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Old 02-01-2012
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Drug Heart Failure + Rheumatoid Arthritis + NSAID

A patient with heart failure has been managed with digoxin and furosemide and is doing well by all measures, for 3 years. He develops acute rheumatoid arthritis and is placed on rather large doses of a very efficacious nonsteroidal anti-inflammatory drug—one that inhibits both cyclooxygenase pathways (COX-1 and -2). Which of the following is the most likely outcome of adding the NSAID?
A. Hyperchloremic acidosis indicative of acute diuretic toxicity
B. Dramatic increase of furosemide's potassium-sparing effects
C. Edema, weight gain, and other signs/symptoms indicative of reduced diuresis
D. Increased digoxin excretion
E. Reduced digoxin effects because the NSAID competes with digoxin for myocyte receptor-binding sites
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Old 02-01-2012
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ans : .......C ...........
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Old 02-01-2012
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C--

ASA and Loop diuretics.. compete with the same anion pump in the PCT.. and hence ASA will enter into the tubular fluid while LOops will not be able to hence decreasing their action



is that correct?
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Old 02-01-2012
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Ya C. its because COX inhibitor result in decrese synthesis of PGE2 which result in afferent vasoconstriction resultin in decrease blood flow that can result in inrease in RAAS system resulting in the present symptoms
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Old 02-01-2012
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Quote:
Originally Posted by mohitkmc View Post
Ya C. its because COX inhibitor result in decrese synthesis of PGE2 which result in afferent vasoconstriction resultin in decrease blood flow that can result in inrease in RAAS system resulting in the present symptoms
c for the same reason above
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Quote:
Originally Posted by mohitkmc View Post
Ya C. its because COX inhibitor result in decrese synthesis of PGE2 which result in afferent vasoconstriction resultin in decrease blood flow that can result in inrease in RAAS system resulting in the present symptoms
yup the right answer
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Old 02-02-2012
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An important element in the renal responses to furosemide is maintenance of adequate renal blood flow. That is, to a degree, prostaglandin-mediated. The NSAIDs, such as the hypothetical one described here, inhibit prostaglandin synthesis. That, in turn, antagonizes the desired effects of the loop diuretic, leading to less fluid and salt elimination: edema, weight gain, and other markers of heart failure are likely to develop as a result. Hyperchloremic alkalosis (a) is incorrect, in part, because chronic or acute excessive effects of loop diuretics are characterized by hypochloremic metabolic alkalosis. Regardless, NSAIDs are not likely to potentiate the effects of these diuretics. "Dramatic increases of furosemide's K-sparing effects (b)" is incorrect. Recall that loop diuretics are K-wasting. Digoxin is eliminated by renal excretion. If we accept the notion that loop diuretics may increase excretion of digoxin, then we should accept the likely possibility that NSAID-induced reductions of diuretic action should reduce the glycoside's renal loss, not increase it (d). The NSAIDs do not bind to and inhibit the myocyte Na+,K+-ATPase, which is digoxin's cellular receptor (e). Do remember that furosemides (and thiazides) are apt to increase the risk or severity of digoxin toxicity. The mechanism mainly involves diuretic-induced hypokalemia, not changes in circulating fluid volume or urine volume per se.
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Old 02-04-2012
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ans is c coz nsaids decrease prostaglandins which are responsible for renal vasodilatation and increase GFR +RBF. decreased diuresis edema and wt gain. would it be true even if a seletive COX-2 inhibitor
were being used?
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