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Glanzmann's thrombasthenia

Etiology: 1) low platelet glycoprotein IIb-IIIa complex 2) fibrinogen will not interlink Epidemiology: most common inherited disease of platelets Pathology: - congenital platelet defects - inability of this integrin alpha-2b to recognize macromolecular or synthetic peptide ligands - type 1: platelets show absence of the glycoprotein IIb/beta-3 complexes at their surface & lack fibrinogen & clot retraction capability - type 2: platelets express the glycoprotein IIb/beta-3 complex at diminishedlevels (5-20% controls), have detectable amounts of fibrinogen, & have low or moderate clot retraction capability - normal or near normal (60-100%) expression of dysfunctional receptors Genetics: - autosomal recessive - associated with defects in ITGA2B (CD41) Clinical manifestations: 1) early hemorrhagic complications in the neonatal period 2) hemorrhagic events perists throughout life a) epistaxis b) purpura c) petechiae d) ecchymoses Laboratory: 1) complete blood count (CBC) - platelet count is normal 2) peripheral blood smear a) normal platelet morphology b) no clumping of platelets 3) platelet aggregation a) defect in the 1st phase of platelet aggregation with: ADP, epinephrine, thrombin or collagen b) normal platelet aggregation with ristocetin cofactor Management: 1) nasal packing & other local hemorrhage control measures 2) when local hemorrhage control measures fail - epsilon-aminocaproic acid [2] - recombinant factor VIIa or platelet transfusion [2] - cryoprecipitate with or without platelets

Related

glycoprotein IIB/IIIA

General

platelet disorder; thromboasthenia

References

  1. Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 439
  2. Medical Knowledge Self Assessment Program (MKSAP) 11, 17, 18. American College of Physicians, Philadelphia 1998, 2015, 2018
  3. UniProt :accession P08514