ChemPath - Potassium and electrolyte cases Flashcards
What are the normal reference ranges for sodium, potassium, urea, and creatinine (and which is the most abundant intracellular cation)
Sodium = 135-145
Potassium = 3.5-5.3 (most abundant intracellular cation)
Urea = 2.5-6.7
Creatinine = 70-100
What are the methods of potassium regulation
Loss through the GI tract
Renal regulation and secretion (Angiotensin II and aldosterone)
Movement from intracellular to extracellular
Describe the renin-angiotensin-aldosterone system
- Angiotensinogen is produced by the liver
- Renin (kidney) converts angiotensinogen → angiotensin I
- Angiotensin-converting-enzyme (ACE) (lung) converts angiotensin I → angiotensin II
- Angiotensin II stimulates the adrenal gland to produce aldosterone (zona glomerulosa)
- Aldosterone stimulates sodium reabsorption by increasing the no. of Na channels in the luminal membrane
- This creates a negative electrical gradient in the lumen
- Potassium is secreted into the lumen
- As sodium is retained, water is also retained
What are the triggers for aldosterone release from the adrenals
Angiotensin II
Potassium (high)
What are the triggers for renin release
Low BP In the renal artery
Low sodium in the macular densa by the JGA
SNS beta-1 receptor activation
What are the causes of hyperkalaemia
- Renal impairment (reduced GFR)
- Renin
- T4 Renal tubular acidosis (diabetic nephropathy)
- NSAIDs - Drugs - ACEi, ARBs, spironolactone
- Addison’s disease
- release from cells - rhabdomyolysis (muscle death), acidosis (H+/K+ exchange)
What ECG changes are seen in hyperkalaemia
Peaked T wave (early)
Broad QRS
Flat P-wave
Prolonged PR (and bradycardia)
Sine wave (latest)
How do you manage hyperkalaemia
- 10ml 10% calcium gluconate (stabilise)
- 100ml of 20% dextrose
- 10U insulin (must be given together)
- Nebulised salbutamol - drives potassium into the cell
- Treat the underlying cause
What are the causes of hypokalaemia
- GI losses (diarrhoea, vomiting, fistulas)
- Renal loss
- Conn’s (Hyperaldosteronism), Cushing’s
- Bartter syndrome, thiazide/loop diuretics (increased Na+ delivery to DCT)
- Hyperglycaemia (osmotic diuresis) - Redistribution into cells
- Insulin/insulinomas
- beta-agonists
- Alkalosis
Rare causes
- Hypomagnesaemia
- Renal tubular acidosis T1, T2
Explain why renal losses cause hypokalaemia
The triple (loop)/co (thiazides)-transporter is blocked → less Na absorbed in the ascending loop → more sodium is transported to the distal convoluted tubule → nephron cortex is more electronegative → more Na is reabsorbed in the distal convoluted tubules → lumen is negative → potassium moves down the gradient through ROMK channels
What are the clinical features of hypokalaemia
Muscle weakness
Cardiac arrhythmias
Polyuria and polydipsia (nephrogenic DI from low K+ or a high Ca2+)
What ECG changes are seen in hypokalaemia
ST depression
Flat T-waves
U waves
What initial investigation should be done for hypokalaemia
Aldosterone:renin ratio
Will differentiate between aldosterone excess (Conn’s) and other causes
Conn’s - A:R ratio will be HIGH (renin very low)
What is the management for hypokalaemia
3-3.5
Oral KCL (2 SandoK tablets, TDS) + recheck K+
<3
IV KCL (max rate 10mmol/h)
Treat the underlying cause
What are the differences between the types of renal tubular acidosis
RTA T1 - distal RTA, less H+ excretion, hypokalaemia
RTA T2 - proximal distal RTA, less HCO3 reabsorption, hypokalaemia
RTA T4 - hypoaldosteronism, hyperkalaemia