Platelet Activation Following Vascular Injury

kmguru

kmguru

Staff member
Platelet Activation and Aggregation Following
Vascular Injury


Immediately following vascular injury, platelets recognize and adhere to the damaged endothelium where they become activated. Activated platelets release prothrombotic factors such as thromboxane A2 and ADP that recruit more platelets to the site of injury, forming a hemostatic plug that seals the injury. However, uncontrolled platelet activation results in further platelet recruitment, further platelet activation, and platelet aggregation that may culminate in thrombus formation. Thus, platelet adhesion and activation, the central pathway to platelet aggregation, if uncontrolled, may result in arterial blockage to the heart or the brain, leading to acute myocardial infarction, stroke, or death.
 
dragon vascular just refers to damage to one of the vain, caperaries or arteries. Not all untreated injuryies will lead to death, if you cut your finger and leave it it will heal itself. However kmguru is correct that a simple cut CAN lead to a platelet cascade that can end in thrombosus. If a thrombosus becomes mobile (ie becomes an embolus) it can lodge in the lungs and kill you

kmguru although possable, its highly unlikly that it will lodge in the coronary arteries or the brain. That really requires an injury in the left side of the heart or in vains leading from the lungs. The chances of a PE however are much higher
 
Cardiovascular disease remains the number one killer in the United States.
In 2004 alone, approximately 1.5 million patients were hospitalized for acute coronary syndrome (ACS), and in 2008, an estimated 500,000 Americans
may have a recurrent coronary attack.

ACS is an umbrella term that encompasses the clinical conditions of acute
myocardial infarction (designated as STEMI or NSTEMI) and unstable
angina.Platelet activation and aggregation play integral roles in these thrombotic complications, which can result from either percutaneous coronary intervention (PCI) or spontaneous plaque rupture.

Which means that in most cases the thrombus is not large enough to cause vascular blockage and is mopped up by body's defense mechanism. The unlucky ones are screwed...
 
Tristearin.gif


It's time we put a taboo on this killer!
 
UMM
An MI generally results from a thrombosis that builds up behind a plague buildup in the coronary arterys. They break off to form an embolis (mobile clot) which travels further into the smaller arterys and blocks the blood flow. Not caused by a cut that results in a platelet cascade

Not sure if thats what you ment though. If it is i am sorry for contridicting you
 
could you please give a link to the case study. I may be wrong but everything we have learnt at uni says that MI's are the result of throbosis that origionate in the corinary arteries. DVT's (ie thrombosis that form in the legs and arms) if they form embolie, result in a polumary embolis PE.
 
ok now i see why you didnt link it, you have to pay to get on that site:p

To be fair your piture is exactly what i have been saying, a thrombosis builds up behind a plaque build up in the coranry artery'
 
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