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Kaplan Qbank USMLE



Author10 Posts
  #1

A 58 year old man experiences a mild MI. His condition improves and he is discharged from the hospital. He is prescribed 325mg of enteric coated aspirin daily. This drug inhibits platelet aggregation by decreasing the production of which of the following?

A. Clotting factors II, VII, IX, and X
B. Cyclooxygenase
C. Prostaglandins
D. Thromboxane A2
E. Uric Acid

Please explain your answer...


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  #2

i dont want to give a bs explanation, so ill say this dinosaur minimizes thromboembolism formation {and probably decreases incidence of colon ca also!} by inhibiting platlet aggregation via **inhibiting cyclooxygenase and preventing endoperoxide formation. laymans would say it "thins the blood"

thromboxane A2 increases platlet aggegation and increases vascular and bronchial tone.
II,VII,IX,X has to do with Wafarin inhibiting gamma carboxylation of these factors

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  #3

whats your answer mjl?

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  #4

cycloxygenase

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  #5

D. Thromboxane A2 (correct answer)

TXA2 enhances platelet aggregation
low dose asprin (60 - 80 mg daily) decrease it's synthesis through its inhibiting effect on Cyclooxygenase enzyme

A. Clotting factors II, VII, IX, and X
vitamin K dependent clotting factors factor, affect clotting and not platelets aggregation,
and can be affected only by toxic doses of asprin.

B. Cyclooxygenase
The enzymy is inhibited by asprin. not decreased.

C. Prostaglandins
PGI2 inhibit platelets aggregation and its production is decreased by asprin (same mechanism as TXA2) so it's decrease should favour platelets aggregation.

E. Uric Acid
Not related to platelets aggregation.

feel free to correct me if I'm wrong on anything


  #6

id say asa inhibits the enyme cyclooxygenase there for blunting TX2.
TX2 is substrate NOT an enzyme. my point is enzymes work on substrates or vice versa. I would think of cyclooxygenase as having low Km in association with ASA.

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  #7

is D

Asa inhibits cyclooxygenase decreasing the production of TXA2. (which directly induce platelet aggregation). think simple, the product decreased is TXA2.


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  #8

The correct answer is D (Q-bank question).

Aspirin is an agent that has analgesic, antipyretic, and anti-inflammatory effects. These effects are due to the irreversible inhibition of COX. Aspirin is indicated for mild to moderate pain, fever, (except in children with chickenpox or flu because of increased incidence of Reye Syndrome) inflammatory conditions (e.g., RA, RF< and OA), as well as reduction in risk for MI and TIAs by irreversibly inhibiting platelet aggregation.

Choice B COX--- Acetylation of platelet COX prevents the synthesis of TXA2, a potent vasoconstrictor and inducer of platelet aggregation that is also involved in the platelet release reaction.

Choice C Prostaglandins----- Although aspirin inhibits the production of prostaglandins, a lower level of prostaglandins does not affect the clotting process.

Choice A... Warfarin is obviously wrong.

Choice E.. Uric acid:..... Aspirin causes URIC ACID levels to INCREASE!




___________________
Our greatest glory is not in never falling, but in rising every time we fall.

  #9

ok so we're talking about the final substrate that actually causes the action. {you got me on that one}

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  #10

D I AGREE










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