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  #1  
Old 11-13-2010
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Q :A 64-year-old female is treated with warfarin for chronic atrial fibrillation. She develops acute pyelonephritis that requires ceftriaxone therapy. Soon after initiation of therapy her laboratory testing reveals significantly increased prothrombin time and increased INR. Warfarin action is enhanced in this patient due to the effect on which of the following?

A. Absorption
B. Hepatic metabolism
C. Plasma protein binding
D. Competitive antagonism
E. Renal excretion

This is a question from UW. Lets see how many of you are getting it right.
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  #2  
Old 11-14-2010
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C. Plasma protein.
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Old 11-14-2010
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I'm sorry Doc. Nice try, but that's not the correct answer. Let me give you little more time to figure it out.
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Old 11-14-2010
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Hepatic metabolism
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Old 11-14-2010
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Quote:
Originally Posted by usmle0987 View Post
Hepatic metabolism
I'm afraid Doc that's not the correct one. Please wait for others. Thank you
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Old 11-14-2010
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D. Competitive antagonism
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Old 11-14-2010
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Quote:
Originally Posted by step1an View Post
D. Competitive antagonism
Wow... you are genius Doc. Here is the explanation for your answer...



Warfarin isthe most commonly used agent for longterm anticoagulation to prevent thromboembolism in patientswith atrial fibrillation. Warfarin inhibits vitamin K dependent -carboxylation of glutamic acid residues of clotting factors II, VII, IX and X resulting in production of dysfunctional coagulation proteins. Warfarin has a large number of interactions with drugs that alter
P-450 activity, protein binding and gastrointestinal absorption.

Prothrombin time (PT) is used for monitoring the therapeutic effect of warfarin. International normalized ratio (INR) standardizes PT assays and typically an INR between 2 and 3 is used as the therapeutic target range. Bleeding from excessive anticoagulation is the most common complication of warfarin therapy. Vitamin K is the antidote given to reverse bleeding from warfarin overdose. Vitamin K occurs in two natural forms, K1 or phylloquinone and K2 or menaquinone. K1 comes from dietary sources, whereas K2 is produced in the gut by bacterial flora. Antibiotic use typically results in a decrease in intestinal bacterial flora and decrease in production of Vitamin K2. This can result in increased activity of warfarin without a change of dosage because of a decrease in competitive inhibition.

Warfarin has a large number of other interactions with drugs that alter P-450 activity, protein binding, gastrointestinal absorption and pharmacodynamic alteration. The elimination of warfarin is almost entirely by hepatic metabolism by microsomal enzymes (cytochrome P-450). Drugs that inhibit cytochrome P450 increase the anticoagulant activity, whereas drugs that increase P450 activity decrease warfarin’s anticoagulant activity.
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Old 11-14-2010
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Quote:
Originally Posted by aktorque View Post
Wow... you are genius Doc. Here is the explanation for your answer...
I think i had already read this question somewhere & remembered the answer....but was clueless about the reason behind it......:sorry:

But i think this explanation also does not explain the "Competitive antagonism".

Can you be more specific in ur explanation..... Thx
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Old 11-14-2010
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Decreased vitamin K synthesis by intestinal flora decreases the effect of competitive antagonism on clotting factor synthesis. This increases the activity of warfarin.
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