Lecture 18 - Renal Physiology: Potassium & Magnesium Flashcards
Key roles of the kidney?
elimination of waste products, control of fluid balance, control of minerals, regulate acid-base balance, produce hormones
Mg Physiology?
bone formation, cofactor in copious amounts of reactions, regulation of vascular tone, cardiac rhythm, platelet-activated thrombosis
Mg Absorption?
10-20% PCT, 60-70% thich ascending LoH, 10% DCT
Mg reabsorption - LoH?
active transport through Claudin 16-19 receptors
Assessments of Mg?
serum Mg, red cell Mg, 24hr excretion, Mg retention test, isotope analysis
Symptom of hypomagnesaemia?
fatigue, cramps, tetany spasm, numbness, seizures, arrhythmias
Causes of hypomagnesaemia?
common condition; diet, malabsorption and loss, hyperaldosteronism, diabetes, SIADH, renal loss
Hypomagnesaemia treatment?
typically oral magnesium, otherwise IV magnesium sulphate
Causes of hypermagnesaemia?
advanced CKD, excessive magnesium salt or drugs, Iatrogenic
Internal balance of K?
buffered by movement of K into or out of skeletal muscles regulated by insulin and catecholamines
pH and K?
acidosis leads to K efflux (as well as hyperglycaemia), alkalosis vice versa
K reabsorption?
60% PCT, 30% thick ascending LoH, variable in collecting ducts
Symptoms of hypokalaemia?
muscle weakness, paralysis, cardiac conduction abnormalities, cramps, constipation
Hypokalaemic Periodic Paralysis?
inherited (rare) or thyrotoxic origin, abnormal K channels, triggered by high carbs (insulin) or SNS activation (stress), excessive K influx -> weakness
K losses - renal?
hyperaldosteronism, licorice, diuretics, renal tubular acidosis
K losses - gut?
vomiting, diarrhoea, laxatives, ileostomy
Conns syndrome?
adrenal adenoma, secretes aldosterone -> hypertension and hyperkalaemia
Symptoms of hyperkalaemia?
fatigue, paraesthesia, nausea, dyspnoea, palpitations
Heart attack?
hyperkalaemia -> ventricular fibrillation -> cardiac arrest
Psuedohyperkalaemia?
caused by haemolysis
Causes of hyperkalaemia?
increased intake, disruption of cell intake (beta blockers, acidosis), decreased excretion (renal failure, hypoaldosteronism)
Addison’s disease?
deficient secretion of aldosterone and cortisol, hyperpigmentation due to excessive ACTH excretion stimulating melanocytes, symptoms: lethargy, weakness, weight loss, hypotension
Addison’s - diagnosis and treatment?
hyperkalaemia, hyponatraemia; use of short synacthen test; treatment: dexamethasome or fludrocortisone
Treatment of hyperkalaemic MI?
stabilise AP, push K into cells, reduce K reabsorption, increase elimination, fix underlying problem
Stabilising AP?
calcium, normalises membrane excitability, lasts 30min, prolongs cardiac arrest
Beta agonists?
ventolin nebuliser, reduces K via influx, 30-60min to work, lasts 6 hr (combine w insulin w dextrose)
Treating acidosis?
oral bicarbonate (IV if emergency)
Reducing K absorption?
cation exchange products, calcium resonium
Increasing K elimination?
K losing diuretic, or dialysis if already dialysis patient or Rhabdomyolysis
