Heme/Onc Flashcards
What is PT?
Prothrombin Time - measures the integrity of the extrinsic & common pathways of coagulation with factors 7, 10, 5, prothrombin, and fibrinogen
What is aPTT?
activated Partial Thromboplastin Time - measures the integrity of the intrinsic & common pathways of coagulation including high-molecular weight kininogen, prekallikrein, factors 12, 11, 9, 8, 10, 5, prothrombin, and fibrinogen.
Implications of prolonged PT or aPTT?
Deficiency in one or more coagulation factors, or presence of an inhibitor (such an antibody to one or more components). This is distinguished with a mixing study of 1:1 to patient’s plasma and normal plasma. Normalizes with deficiency, stays the same with inhibitor. Deficiency should measure each level, and inhibitor consider lupus anticoagulant, etc.
Difference between arterial and venous thrombosis
Arterial is in the absence of apparent risk factors and more likely related to vasculitis, myeloproliferative disorders, hyperhomocysteinemia, antiphospholipid syndrome, etc.
VTE - more likely to be secondary to mixture of risk factors + inherited hypercoagulability
Characteristics of patients with platelet vascular disorders
- Superficial surfaces
- Petechiae, ecchymoses
- Mucous membranes include oral, nasal, GI, GU
- Bleeding onset is likely spontaneous or after trauma
- Examples: thrombocytopenia, functional platelet disorder, vascular fragility, DIC, liver disease
Characteristics of patients with coagulation factor deficiency
- Involves deep tissues with hematomas
- Does not involve mucous membranes
- Likely also have joint, muscle retroperitoneal involvement
- Bleeding is delayed after trauma
- Examples: inherited coagulation factor deficiency, hemophilia, acquired inhibitor, anticoagulation, DIC, liver disease
What characteristics lead to malignancy as part of the differential for VTE?
If the thromboembolism is migratory, superficial thrombophlebitis (Trousseau’s syndrome), non-bacterial thrombotic endocarditis, hepatic vein thrombosis (Budd-Chiari), portal-vein thrombosis, and paroxysmal nocturnal hemoglobinuria.
Which product is associated with pseudothrombocytopenia?
EDTA - ethylenediaminetetraacetic acid - causes platelets to accumulate with the sample and cause a reduction in platelet count. (Also happens at cool temperatures).
Three mechanisms for thrombocytopenia
1 - destruction
2 - lack of production
3 - sequestration
Characteristics of platelet destruction
- rapid onset (such as during hospitalization)
- may be non-immune or immune
- Nonimmune : sepsis, DIC< TTP, HUS, pre-eclampsia/eclampsia, CABG, giant cavernous hemangioma
- Immune : drugs, alloimmune sensitization, or autoimmunity
- Platelet transfusion rarely necessary for non-immune, however may be needed in immune cases
- Treat underlying cause
Thrombocytopenia associated with thrombosis?
TTP, HUS, HIT, DIC, PNH, vasculitis, antiphospholipid syndrome
Medications associated with thrombocytopenia
- quinine
- quinidine
- sulfonamides
- gold salts
Characteristics of decreased platelet production
Associated with primary disease of bone marrow such as acute leukemia, aplastic anemia, metastatic carcinoma, fibrosis, other clonal hematopoietic disorder, chemotherapy/radiation therapy, Etoh, HIV, CMV, EBV, varicella
How much does a platelet transfusion change platelet count?
1 Unit should change platelet count by 10-12,000
What is the PLADO trial?
Platelet Dose trial - multicenter. Randomized to receive low, med, high dose platelets while recovering from hematopoietic stem cell transplantation. Low dose received transfusion more frequently, however notably less transfusions overall. With the same bleeding complications across all groups.
What are some of the risks associated with platelet transfusion?
- Allo-immunization - prompting a patient to become refractory to platelet transfusion in the future.
- Bacterial contamination of stored platelets is more common compared to RBC transfusions due to being temperature sensitive and stored at room temperature.
- Short life span - typically only 5-7 days
