hgheith Forum Elite

Topics: 39 Posts: 268
| | 06/13/05 - 10:15 PM  
 
   
 
|   #1 |
If a pt had a genetic problem with plasmin (it did not work right), and had surgery on his thigh, what will he have? Systemic thrombolysis, thrombolysis at the site of surgery only, systemic thrombosis, thrombosis at the site only? I don't have the answer but anyone can help I would appreciate it thanks
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| 99doc Forum Elite
Topics: 52 Posts: 370
| | 06/14/05 - 12:51 AM  
 
   
 
|   #2 |
plasmin is linked to clot dissolution,so def. will lead to thrombosis in body,because normally it prevents any clot forming at any absurd site where it should not be forming.
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| ssrpk Forum Fanatic

Topics: 154 Posts: 2,819
| | 06/14/05 - 01:13 AM  
 
   
 
|   #3 |
i don't think surgery wud exacerbate the situation as suppression of plasmin activity is generally desirable during surgery or it wud lead to excessive bleeding later on!
___________________ life is guud
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| hgheith Forum Elite

Topics: 39 Posts: 268
| | 06/14/05 - 09:36 AM  
 
   
 
|   #4 |
Right, but wouldn't this pt have problems after the surgery? Won't this pt have excess thrombosis extending beyond the surgry site since the plasmin is not working to limit it to the site of injury?
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| mildus Forum Guru
Topics: 19 Posts: 614
| | 06/14/05 - 09:45 AM  
 
   
 
|   #5 |
As far as I know, there are two systems important for anticoagulation. 1. one is in charged to prevent any clot forming when not necessary (antitrombin III, trombomodulin) 2. the other is in charged to dissolve already formed clot (plasmin) So, plasmin has a very important role in clot dissolution. So, the clot is produced during coagulation, and a few days after plasmin dissolves it.
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| hgheith Forum Elite

Topics: 39 Posts: 268
| | 06/14/05 - 10:24 AM  
 
   
 
|   #6 |
I agree, but it also states in robbins that plasmin is also part of the counter regulatory mechanisms that limit the hemostatic plug to the site of injury, also once the coagulation cascade is activated, clotting is controlled by 3 groups of natural anticoagulants (to prevent clotting of the entire vascular tree), one of them being the plasminogen-plasmin system. This is a strange q, but an important one, so what would happen to this pt? He has a problem with his plasmin, he had surgery on his thigh, now what is going to face? His clot won't dissolve and it might spread beyond the site? if anyone knows please help
Edited by hgheith on 06/14/05 - 10:29 AM
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| mesh Forum Guru
Topics: 77 Posts: 401
| | 06/14/05 - 06:29 PM  
 
   
 
|   #7 |
i think it will be thrombosis at the site only.cause the cascade system is will be inhibited by the anticoagulants(antithrombin III,proteinC and proteinS). excess of thrombin binds to the cell surface receptor called the thrombomodulin which activates protein C and proteinS inhibiting further thrombin formation. so i think the clot formed will nt be dissolved but it wont certainly lead to systemic thrombosis.
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| Galaxum Forum Newbie
Topics: 3 Posts: 33
| | 06/14/05 - 09:50 PM  
 
   
 
|   #8 |
Very interesting!!!!! so far, i dont know genetic problem of plasmin..... Clinically, for preoperative preparation, no test to evaluate plasmin is obligatory. So it is not really important for surgery, at least in minor surgery. _ In your case, just a local operation on the thigh, so if thrombosis occurs, it's only at that place. And you have some factors named antithrombin III,proteinC and proteinS that prevent a trigger of DIC.... and we dont see the cause or risk factor of DIC including plasmin abnormalities, despite plasmin problem aggravates DIC _ Otherwise Presence or thrombosis at this site is of microvasculature, the development of collateral vessle will help..... so we dont worry about the would healing in this case.......
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| Galaxum Forum Newbie
Topics: 3 Posts: 33
| | 06/14/05 - 10:38 PM  
 
   
 
|   #9 |
The fibrinolytic system and thrombotic tendency. Kluft C. Gaubius Laboratory, TNO-PG, Leiden, The Netherlands. c.kluft@pg.tno.nl The deposition of the insoluble protein matrix, fibrin is temporary. The mainly known mechanism of proteolytic removal is orchestrated by a cascade type of proteolytic process involving ultimately the formation from plasminogen of the active degradation enzyme plasmin. The occurrence of plasminogen deficiency without a massive deposition of fibrin and thrombotic events indicates the occurrence of alternate routes of fibrin degradation. In the literature, data have been reported about the direct fibrinolytic activity of various other enzymes including leucocytal elastase and cathepsin G and three metalloproteinases (MMP-3,MMP-7, MT1-MMP). The importance of each of these pathways and the possible differences in importance in various diseases, in acute situations and at different locations in the circulation, in tissues and organs is not known in detail. It is suggested that multiple combined knock-outs be created to evaluate the situation for various well-defined phenotypes. It is concluded that fibrin removal is an important biological process with various buffering mechanisms and only combinations of abnormalities in the various mechanisms and special situations will lead to fibrin accumulation and thrombotic events.
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| ssrpk Forum Fanatic

Topics: 154 Posts: 2,819
| | 06/14/05 - 11:02 PM  
 
   
 
|   #10 |
hey galaxum tht's an excellent refrence, keep it up buddy
___________________ life is guud
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| hgheith Forum Elite

Topics: 39 Posts: 268
| | 06/15/05 - 11:30 AM  
 
   
 
|   #11 |
Thank you all, I do agree with you Mesh, it's a great explanation, and galaxum thank you for the refrence, it is very helpful. I think this q is brought up to test our knowledge of the clotting system and our knowledge of plasmin (theoretically), otherwise in practicle use it might not be significant. Again thanks to you all
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