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Haematological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The function of blood platelets is to prevent haemorrhage by forming platelet plugs at sites of blood vessel damage. Normal platelet count: 150–400 × 109/LIncreased platelet count: >400 × 109/L = thrombocytosisDecreased platelet count: <150 × 109/L = thrombocytopenia
Blood Transfusion
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
One unit of platelet concentrates contains approximately 6 × 1010 platelets. Although platelets express only HLA class I antigens, contamination by leukocytes and red blood cells can cause alloimmunization. Thus, ABO- and Rh-compatible platelets are usually used, but HLA-matched platelets are used for patients with HLA antibodies. Nearly one-third of transfused platelets are sequ estered in the normal spleen. One unit of platelet concentrate increases the blood platelet count by 10 × 109/L/m2 body surface area.
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Blood platelets contain high amounts of ADP and ATP. The concentration of ADP in platelets decreases during the clotting of the platelet-rich plasma. When the thrombus is first formed, platelets, red, and white cells are disrupted and release ADP into the plasma (Figure 4). This released ADP triggers the adhesion of platelets, probably initiating the first step in the production of hemostatic plugs and thrombi. The size of platelet aggregates is related to the amount of ADP released and to the pattern of blood flow. Large platelet aggregates form in areas where there is disturbed blood flow. The platelet mass formed by the action of ADP is unstable and will fragment and not adhere unless fresh platelets arrive at the site. The platelet aggregation phenomenon is independent of the clotting mechanism and does not necessarily promote fibrin formation. When platelets aggregate under the influence of ADP, proteins and a specific phospholipid are released. This phospholipid seems to be essential for the normal clotting mechanism. Certain saturated fatty acids also elicit aggregation of platelets and activate blood clotting. The rapid infusion of saturated fatty acids produces thrombosis in experimental animals; subsequently, the formation of fibrin stabilizes the platelet mass.
Stimulation of mTORC2 by integrin αIIbβ3 is required for PI3Kβ-dependent activation of Akt but is dispensable for platelet spreading on fibrinogen
Published in Platelets, 2020
Mauro Torti, Daria Manganaro, Caterina Visconte, Marta Zarà, Jessica Canino, Mauro Vismara, Ilaria Canobbio, Gianni Francesco Guidetti
Circulating blood platelets are critical players in hemostasis and represent a major pharmacological target for antithrombotic therapies. A complex interplay among membrane receptors and intracellular signaling proteins governs platelet reactiveness, promoting adhesion, secretion and aggregation [1,2]. Integrin αIIbβ3 mediates the interaction with fibrinogen, fibronectin and von Willebrand factor and supports both platelet aggregation and firm platelet adhesion to the subendothelial matrices exposed upon vessel damage [3]. In resting platelets, integrin αIIbβ3 is maintained in a low-affinity state and it is converted to a high-affinity conformation for its ligands upon platelet activation, through an inside-out signaling pathway [4]. The interaction of integrin αIIbβ3 with specific ligands initiates an outside-in signaling pathway, which is essential for thrombus stabilization and subsequent clot retraction [5,6].
Multifocal avascular necrosis in a patient with refractory immune thrombocytopenia and antiphospholipid antibodies; case report and review of literature
Published in Platelets, 2019
Hala El-Gendy, Rasmia M. El-Gohary, Safaa Mahfouz, Hamdy M.A. Ahmed, Doaa M. El Demerdash, Gaafar Ragab
Dear editor(s), as you know, avascular necrosis (AVN), also known as ischemic necrosis, osteonecrosis and aseptic necrosis, was first described in 1738 by Alexander Munro and is defined as necrosis of a localized area of bone [1]. Immune thrombocytopenia (ITP) and antiphospholipid syndrome (APS) are two different autoimmune diseases that are rarely associated with AVN. ITP is characterized by low peripheral blood platelet count (< 100 × 109/L) and may present with petechiae and bleeding. It may occur in isolation (primary) or in association with other disorders (secondary) [2]. In ITP, anti-platelet antibodies directed against single or multiple platelet membrane glycoproteins (GP) lead to acceleration of platelet destruction and inhibition of their production [3]. Secondary causes include autoimmune disorders such as systemic lupus erythematosus (SLE) and APS; viral infections including hepatitis C virus (HCV) and human immunodeficiency virus (HIV); and certain drugs [4]. APS is caused by antiphospholipid antibodies (aPLs) and results in a hypercoagulable state which can clinically present with arterial, venous, or small vessel thrombosis and/or pregnancy morbidities [5].
Seasonal Variation of Phyto-Constituents of Tea Leaves Affects Antiproliferative Potential
Published in Journal of the American College of Nutrition, 2019
Sayantan Maitra, Arnab De, Bhaskar Das, Sudipendra Nath Roy, Ranadhir Chakraborty, Amalesh Samanta, Subhrajit Bhattacharya
There was a significant (p < 0.01) increase in the level of WBC and significant (p < 0.01) decrease in level of RBC and hemoglobin (Hb) in the EAC control group as compared to the normal control group (Table 4). However, treatment with MECR and MECA at the doses of 20 and 40 mg/kg in EAC-bearing mice have produced significant increase in both the RBC count and the Hb content (p < 0.01 for MECR at 40 mg/kg and p < 0.01 to p < 0.05 for other test groups), while WBC count decreased significantly (p < 0.01 for MECR at 40 mg/kg and p < 0.01 to p < 0.05 for other test groups) when compared with the EAC control group. The group treated with MECR at 40 mg/kg showed almost similar efficacy in the case of the standard group and better than other test groups in restoring the blood parameters. Interestingly, blood platelet count diminished primarily in the standard drug (5-fluorouracil)-treated group but remained almost unaltered and within the normal range for all other experimental groups including MECR-treated mice. One of the major complications encountered in cancer chemotherapy is myelosuppression, leading to pancytopenia. Transient increase in leucocyte count in EAC control group evidenced the transplantation of tumor cells. However, the incidence of leucopenia, erythropenia, and thrombocytopenia was comparatively less or negligible in the MECR at 40 mg/kg treatment group compared to other tests and standard drug-treated mice groups and was devoid of chemotherapy-induced myelosuppression.