A Study On Prevention And Treatment Of A Platelet Activation Marker And Markers Of Evidence Of Thrombotic Risk

The WBC and platelets are high because the Pt.’s body is trying to fight an infection.

In Cardone presentation, His main focus was on Platelet-rich plasma (PRP), (plasmas that come from the patient’s body, and is centrifuged to increase the concentration of platelets combined with remaining blood). He also discussed the potential advantages as well as potential drawbacks and uncertainties regarding the use of PRP injections to treat

A person with a normal platelet count has between 150,000 to 450,000 per each microliter of blood in the body. With Thrombocytopenia, patients have platelet counts that are less than 150,000 per microliter of blood. Platelets help to promote blood clotting. When a person receives a cut, or injures themselves, platelets come to the site of injury and bind to damaged vessel, thus causing a blood clot and helping to stop the bleeding that accompanies the injury (Williams). However, with a reduced platelet count, this function can be impaired. Patients can easily bruise or bleed due to even a slight bump, as well as experience nosebleeds. Bleeding gums are another symptom of Thrombocytopenia (MDS Foundation). Based on symptoms, doctors might decide to test a patient for Myelodysplastic

Platelets are not really cells in a way. As Marieb (2012) mentions,” They are fragments of bizarre multinucleate cells called megakaryocytes (meg″ah-kar′e-o-sītz), which pinch off thousands of anucleate platelet “pieces” that quickly seal themselves off from the surrounding fluids” (p. 344) The liver helps produce blood clotting factors. If it is not in working order then the person is not able to stop bleeding as easily as someone who has a properly working liver. There is a correction to help produce the proper amount of blood clotting factors and that is to take Vitamin K.

October 17, 2009, my world changed. My little brother, Brennan, was diagnosed with idiopathic thrombocytopenia purpura, in short known as ITP. Normally, platelets are made in bone marrow and make their way through the blood stream and filtered out by the spleen. In Brennan’s case, his platelets are destroyed by his body causing his platelet count to drop to life threatening levels. Brennan’s platelet count from 2009, to today in 2016, has never gotten higher than 20,000; which means that he is at risk for spontaneous bleeding at any time. Due to this, Brennan is not allowed to participate in sports and many other physical activities.

Leads to a reduced ability to form blood clots due to a decreased number of platelets.

Clopidogrel is a second-generation thienopyridine antiplatelet agent used in humans and other species including cats to reduce the risk of thromboembolic diseases secondary to cardiovascular diseases and other systemic diseases. Once it’s converted to clopidogrel active metabolite by Cytochrome P450 isoenzymes, clopidogrel irreversibly inhibits one of the platelet ADP receptors leading to an inhibition of platelet activation and aggregation. Several large clinical trials revealed that clopidogrel administration in human patients significantly reduced the platelet activation and aggregation in vivo, and decreased the frequency of developing thromboembolic events (Sabatine MS et al. JAMA 2005, Yusuf S et al. NEJM 2001, Chen ZM et al. Lancet 2005).

People with ITP often have platelet counts below 20,000. As the number of platelets decreases, your risk of bleeding increases. The greatest risk is when your platelet count falls very low -- below 10,000 platelets per microliter. At this point, internal bleeding may occur despite a lack of any injury.

Research by the Mayo Clinic (2014) has shown that this does not necessarily benefit the diagnosis, and it can also increase the risk of blood clots, as well as impact the socioeconomic aspect of the patient. For these reasons, bedrest is no longer recommended in most cases.

Adhering platelets release growth factors that enhance smooth muscle proliferation in the vessel wall. Consequently, platelet aggregation is able to contribute to the development and progression of atherosclerosis

This chronic myeloproliferative disorder (MPD) is associated with mass quantity of platelets that are put out by megakaryocytes

The MPL gene provides instructions for making the thrombopoietin receptor protein, which promotes the growth and division (proliferation) of cells. This receptor is especially important for the proliferation of certain blood cells called megakaryocytes, which produce platelets, the cell fragments involved in blood clotting. Research suggests that the thrombopoietin receptor may also play a role in the maintenance of hematopoietic stem cells, which are stem cells located within the bone marrow that have the potential to develop into red blood cells, white blood cells, and platelets.

,platelet count at cutoff less than 74000 mm3 is significant in prediction of variceal bleeding risk with sensitivity 82.5% and specificity 55%. and platelet count/spleen diameter ratio (PC/SD) at cutoff 851.6 is significant in prediction of variceal bleeding risk with sensitivity 45% and specificity 90%.(table 5)

Activated platelets facilitate recruitment of leukocytes to regions of injury or inflammation. Platelets bind circulating leukocytes to form platelet-leukocyte aggregates in the circulation, which are subsequently recruited to the vessel wall. Initial interactions between platelet P-selectin and leukocyte PSGL-1 lead to signaling through a Src family tyrosine kinase pathway, which enhances leukocyte 2 integrin expression. [212]. Furthermore, ligation of platelet P-selectin activates IIb3 through inside-out signaling, which stabilizes platelet-leukocyte aggregate formation. These aggregates occur either in circulation or via platelet binding to the endothelial surface, and facilitate leukocyte recruitment through leukocyte 2 integrin and platelet IIb3 co-interactions with fibrinogen [213, 214][215]. In contrast, adherent neutrophils within venules have been shown to interact with P-selectin- and IIb3-expressing platelets, although a specific role for IIb3 was not identified

Platelets are the cells that circulate within our blood and bind together when they recognized damaged blood vessels. They are the smallest of our blood cells, and can only be seen under a microscope. Platelets are made in your bone marrow with your white and red blood cells. They are tiny blood cells that help your body form clots to stop bleeding. If one of your blood vessels gets damage, it sends out signals that are picked up by platelets. Platelets rush to the damage blood vessel to stop the bleeding, by growing sticky long tentacles that help them adhere. As well as send out chemical signals to attract more platelets to pile onto the clot in a process called aggregation. It is amazing how platelets can help our damage blood vessels and stop bleeding, so what other ways can our platelets do for us? This is a question one researcher and his colleagues asked and put to the test.