thrombosis Flashcards
1
Q
name 4 deep veins? 4
A
- iliac vein
- femoral vein
- popliteal vein
- tibial vein
2
Q
what is virchow’s triad and what does it show?
A
- factors clinically important in the development of a thrombosis
- circulatory stasis
- endothelial injury
- hypercoagulable state
3
Q
what are the thrombotic risk factors? 8
A
- post-operative, especially orthopaedic
- hospitalisation
- cancer
- pregnancy
- OCP (oral contraceptive pill)
- long-haul flights
- obesity
- intravenous drug abuse
4
Q
how can DVT be presented? 4
A
- can be clinically silent (no symptoms)
- unilateral calf swelling/ heat/ pain/redness/ hardness
- differential diagnosis= cellulitis, bakers cyst, muscular pain
- potentially fatal if missed
5
Q
what is the investigation of choice for DVT? 4
A
- doppler ultrasound
- ultrasound transducer produces a real-time two dimensional image of soft tissue structure
- colour duplex shows velocity and direction of blood flow
- veins are non-compressible by probe
6
Q
what is the D-dimer test? 4
A
- likelihood of having a DVT can be assessed using the Wells risk score and doing a D-dimer test
- indicate activation of the clotting cascade
- low Wells score and negative D-dimer test have a high negative predictive value
- if high wells score or positive D-dimer then proceed to ultrasound scan to confirm DVT
7
Q
what is initial treatment for above the knee DVT? 3
A
- therapeutic anticoagulation using sub-cut LMW (low molecular weight) heparin (anti-coagulant)
- dose of LMW heparin according to patient’s weight
- no monitoring required
8
Q
what happens when we switch patients to warfarin? 6
A
- load patient with oral warfarin for 3-5 days
- stop LMV heparin once INR (internationalised normal ratio) is lower than 2 for 2 days
- 1st DVT= anticoagulation for 6 months
- 2nd DVT/ PE= lifelong anticoagulation
- want to maintain INR between 2 and 3
- monitor INR every 3 weeks
9
Q
describe the clinical spectrum of Pulmonary Embolism? 8
A
- micro-emboli= asymptomatic
- pleuritic pain
- dyspnoea
- haemoptysis
- massive PE= syncope, death
- tachycardia
- tachypnoea
- hypotension
10
Q
what is a CTPA scan?
A
CT pulmonary angiogram
11
Q
what does a V/Q scan for PE show? 2
A
- underperfusion~ V/Q mismatch
- limitation= underlying lung disease
12
Q
what does an ECG for pulmonary embolism show? 4
A
- sinus tachycardia
- atrial fibrillation
- right heart strain (RBBB)
- classic SI, QIII, TIII (rare)
13
Q
what does a CXR (chest x-ray) for a pulmonary embolism show? 3
A
- usually normal
- linear atelectasis
- small effusions
14
Q
what are the outcomes of PE? 5
A
- 5% mortality rate despite treatment
- 4% develop pulmonary hypertension
- cause of death in 10-30% of in-patient post mortems
- up to 60% have micro-emboli at post mortem
- a leading cause of ‘preventable death’
15
Q
what are the treatments of a massive PE? 3
A
- thrombolysis with tPA (Alteplase)
- tissue plasminogen activator (fibrinolytic) 2-6% risk of serious bleeding
- iv unfractionated heparin (monitor with APTR (Activated Partial Thromboplastin Time Ratio))
16
Q
what is the standard treatment for PE? 6
A
- LMW (low molecular weight) heparin injections
- warfarin for 6 months
- consider underlying causes
- LMW heparin is better if there is underlying cancer
- IVC filter (inferior vena cava filter)
- consider a DOAC as an alternative
17
Q
when do we do a thrombophilia screen? 3
A
- consider in young patients with a spontaneous venous thromboembolism
- inherited causes: factor V leiden, deficiency of natural anticoagulants, antithrombin deficiency, protein C and protein S deficiency
- acquired causes: antiphospholipid syndrome (tests for lupus anticoagulant (DRVVT))
18
Q
name some antithrombotic drugs? 6
A
- warfarin
- heparin (unfractionated heparin, LMW heparin)
- newer agents- dabgatran (oral direct thrombin inhibitor)- rivaroxaban/ apixaban (oral direct factor Xa inhibitors)
- anti-platelet drugs
- fibrinolytic agents
19
Q
what is warfarin and what does it do? 5
A
- vitamin K antagonist
- prevents gamma-carboxylation of factors, II, VII, IX, X
- required for functional maturation of these factors
- prolongs the extrinsic pathway
- monitored by INR
20
Q
how long can warfarin take to achieve therapeutic levels?
A
over 3 days
21
Q
what warfarin interactions should we beware? 2
A
- drug interactions due to cytochrome P450 (enzyme inhibitors potentiate warfarin, enzyme inducers inhibit warfarin)
- interaction with alcohol, binge drinking can potentiate warfarin and chronic alcoholism can inhibit warfarin
22
Q
what can warfarin control be affected by? 4
A
- binding to albumin
- absorption of vitamin K from GI tract
- synthesis of vitamin K factor by liver
- hereditary resistance
23
Q
what are the side effects of warfarin? 5
A
- teratogenic (may cause birth defects)
- significant haemorrhage risk
- minor bleeding
- skin necrosis
- alopecia
24
Q
how do we reverse warfarin? 3
A
- if life threatening bleed, give activated prothrombin complex (octaplex or beriplex) which contains vitamin K dependent factors II, VII, IX, X
- dose is 25-50 units per kg depending on INR level
- give vitamin K 2-10mg depending on INR level
25
Q
what is heparin? 6
A
- mucopolysaccharide that works by potentiating anti-thrombin
- irreversibly inactivates factor Ia (thrombin) and factor Xa
- injected
- unfractionated heparin (iv infusion)
- LMW heparin (sc injections)
- safe in pregnancy
26
Q
what is unfractionated heparin used? 4
A
- not often due to inconvenience of administration
- safe in renal failure as unfractionated heparin is metabolised by the liver and not renally excreted
- if bleeding , protamine sulphate can partially reverse heparin
- heparin-induced thrombocytopenia (HIT) is a rare complication of heparin (suspect if platelet count falls on heparin, this is a prothrombotic condition which can cause VTE)
27
Q
when is low molecular weight heparin used? 4
A
- very convenient due to once daily injections
- prescribed according to weight
- not usually monitored
- used for thromboprophylaxis for hospital inpatients
28
Q
when are direct oral anticoagulants used? 6
A
- developed as oral alternatives to warfarin
- no monitoring required
- direct thrombin (IIa) inhibitor
- direct factor Xa inhibitor
- trials show clinical non-inferiority of DOACs when compared to warfarin and LMW heparin
- should not be used for cardiac valves as here it is inferior to heparin
29
Q
what is rivaroxaban? 6
A
- direct factor Xa inhibitor
- causes irreversible anticoagulation
- VTE prophylaxis
- used for DVT and PE treatment
- stroke prevention in AF
- apixaban is an alternative anti Xa drug and is less affected by renal function
30
Q
what is dabigatran? 4
A
- a direct thrombin inhibitor - VTE prophylaxis
- treats DVT and PE
- stroke prevention in AF
- can be reversed by Prabind
31
Q
name some types of antiplatelet drugs? 5
A
- aspirin (cyclooxygenase inhibitor)
- clopidogrel (ADP receptor blocker)
- Dipyridamole (inhibits phosphodiesterase)
- prostacyclin (stimulates adenylate cyclase)
- glycoprotein IIb/IIIa inhibitors used in angioplasty procedures
32
Q
what are fibrinolytic agents? 5
A
- thrombolytic agents used to lyse fresh thrombi by converting plasminogen to plasmin
- tissue plasminogen activator (tPA)
- streptokinase and urokinase
- administered systemically in acute MI, recent thrombotic stroke , major PE and massive iliofemoral thrombosis
- need to look at risk-benefit ratio
