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  #1  
Old 01-25-2012
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Drug Too much Aspirin!

A 50-year-old man is well aware of the benefits of aspirin in terms of reducing the risk of death from an acute myocardial infarction, mainly because he has seen and carefully studied many of the ads and internet posts about this. He notices that the usual recommended dose of aspirin for cardioprotection is 81 mg/day, but reasons that the bigger the dose, the bigger the protective effect. He has taken "at least" 1000 mg of aspirin twice a day for the last 6 months. While he is fortunate in terms of having no apparent gastrointestinal adverse effects, he suffers an MI. Autopsy results show considerable platelet occlusion of several coronary vessels. Which of the following most likely explains the mechanism by which aspirin triggered these events?

A. Acetylated platelet glycoprotein IIb/IIIa receptors, triggering aggregation
B. Favored adhesion of platelets to the vascular (coronary) endothelium
C. Ruptured atherosclerotic plaque in the coronaries, exposing platelets to collagen
D. Suppressed hepatic synthesis of vitamin K–dependent clotting factors
E. Triggered excessive activation of platelets by ADP
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  #2  
Old 01-25-2012
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wow, ummm B? or D?
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Old 01-25-2012
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I feel its B ....... aspirin inhibits COX thus the arachinoid acid pathway diverts to lipo oxygenase pathway making leukotrienes that cause platelet aggregration ......and increased attachment to endothelium ....
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  #4  
Old 01-25-2012
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i think B too
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  #5  
Old 01-25-2012
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hey scopusmount, what's the answer and why??

This was a good question.
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  #6  
Old 01-25-2012
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excessive aspirin will cause a decrease of PROSTACYCLIN or PGI2 too which is an anti thrombotic naturally produced in the body.
hence i will go with B
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Old 01-25-2012
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here are some helpful links

http://www.ncbi.nlm.nih.gov/pubmed/19293355
http://en.wikipedia.org/wiki/Prostaglandin
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  #8  
Old 01-26-2012
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Quote:
Originally Posted by mbbs2010 View Post
excessive aspirin will cause a decrease of PROSTACYCLIN or PGI2 too which is an anti thrombotic naturally produced in the body.
hence i will go with B

is this correct???
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  #9  
Old 01-26-2012
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Default Distractor?

I remember doing a question once: which of the following is the most likely autopsy finding in a bedridden patient (secondary to a broken hip) who died of a sudden death. The options included

  1. Pulmonary embolus
  2. Embolus in the coronary vessels
  3. DVT

The answer was a DVT because it is the most likely autopsy finding- they did not ask about the cause of death. (This is stuck in my head because I got it wrong )

Similarly- could it be that too much aspirin is simply a distractor- and that the answer is something mundane like: C. Ruptured atherosclerotic plaque in the coronaries, exposing platelets to collagen?

Last edited by Moloch; 01-26-2012 at 10:27 PM. Reason: NoScript acting up
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  #10  
Old 01-27-2012
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Quote:
Originally Posted by Moloch View Post
Similarly- could it be that too much aspirin is simply a distractor- and that the answer is something mundane like: C. Ruptured atherosclerotic plaque in the coronaries, exposing platelets to collagen?
Don't think its a distractor.

The question asks....Which of the following most likely explains the mechanism by which aspirin triggered these events?

So aspirin has something to do with it.
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  #11  
Old 01-28-2012
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Quote:
Originally Posted by mbbs2010 View Post
excessive aspirin will cause a decrease of PROSTACYCLIN or PGI2 too which is an anti thrombotic naturally produced in the body.
hence i will go with B
this is the explanation
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  #12  
Old 01-28-2012
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Quote:
Originally Posted by scopusmount View Post
this is the explanation
yay!!
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  #13  
Old 01-28-2012
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the reason for it is-

in low doses, only the COX enzyme in platelets is inhibited, irreversibly, and new enzyme is synthesized when new platelets are formed
whereas turnover rate of the endothelium is high, so COX inhibition is not apparent enough

platelets are the main source of TXA-2
endothelium is the main source of PGI-2

in case of high doses, both of these are inhibited, so the beneficial effect is negated, thus causing MI
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  #14  
Old 01-29-2012
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on doing a little research.. a friend of mine found this out


Liver function should be monitored in patients receiving large doses of aspirin (e.g., for treatment of rheumatoid arthritis) or in patients with preexisting hepatic disease in order to prevent reversible, dose-dependent hepatotoxicity. Large doses also can cause hypoprothrombinemia, which can be reversed by vitamin K. Similarly, patients with renal insufficiency, renal failure, or vitamin K deficiency should be closely monitored if taking large doses of aspirin.

so if the same case was a patient with heammorrhagic stroke etc.. the answer could also be D.

Last edited by mbbs2010; 01-29-2012 at 10:40 AM.
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  #15  
Old 01-29-2012
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Aspirin is also an acetylating agent- so A. Acetylated platelet glycoprotein IIb/IIIa receptors, triggering aggregation is not off the table
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  #16  
Old 01-30-2012
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Default Aspirin Overdose

Aspirin Overdose can affect platelet aggregation due to the lack of ATP and increase in ADP. The answer is D.
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  #17  
Old 01-30-2012
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I ll go with E.
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  #18  
Old 01-30-2012
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Brilliant explanation of the choice B. By the way, what is the source of this question?
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