1/47
A collection of vocabulary flashcards covering coagulopathies, the coagulation cascade, hematologic disorders, and blood transfusion management for anesthetic practice.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai | Chat |
|---|
No analytics yet
Send a link to your students to track their progress
Tunica Intima
The layer of blood vessels made up of endothelial cells that produce procoagulants, anticoagulants, mediators, and fibrinolytics, acting as a barrier between blood and the vessel.
Von Willebrand factor (vWF)
A mediator that acts as a cofactor for the coagulation cascade.
Tissue factor (TF)
Also known as factor 3, it activates the clotting cascade pathway during vessel injury.
Thromboxane A2 and Adenosine Diphosphate (ADP)
Mediators that cause vasoconstriction of blood vessels and promote platelet activation during hemostasis.
Nitric oxide (NO)
A mediator that inhibits platelet adhesion and aggregation while promoting smooth-muscle relaxation and vasodilation.
Prostacyclin
A mediator that promotes vasodilation and interferes with platelet formation and aggregation.
Collagen
A substance that stimulates platelet attachment to the injured vessel wall when the endothelial layer is damaged.
Fibronectin
A mediator that facilitates anchoring of fibrin during the formation of a hemostatic plug.
Primary Hemostasis
The process of forming a platelet plug, involving three steps: adhesion, activation, and aggregation.
Adhesion
The step in primary hemostasis where Von Willebrand Factor (vWF) binds to GpIb receptors on platelets to anchor them to the sub-endothelium.
Von Willebrand Disease
A condition caused by decreased, absent, or dysfunctional vWF, often leading to reduced factor 8, increased PTT, and increased bleeding time.
Desmopressin
The treatment of choice for type 1 Von Willebrand disease that causes the body to release more vWF.
Activation (Platelets)
The process where platelets bind to collagen and release thromboxane A2 and ADP to activate other platelets.
Aggregation
The step in primary hemostasis where activated platelets use GpIIIa and GpIIb receptors to bind to fibrinogen and form a platelet plug.
Bleeding Time
A measure of platelet function based on the time required to form a plug, normally up to 10minutes.
Normal Platelet Count
Typically between 150,000 and 300,000/mm3.
Secondary Hemostasis
The coagulation cascade consisting of the extrinsic and intrinsic pathways that converge on a final common pathway leading to fibrin formation.
Extrinsic Pathway
A coagulation pathway activated by tissue factor (outside the vessel) and calcium, measured by PT and INR.
Prothrombin Time (PT)
A measure of the extrinsic pathway; normal is approximately 12−14seconds.
International Normalized Ratio (INR)
A standardized measure of the extrinsic pathway; normal is less than 1.1 (or 2−3 for patients on Warfarin).
Warfarin
An anticoagulant that inhibits vitamin K activation and prevents clotting factors II, VII, IX, and X; reversed by Vitamin K or FFP.
Intrinsic Pathway
A coagulation pathway activated by internal vessel damage and factor 12 (Hageman factor); measured by PTT and ACT.
Heparin
An anticoagulant that binds to antithrombin to block thrombin and factors 2 and 9-12; it is reversed by protamine.
Heparin Induced Thrombocytopenia (HIT) Type II
An immune response involving IgG antibodies that activate platelets, causing a hypercoagulable state and a fall in platelet count.
C-serotonin Release Assay
The gold standard diagnostic test for Heparin Induced Thrombocytopenia (HIT).
aPTT (Activated Partial Thromboplastin Time)
A measure of the intrinsic pathway typically around 30seconds; it increases by 2 times with heparin use.
ACT (Activated Clotting Time)
A test typically used intraoperatively to adjust heparin doses, with a normal range of 100−120seconds.
Final Common Pathway
The pathway starting with factor 10 that converts factor 2 (prothrombin) into thrombin and factor 1 (fibrinogen) into fibrin.
Prothrombin Activator
A complex formed by activated factor 10, factor 5, and factor 4 that converts prothrombin into thrombin.
Initiation Phase
The first phase of the cell-based coagulation cascade where injury causes tissue factor to activate factor 7 and factor 10.
Amplification Phase
The second phase where a small amount of thrombin activates platelets and factors 5 and 9 to increase thrombin production.
Propagation Phase
The final phase of the cell-based cascade where large amounts of thrombin lead to the formation of a secondary hemostatic plug.
Fibrinolysis
The breakdown of a fibrin clot by plasmin.
Plasmin
The enzyme responsible for breaking down fibrin clots, activated from plasminogen by tissue plasminogen activator (tPA) or urokinase.
Protein C and S
Anticoagulants that inhibit factors 3, 5, and 8; Protein S augments the effect of Protein C.
Hemophilia A
An X-linked deficiency of factor 8 causing increased PTT; preferred treatment is cryoprecipitate or factor 8 concentrate.
Hemophilia B
A deficiency of factor 9 (Christmas factor) causing prolonged PTT; treated with factor 9 replacement or FFP.
Sickle Cell Disease
A condition with altered HgbS causing RBCs to become lodged in small spaces; triggers include hypoxia, hypothermia, and acidosis.
Disseminated Intravascular Coagulation (DIC)
A state where systemic coagulation causes micro-clots, depletion of clotting factors and platelets, and eventual hemorrhage; characterized by increased D-Dimer.
Anemia
A condition where the body has insufficient red blood cells to carry oxygen, most commonly caused by iron deficiency.
Platelet Transfusion
Indicated when counts are below 50,000/mm3; one unit increases platelets by 5,000−10,000.
Fresh Frozen Plasma (FFP)
Contains all clotting factors; used for PT/PTT above 1.5 times normal or to reverse warfarin.
Cryoprecipitate
A blood product containing fibrinogen, factor 8, factor 13, vWF, and fibronectin.
Packed Red Blood Cells (PRBC)
One unit raises hemoglobin by 1g/dL or hematocrit by 3%.
Febrile Non-Hemolytic Reaction
The most common transfusion reaction, caused by recipient antibodies interacting with donor leukocytes or platelets.
Hemolytic Reaction
A severe reaction occurring when the wrong blood type is given, characterized by dyspnea, lumbar pain, and hemoglobinuria.
TRALI (Transfusion Related Acute Lung Injury)
Pulmonary edema caused by donor leukocyte antigens injuring the lung capillary membrane.
TACO (Transfusion Associated Circulatory Overload)
Pulmonary edema due to fluid volume overload exceeding the heart's pumping capacity.