High Potassium handling - Amir Sam

Question 1

Explain the RAAS system

Answer 1

Liver produces ANGIOTENSINOGEN

Kidney JGA produces renin, which converts angiotensinogen to ANG 1

ANG 1 gets converted into ANG 2 by ACE, which is produced by the lungs

ANG 2 acts on the adrenal glands to produce aldosterone

Aldosterone downstream effects include sodium retention and potassium excretion

Question 2

Which part of the kidney produces renin and what does renin do?

Answer 2

Juxtaglomerular apparatus

Renin converts aNgIoTeNsInOgEn to ANGIOTENSIN ONE

Question 3

What does Angiotensin 2 do? Where does it act (specifically)?

Answer 3

Ang 2 works on the adrenal gland - zona glomerulosa to produce aldosterone

Question 4

What does aldosterone bind to and where does it act in the kidney?

Answer 4

Aldosterone binds to mineralocorticoid receptors in the PRINCIPAL CELLS in the CORTICAL COLLECTING TUBULE, and also the intercalated cells (H+ATPase)

Question 5

What are the downstream effects of aldosterone (in detail)?

Answer 5

Aldosterone binds to mineralocorticoid receptor (MR).

MR stimulates transcription of ENaC (epithelial sodium channels) and ROMK (potassium channels).

This means that aldosterone leads to an increased number of OPEN SODIUM CHANNELS. Sodium moves in from the urine into the tubular cells. blood.

Aldosterone activates the sodium potassium ATPase on the basal side/the side of the bloodstream, so sodium is pumped out in exchange for potassium.

The lumen is now more negatively charged due to the loss of sodium, so potassium moves DOWN / OUT (into the urine) via an electrochemical gradient.

Question 6

What do you call the sodium and potassium channels on the principal cells?

Answer 6

Epithelial sodium channels - ENaC
ROMK potassium channels

Question 7

Renal causes of hyperkalemia + explain why

Answer 7

Reduced GFR
Type 4 renal tubular acidosis
NSAIDS

All cause reduced renin production, therefore reduced downstream aldosterone production, therefore less potassium is excreted, leading to hyperkalemia.

Question 8

Drugs that cause hyperkalemia + why

Answer 8

ACE inhibitors (lisinopril)
Angiotensin 2 receptor blockers (losartan)
Aldosterone receptor antagonists

First two cause less aldosterone production, last one causes less aldosterone activity therefore more sodium peed out, more potassium retained

Question 9

Other causes of hyperkalemia

Answer 9

Rhabdomyolysis (intracellular potassium released from cells)
Acidosis (potassium is released in exchange for accommodating excess hydrogen into cells)

Question 10

Adrenal causes of hyperkalemia

Answer 10

Addison’s disease

Question 11

What two hormones regulate potassium?

Answer 11

Angiotensin 2 and aldosterone

Question 12

What is the normal serum concentration of potassium?

Answer 12

3.5-5.0mmol/L

Question 13

Potassium is the most abundant _________ cation?

Answer 13

Intracellular cation

Question 14

Management of HYPERkalemia

Answer 14

10ml 10 percent calcium gluconate
100ml 20 percent dextrose + 10 units of insulin
Salbutamol inhaler
Treat underlying cause

Question 15

Main mechanisms of hyperkalemia

Answer 15

Renal impairment
Drugs
Low aldosterone (Addisons/T4RTA)
Release from cells

Question 16

What ECG changes do you see in hyperkalemia?

Answer 16

Tall tented T waves
Prolonged PR interval
Loss of p waves
Broad / weird QRS complex
VF

Question 17

Management of HYPERkalemia - why do we give IV calcium gluconate?

Answer 17

To stabilise the heart

Question 18

Management of HYPERkalemia - why do we give dextrose + insulin + nebulised salbumatol?

Answer 18

To drive the excess potassium INTO cells

Question 19

How do you manage refractory hyperkalemia?

Answer 19

Calcium resonium (to chelate the potassium)

Given orally or rectally - as potassium is also secreted by the rectum

Loop diuretics (but not in AKI)

Dialysis - haemofiltration/haemodialysis

Question 20

Explain how Type 4 renal tubular acidosis causes hyperkalemia (and acidosis). Think about which two renal cells are involved.

Answer 20

Type 4 renal tubular acidosis results from a lack of aldosterone.

Hypoaldosterism means there there is a reduced potassium excretion in the principal cells of the collecting duct.

(Note the acidosis results from there being no aldosterone to activate the hydrogen ATPase pump on the apical side of tubular cells in the intercalated cells, so hydrogen can’t leave.

Question 21

Clinically, state the most likely cause of hyperkalemia in order of most likely mechanism to less common mechanism.

Answer 21

Renal impairment (causing reduced GFR and reduced renin)
Drugs (ACEi, ARBs, Aldosterone receptor antagonists)
Low aldosterone (addisons/T4RTA)
Release from cells (rhabdomyolysis, acidosis)