Other Disorders of Hemostasis Flashcards
Describe the mechanism of Heparin-Induced Thrombocytopenia
Heparin binds to platelet factor 4 (PF4) on surface of platelets. Body mounts IgG response against platelet complexes. Fragmented platelets may activate remaining platelets causing thrombosis.
What is Disseminated Intravascular Coagulation?
Pathologic activation of the coagulation cascade characterized by widespread microthrombi resulting in ischemia and infarction. Consumption of platelets and factors results in bleeding from mucosal surfaces and IVs.
What are common causes of DIC?
Obstetric complications (Tissue thromboplastin in amniotic fluid activates coagulation), Sepsis (E. Coli, N. meningitidis) - Endotoxins from bac wall and cytokines (TNF-Alpha, IL-1), Adenocarcinoma (Mucin activates coag), Acute promyelocytic leukemia (Primary granules activate coagulation), Rattle snake bites
What are the laboratory findings for DIC?
Decreased platelet count, Increased PT/PTT, Decreased Fibrinogen, Microangiopathic hemolytic anemia, elevated fibrin split products (particularly D Dimer)
From what is D-dimer derived and for deciding between what two diagnoses is it useful?
D-dimer is formed from the lysis of crosslinked fibrin. Presence of D-dimer and fibrin split products means that clots are being fibrinolysed. If fibrinogen split products are present without D-dimer, that indicates that there is an elevation of plasmin activity. Both plasmin hyperactivity and DIC present the same way.
Tx for DIC
Treat underlying cause then transfuse blood products and cryoprecipitate (coag factors)
What is fibrinolysis? Describe the mechanism of action.
Removal of thrombus after damaged vessel heals. Plasminogen is converted to plasmin by tissue Plasminogen Activator (tPA). Plasmin then cleaves fibrin and serum fibrinogen, destroys coag factors, and blocks platelet aggregation. Alpha2-antiplasmin inactivates plasmin.
Describe fibrinolysis pathology, name two associated scenarios and their mechanism of pathology.
Plasmin overactivity resulting in the excessive cleavage of serum fibrinogen. 1) Radical prostatectomy - release of urokinase which activates plasmin 2) Cirrhosis of the liver - reduced production of Alpha2-antiplasmin
How are DIC and plasmin hyperactivity the same? What is an important differentiating factor between these conditions?
They present the same. Increased PT/PTT, increased bleeding time. DIFFERENCE: Plasmin hyperactivity has increased fibrinogen split products without D-dimers whereas DIC shows fibrin split products and D-dimers
Tx for plasmin hyperactivity
Administer amino caproic acid which blocks activation of plasminogen
