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Kaplan Qbank USMLE



Author11 Posts
  #1

64 yr. old man has MI due to thrombotic occlusion of the left circumflex coronary artery. He's admitted to intensive coronary unit 1 hour after onset of his symptoms. At this stage a thrombolytic agent is administered to prevent further extension of myocardial ischemic necrosis. Which of the following measurement is/are most likely to be affected by giving this medication?

A. Platelet count
B. Prothrombin time (PT)
C. PTT
D. PT & PTT
E. PT, PTT, and platelet count

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  #2

Monitoring is of Heparin is done by aPTT or PTT while PT is done for warfarin and while Platelets will be a later seen complication of Heparin usage.


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FORUM RULES-- Those who believe in telekinesis, raise my hand. I get enough exercise just by pushing my luck --P4U World.." The pure and simple truth is rarely pure and never simple."

  #3

D.??

  #4

Choice A - I'm thinking he was treated with tPA or streptokinase which are thrombolytic agents and are what is given when a patient presents with MI. Heparin's not a thrombolytic. So platelets should be checked.


  #5

D


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  #6

not sure , but I would go with E !

thrombolytic therapy works on plasminogen -----> plasmin which cleaves thrombin and fibrin clots , depleting circulating fibrinogen and factor V and VIII , so that' why I'm thinking this way ????
they should be adm.early (>60% decrease in Mortality rate post MI if used with 3 hs)
No antiplatelet or anticoagulant therapy should be administered for 24 hours following throbolytis therapy .since nothing specific in this patient's scenario I'll go with E.

  #7

I am thinking of PTT.

thrombolytics like tPA and streptokinase activate plasmin->plasmin degrades von Willebrand factor. B/C von Willebrand factor binds factor VIII to stablize it -> this will lead to a decrease in VIII reserve --> by this thinking, thrombolytics should decrease PTT.nod

  #8

C. PTT


  #9

Misrati wrote:


thrombolytic therapy works on plasminogen -----> plasmin which cleaves thrombin and fibrin clots , depleting circulating fibrinogen and factor V and VIII , so that' why I'm thinking this way ????
they should be adm.early (>60% decrease in Mortality rate post MI if used with 3 hs)
No antiplatelet or anticoagulant therapy should be administered for 24 hours following throbolytis therapy .


patient not on antiplatelet or anticoagulant therapy , also
since co-factors V,VIII are involved " extrensic pathway " APTT is a good possible answer though.

Answe C "APTT" mostly accepted for me ..smiling face

  #10

CORRECT ANSWER: D

Thrombosis is an important pathological process that may lead to acute MI. Among anticoagulant mechanisms are fibrinolytic factors, including plasmin. This fibrinolytic enzyme derives from cleavage of the circulating precursor plasminogen by plasminogen activators. There are 2 types of plasminogen activators, urokinase-like PA (uPA) and tissue PA (tPA). The latter is produced by endothelial cells and has been used extensively in early treatment of MI to promote lysis of newly formed thrombi. Since thrombolytics like tPA lead to direct degradation of fibrin and fibrinogen, which are common to both the extrinsic and intrinsic pathways, both PT and PTT should be prolonged.

Since tPA doesn't act on platelets, platelet count should not be affected (choices A & E).










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Expecting the world to treat you fairly because you are a good person, is like expecting the lion not to attack you because you are a vegetarian.

  #11

Thanks silver for posting the correct answer. Is fibrinogen a plasmin substrate? where is your source? From my reading, plasmin cleaves fibrin, fibronectin, laminin, von Willebrand factor..







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