K & Mg physiology Flashcards
role of Mg
- bone formation
- enzyme co-factor = ATP metabolism, muscle contraction/relaxation, neurological function
- regulation of vascular tone
- cardiac rhythm
- platelet activation
Mg reabsorption
glomerulus
- freely filtered
proximal tubule
- 15% reabsorption
Loop of Henle
- 70% reabsorption in thick ascending limb
- paracellular channel formed by claudin
Distal tubule
- 10% reabsorption
- by transient receptor potential channels (TRPC6)
- mutations give hypomagnesaemia & hypercalcaemia
Assessing Mg
- serum Mg
- red cell Mg
- 24 hour excretion
- Mg retention test
- isotope analysis
causes of hypomagnesemia
- decreased dietary intake
- GI malabsorption
- endocrine (hyperaldosterone, SIADH)
- renal loss (congenital, drug-induced)
- proton pump inhibits, amphotericin B
symptoms of hypomagnesemia
- weakness, fatigue
- fasciculations, cramps, tetany
- numbness
- seizures
- arrhythmias
treatment for hypomagnesemia
- oral (most cases)
- IV magnesium sulphate
hypermagnesaemia
- less common
- cause = excessive oral administration of Mg / Mg-containing drugs (in GORD drugs)
- advanced CKD possible, less common
homeostasis of K
- initial changes buffered by movement in/out of skeletal m (regulated by insulin, catecholamines)
- hyperglycemia & acidosis cause K efflux from cell
- serum K affected by intake, losses, redistribution from ECF/cells
K reabsorption
glomerulus
- freely filtered
proximal tubule
- 60% reabsorption - passive paracellular movement with water (due to Na/K exchanger)
Loop of Henle
- 30% reabsorption in thick ascending limb - active reabsorption by NKCC2 channel - ROMK channel & Na/K/ATPase also involved
Distal tubule & CD
- variable reabsorption/secertion - influenced by aldosterone, angiotensin
hypokalaemia and its symptoms
- serum K <3.5mmol/L
- symptoms = muscle weakness, paralysis, cramps, cardiac conduction abnormalities, constipation
causes of hypokalaemia
GI loss
-vomiting, diarrhea, laxatives, ileostomy
renal loss
- hyperaldosterone
- diuretics (e.g. loop diuretics - furosemide)
- renal tubular acidosis
- liquorice (produces enzymes w/ aldosterone-like effect)
treatment for hypokalaemia
- treat underlying cause
- mild hypokalemia (3-3.5) = use oral K
- sever (<3) = use IV replacement
hyperkalemia and its symptoms
- serum K > 5mmol/L
- symptoms = fatigue, weakness, paresthesia, nausea, vomiting, dyspnoea, palpitations
- pseudo-hyperkalemia = breakdown of RBCs in sample raises K
causes of hyperkalemia
- increased intake (usually in kidney disease)
- disruption of cell intake
- acidosis
- beta blockers
- rhabdomyolysis - decreased excretion
- renal failure
- hypoaldosteronism (spironolactone)
- drugs = ACEi, AIIA
Addison’s disease
- deficient adrenal cortex hormones (aldosterone, cortisol)
- gives characteristic hyper-pigmentation (excessive ACTH & MSH production)
- lethargy, weakness, weight loss, low BP
- electrolytes = low Na, high K
- diagnosis by synacthen test
- treated w/ synthetic hormones (e.g. dexamethasone)