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  #1  
Old 02-11-2013
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Arrow Billy Step1 Questions # 111

Patients with extensive endothelial injury from Escherichia coli sepsis have consumption of coagulation factors as wellas an extensive inflammatory response. Administration of activated protein C decreases this inflammatory response byreducing the amount of a substance that normally binds toprotease-activated receptors to trigger expression of adhesion molecules, cytokines, and chemokines. What is this substance most likely to be?


□ (A) Complement
□ (B) Fibrin
□ (C) Kallikrein
□ (D) Plasmin
□ (E) Thrombin
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Old 02-11-2013
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E. Thrombin

From wiki:

Thrombin in turn acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin, as well as catalyzing many other coagulation-related reactions.

Beyond its key role in the dynamic process of thrombus formation, thrombin has a pronounced pro-inflammatory character, which may influence the onset and progression of atherosclerosis.
Acting via its specific cell membrane receptors (protease activated receptors: PAR-1, PAR-3 and PAR-4), which are abundantly expressed in all arterial vessel wall constituents, thrombin has the potential to exert pro-atherogenic actions such as inflammation, leukocyte recruitment into the atherosclerotic plaque, enhanced oxidative stress, migration and proliferation of vascular smooth muscle cells, apoptosis and angiogenesis.
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Old 02-11-2013
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I'm totally guessing this one. Not sure what is this. But here I go. So you give Protein C. That Protein C inhibits something. From my way, Protein C inhibits Factor 5 and 8. No factor 5 then Factor 10 can not convert prothromin into thrombin. No thrombin then there's no fibrin and therefore no clotting.

With that I am going narrow it down to Fibrin and Thrombin. Protein C inhibits cofactors 5 and 8. No Factor 8, Factor 10 won't be activated. No Factor 5, Thrombin won't be activated. No Thrombin, Fibrin won't be activated. No Fibrin, there's no clotting.

So if I go in that order, meaning start from Factor 5 being inhibited by Protein C. When there's no Factor 5, Thrombin won't form. Therefore I will pick Thrombin as an answer. Again, I'm just entirely guessing by looking how pathway runs here.

My final answer is E - Thrombin.
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Old 02-12-2013
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Old 02-12-2013
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Complement . . . .

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I think its C. Kallikrein

Don't know why though? lol.
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Old 02-24-2013
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So, what's the correct answer?
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Old 02-24-2013
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Arrow E is correct

Ongoing activation of coagulation generates an inflammatory response that further amplifies coagulation, creating a vicious cycle. Protein C antagonizes coagulation factor V, which catalyzes activation of prothrombin to thrombin, thereby breaking the cycle of thrombin generation. Complement components can become activated by plasmin (C3) and kallikrein (C5) forming anaphlytoxins (C3a and C5a) that promote inflammation. Fibrin is the end product of coagulation pathways that forms a meshwork entrapping platelets and forming a plug. Kallikrein is generated by activation of Hageman factor (XII) and leads to formation of bradykinin. Plasmin is generated from plasminogen activated by thrombosis to promote clot lysis.
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Old 02-24-2013
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Quote:
Originally Posted by billy View Post
Patients with extensive endothelial injury from Escherichia coli sepsis have consumption of coagulation factors as wellas an extensive inflammatory response. Administration of activated protein C decreases this inflammatory response byreducing the amount of a substance that normally binds toprotease-activated receptors to trigger expression of adhesion molecules, cytokines, and chemokines. What is this substance most likely to be?


□ (A) Complement
□ (B) Fibrin
□ (C) Kallikrein
□ (D) Plasmin
□ (E) Thrombin
E. Thrombin???
Protein C is anti thrombotic and may suppresses activation of prothrombin to thrombin..
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