K and electrolytes Flashcards
what is the most abundant intracellular cation
K
normal serum K
3.5-5 mmol/L
what hormones are involved in reg of K in kidney
- Aldosterone
- Angiotensin II
summarise the renin-angiotensin-aldosterone system
- Angiotensin produced in liver - converted to ang 1 and then ang II by ACE in lung
- Ang II stim adrenal cortex -> aldosterone
- -> Na in and K out through urine
- Happens in principle cells in cortical collecting tubules
If a lot of aldosterone = low K
K also stim aldosterone release = lose K in urine
summarise how Na movement alters K movenment
- More Na comes in = lumen more -ve = loss of K down the electrical gradient
- Na and K don’t move in same transporter
- It is the fact that the na makes the lumen -ve which pushes the K out down the electrical gradient
how does aldosterone alter K movement
Aldosterone = increase number of open Na channels = reabsorb more Na = more -ve lumen = electrical gradient = more K secreted into lumen
what are the stimuli for aldosterone secretion
K
Angiotensin II
causes of hyperkalaemia
- Reduced GFR ie renal failure
- Low renin - ie diabetic nephropathy, NSAIDs - less Angiotensin to ANg1 = less aldosterone = less K secretion. renin produced in juxtaglomerula apparatus
- ACEi - less Ang1->ANg2 = less K loss
- ARB - losartan. Block ang2 receptor = less ang2 action = less loss K
- Addisons -> low aldosterone
- Aldosterone antagonist - spirionolactone = less aldosterone action = less K secretion
Release from cells
- rhabdomyolysis
- Acidosis - H ions move into cells - K lost to maintain electroneutrality = high k
ECG with hyperkalaemia
peaked T waves
mx of hyperkalaemia - need to know dose
- 10ml 10% ca gluconate - stabalise myocardium
- 100ml 20% dextrose and 10 units insulin
- Nebulised salbutamol
- Treat underlying cause
causes of hypokalaemia
GI loss - vomiting
Renal loss
* excess cortisol (bind mineralocorticoid receptor) or excess aldosterone (Conn’s or bilateral hyperplasia)
* Increase na distally
* Osmotic diuresis
Redistribution into cells
* B cell agonist stim K uptake into cells
* Insilin
* Alkalosis - H move out of cell, and K move into the cell.
Rare cayuses - renal tubular acidosis type 1 and 2, hypomagnesia
summarise renal loss of K
If block resporption with loop diuretics eg furosemide - more Na will go to DCT - so more K will be lost. Eg with loop diuretics or bartter syndrome
Thiazide diuertics and gitelman syndrome - same thing more distally - more Na reabsorbed more distally -> more -ve lumen -> more k lost
ie deliver more na to distal tubles
sx of hypokalaemia
- Muscle weakness
- Cardiac arrhythmia
- Polyuria and polydupsia - hypok gives you nephrogenic DI
Screening test if low K and htn
aldosterone:renin ratio
mx of hypokalaemia
Serum potassium 3.0-3.5 mmol/L
* Oral potassium chloride (two SandoK tablets tds for 48 hrs)
* Recheck serum potassium
Serum potassium < 3.0 mmol/L
* IV potassium chloride
* Maximum rate 10 mmol per hour
* Rates > 20 mmol per hour are highly irritating to peripheral veins
Treat the underlying cause e.g. spironolactone