13-Haemostasis Flashcards
What type of heart injury can a partial artery occlusion cause?
NSTEMI - white thrombus in a coronary artery
Describe Virchow’s Triad
1-Rate of blood flow (replenishes and rebalances pro vs antithrombotic components). Stagnant=clot
2-Consistency of blood (natural imbalance between pro and anti-thrombotic components)
3-Vessel wall damage - exposes collagen and causes aggregation
Describe initiation of coagulation
TF helps 7a activate 10 to 10a, and 5 to 5a, forming the prothrombin complex
Prothrombin complex activates 2 (prothrombin) to 2a (thrombin), while antithrombin inhibits 2a
How do you treat initiation of coagulation and restore levels of anticoagulants?
Dabigatran - 2a inhibitor
Rivaroxaban - 10a inhibitor
Heparin - activates antithrombin 3 (AT-III)
LMWH (-parin) - Activates AT-III AND inhibits 10a
Warfarin - vitamin K antagonist, needed for factors 2, 7, 9 and 10
Explain step 2 - activation/aggregation of platelets
Thrombin binds to PAR receptor, activates platelets to change shape, become sticky
PAR -> rise in Ca2+
Ca2+ causes ADP release
ADP bind to P2Y12 receptors - liberates arachidonic acid
COX acts on AA to make thromboxane A2
Thromboxane upregulates GpIIb/IIIa receptor for platelet aggregation
Explain step 3 - propagation/generation of fibrin strands
Activated platelets causes large scale thrombin production
Thrombin cleaves fibrinogen to fibrin strands - stabilising clot
How do you treat NSTEMI?
Stop further occlusion
Clopidogrel - P2Y receptor (ADP receptor) antagonist
Aspirin - irreversibly inhibits COX (platelets only have COX-1, so stops thromboxane production)
Abciximab - blocks GpIIb/IIIa receptor for aggregation
What kind of heart injury does a full artery occusion cause?
STEMI?
How do you treat STEMI?
Stop platelet activation/aggregation
Anti-platelets, anticoagulants
Dissolve clot via thrombolytics
Streptokinase, tissue plasminogen activator
