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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 ]
[2] [10] In 1937 periodic paralysis was linked with hypokalemia, as well as precipitation of attacks with glucose and insulin. [11] [12] This phenomenon has been used as a diagnostic test. [12] In 1974 it was discovered that propranolol could prevent attacks. [13]
Standard EMG testing cannot diagnose a patient unless they are in a full blown attack at the time of testing. Provoking an attack with exercise and diet then trying oral potassium can be diagnostic, but also dangerous as this form of PP has an alternate form known as hyperkalemic periodic paralysis. The symptoms are almost the same, but the ...
The Chvostek sign (/ ˈ k v ɒ s t ɪ k /) is a clinical sign that someone may have a low blood calcium level (a decreased serum calcium, called hypocalcemia).The Chvostek sign is the abnormal twitching of muscles that are activated (innervated) by the facial nerve (also known as Cranial Nerve Seven, or CNVII). [1]
Diagnosis of Gitelman syndrome can be confirmed after eliminating other common pathological sources of hypokalemia and metabolic alkalosis. [16] A complete metabolic panel (CMP) or basic metabolic panel (BMP) can be used to evaluate serum electrolyte levels. Electrolyte measurement and aldosterone levels can be done via urine. [16]
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]
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.
Diagnosis of contraction alkalosis is made by correlating laboratory data with clinical history and examination. Metabolic alkalosis in the presence of decreased effective circulatory volume, loop diuretic use, or other causes of intravascular depletion such as profound diarrhea should raise suspicion for contraction alkalosis as a likely etiology in the absence of other causes.