Plaque Synthesis

The body views the platelets as a foreign body and causes a response that produces antibodies that marks the spleen to destroy and remove the platelets. The platelet count is affected by antibodies produced by individuals with ITP. The antibody produced covers the surface of the platelets making them easily destructible by macrophages. Once the macrophages destroy the platelets faster than they are produced, the number of platelets are greatly reduced causing a decrease in blood clotting.

This organ system has a number of functions namely, to keep a constant body temperature as well as to ensure coagulation occurs specifically at the site of injury, as well as to ensure no added blood loss occurs to cause life-threatening effects. This process of blood coagulation is explained in three interconnected phases. In the first phase, the enzyme thrombokinase is activated due to the damage of tissue and the breaking down of platelets. Prothrombin is converted into thrombin by the disintegration of the thrombocytes, electrically charged calcium ions and other coagulation factors, as well as the blood activator and tissue activator which become involved in the coagulation process. The second phase includes production of the thrombin that transforms fibrinogen in the blood plasma into fibrin. The thrombus (or blood clotting) is formed by a fibrilliform mesh that encloses the blood cells. Lastly, the third phase, which takes place as retraction occurs of the fibres of the fibrin mesh. Solidification of the fibrous mesh takes place which closes the defect in the vascular wall. Coagulation is then followed by fibrinolysis (re-dissolution of the clot).

Atherosclerosis a chronic, inflammatory disease of the medium and large arteries, peripheral arteries, carotid and the aorta is a major contributor to the development of cardiovascular disease and the leading cause of death worldwide. Aherosclerotic plaque formation is a local process in the vessel wall with symptoms in the specific area, though the possibility of plaque formation at the same time and in different areas of the vasculature, regards the disease as systemic one1-3. Furthermore it is recognized that atherosclerotic carotid arteries pose a substantial risk of ipsilateral cerebrovascular events, with reported annual ischemic stroke rates ranging from .35% to 1.3% in asymptomatic patients with moderate stenosis4,5 and from .5% to

The occlusion, caused by a haemostatic plug or thrombus is comprised of a fibrous protein called fibrin. This protein polymerises to create a tightly woven mesh, trapping platelets within the fibrin fibre meshwork, resulting in the

Coronary Artery Disease (CAD) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries that supply the myocardium with oxygen and nutrients. While the symptoms and signs of (CAD) are noted in the advanced state of disease, most individuals with (CAD) show no evidence of disease for decades as the disease progress before the first onset of symptoms, often a “Sudden” heart attack, After decades of progression, some of these atheromatous plaques may rupture (along with the activation of the blood clotting system) limiting blood flow to the heart muscle.

Impaired platelet function has been described prospectively by Kutcher et al. in response to traumatic tissue injury. This describes the primary hemostatic mechanism in which platelet dysfunction can alter platelet adhesion

Platelets are tiny fragments that play a critical role in forming blood clots to stop bleeding. As states plaque can rapture during the first hour of a heart attack, and platelets assume it is an injury needing clotting, begin forming a clot in the vessel. This can cause a blockage of blood flow, which can kill a portion of the heart muscle.

Atherosclerosis begins when an accumulation of white blood cells form plaque on the artery wall. These plaques are made up of both live and dead cell, including cholesterol and triglycerides, this can create an inflammatory response in the tissue of the artery wall. These atherosclerosis plaques can be divided into two categories, stable and vulnerable. The stable plaques tend to be asymptomatic and are characterized by smooth muscle cells and have a stronger cell matrix. The second category is vulnerable plaques; these tend to be unstable and have higher levels of macrophages and foam cells. The extracellular matrix creates breaks in the fibrous cap and can lead to ruptures.

“Qualitative or quantitative abnormalities interfere with or prevent enzymatic reactions that transform clotting factors, circulating as plasma proteins into a stable fibrin clot” (Huether and McCance 544). Some defects are caused by a single factor, these would be hemophilias and von Willebrand disease and some are acquired and result from “deficient synthesis of clotting factors by the liver” which is caused by liver disease and vitamin K deficiency (Huether and McCance 544). Other abnormalities in coagulation disorders are caused by “pathologic conditions” such as a cardiovascular abnormality that alters blood flow. An example of this is thromboembolic disease where blood clots block vessels (Huether and McCance 544). Vasculitis and damage to vessels activates platelets which activates coagulation (Huether and McCance 544). Prolonged vasculitis leads to clogging of the

Collagen and von Willebrand factor can initiate coagulation by causing platelet activation which triggers coagulation.

After VWF is made, it can follow a number of pathways. It can either be released into the plasma, released into the subendothelium or it can also be stored in organelles in the cytoplasm. If VWF is stored, it can be released when it is needed depending on the physiological status of the individual10. When VWF is exposed to an injury in the blood vessel in the endothelium, the platelet receptors will be activated. This activation, will

Thrombus formation is generated by vessel damage and the subsequent thrombogenic stimuli exposure and consists of activated platelets and fibrin protein. 3 This barrier that is created limits the blood flow through coronary vessels causing myocardial ischemia. Thus coronary blood vessel thrombosis is related to pathologic events of acute coronary syndromes which include unstable angina, myocardial infarction, and sudden ischemic death. 3,4

Farrell & Dempsey (2014) suggests that the main cause of myocardial infarction (MI) is the underlying coronary artery disease (CAD), such as atherosclerosis. Atherosclerosis, is the abnormal accumulation of lipids, fatty substances or fibrous tissue in the lining of arterial blood vessels. These deposits, called atheromas, cause a narrowing or blockage of the arterial lumen which reduces blood flow to the myocardium. If the atheroma becomes too large it may rupture or haemorrhage into a plaque. The ruptured plaque becomes a site for thrombus formation, and this thrombus may then obstruct coronary blood flow resulting in an AMI

with wounds that have broken through the skin, WBCs will gather around the point of entry to fight infection and prevent any further damage to systems (Tortura 699). However, in the case of hemostasis, the most important contributors are the Platelets, cell fragments that are held together with a membrane (702). As bleeding occurs, various chemicals and enzymes that are contained within platelets activate, causing the cells to become sticky and encourage accumulation to one another. This coagulation of platelets at the broken vessel’s entry site will eventually form a solid plug, resulting in effective clotting. . Clotting is essential to stop major bleeding of vessels throughout the body, especially in the case of hemorrhagic or hypovolemic shock

During early atherogenesis, endothelial activation results in platelet activation and recruitment of platelets to the vessel wall. This early recruitment establishes a positive feedback loop in which the platelets release substances that cause further endothelial activation. Inhibiting early platelet adhesion decreased atherosclerotic plaque formation and is therefore thought to be a key step in the initiation of atherogenesis [209, 210]. While a number of receptor-ligand pairs are important, platelet integrins play a key role in firm adhesion. After rolling along the endothelium, platelets become activated leading to inside-out signaling which causes a conformational change in IIb3. This activated form of IIb3 facilitates the firm adhesion of platelets to the endothelium through a fibrinogen cross-bridge with endothelial v3