coags Flashcards
What initiates thrombogenesis?
Vascular injury exposing collagen and von Willebrand factor (vWF).
What platelet receptors bind to collagen and vWF?
GP Ia binds collagen; GP Ib binds vWF.
What happens when platelets adhere during thrombogenesis?
Platelets activate and release ADP, TXA₂, and 5-HT.
What is the role of ADP in thrombogenesis?
ADP enhances platelet aggregation.
What is the role of TXA₂ in thrombogenesis?
TXA₂ enhances platelet aggregation.
How does serotonin (5-HT) aid thrombogenesis?
It promotes vasoconstriction, reducing blood flow.
How do platelets form a plug in thrombogenesis?
Fibrinogen binds to GP IIb/IIIa receptors on platelets.
What stabilizes the platelet plug in thrombogenesis?
Thrombin converts fibrinogen to fibrin.
What is the role of prostacyclin (PGI₂) in thrombogenesis?
It inhibits platelet aggregation in uninjured areas.
What activates the intrinsic coagulation pathway?
Collagen exposure.
Outline the steps in the intrinsic coagulation pathway.
Factor XII → XIIa → XI → XIa → IX → IXa (+ Factor VIII and Ca²⁺) → X.
What activates the extrinsic coagulation pathway?
Tissue damage.
Outline the steps in the extrinsic coagulation pathway.
Tissue factor (TF) + Factor VII → VIIa → Factor X.
What are the steps in the common coagulation pathway?
Factor X → Xa (+ Factor V and Ca²⁺) → Prothrombin → Thrombin → Fibrinogen → Fibrin (+ Factor XIII) → Stable clot.
What are the causes of DVT?
Stasis (immobility), hypercoagulability, and endothelial injury.
How do white thrombi form?
In high-pressure arteries, mainly composed of platelets and fibrin.
How do red thrombi form?
In low-pressure veins, with red cells around a fibrin-platelet core.
What is the danger of red thrombi?
Their ‘tail’ can detach and cause embolism.
What are the inherited risk factors for DVT?
Antithrombin III deficiency, protein C/S deficiency, sickle cell anemia, activated protein C resistance.
What are acquired risk factors for DVT?
Bedridden, surgery/trauma, obesity, estrogen use, malignancies, chronic venous insufficiency.
What is DIC?
Disseminated intravascular coagulation involves overstimulation of clotting, leading to excessive clot formation and bleeding.
What causes DIC?
Massive tissue injury, malignancy, and sepsis.
How is DIC treated?
Plasma transfusion and addressing the underlying cause.
What is HIT?
Heparin-induced thrombocytopenia, an immune response to heparin causing low platelets.
How is HIT treated?
Discontinuing heparin and possibly using alternative anticoagulants.
What is TTP?
Thrombotic thrombocytopenic purpura, involving widespread platelet aggregation and microvascular clots.
How is TTP treated?
Plasma exchange therapy.
Outline the steps in fibrinolysis.
t-PA, urokinase, or streptokinase bind plasminogen → convert to plasmin → break fibrin into degradation products (e.g., D-dimers).
What are examples of anticoagulants?
Warfarin, heparin, hirrudin, argatroban, apixoban
What are examples of antiplatelet drugs?
Aspirin, clopidogrel, abcuximab
What are examples of thrombolytics?
Streptokinase, urokinase.
What are examples of hemostatic/antifibrinolytic drugs?
Aminocaproic acid, tranexamic acid.
How do indirect thrombin inhibitors work?
Heparin and LMWH enhance antithrombin activity, inactivating thrombin and Factor Xa.
How do direct thrombin inhibitors work?
Bind directly to thrombin’s active sites, inhibiting thrombin without needing antithrombin.
What are the differences between HMW, LMW, and fondaparinux heparins?
HMW: Broad activity, less specific for Factor Xa. LMW: More specific for Factor Xa, fewer side effects. Fondaparinux: Synthetic, selectively inhibits Factor Xa, useful in HIT patients.
What are the toxicities of HMW heparin?
Bleeding and thrombocytopenia.
What are contraindications for HMW heparin use?
Active bleeding, hemophilia, severe hypertension, intracranial hemorrhage, TB, hepatic disease.
How is HMW heparin toxicity treated?
Discontinue heparin and use protamine sulfate for reversal. Protamine is a positive charge and heparin is negative so it binds to it and inactivates it.
What does prothrombin time (PT) assess?
The extrinsic and common coagulation pathways.
What is the normal INR range?
0.8–1.2.
What does aPTT assess?
The intrinsic and common coagulation pathways.
What is the normal aPTT range?
35–45 seconds.
How does warfarin work?
It blocks vitamin K recycling, reducing clotting factor synthesis.
What are treatment considerations for warfarin?
Monitor INR and adjust dose to balance efficacy and bleeding risk.
What are some non-warfarin anticoagulants?
Factor Xa inhibitors: Apixaban, rivaroxaban. Direct thrombin inhibitors: Dabigatran.
What are fibrinolytic drugs, and how do they work?
Streptokinase, urokinase, and tPA activate plasminogen to plasmin, breaking down fibrin clots.
