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Hypokalemia which is recurrent or resistant to treatment may be amenable to a potassium-sparing diuretic, such as amiloride, triamterene, spironolactone, or eplerenone. Concomitant hypomagnesemia will inhibit potassium replacement, as magnesium is a cofactor for potassium uptake.
[1] [2] The causes, severity, treatment, and outcomes of these disturbances can differ greatly depending on the implicated electrolyte. [3] The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium or calcium. Other electrolyte imbalances are less common and often occur in conjunction with major ...
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.
NICE publishes guidelines in four areas: the use of health technologies within England's National Health Service (NHS) (such as the use of new and existing medicines, treatments and procedures) clinical practice (guidance on the appropriate treatment and care of people with specific diseases and conditions)
Treatment of the low levels of potassium in the blood, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks. It occurs predominantly in males of Chinese, Japanese, Vietnamese, Filipino, and Korean descent. [1] TPP is one of several conditions that can cause periodic paralysis. [4]
In 1935 the Scottish physician Dr Mary Walker was the first to recognise the association between familial periodical paralysis and hypokalaemia. She also described the glucose challenge test used in diagnosing hypokalaemic periodic paralysis and the use of intravenous potassium in its treatment. [13] [14] [15]
Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance.Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. [5]
"The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline". The Journal of Clinical Endocrinology and Metabolism. 101 (5): 1889– 1916. doi: 10.1210/jc.2015-4061. PMID 26934393