Co-agulation 2 Flashcards
• What 4 VTE disorder do we need to know about?
- Deep vein thrombosis
- Pulmonary embolism
- Factor V Leiden
- Antiphospholipid syndrome
which one is most common?
- Deep vein thrombosis (60% of VTE)
2. Pulmonary embolism (30% of VTE)
Deep vein thrombosis, DVT
Initial investigations?
when does d-dimer increase?
Management?
- Well’s score (if >1 – DVT likely, do Doppler USS).
(if <1, - D dimer test and Doppler USS if recommended).
- D-dimer ⇑ (as it’s a protein product of clot breakdown)
- Immediate rivaroxaban
- Long term anticoagulation
Pulmonary embolus, PE
Investigations?
- ECG?
- ABG?
- CXR?
- D-dimer?
- diagnostic imaging?
- mx?
- ECG (you’ll find evidence of R heart strain + tachycardic)
- Blood gasses (low sats)
- CXR (can sometimes see wedge infarcts)
- D-dimer ⇑
- CT pulmonary angiogram (CTPA) = definitive diagnostic imaging
- Immediate rivaroxaban (see later)
- Long term anticoagulation
• What were the 2010 NICE reccomdations regarding VTE prevention?
noted that 25,000 died every year due to hospital acquired VTE (just because they were lying in bed immobile). NICE recommended that all patients at risk of VTE should mobilise early and given thromboprophylaxis (enoxaparin, LMWH).
• What are the risk factors for acquiring DVT/PE?
- Immobility (as venous stasis ⇑ risk of clot formation)
- Trauma/surgery (as clotting factors are upregulated)
- Pregnancy
- Oestrogen therapy (COCP or HRT)
- Inflammatory disease
- Malignancy
- Antiphospholipid syndrome (see below)
- Genetic risk factors (DVT risk runs in the family but is usually a complex trait):
i. Factor V Leiden
- What is Factor V Leiden?
* Why don’t we test for Factor V Leiden and treat those with it prophylactically?
Factor V gene (F5), which reduces inactivation of Factor V by activated protein C, which makes you 4x more likely to develop a VTE.
many other genetic components to VTE so it doesn’t really matter if you have it or not. Therefore, being Factor V Leiden negative doesn’t mean you are at reduced risk of VTE
• What is antiphospholipid syndrome?
Antibodies do you find ?
Autoimmune
generate antibodies to phospholipids on blood cells like platelets – > activates them –> prothrombotic
Anti-cardiolipin + lupus anticoagulant
• What is weird about lupus anticoagulant antiphospholipid antibodies?
They interfere with the lab testing and so you actually get a long aPTT! (So it’s a pro-thrombotic condition where you get a long aPTT which usually means it’s a coagulation problem…weird)
• What is antiphospholipid syndrome often associated with?
Connective tissue disorders (e.g. SLE)
• What are the clinical features of antiphospholipid syndrome?
Mx?
DVT/PE
Livedo reticularis (net like skin rash)
thrombocytopenia
pregnancy loss
- Anti-coagulation and thromboprophylaxis.
• What are the types of anti-thrombotic drugs?
- Antiplatelets?
- Anticoagulants?
- Inhibits platelet activation and aggregation
- Important in treat/prevent arterial thrombosis (ACS, PVD, CVD)
- Aspirin, clopidogrel, abciximab
- Inhibits coagulation pathway (i.e. production of thrombin)
- Important in venous thrombosis or low pressure thrombosis (DVT, PE
- Warfarin, unfractionated heparin LMWH, rivaroxaban
• What are the contraindications of giving anti-coagulants?
- Renal impairment
- Previous life threatening bleeding
- On anti-platelet drugs
- Age >75, frequent falls, low body weight
• What are the general rules for peri-operative management of anticoagulation?
when do you take them off warfarin?
BRIDGING THERAPY:
- LOW RISK
- HIGH RISK
- VERY HIGH RISK
- INR goal?
o Take patient off anticoagulation/warfarin 4 days before surgery
o Treat with bridging therapy according to risk of thrombosis:
- Low = no bridging therapy
- High risk = prophylactic dose of bridging therapy (40mg enoxaparin/day)
- Very high risk = treatment dose of bridging therapy (1mg/kg, twice a day)
o Check INR on day of surgery, if it is <1.5 the surgery can go ahead.
Aspirin
- how does it work:
- COX1 inhibitor?
- COX2 inhibitor?
- Inhibiting COX2 has anti-inflammatory effects
- Inhibiting COX1 blocks the formation of thromboxane A2, producing an inhibitory effect on platelet aggregation
Clopidogrel
inhibits which ADP receptor?
- Inhibits P2Y12, an ADP receptor responsible for the activation of platelets
