User:Mr. Ibrahem/Hypokalemic periodic paralysis

Hypokalemic periodic paralysis (hypoKPP) is a genetic condition characterized by episodes of severe muscle weakness. While the underlying cause is present at birth, attacks do not generally begin until the age of 10 to 30. Before the onset of weakness, tiredness, tingling, or behavioral changes may occur. Onset is over minutes to hours and symptoms may last hours to days. The frequency of attacks is variable. Complications may include aspiration pneumonia, heart arrhythmias, and long term muscle damage.

Most cases are due to a mutation in the CACNA1S gene and are autosomal dominant. This mutation may be inherited from a parent or occur during early development. Other cases may arise due to high thyroid, which is known as thyrotoxic periodic paralysis. Attacks may be triggered following strenuous exercise or by a high carbohydrate diet, salt, alcohol, cold, psychological stress, or corticosteroids. The underlying mechanism involves a defect in an ion channel which results in periods of low blood potassium. The diagnosis is suspected based on symptoms and either a family history or low potassium during an attack.

Efforts to prevent attacks include avoiding triggers, potassium supplementation, acetazolamide, and potassium-sparing diuretics. Attacks are treated by giving potassium chloride at doses of 0.5 to 1 mEq/kg by mouth. Further doses at 0.3 mEq/kg may be given ever 30 minutes if the symptoms do not improve to a maximum of 200 mEq per 24 hours. Intravenous potassium may given, preferably in mannitol, for those who cannot swallow or have a heart arrhythmia.

HypoKPP is rare, affecting about 1 in 100,000 people. Women are less seriously affected than men. Cases due to high thyroid occur more commonly in Asians and Latinx. It was first described in 1727 by Musgrave.