Potassium and Electrolytes Flashcards
which is the most abundant intracellular cation
Potassium
normal range of Potassium
3.5-5.0mmol/L
main source of K+
dietary intake: fruit and vegetables mainly
hormones involved with renal regulation of K+
- Angiotensin II
- Aldosterone
where is renin released from
juxtaglomerular apparatus in kidney
what stimulates renin release
reduced perfusion pressure
low Na
what does renin do
causes angiotensinogen to be cleaved to form angiotensin I in the liver
how is Angiotensin II formed
Angiotensin I is converted to Angiotensin II via angiotensin converting enzyme (ACE) in the lung
role of Angiotensin II
AT II acts on the adrenal gland to stimulate the production of aldosterone
role of aldosterone
Aldosterone causes excretion of K+ and reabsorption of Na+.
acts on principle cells of collecting duct to reabsorb Na + water and excrete K+.
It also increases Na reabsorption via reduced degradation of Na channels
what happens if If K+ levels are too high
stimulate increased aldosterone release so K+ excreted in urine
net effect will be loss of K+ and retaining Na and water to maintain BP.
relationship between aldosterone and potassium and sodium (plasma)
high aldosterone–>high sodium (directly proportional)
high aldosterone–>low potassium (inversely proportional)
Causes of HyperK+
1. renal impairment (reduced GFR) - AMIR SAM- THINK OF THIS FIRST
2. Reduced renin: NSAIDS + Type 4 renal tubular acidosis
- ACEi (i.e, ramipril, lisinopril)
- ARBs (i.e. losartan, candesartan)
- Addison’s disease
- Aldosterone antagonists (e.g. spironolactone, eplerenone
- *7. Potassium release from cells:**
- biggest intracellular cation = any cell injury and cell death can cause a big release of K+ (rhabdomyololysis)
- acidotic states acidotic state (an abundance of H+ and low pH),
Main causes of HyperK+
- Renal impairment- reduced renal excretion
- Drugs- ACEi, ARBs, spironolactone
- Low aldosterone
o Addison’s disease
o Type 4 renal tubular acidosis (low renin, low aldosterone) - Release from cells: rhabdomyolysis, acidosis
((See picture- Nidhish’s pathsoc lecture))
Main ECG changes associated with hyperK+ and other findings:
main: Peaked T waves
other findings:
- Bradycardia
- Widened QRS
- Prolonged PR interval
- Late change= sine wave
Management of Hyperkalaemia
- 10ml 10% calcium gluconate: note: does not reduce K+ but stabilises cardiac membrane
- 50ml 50% dextrose (Amir sam: 100 ml of 20% dextrose…) + 10 units of insulin
- Nebulised salbutamol
- Treating the underlying cause
Causes of HYPOkalaemia (3)
- GI loss- D&V, Diarrhoea > vomiting
**- Renal loss:** Anything that increases renal aldosterone will increase K+ loss: o Hyperaldosteronism (Conn's syndrome), Excess cortisol (has promiscuity for MRs) o Increased Na delivery to distal nephron (Drugs- Loop diuretics, Thiazides; conditions- barter's and gilteman's) o Osmotic diuresis
- Redistribution into cells:
- Insulin
- BETA agonist (salbutamol)
- Alkalosis
______________________
Barters: LOH
Gitleman’s: DCT
ECG finding in hypoK+
NOTE: in HypoK+, get U waves
**INCREASED RISK OF VT AND TORSADES DE POINTES
Loop diuretics + potassium
Diuretics increase the loss of K+
Loop diuretics act on the triple transporter. and block the reabsorption of Na+ so more Na+ in distal nephron.
This will stimulate renin release and eventually aldosterone release
Thiazide diuretics + potassium
Diuretics increase the loss of K+
These work in the DCT- block Na reabsorption via the NaCl transporter. so more more Na delivered to the distal nephron.
So more Na is crossing through the epithelial Na channels >>>> MORE K+ is LOST by maintaining the electrochemical gradient
Clinical Features of HypoK+
- Muscle weakness
- Cardiac arrhythmia: Increased risk of VT and Torsades de pointes
- Polyuria and polydipsia (nephrogenic DI)
Management of Hypokalaemia if Serum K+ 3.0-3.5mmol/L
o PO potassium chloride (two SandoK tablets TDS for 48 hours)
o Recheck serum K+
Management of Hypokalaemia if Serum K+ < 3.0mmol/L
o IV potassium chloride + Maximum rate 10mmol per hour
Screening Test for Hypokalaemia with Hypertension
- Aldosterone: renin ratio: Primary hyperaldosteronism- High aldosterone: renin ratio (as high aldosterone will suppress renin)
Rmb: in conn’s syndorme, you get HYPERTENSION and HYPOKALAEMIA (may not necessarily have hypernatraemia)
Conn’s syndrome can be due to
- bilateral adrenal hyperplasia
- Aldosterone producing adenomas (autonomous production of aldosterone is produced)
What is the cause of the electrolyte abnormaities here?
Not ramipril because creatinine is also high
therefore it’s because of REDUCED GFR
What happens in barter syndrome?
autosomla recessive
hypokalaemia
hypotension
metabolic alkalosis
hypercalciuria
**affects the ascending limb of loop of henle
what effect does spurious blood sampling have on potassium?
can lead to hyperkalaemia because the needle you use can lead to haemolysis–>potassium leaks out
when to suspect renal tubilar acidosis?
if you have hypokalaemia and acidosis
**rmb usually you get hypokalaemia with alkalosis, so when you see hypolalaemia with acidosis think renal tubular acidosos*
mechanism: failure to excrete H+ into the kidneys, so you excrete K+ instead to enable Na+ reabsorption
*NB: type 4 causes hyperkalaemia so ignore that
