Wk 6 Anticoagulants & Atrial Fibrillation Flashcards
Describe the three stages of haemostasis
Vascular spasm - vasoconstriction
Platelet aggregation - plug formation
Coagulation - clot formation
Anticoagulant targets:
i. Deep venous thrombosis (DVT)
ii. Prophylaxis for venous thromboembolism
iii. Pulmonary embolism (PE)
iv. Atrial fibrillation (AF)
- Thrombus:宅着附着血管壁
- Embolus:旅行
- Thromboxane:缩血管《。》
- Prostacyclin:开血管《O》
Explain how low dose aspirin exerts its antiplatelet effect
MOA: inhibits platelet coagulation by ↓ the production of thromboxane A2 (COX1 → TXA2)
Understand the difference between a thrombus and an embolus
o Thrombus — a clot that forms in a vessel and remains there
o Embolus — a clot that forms in one location and travels to another
Discuss the mechanism of action of Heparin
MOA: combined with antithrombin III to promote its effect of inhibiting thrombus formation
NP: prophylaxis of VTE for surgical PT, treatment for MI
CON: platelet depletion, hepatorenal impairment
AEs: bleeding/bruising, hyperkalemia (heparin inhibits aldosterone), platelet depletion
Discuss the mechanism of action of Warfarin
Drug class: anticoagulants
MOA: inhibits the synthesis of Vit K and Vit K dependent clotting factors
NP:
- monitor INR (international normalised ratio) to be within 2~3
- keep a normal diet and steady intake of Vit K
CON: alcoholism (affect warfarin effects), platelet depletion, surgery/pregancy
AEs: bleeding
Discuss the mechanism of action of DOACs
DOACs - direct oral anticoagulants
Benefits: fast onset (30 mins), convenient with no ongoing monitoring
Dabigatran
MOA: inhibits the action of thrombin in converting the fibrinogen to fibrin, and thus ↓ clot formation
CON:
- risk of bleeding, ie haemorrhagic stroke
- hepatorenal impairment
- AF/heart valve disease
AEs: gastritis, dyspepsia, GI bleeding
Factor Xa Inhibitor MOA: selectively inhibit factor Xa, and inhibit conversion of fibrinogen to fibrin → ↓thrombus development. Apixaban CON: - risk of bleeding, ie haemorrhagic stroke - hepatorenal impairment - AF/heart valve disease AEs: nausea, platelet depletion
Rivaroxaban CON: - risk of bleeding, ie haemorrhagic stroke - hepatorenal impairment - AF/heart valve disease AEs: nausea, platelet depletion
Discuss the monitoring required with anticoagulant therapy
- watch for the warning signs of bleeding, ie bruising, dark urine
- monitor INR, target 2~3
Be aware of the major drug interactions which may occur with anticoagulant therapy
Warfarin drug interaction:
- NSAIDs, ie aspirin, ibuprofen
- SSRIs
- paracetamol
- statins
- St John’s wort
- garlic/cranberries/alcohol
Avoid a low vitamin K diet – eat a normal, balanced diet
Dabigatran, Rivaroxaban, Apixaban: less drug interactions than warfarin
Describe atrial fibrillation, discuss its treatment options and explain why it may lead to ischaemic stroke
Def.: a heart dysrhythmia in which the heart beats irregularly (atrium quivers)
Treatment:
- Rhythm control: use ‘Atrial Fibrillation Ablation’ method to reverse AF to sinus rhythm
- Rate control: using drugs to slow the conduction rate of AV node
> BB: atenolol, AE hypotension
> CCB: verapamil, AE bradycardia, hypotension
> Digoxin: impede Na+/Ca++ pump, cause Ca++retention, AE bradycardia
Risk of IS:
- clots/thrombus formed in the atrium (always left-sided atrium)
- every person with rate control AF must be on an anticoagulant e.g. warfarin or a DOAC to stop the clotting that happens in AF
What is the stroke risk assessment in people with non-valvular AF?
CHA2DS2-VASc score: 1 - congestive HF/or history 1 - HTN 1 - > 75 y/o 1 - DM 2 - stroke or transient IS history
0 means “low risk”, 1 means “moderate risk”, >1 means “high risk”