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A handful of published reports describe individuals with severe hypokalemia related to chronic extreme consumption (4–10 L/day) of cola. [20] The hypokalemia is thought to be from the combination of the diuretic effect of caffeine [ 21 ] and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.
Hypokalemic periodic paralysis (hypoKPP), also known as familial hypokalemic periodic paralysis (FHPP), [1] is a rare, autosomal dominant channelopathy characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood (hypokalemia).
ICD-10 is the 10th revision of the International Classification of Diseases (ICD), a medical classification list by the World Health Organization (WHO). It contains codes for diseases, signs and symptoms, abnormal findings, complaints, social circumstances, and external causes of injury or diseases. [1]
[9] [10] The first English-language report, in 1931, originated from Dunlap and Kepler, physicians at the Mayo Clinic; they described the condition in a patient with features of Graves' disease. [ 2 ] [ 10 ] In 1937 periodic paralysis was linked with hypokalemia, as well as precipitation of attacks with glucose and insulin.
Under the proposal, the ICD-9-CM code sets would be replaced with the ICD-10-CM code sets, effective October 1, 2013. On April 17, 2012, the Department of Health and Human Services (HHS) published a proposed rule that would delay the compliance date for the ICD-10-CM and PCS by 12 months-from October 1, 2013, to October 1, 2014. [ 4 ]
Adoption of ICD-10-CM was slow in the United States. Since 1979, the US had required ICD-9-CM codes [11] for Medicare and Medicaid claims, and most of the rest of the American medical industry followed suit. On 1 January 1999 the ICD-10 (without clinical extensions) was adopted for reporting mortality, but ICD-9-CM was still used for morbidity ...
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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.