The causes of<unk>  can be divided into two categories, depending upon urine chloride levels. Chloride-responsive (Urine chloride 40 mEq/L) * Retention of bicarbonate – retention of bicarbonate would lead to alkalosis * Shift of hydrogen ions into intracellular space – Seen in hypokalemia. Due to a low extracellular potassium concentration, potassium shifts out of the cells. In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH. *Hyperaldosteronism – Loss of hydrogen ions in the urine occurs when excess aldosterone (Conn's syndrome) increases the activity of a sodium-hydrogen exchange protein in the kidney. This increases the retention of sodium ions whilst pumping hydrogen ions into the renal tubule. Excess sodium increases extracellular volume and the loss of hydrogen ions creates a<unk> . Later, the kidney responds through the aldosterone escape to excrete sodium and chloride in urine. * Excess glycyrrhizin consumption * Low levels of magnesium in the blood * Severely high levels of calcium in the blood * Bartter syndrome and Gitelman syndrome – syndromes with presentations analogous to taking diuretics characterized with normotensive patients *Liddle syndrome – a gain of function mutation in the genes encoding the epithelial sodium channel (ENaC) which is characterized by hypertension and hypoaldosteronism. * 11β-hydroxylase deficiency and 17α-hydroxylase deficiency – both characterized by hypertension *Aminoglycoside toxicity can induce a hypokalemic<unk>  via activating the calcium sensing receptor in the thick ascending limb of the nephron, inactivating the NKCC2 cotransporter, creating a Bartter's syndrome like effect.
Metabolic alkalosis
Metabolic acidosis
Acidosis
Hypercapnia
Respiratory acidosis
Contraction alkalosis
Respiratory alkalosis
Alkalosis