low aldosterone)
5. Release from cells in rhabdomyolysis (cell damage) and acidosis (to maintain electroneutrality)

Question 9

What is the main ECG change associated with hyperkalaemia?

Answer 9

Peaked T waves

Question 10

How would you manage a patient with hyperkalaemia (pretty much >6.5mmol/Lor ECG changes)?

Answer 10

10 ml 10% calcium gluconate (to stabilise myocardium)

(not now but historically 50 ml 50% dextrose) More commonly 100ml of 20% dextrose to reduce damage + 10 units of insulin

Nebulized salbutamol

Treat the underlying cause

Question 11

What are the causes of hypokalaemia?

Answer 11

GI loss

Renal loss (High aldosterone/ Cushing’s, increased sodium delivery, osmotic diuresis)

Redistribution into cells (Insulin, beta agonists, alkalosis)

Rare: renal tublar acidosis T1&2, hypomagnesia

Question 12

Where is Na, K and Cl lost from the nephron?

Answer 12

Na, Cl = (Asc.) Loop of Henle and DCT

K = (Asc. ) Loop of Henle

Question 13

What stops the triple transporter in the ascending Loop of Henle? (cause more Na to distal nephron)

Answer 13

Loop diuretics and Bartter syndrome

Question 14

What are the clinical features hypokalaemia?

Answer 14

Muscle Weakness

Cardiac arrhythmia

Polyuria & polydipsia (nephrogenic DI)

Question 15

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

Answer 15

Aldosterone: Renin ratio which may indicate Conn’s (primary hyperaldosteronism if high)

Question 16

How would you manage a patient with mild (3-3.5) hypokalaemia?

Answer 16

Oral potassium chloride (two SandoK tablets tds for 48 hrs)

Then recheck serum potassium

Question 17

How would you manage a patient with severe (<3) hypokalaemia?

Answer 17

IV potassium chloride

Maximum rate 10 mmol per hour

Rates > 20 mmol per hour are highly irritating to peripheral veins - need to use a central line

Question 18

Hyperkalaemia is a side-effect of which of the following drugs?

Furosemide
Bendroflumethiazide
Salbutamol
Ramipril

Answer 18

Ramipril

Question 19

Hypokalaemia is a side-effect of which of the following drugs?

Spironolactone
Indomethacin
Perindopril
Furosemide

Answer 19

Furosemide

Question 20

What are the two stimuli for aldosterone?

Answer 20

high potassium

Angiotensin II

Question 21

How does potassium move?

Answer 21

K moves down the electrical gradient through ROMK (potassium channel)

Aldosterone binds to MR receptor which increases ENaC channels (sodium reabsorbed more and lumen is more negative allowing K to move)

Question 22

How does Aldosterone affect ENaC?

Answer 22

Aldosterone binds to mineralocorticoid Receptor which leads to expression of Sgk-1 which stops Nedd4-2

Kinase phosphorylates Nedd4-2 which degrades sodium channels (ENaC) is stopped (less degradation of ENaC)

Question 23

How is polyuria and polydipsia caused in Conn’s syndrome (low K)?

Answer 23

It causes nephrogenic DI (ADH resistance)

Question 24

What is the order of likelihood of hyperkalaemia causes?

Answer 24

Renal impairment (AKI/ CKD)

Drugs (ACEI/ARBs/Aldo Ant)

Low aldosterone (Addisons, T4 Tubular acidosis)

Release from cells

Question 25

How does increased sodium delivery to distal nephron result in renal loss of K?

Answer 25

More sodium comes in and is reabsorbed which makes the lumen more negative and gradient causes more K loss