Hypokalamia is associated with ?
Pathophysiology Hypokalaemia is generally indicative of abnormal potassium loss from the body, through either the kidney or the gastrointestinal tract. Renal causes of hypokalaemia can be divided into those with and those without hypeension. Hypokalaemia in the presence of hypeension may be due to increased aldosterone secretion in Conn's syndrome (p. 674) or a genetic defect affecting sodium channels in the distal nephron (Liddle's syndrome). Excessive intake of liquorice or treatment with carbenoxolone may result in a similar clinical picture, due to inhibition of the renal 11bHSD2 enzyme, which inactivates coisol in peripheral tissues. associated with organophospharus poisoning If blood pressure is normal or low, hypokalaemia can be classified according to the associated change in acid-base balance. Inherited defects in tubular transpo should be suspected when hypokalaemia occurs in association with alkalosis, provided that diuretic use has been excluded. One such disease is Bater's syndrome, in which sodium reabsorption in the thick ascending limb of Henle is defective, usually due to a loss-of-function mutation of the NKCC2 transpoer. The clinical and biochemical features are similar to those in chronic treatment with furosemide. In Gitelman's syndrome there is a loss-of-function mutation affecting the NCCT transpoer in the early distal tubule. The clinical and biochemical features are similar to chronic thiazide treatment. Note that while both Bater's and Gitelman's syndromes are characterised by hypokalaemia and hypomagnesaemia, urinary calcium excretion is increased in Bater's syndrome but decreased in Gitelman's syndrome, analogous to the effects of the loop and thiazide diuretics, respectively, on calcium transpo (see Box 14.9). If hypokalaemia occurs in the presence of a normal blood pressure and metabolic acidosis, renal tubular acidosis (proximal or 'classical' distal) should be suspected (p. 364). When hypokalaemia is due to potassium wasting through the gastrointestinal tract, the cause is usually obvious clinically. In some cases, when there is occult induction of vomiting, the hypokalaemia is characteristically associated with metabolic alkalosis, due to loss of gastric acid. If, however, potassium loss has occurred through the surreptitious use of aperients, the hypokalaemia is generally associated with metabolic acidosis. In both cases, urinary potassium excretion is low unless there is significant extracellular volume depletion, which can raise urinary potassium levels by stimulating aldosterone production. Hypokalaemia can also be caused by redistribution of potassium into cells as the result of insulin, b-adrenoceptor agonists and alkalosis, or as the result of K+ flux into muscle in hypokalaemic periodic paralysis, which is associated with mutations in several genes that regulate transmembrane ion flow into muscle cells. Finally, reduced dietary intake of potassium can contribute to hypokalaemia but is seldom the only cause, except in extreme cases. Ref Davidson 23rd edition pg 361
Alkalosis
Periodic paralysis
Type 1 A
Organophosphate poisoining
Fluid and electrolytes