Potassium and Electrolytes Flashcards
What is the normal range of potassium?
3.5-5.0
What are the two hormones involved in potassium regulation?
Angiotensin II
Aldosterone
Explain the RAS system
Angiotensinogen is converted by RENIN to angiotensin I
Angiotensin I is coverted by ACE to angiotensin II
Angiotensin II stimulates the adrenal to produce aldosterone
Aldosterone stimulates sodium and water retention and potassium excretion in the kidney
Where is angiotensinogen produced?
liver
where is renin produced?
juxtoglomerular apparatus
Where is Angiotensin II produced
lung
Where is ALDOSTERONE produced?
liver
Which two molecules stimulate aldosterone release?
Angiotensin II
K+
How does aldosterone work?
It binds to MC receptors
This stimulates transcription of ENaC (sodium) channels
More Na+ from the lumen is reabsorbed
The lumen becomes negative
Subsequently, K+ moves down electrochemical gradient into the lumen
What are the main causes of hyperkalamia?
REDUCED EXCRETION OF POTASSIUM Reduced GFR from renal impairment Reduced renin activity (NSAIDs, T4RTN) Drugs: ACE inhibitors, ARB, Aldosterone antagonists (spironolactone) Addisons (so less. aldosterone)
EXTRACELLULAR SHIFT
Potassium release from cells (rhabdomyolysis, acidosis)
How does acidosis cause hyperkalaemia?
High H+ in plasma means cells try to take in Moree H+ ions to normalise pH
To maintain electroneutrality, K+ comes out of cels
What are examples of diseases causing reduced renin activity?
Type 4 tubular necrosis
NSAIDs
What is the main ECG change with hyperkalaemia?
Peaked T waves
What is the management of hyperkalaemia?
10mL 10% calcium glutinate — for K+ > 6.5 or any ECG changes
50mL 50% dextrose + 10 units of insulin
Nebulised salbutamol
What are causes of hypokalaemia?
GI loss (loss of K+ through GI tract) Renal loss (hyperaldosteronism: Conn's, Cushing's, osmotic duiuresis: Loop and thiazide diuretics) Redistribution into cells (insulin, beta agonists, alkalosis) Rare causes: renal tubular acidosis1&2, hypomagnaesaemia
What are clinical ft of hypokalaemia?
Muscle weakness
Cardiac arrhythmia
Polyuria, polydipsia
How do you manage hypokalaemia?
If K: 3.0-3.5 give oral KCl (SANDO-K)
If K: <3: IV KCl (max 10mmol/L otherwise irritating to peripheral veins)
what drug and syndrome block the triple transporter in the loop of henle, preventing Na, K, Cl reabsorption
Loop diuretics
Bartter syndrome
Give an example of a loop diuretic
Furosemide
What drug and syndrome block the Na/Cl channel in the loop of henle, causing more Na to reach the distal nephron > change in electrochemical gradient > more K+ loss ?
Gitelman syndrome
THiazide diuretic
What stimuli cause aldosterone release
low sodium
high k+
what investigations should you get for hyperkalaemia and why
- Repeat sample (check for spurious sample)
- CK for rhabdomyolysis
- Creatinine, Urea
- Cortisol, short synachten test (addisons)
give an example of a loop diuretic
Furosemide
Explain renal tubular acidosis 1&2(&3)
Defect in hydrogen ion secretion into renal tubules > cannot secrete H+ into tubule
So secretes K+ instead to balance change with Na+ > hypokalaemia with acidosis
T1,2,3 differ in terms of where in the tubule the defect is (1: distal, 2: proximal, 3: both)
Explain renal tubular acidosis T4
defect is in adrenal
ACIDOSIS with HYPERKALAEMIA
what blocks the triple transporter in the loop of henle, preventing reabsorption of Na, K+, Cl and thereby causing hypokalaemia
Bartter syndrome
Loop diuretics e.g. furosemide
what blocks the NaCl channel in the kidney preventing Na+ reabsorption and thereby causing hyponatraemia
Thiazide diuretic
How do you work out the anion gap
Na + K - Cl - HCO3
What is a normal anion gap
18-20
what does a high anion gap suggest
that there is some other form of toxins in the patient’s blood (ketones, lactic acid)
what is a form of poisoning responsible for a high anion gap
ethylene glycol poisoning
