The Half-Life Of Platelets

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

The liver becomes so diseased and damaged that it can no longer produce appropriate amounts of clotting factor and hormones to make platelets. “Vitamin K must be present in order for the liver to synthesize some of the clotting factors, including prothrombin, interleukin-6, multi-CSF, and fibrinogen.” p 664 If the blood is unable to clot then the patient will continue to bleed to the point that a liver transplant is necessary. Prothrombin a peptide hormone produced in the kidneys that accelerates platelet formation. Interleukin-6 is a hormone that stimulates platelet formation. Multi-CSF is a hormone that stimulates platelet production by promoting the formation and growth of megakaryocytes. p.660 If all of these hormones are

Using your measuring spoons, scoop out a leveled 1/2 teaspoon of rice. These will represent the platelets. Carefully pour the rice into the plasma.

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.

A 13 year old is studying blood in school, and has asked some questions that haven't been answered in class. I will answer

The normal platet count is 150,000 to 200,000, but when i was hospitalized my platelet count was at a signicantly low level of 3,000.

Venous thrombi, composed predominately of red blood cells but also platelets and leukocytes bound together by fibrin, form in sites of vessel damage and areas of stagnant blood flow such as the valve pockets of the deep veins of

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.

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

APCs are hemocomponents prepared by centrifugation of a blood sample of the patient. The basic concept of this technology is to collect the most active components of the blood sample (eg, platelets, fibrin, and in certain cases leukocytes). This process produces a very high-concentration gradient of platelets whose granules are rich with many substances fundamental to promote the healing process including adhesive proteins; procoagulant factors; cytokines and chemokines; antimicrobial proteins; and a number of mitogenic growth factors , which may trigger angiogenesis and improve tissue

There are several ways to treat Myelodysplastic Syndromes. The plan of action of one’s treatment depends on the severity of the syndrome and age. Types of standard treatment are supportive care, drug therapy, and chemotherapy with stem cell transplant. Supportive care is used to reduce problems or side effects associated with the syndrome or its treatment. One supportive care option is blood transfusion. Transfusions can be specific to the type of cytopenias. For example, if a patient is experiencing anemia, a red blood cell transfusion is given. Platelet transfusions are given when a patient is bleeding easily, platelet count is low, or when the patient is having a procedure that may cause bleeding. Patients can also receive transfusions to

Plasma cells are a type of white blood cell formed from B cells produced in a person’s bone marrow. B cells mainly stay within the bone marrow and are responsible for a specific defense mechanism that involves the production of antibodies by plasma cells. These antibodies are able to move

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

A platelet is a disk-shaped structure found in the blood of all mammals, playing a major role in the coagulation of blood 1; platelets are transfused to patients to treat or prevent bleeding during surgery and other medical conditions associated with platelet deficiency or function defect. Platelets shelf life for transfusion purposes is up to six days; however, due to testing, platelets are generally not released to inventory until 24 hours after the collection time. Therefore, usable platelet shelf life is generally five days. This is an extremely short product shelf life compared to other blood products. This makes inventory management of platelets

Diagnosing prothrombotic diseases early and preventing its complications are significantly essential. Therefore, this study sought to investigate whether MPV contain diagnostic value that can prompt it to be utilized as a platelet activation marker and as marker of evidence of thrombotic risk. Platelet activation is widely acknowledged to be an indicator of likely prothrombotic diseases. Platelet size, measured as MPV, has been shown to be an indicator of platelet function and is positively linked to platelet activity indicators (Tsiara et al., 2003). The correlation between platelet size and function can be attributed to the larger platelets that activated megakaryocyte produce in the bone marrow likely to be more reactive and easier to aggregate than the normal platelets. Such is because the larger platelets secret more β-thromboglobulin and serotonin, have denser granules, generate more thromboxane in comparison to the smaller platelets while also showing more activity than the smaller platelets (Dastjerdi et al., 2006). Therefore, the hyperactive large platelets contribute considerably in speeding the formation and spread of intracoronary thrombus. This causes acute thrombotic events to occur (Smith et al., 1999). Increased MPV levels are exhibited to constitute an independent predictor for recurrent MI, ischemic vascular events or even death caused by coronary artery disease (Wang et al., 2011; Chu et al., 2010; Huczek et al., 2005). Dogan et al. (2012) linked MPV