03-10-2009, 02:46 PM
anyone knows MOA for thiazide increasing digitalis toxicity? same as lithium by increasing reabsorption in PCT?
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Digitalis toxicity - doc_vic
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03-10-2009, 02:56 PM
hypokalemia caused by thiazides causes digitalis toxicity
03-10-2009, 02:57 PM
hi vikisin.
how hypokalemia enhance digitalis activity? anybody pls explain?
03-10-2009, 03:47 PM
both hyper and hypokalemia can cause arrhythmia.
I dont know how but this is my guess. In hypokalemia extracellular k is low so more potassium would rush out or less would go out leading to defect in phase 3 and 4 and can lead to defective or less repolarization and premature beats or delayed after depolarizations. wild 2 min guess.
03-10-2009, 03:48 PM
both hyper and hypokalemia can cause arrhythmia.
I dont know how but this is my guess. In hypokalemia extracellular k is low so more potassium would rush out or less would go out leading to defect in phase 3 and 4 and can lead to defective or less repolarization and premature beats or delayed after depolarizations. wild 2 min guess.
03-10-2009, 03:50 PM
both hyper and hypokalemia can cause arrhythmia.
I dont know how but this is my guess. In hypokalemia extracellular k is low so more potassium would rush out or less would go out leading to defect in phase 3 and 4 and can lead to defective or less repolarization and premature beats or delayed after depolarizations. wild 2 min guess.
03-10-2009, 03:50 PM
both hyper and hypokalemia can cause arrhythmia.
I dont know how but this is my guess. In hypokalemia extracellular k is low so more potassium would rush out or less would go out leading to defect in phase 3 and 4 and can lead to defective or less repolarization and premature beats or delayed after depolarizations. wild 2 min guess.
03-10-2009, 03:52 PM
SORRY...I HAVE NO IDEA WHY IT POSTED IT SO MANY TIMES SORRY
03-10-2009, 03:57 PM
I am just copy/pasting. According to Katzung, 'INTERACTIONS WITH POTASSIUM, CALCIUM, AND MAGNESIUM Potassium and digitalis interact in two ways. First, they inhibit each other's binding to Na+/K+ ATPase; therefore, hyperkalemia reduces the enzyme-inhibiting actions of cardiac glycosides, whereas hypokalemia facilitates these actions. Second, abnormal cardiac automaticity is inhibited by hyperkalemia (see Chapter 14). Moderately increased extracellular K+ therefore reduces the effects of digitalis, especially the toxic effects.' |
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