| 01/22/08 - 04:52 PM  
 
   
 
|   #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 ..
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| SILVER DoWhatYouGotToDo!

Topics: 22 Posts: 887
| | 01/23/08 - 09:28 AM  
 
   
 
|   #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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| fluoxetin Forum Newbie
Topics: 0 Posts: 5
| | 01/23/08 - 04:51 PM  
 
   
 
|   #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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