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The primary treatment of digoxin toxicity is digoxin immune fab, which is an antibody made up of anti-digoxin immunoglobulin fragments. This antidote has been shown to be highly effective in treating life-threatening signs of digoxin toxicity such as hyperkalemia, hemodynamic instability, and arrhythmias. [ 11 ]
Hypokalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness typically beginning in childhood or adolescence. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Attacks cause severe weakness or paralysis that usually lasts from hours to days.
Digoxin may be prescribed for a child to treat heart defects. Possible side effects in children are: dysrhythmia, nausea, vomiting, a slower-than-normal heart rate and anorexia. [4] Children may demonstrate side effects if they are breastfed. Digoxin is also absorbed by the infant in utero. [5]
Digoxin increased the risk of death in women by 23%. There was no difference in the death rate for men in the study. [38] Digoxin is also used as a standard control substance to test for P-glycoprotein inhibition. [39] Digoxin appears to be a peripherally selective drug due to limited brain uptake caused by binding to P-glycoprotein. [40] [41]
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] Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest. [1] [3]
This disease is encountered typically after the 1st decade of life, i.e., during adolescence or adulthood. However, it can occur in the neonatal period. Heterozygous carriers of the SLC12A3 gene mutations are 1% of the population. [16] A person with Gitelman syndrome has a low probability of passing the disease to their offspring.
Fanconi syndrome or Fanconi's syndrome (English: / f ɑː n ˈ k oʊ n i /, / f æ n-/) is a syndrome of inadequate reabsorption in the proximal renal tubules [1] of the kidney.The syndrome can be caused by various underlying congenital or acquired diseases, by toxicity (for example, from toxic heavy metals), or by adverse drug reactions. [2]
Hypokalemia (a decreased potassium level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the breathing muscles leads to respiratory failure, or if the low potassium levels lead to abnormal heart rhythms. [1] [2] If untreated, it is typically recurrent in nature. [1]