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Resident/Fellow Levels of Training as Defined by Specialty. Residents PGY-2. PGY-3 and beyond. Emergency medicine subspecialties. None. None. All.

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1. Percentage = CGPA X 10.
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TTP is a serious disease in which small clots can cause problems in the blood vessels and impair oxygenation to vital organs. TTP is characterized by purpura, anemia, and possibly renal failure. There are two forms of TTP: the acquired form, which is acquired during life as a result of infections, or the inherited form, which is due to a genetic defect. The symptoms are the same in both cases, but the circumstances and age of onset change.

ITP is a blood disorder in which there is a flare of autoantibodies, which can cause a range of symptoms.

Severe and life-threatening bleeding can occur in patients with few or no symptoms. There is no known reason for the formation of the antibodies. ITP occurs in children after a viral infection. In children, the disease can be cured in a few weeks.

In 1/3 of the cases, it lasts more than a year, as it becomes chronic in adults. When TTP or ITP is suspected, treatment is immediately instituted to ensure the safety of patients.

The first goal of treatment is to raise the platelet count to a normal level. Low levels of platelets can be fatal. The treatment aims to improve the symptoms.

The recommended drugs for the treatment of ITP are steroids. The doctor can gradually stop the platelet count once they return to normal. Corticosteroids are not recommended for long-term use because of their side effects. In the second line, immunoglobulins are prescribed.

They are prescribed in case of bleeding or when it is necessary to rapidly increase platelet levels before an operation, since their effect is immediate. elmiplostim and eltrombopag are drugs that increase the production of platelets. The production of platelets by the bone marrow is regulated by the production of thrombopoietin. rituximab is also recommended.

Rituximab works by suppressing the immune system. The patient may be prone to infections due to its immunosuppressive mechanism. The removal of the spleen may be proposed. It is the main organ where cells called macrophages destroy platelets, and it is also the main organ where the antibodies that destroy platelets are made.

The first-line treatment for TTP is the use of a blood product. The latter is used to remove the ADAMTS13 enzyme that is responsible for regulating platelet aggregation and reintroduce the functional enzyme.

In some cases, the ADAMTS13 protease can be removed and a functional ADAMTS13 protein reintroduced with the use of plasmapheresis. There is a prescription for corticosteroids for patients to increase their levels of platelets. Rituximab can be used to prevent the production of antibodies against the ADAMTS13 protease. Caplacizumab is approved for the treatment of TTP. It is usually proposed for acquired TTP.

Symptomatic and supportive treatments are available.

Current standard treatments and rapid diagnosis have an excellent prognosis. In the case of TTP, patients may experience relapses. Neurological disorders can affect the quality of life for patients. The work888-607-888-607-3166 is being done at an international level to better understand the mechanisms and causes of resistance to the various currently available treatments in order to develop new molecule and therapies.

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