Renal physiology - magnesium and potassium Flashcards
Magnesium
- how is it absorbed?
- where is it absorbed?
is often bound to water, cannot get it absorbed without removing it from water first
- and is hard to get intracellular absorption
- it is absorbed in the thick ascnedign limb of loop of henle after water is absorbed from descending limb - increases conc of electrolytes
Hypomagnesimia
- Can occur in some of the transporters for magneisium in kidney so dont get reabsorpition
- present in childhood
How to test this?
- serum Mg
- red cell Mg
- 24 hour excretion
Causes of hypomagneisa
- decreased dietary intake
- GI malabsorption and loss
- endocrine - hyperaldosterronism , SIADH
- renal loss - congential, aquired, drug
Symptoms of hypomagnesia
and treatment
- weakness and fatigue
- teetany
- seizures, arrhythmias
-IV - magensium sulphate
Hypermagnesaemia
in advanced CKD - the compensatory mechanism start to become inadequate and hypermagnesaemia may develop
-excessive oral administration of magnesium salts or magnesium containing drugs
Initial changes in potassium into extracellular compartment
-extracellular K are initially buffered by movement of K into or out of skeletal muscle regulated by insulin and catecholamines
Hyperglycaemia what can this do to potassium
-can lead to K efflux from the cell
Acidosis and alkalosis on potassium
- acidosis can drive K effulux (hydrogen will be pushed into cells and K out)
- alkalosis - (H will be pushed out of cells and K will go in)
How is it absorbed
active reabsoprtion of potassium with sodium potassium chloride channel
- also has aROMK channel
- also a sodium potassium atapse pump
Aldosterone
-works on principle cells in the distal tubule and collecting duct
will increase absorption of sodium and increase secretion of potassium via sodium ptoassium atpase
-is stimulated by having increased potassium or by angiotensin 2 due to reduced extracellular volume
Hypokalaemia
-muscle weakness paralysis cardiac conduction abnormalities cramps constipation
K loses
Renal - hyperaldosteronism (aldosterone secreting turour) , liquorice, diuretics (some cause increase K some caused decreased) , renal tubular acidosis
Gut
-vomiting, diarrhoea, laxatinves, ileostomy
Conns syndrome
- adrenal adenoma
- secretes aldosterone
- hypertension
- hypokalaemia
Licorice
contains glycyrrhizin, acts like aldosterone by activiating mineralcorticoid receptors in the kdiney
- results in hypokalaemia and HTN
- psudohyperaldosteronism
Sprinolactone
- mineralocorticoid antagonist (stops action of aldosterone)
- will reduce amount of sodium absorption and result in a decrease in potassium secretion
Treatment
- treat underlying problme
- oral tablets
- sever - IV replacement
Hyperkalemia
-symptoms - fatigue or weakness
parasthesia, nausea or vomitign, palpatatiosn
-can get ventricular fibrilaiton and cardiac arrest
Causes - ncrease intake
disruption of cell intake - beta blockers, acidosis
Decrease exceriton - renal failure, hypoaldosternoism, ACEi/arb
-adisons disease
psuedo-hyperkalemia
-can get false result due to haemolysed sample
Addisons disease
Deficient secretion of adrenocortical hormones - aldosterone and cortisol
- tanned skin appearance
- symptoms- lethargy, waekness, weight loss, low BP
- hyperkalaemia, hyponatraemia
- can get VF
Treatment - stabilise AP
- push K into cells
- reduce K absorption
- increase elemination
- fix underlying problem
Treatment for hyperkalemia resutling in VF
- IV calcium can stabilise the AP
- want reduced potassium absorption , increase elemination , fix underlying probleme
- can give insulin - drive potassium to get into cells (also give dextrose so dont make patient hypoglyacemic)
- treat acidosi s- bicarbonate
- can give somethign to bidn to K so get more elimination
