Immune thrombocytopenia

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Immune thrombocytopenia

BIIC

BIIC

Thymus histology
Spleen histology
Lymph node histology
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Blood histology
Blood components
Blood groups and transfusions
Platelet plug formation (primary hemostasis)
Coagulation (secondary hemostasis)
Role of Vitamin K in coagulation
Clot retraction and fibrinolysis
von Hippel-Lindau disease
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Pyruvate kinase deficiency
Hereditary spherocytosis
Beta-thalassemia
Alpha-thalassemia
Iron deficiency anemia
Anemia of chronic disease
Sickle cell disease (NORD)
Erythropoietin
Hemophilia
Vitamin K deficiency
Von Willebrand disease
Sideroblastic anemia
Autoimmune hemolytic anemia
Paroxysmal nocturnal hemoglobinuria
Aplastic anemia
Fanconi anemia
Folate (Vitamin B9) deficiency
Vitamin B12 deficiency
Megaloblastic anemia
Diamond-Blackfan anemia
Lead poisoning
Bernard-Soulier syndrome
Hemolytic-uremic syndrome
Thrombotic thrombocytopenic purpura
Immune thrombocytopenia
Glanzmann's thrombasthenia
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Antithrombin III deficiency
Protein C deficiency
Antiphospholipid syndrome
Factor V Leiden
Protein S deficiency
Polycythemia vera (NORD)
Mixed platelet and coagulation disorders: Pathology review
Coagulation disorders: Pathology review
Macrocytic anemia: Pathology review
Intrinsic hemolytic normocytic anemia: Pathology review
Microcytic anemia: Pathology review
Non-hemolytic normocytic anemia: Pathology review
Extrinsic hemolytic normocytic anemia: Pathology review
Heme synthesis disorders: Pathology review
Platelet disorders: Pathology review
Thrombosis syndromes (hypercoagulability): Pathology review
Myeloproliferative disorders: Pathology review
Anticoagulants: Heparin
Anticoagulants: Warfarin
Thrombolytics
Hematopoietic medications
Protein synthesis inhibitors: Tetracyclines
DNA synthesis inhibitors: Fluoroquinolones
Cell wall synthesis inhibitors: Cephalosporins
Cell wall synthesis inhibitors: Penicillins
Protein synthesis inhibitors: Aminoglycosides
Yellow fever virus
Dengue virus
Ebola virus
Hantavirus
Salmonella typhi (typhoid fever)
Yersinia pestis (Plague)
Borrelia burgdorferi (Lyme disease)
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Coxiella burnetii (Q fever)
Ehrlichia and Anaplasma
Hodgkin lymphoma
Non-Hodgkin lymphoma
Chronic leukemia
Acute leukemia
Myelodysplastic syndromes
Myelofibrosis (NORD)
Essential thrombocythemia (NORD)
Multiple myeloma
Waldenstrom macroglobulinemia
Leukemias: Pathology review
Lymphomas: Pathology review
Plasma cell disorders: Pathology review
Ribonucleotide reductase inhibitors
Topoisomerase inhibitors
Platinum containing medications
Anti-tumor antibiotics
Microtubule inhibitors
DNA alkylating medications
Monoclonal antibodies
Antimetabolites for cancer treatment
HIV and AIDS: Pathology review
HIV (AIDS)
Integrase and entry inhibitors
Protease inhibitors
Nucleoside reverse transcriptase inhibitors (NRTIs)
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

Transcript

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Immune thrombocytopenic purpura or ITP is an autoimmune condition in which the body produces antibodies against its own thrombocytes or platelets, which are destroyed. And this result in purpura, or small bleeding spots beneath the skin.

Normally, when there’s any kind of damage to the blood vessel, hemostasis occurs, which is the process that stops the bleeding and plugs the damaged vessel to limit the blood loss.

And there are two steps: primary and secondary hemostasis. During primary hemostasis, platelets aggregate to form a plug at the site of an injured blood vessel.

Platelet aggregation is mediated by surface proteins found on platelets, called GP2B3A receptors. While these platelets are aggregating, secondary hemostasis kicks in.

Secondary hemostasis is also called coagulation, because that’s when clotting factors come into play one after another, with a view to cleaving fibrinogen into fibrin.

Then, fibrin forms a protein mesh, kinda like a giant net that covers the platelet plug and stabilizes it.

Now, in ITP, the spleen produces certain IgG autoantibodies which bind to the platelet receptor Gp2B3A, and target the platelet-antibody complexes for destruction in the spleen.

This leads to lowering of platelet counts in the blood, which makes it harder for bleeding to stop. Now, ITP can be acute or chronic.

Acute ITP usually affects children, a couple of weeks after a viral infection, and resolves spontaneously within two months.

Chronic ITP usually affect females of reproductive age, and persist more than six months. Chronic ITP can also be primary, when it occurs without an underlying trigger, or secondary, when it’s triggered by another condition like hepatitis C, HIV, or lupus.

Most of the time, ITP is asymptomatic. In some cases, it can cause purpura, which are red or purple spots on the skin, measuring 0.3 to 1 cm in diameter.

In severe cases of ITP, when platelet levels get very low, there may be frequent mucosal bleeding, which most commonly presents as epistaxis, meaning nose bleeds.

Sources

  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  3. "Harrison's Principles of Internal Medicine" McGraw-Hill (2004)
  4. "Purpura thrombopénique immunologique [Immune thrombocytopenic purpura]" Rev Prat (2019)
  5. "Immune Thrombocytopenic Purpura" New England Journal of Medicine (2002)
  6. "[TREATMENT OF IMMUNE THROMBOCYTOPENIC PURPURA IN ADULTS: UPDATE]" Harefuah (2019)