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Hypokalemia is a low level of potassium (K +) in the blood serum. [1] Mild low potassium does not typically cause symptoms. [ 3 ] Symptoms may include feeling tired , leg cramps , weakness , and constipation . [ 1 ]
Bartter syndrome (BS) is a rare inherited disease characterised by a defect in the thick ascending limb of the loop of Henle, which results in low potassium levels (hypokalemia), [2] increased blood pH , and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic.
Excretion is the most common cause of hypokalemia and can be caused by diuretic use, metabolic acidosis, diabetic ketoacidosis, hyperaldosteronism, and renal tubular acidosis. [3] Potassium can also be lost through vomiting and diarrhea. [14]
Gitelman syndrome; Other names: Primary renal tubular hypokalemic hypomagnesemia with hypocalciuria: A model of transport mechanisms in the distal convoluted tubule.Sodium chloride (NaCl) enters the cell via the apical thiazide-sensitive NCC and leaves the cell through the basolateral Cl − channel (ClC-Kb), and the Na + /K +-ATPase.
For the medical condition in humans, see hypokalemia; Potassium deficiency (plants), the disorder in plants This page was last edited on 29 ...
Emaciation manifests physically as thin limbs, pronounced and protruding bones, sunken eyes, dry skin, thinning hair, a bloated stomach, and a dry or coated tongue in humans. Emaciation is often accompanied by halitosis, hyponatremia, hypokalemia, anemia, improper function of lymph and the lymphatic system, and pleurisy and edema. [2]
Secondary hyperaldosteronism (also hyperreninism, or hyperreninemic hyperaldosteronism) is due to overactivity of the renin–angiotensin–aldosterone system (RAAS).. The causes of secondary hyperaldosteronism are accessory renal veins, fibromuscular dysplasia, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, and cor pulmonale.
Hyperkalemic periodic paralysis causes episodes of extreme muscle weakness, with attacks often beginning in childhood. [1] Depending on the type and severity of the HyperKPP, it can increase or stabilize until the fourth or fifth decade where attacks may cease, decline, or, depending on the type, continue on into old age.