Often referred to as ITP, Immune Thrombocytopenic Purpura is a type of blood clot that causes bruising and swelling of the skin. It can also lead to hemorrhaging and is usually treated with anticoagulant medication. The treatment for ITP can depend on the patient’s age and other factors.
Symptoms
Symptoms of immune thrombocytopenia are a result of the body’s immune system malfunctioning and destroying platelets. These are essential for clotting the blood. A lower platelet count can result in excessive bruising. In people with ITP, platelet levels are usually lower than ten thousand per microliter. A lower count can also lead to anemia. A platelet count below ten thousand per microliter can also affect a person’s menstrual cycle.
Immune thrombocytopenia is a rare disease. The cause is not clear. It is most common in young children. However, it can also occur in adults. Symptoms can include bloody stools, easy bruising, and gingival bleeding. A physician will perform a physical exam and review recent infections. If the condition is found to be due to an infection, treatment can be aggressive to relieve symptoms.
A smear of the peripheral blood is taken as a follow-up test to an abnormal CBC. It is used to measure the platelet count, and to identify any infections. It is also used to rule out other causes of the condition.
The symptoms of immune thrombocytopenia can include easy bruising, gingival bleeding, and hematuria. People with this condition are also prone to deep subcutaneous hematomas. Deep subcutaneous hematomas occur when there is moderate trauma to the area.
Some people with ITP also have bloody stools and nose bleeds. If you have these symptoms, you should see your doctor immediately. Your doctor may perform blood and urine tests to find the cause of the bleeding. Depending on the condition, you may also need to take medications. Some medications used in the treatment of this condition include cyclophosphamide, IVIG, and prednisone.
Immune Thrombocytopenia can be a lifelong condition. It usually affects women more than men. It can be caused by an autoimmune disease, infection, or neoplasm. Depending on the type of ITP, it can be treated using medications and lifestyle modifications.
Symptoms of immune thrombocytopenia can be severe and life-threatening. A person with ITP can develop intracranial hemorrhage, which is life-threatening. If you have any of the symptoms of immune thrombocytopenia, you should contact your doctor immediately.
Diagnosis
Thrombocytopenic purpura is a common hematological disease characterized by the presence of low circulating platelets. The clinical course of the disease may be acute or chronic. It may be autoimmune in nature, or it may result from viral infections.
The first and most important step in the diagnosis of thrombocytopenic purpura is to obtain a complete blood count. This is done to determine the total number of red blood cells, white blood cells, and platelets. If the count is less than 1000 per mm3, then thrombocytopenia is present. A smear of the peripheral blood may be used to examine platelets. It is essential to exclude other pathologies, such as myeloproliferative disorders, pseudo thrombocytopenia by ethylene-diamine-tetra-acetic acid (EDTA), and leukemia.
If the smear is positive for ITP, the diagnosis is made. It is then important to exclude other viral infections, lymphoproliferative disorders, and platelet deficiency due to other conditions.
A peripheral blood smear is the most common diagnostic method for immune thrombocytopenic purpura. The smear shows decreased numbers of platelets and immature leukocytes. The smear also shows normal-appearing neutrophils.
The second step in the diagnosis of immune thrombocytopenic purpura involves performing a bone marrow aspiration. This may be done for selected cases to exclude other pathologies, including myeloproliferative disorders, leukemia, and cytopenia. A bone marrow biopsy may be conducted for selected patients who have poor sensitivity to the first-line treatments.
The third step in the diagnosis of immune thrombocytopenic purpura involves using a peripheral blood smear to evaluate the platelet count and other blood cell counts. A peripheral blood smear is also used to follow up on patients who have an abnormal CBC. The smear may also be used to determine if there are concomitant medical conditions.
In some cases, the diagnosis of immune thrombocytopenic Purpura may be based on a peripheral blood film stained with Wright’s. This is especially important if the patient has signs or symptoms of immune thrombocytopenia. This test can also be used to determine the platelet size.
Treatment for immune thrombocytopenic purpura depends on the level of platelets. Patients with a low platelet count will not need treatment, whereas patients with a high platelet count will need medication.
Treatment
Typical treatment for immune thrombocytopenic purpura (ITP) includes intravenous immunoglobulin, splenectomy, and corticosteroids. However, these treatments may not work for some patients or may cause side effects. For example, steroids can cause acne, weight gain, and stomach irritation. This means that the decision to treat a patient should be based on the severity of symptoms, risk factors for bleeding, and patient preference.
A four-day course of high-dose oral dexamethasone is an effective first-line therapy for adult patients with immune thrombocytopenic purpura. However, the use of high-dose dexamethasone is controversial. It is also unclear whether patients with refractory ITP respond to high-dose therapy.
ITP is an autoimmune disease that causes the destruction of platelets by autoantibodies. These antibodies are produced by plasma B-cells in the bone marrow. They interact with liver and monocyte-macrophages and remove platelets from circulation. They are typically autoantibodies to glycoproteins expressed on megakaryocytes.
Platelet counts are usually low, resulting in an increased risk of bleeding. If the bleeding becomes severe, a platelet transfusion may be required. In addition, steroids are used to slow the destruction of platelets. They inhibit the CD8+ cytotoxic T-cell (CTL) killing of autoantibody-coated platelets and inhibit the hepatic cell clearance of desialylated platelets.
The diagnosis of ITP is based on the platelet count in the peripheral blood and other laboratory findings. A peripheral blood smear is used to check the platelet count and other types of blood cells. In addition, other blood and urine tests may be used to measure bleeding time.
Immune thrombocytopenic purpura may be a primary disease or may occur as part of a secondary illness. In most cases, treatment is not necessary. However, patients with chronic ITP may require a second course of therapy, or surgery may be necessary.
ITP can affect both children and adults. In adults, it is more common than in children. Chronic ITP is more common in women. Chronic ITP may last for years or even a lifetime. Typical symptoms include bruising at knee joints, elbow joints, or under the skin, which may be caused by movement or injury. Patients may experience fatigue and a decreased health-related quality of life.
Secondary hemostasis
Thrombocytopenic purpura (IPP) is an autoimmune disease that causes the destruction of platelets and thrombocytes. The clinical manifestations include purpura and bruising. A patient with IPP has a low platelet count and a normal prothrombin time (PTT). Symptoms of the disease usually improve within three to 10 days. However, in some cases the disease can progress to a more severe form, resulting in frequent mucosal bleeding.
In order to understand the pathogenesis of ITP, it is important to study the factors that are involved in hemostasis. There are several types of coagulation factors. Some are enzymatic while others are non-enzymatic. These factors are required to be activated before they can exert their cleavage activities. Activated coagulation factors will generate thrombin, phosphatidylserine, and Factor XI. These factors will then cleave fibrinogen into fibrin and stabilize a platelet plug. These coagulation factors have a complex interaction, which keeps the hemostatic balance in place.
Von Willebrand factor (VWF) plays an important role in primary hemostasis. VWF has multiple binding sites for platelet receptors. It also acts as a bridge for platelet adhesion. VWF is produced by endothelial cells and is found in plasma. VWF is important in primary hemostasis because it increases the plasma half-life and protects the activity of procoagulant factor VIII. It is also essential in secondary hemostasis because it provides a bridging molecule for platelet aggregation.
There are two types of VWF multimers: high molecular weight (HMWM) and low molecular weight (LMWM). HMWM multimers are high molecular weight and are more effective in collagen interaction. LMWM multimers are low molecular weight and are mainly effective in wound healing under shear stress.
The size of VWF multimers also affects their adhesive activity. VWF multimers range in size from 500 to over 10 000 kDa. ADAMTS13 regulates the size of VWF multimers. A deficiency of ADAMTS13 leads to an abnormal accumulation of UL-VWF multimers. These multimers may then be spontaneously aggregated and lead to thrombotic thrombocytopenic purpura.
In addition, there are certain factors that can inhibit the activation of coagulation factors. For example, antithrombin inhibits the activity of FVIIa. Other inhibitors include proteins C and S.
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