ChemPath 13: Potassium Flashcards
What is the normal range for serum potassium?
3.5-5.0 mmol/L
What are the two main hormones involved in the regulation of potassium?
Angiotensin II
Aldosterone
Outline how the renin-angiotensin-aldosterone system works
Reduced perfusion or low sodium will stimulate the production of renin from the juxta-glomerular cells
This cleaves angiotensinogen to angiotensin I
This is then converted by ACE in the lungs to angiotensin II
Angiotensin II stimulates aldosterone production from the adrenals
Aldosterone stimulates sodium reabsorption and potassium excretion in the principal cells of the cortical collecting tubule (CCT)
NOTE: water will also be drawn in with the sodium so aldosterone should not greatly affect sodium concentration
Outline the mechanism of action of aldosterone
- Aldosterone binds to MR (mineralocorticoid receptor) and stimulates the transcription of ENaC channels + increased Sgk1 which inhibits Nedd4
Nedd4 usually ubiquitinates sodium channels and degrades them
Inhibition of Nedd4 leads to preservation of sodium channels thereby increasing sodium reabsorption
As you reabsorb more sodium, the lumen becomes more negative and K+ will move down the electrochemical gradient into the lumen via ROMK (renal outer medullary potassium) channels
What are the main stimuli for aldosterone release?
Angiotensin II
Low potassium
List some causes of hyperkalaemia.
Drugs:
- NSAIDs - Reduced renin activity
- ACEi - Blocks conversion of angiotensin 1-> 2
- ARB - Block ang 2 recptors
- Aldosterone antagonists (Spironalactone)
Conditions:
- Type 4 Renal Tubular Acidosis (Reduced renin activity)
- Addisons (adrenal insufficiency)
- Renal failure (Reduced GFR)
Intracellular spillage:
- Rhabdomyolysis - Potassium release from cells
- Acidosis - Potassium release from cells
Explain how acidosis leads to hyperkalaemia
When plasma H+ concentration is high, the cells try to take in more H+ from the plasma
To maintain electrochemical neutrality, K+ must leave the cell when H+ enters
This leads to hyperkalaemia
Outline the management of hyperkalaemia
10 mL 10% calcium gluconate - protect cardiomyocytes
1st line = 50 mL 50% dextrose + 10 U insulin - drive K+ back into cells
2nd line = Nebulised salbutamol
Treat the cause - if started new meds stop it, if condition present treat it
List some causes of hypokalaemia
GI loss
Renal loss
- Hyperaldosteronism, Cushing’s syndrome
- Increased sodium delivery to distal nephron
- Osmotic diuresis
Redistribution into cells
- Insulin
- Beta-agonists
- Alkalosis
Rare causes
- Renal tubular acidosis (type 1 and 2)
- Hypomagnesaemia
Name two conditions that can block the triple transporter (Na / K / Cl)
Loop diuretics
Bartter syndrome (mutation in triple transporter)
These both increase Na+ in the lumen of CCT hence more K+ gets excreted there leading to hypokalaemia
Name two conditions that can block the Na+/Cl- cotransporter
Thiazide diuretics
Gitelman syndrome (mutation in Na+/Cl- cotransporter)
These both increase Na+ in the lumen of CCT hence more K+ gets excreted there leading to hypokalaemia
Explain how increased delivery of sodium to the distal nephron can cause hypokalaemia
Increased delivery of Na+ to the distal nephron (e.g. because of blocking/ineffective triple transporter or Na+/Cl- cotransporter) leads to increased reabsorption of Na+ in the distal nephron
This leads to the lumen of the distal nephron becoming more negative
This results in the movement of K+ down the electrochemical gradient through ROMK channels into the lumen
What are the clinical features of hypokalaemia?
Muscle weakness
Arrhythmia
Polyuria and polydipsia (due to DI)
What screening test should be done in a patient with hypokalaemia and hypertension?
Aldosterone: renin ratio (primary hyperaldosteronism will show high aldosterone and low renin)
Outline the management of hypokalaemia:
3-3.5 mmol/L
- Oral potassium chloride (2 x SandoK TDS for 48 hours)
- Re-check serum K+ concentration
< 3 mmol/L
- IV potassium chloride infusion
- Maximum rate: 10 mmol/hr
- NOTE: rates > 20 mmol/hr irritate the superficial veins
TREAT THE CAUSE
ECG finding w/ hyperkalaemia? inital mx?
Peaked T waves (GLOBAL CHANGE IN ALL LEADS)
10 ml 10% calcium gluconate
You are bleeped to review Jane Doe. A 56-year-old lady on the Endocrinology ward admitted with severe hypothyroidism. Her Past Medical History includes Hypertension and Type 2 Diabetes Mellitus. She is currently taking Levothyroxine, Ramipril, Metformin and Gliclazide.
Has hyperlkalaemia and nothing else
Which of the following is the most likely to be causing Jane’s electrolye abnormality?
Levothyroxine
Ramipril
Metformin
Gliclazide
None of the above.
Ramipril - blocks conversion of Ang I to Ang II -> less aldosterone -> hyperkalaemia (reduced reabsorption of Na)
You are bleeped to review John Doe. A 45-year-old male following an Asthma attack, after a long history of poorly controlled asthma.
Hypokalaemia, rest is normal
Which of the following is the most appropriate to correct John’s electrolye abnormality?
Oral Potassium Chloride i.e. SandoK
Ramipril
IV Potassium Chloride
10ml 10% Calcium Gluconate
Nebulised Salbutamol
IV Potassium Chloride - hypokalaemia likely percipitated by salbutamol use
You attend to a patient in Resus. The initial ECG shows the following;
Given the likely electrolye abnormality, what is the most appropriate initial management?
Peaked T Waves = Hypokalaemai mx => 10ml 10% Calcium Gluconate
