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Common symptoms of IMT include lethargy, anorexia, pyrexia, haemorrhage, and bruising. [1] Destruction of platelets occurs when immunoglobins attach to the surface of the platelet, which causes macrophages to initiate phagocytosis. [2] IMT is differentiated from other forms of thrombocytopaenia by the immune-mediated component of the condition. [3]
Immune thrombocytopenic purpura is a condition in which platelets are destroyed by an autoimmune process. Platelets are a component of blood that contribute to the formation of blood clots in the body to prevent bleeding. The syndrome was first described in 1951 by R. S. Evans and colleagues. [1]
Light transmission aggregometry is widely accepted as the gold standard diagnostic tool for assessing platelet function, and a result of absent aggregation with any agonist except ristocetin is highly specific for Glanzmann's thrombasthenia. [9] Following is a table comparing its result with other platelet aggregation disorders:
Aspergillosis* is a fungal disease that in dogs is caused primarily by Aspergillus fumigatus. Infection is usually in the nasal cavity. Typical signs in dogs include sneezing, nasal discharge, bleeding from the nose, and ulcerations of the nose. [23] Pythiosis is a disease caused by a water mould of the genus Pythium, P. insidiosum. It occurs ...
Unlike ITP, the platelet count in gestational thrombocytopenia rarely goes below 100,000, and a platelet count below 80,000 is even more rare (seen in less than 0.1% of cases of gestational thrombocytopenia). Also unlike ITP, gestational thrombocytopenia is not a cause of neonatal or maternal bleeding, or neonatal thrombocytopenia. [63]
Thrombotic thrombocytopenic purpura (TTP) initially presents with a range of symptoms that may include severe thrombocytopenia (platelet count usually < 30,000/mm³), microangiopathic hemolytic anemia (evidenced by schistocytes in the blood smear), and various clinical signs such as petechiae, purpura, neurologic symptoms, myocardial ischemia ...
Platelet storage pool deficiency is a family of clotting disorders characterized by deficient granules in platelets. Individuals with these disorders have too few or abnormally functioning alpha granules , delta granules , or both alpha and delta granules and are therefore unable to form effective clots, which leads to prolonged bleeding.
U46619 is a stable synthetic analog of the endoperoxide prostaglandin PGH 2 first prepared in 1975, [1] and acts as a thromboxane A 2 (TP) receptor agonist. It potently stimulates TP receptor-mediated, but not other prostaglandin receptor-mediated responses in various in vitro preparations and exhibits many properties similar to thromboxane A 2, including shape change and aggregation of ...