Chempath 13: Potassium And Electrolytes

Question 1

Which cells release renin ?

Answer 1

Junta-glomerular cells in the kidneys

Question 2

What is the role of renin ?

Answer 2

Cleaves angiotensinogen to angiotensin 1

Question 3

Which enzyme cleaves angiotensin 1 to angiotensin 2 ?

Answer 3

ACE

Question 4

Where is ACE produced ?

Answer 4

The lungs

Question 5

What is the role of angiotensin 2 ?

Answer 5

Stimulate adrenal cortex to produce aldosterone
Causes vasoconstriction
Stimulates the CNS to release ADH (vasopressin)

Question 6

What causes renin release ?

Answer 6

Low sodium conc.

low perfusion pressure

Question 7

Which section of the adrenal cortex produces aldosterone ?

Answer 7

Zona glomerulosa

Question 8

Where in the nephron does aldosterone act ?

Answer 8

Collecting duct (principal cells)

Question 9

Other than Angiotensin 2 what else can stimulate Aldosterone directly ?

Answer 9

Hyperkaelaemia

Question 10

List 6 causes of hyperkalaemia ?

Answer 10

EXCESSIVE INTAKE - fasting, parenteral, stored blood transfusion

TRANSCELLULAR MOVEMENT - acidosis, DKA,rhabdomylosis

DECREASED EXCRETION - acute renal failure, CRF (late), K sparing diuretics (spironolactone), mineralocorticoid deficiency (Addisons), NSAIDs, ACEi, ARBs

Question 11

Order these ECG changes based on severity of hyperkalaemia ?

Tall tented T waves
Broad QRS complex
Absent P waves
VF

Answer 11

Tall tented T waves > absent P waves > Broad QRS complex > VF

Question 12

List 4 treatments of hyperkalaemia ?

Answer 12

10 mL 10% calcium Gluconate
100 mL 20% Dextrose with 10 units of insulin
Nebulised salbutamol
Calcium resonium PO

Insulin and salbutamol drive K+ into cells

Question 13

How does Cushing’s disease cause hypokalaemia ?

Answer 13

The excess cortisol binds to the mineralocorticoid receptors on the nephron causing increased sodium reabsorption and increased potassium loss

Question 14

List 6 causes of hypokalaemia ?

Answer 14

1. GI loss
2. Renal loss - hyperaldosteronism (high PB and low K+), increased sodium delivery to distal nephron (thiazide and loop diuretics), osmotic diuresis
3. Redistribution into the cells - insulin, beta agonsists, metabolic alkalosis
4. Rare causes - RTA type 1+2, hypomagnesaemia

Question 15

Name the ion channels do K+ ions travel through to enter the tubule of the nephron ?

Answer 15

ROMK channels

Question 16

List 2 causes of blockade/dysfunction of the Na+ k+ cl- triple ion transport channels in the ascending limb of the loop of henle ?

Answer 16

Loop diuretics
Bartter’s syndrome

This causes hypokalaemia
More sodium goes to the distal nephron and is reabsorbed there. This makes the tubule more negatively charged, causing K+ influx via ROMK channels.

Question 17

List 2 causes of blockade/dysfunction of the Na+cl- ion channels in the distal convoluted tubule ?

Answer 17

Thiazide diuretics
Gitelman syndrome

This causes more Na+ reabsorption in the distal part of the nephron. This causes increased negative charge of lumen. This causes influx of pottasium via ROMK channels.

Question 18

Which screening test can be used to diagnose primary Hyperaldosteronism in a patient with hypokalaemia and hypertension ?

Answer 18

Aldosterone: renin ratio

In primary hyperaldosteronism there is excess aldosterone which causes suppression of renin. This means you expect to see a high aldosterone: renin ratio

Question 19

List 3 clinical features of hypokalaemia ?

Answer 19

Muscle weakness
Arrhythmias
Polyuria + polydipsia (Nephrogenic DI)

Question 20

How is hypokalaemia treated ?

Answer 20

If serum k+ 3-3.5 mmol/L: Oral pottasium chloride (KCL)

If serum k+ <3 mmol/L: IV Pottasium chloride (KCL)

Question 21

How does ramipril cause hyperkalaemia ?

Answer 21

Ramipril inhibits ACE
This causes reduced conversion of AT1 to AT2
This causes reduced aldosterone
This means less K+ is excreted

Question 22

Where in the nephron is the defect in
A) Barter’s syndrome
B) Gitelman syndrome

Answer 22

A- Na+/K+/Cl- co-transporter Ascending limb of the loop of hence
B- DCT