Potassium and Electrolytes Flashcards
What is the most abundant intracellular cation?
Potassium
What is the normal serum concentration of potassium?
3.5-5.0 mmol/L
Which hormones are involved in renal regulation of potassium?
Angiotensin II
Aldosterone
How does RAAS work?
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
Which cells does aldosterone work on?
Principal cells (in corticol collecting tubule)
How is potassium secreted?
Na reabsorption through ENaC (stimulated by aldosterone) (epithelial sodium channels) leads to tubular lumen negative electrical potential, driving potassium secretion into lumen
What are the stimuli for aldosterone secretion?
Angiotensin II
Potassium
What are the main causes of hyperkalaemia?
- Renal Impairment (low GFR)(Glomerulus)
- Reduced renin (Type 4 renal tubular acidosis (diabetic nephropathy) or NSAIDs)
- Drugs (ARBs (losartan), ACEi (ramipril), spironolactone (aldosterone antagonist))
- Low aldosterone (Addison’s disease, Type 4 renal acidosis w/ low renin and low aldosterone)
- Release from cells in rhabdomyolysis (cell damage) and acidosis (to maintain electroneutrality)
What is the main ECG change associated with hyperkalaemia?
Peaked T waves
How would you manage a patient with hyperkalaemia (pretty much >6.5mmol/Lor ECG changes)?
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
What are the causes of hypokalaemia?
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
Where is Na, K and Cl lost from the nephron?
Na, Cl = (Asc.) Loop of Henle and DCT
K = (Asc. ) Loop of Henle
What stops the triple transporter in the ascending Loop of Henle? (cause more Na to distal nephron)
Loop diuretics and Bartter syndrome
What are the clinical features hypokalaemia?
Muscle Weakness
Cardiac arrhythmia
Polyuria & polydipsia (nephrogenic DI)
What screening test would you order in a patient with hypokalaemia and hypertension?
Aldosterone: Renin ratio which may indicate Conn’s (primary hyperaldosteronism if high)
How would you manage a patient with mild (3-3.5) hypokalaemia?
Oral potassium chloride (two SandoK tablets tds for 48 hrs)
Then recheck serum potassium
How would you manage a patient with severe (<3) hypokalaemia?
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
Hyperkalaemia is a side-effect of which of the following drugs?
Furosemide
Bendroflumethiazide
Salbutamol
Ramipril
Ramipril
Hypokalaemia is a side-effect of which of the following drugs?
Spironolactone
Indomethacin
Perindopril
Furosemide
Furosemide
What are the two stimuli for aldosterone?
high potassium
Angiotensin II
How does potassium move?
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)
How does Aldosterone affect ENaC?
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)
How is polyuria and polydipsia caused in Conn’s syndrome (low K)?
It causes nephrogenic DI (ADH resistance)
What is the order of likelihood of hyperkalaemia causes?
Renal impairment (AKI/ CKD)
Drugs (ACEI/ARBs/Aldo Ant)
Low aldosterone (Addisons, T4 Tubular acidosis)
Release from cells
How does increased sodium delivery to distal nephron result in renal loss of K?
More sodium comes in and is reabsorbed which makes the lumen more negative and gradient causes more K loss
