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Cardiovascular > Venous thromboembolism > Flashcards

Venous thromboembolism Flashcards

1
Q

What are the points of the Virchow’s triad?

A

Hypercoagulability
Stasis
Vascular injury

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2
Q

What is the purpose of natural inhibitors in the regulation of the coagulation cascade?

A

Prevention of over-activity

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3
Q

What are the natural inhibitors of the coagulation cascade?

A

Tissue factor pathway inhibitor= TF-V11a complex/fXa
Antithrombin= thrombin and fXa activity
Protein C pathway= fVa and fV111a

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4
Q

What are the enzymes involved in coagulation cascade regulation?

A

Extrinsic Tenase
Intrinsic Tenase
Prothrombinase

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5
Q

Describe prothrombinase

A

complex consists of the serine protease, Factor Xa, and the protein cofactor, Factor Va
assembles on negatively charged phospholipid membranes in the presence of calcium ions
catalyses the conversion of prothrombin (Factor II), an inactive zymogen, to thrombin (Factor IIa), an active serine protease

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6
Q

Describe Extrinsic Tenase

A

complex is made up of tissue factor, factor VII, and Ca2+ as an activating ion

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7
Q

Describe Intrinsic Tenase

A

contains the active factor IX (IXa), its cofactor factor VIII (VIIIa), the substrate (factor X), and they are activated by negatively charged surfaces (such as glass, active platelet membrane, sometimes cell membrane of monocytes).

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8
Q

Which inhibitors affect which enzyme?

A

TFPI- Extrinsic Tenase
Protein C pathway- Intrinsic Tenase, (pro)
Antithrombin- Prothrombinase

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9
Q

Describe the epidemiology of Venous Thromboembolism

A
  • Incidence= 1 per 1000 per annum
  • May present as sudden death (up to 30% of pulmonary embolism)
  • 30% develop recurrent venous thrombosis in 10 years
  • 28% develop post thrombotic syndrome
  • Mortality of promptly diagnosed and adequately treated pulmonary embolism is 2%
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10
Q

Why is VTE a major international health problem?

A

Overall deaths from pulmonary embolism exceed the combined total of deaths from breast cancer, AIDs and traffic accidents
5x the number of deaths from a total of all hospital acquired infections

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11
Q

What are the risk factors for VTE?

A 
Age
Obesity
Varicose veins
Previous VTE
Family history of VTE
Thrombophilia
Cancer
Other thrombotic states- stroke, heart failure
Hormone therapy
Pregnancy
Immobility- during/ not during travel
Hospitalisation
Anaesthesia
Central venous catheters
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12
Q

Why is VTE frequently unrecognised?

A

80% DVT clinically silent

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13
Q

At what age does incident rates of VTE rise dramatically?

A

55
By age 80, nearly 1:100 per year
Rates of PE rise faster than DVT in elderly

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14
Q

What are the types of venous thrombosis?

A

Deep venous thrombosis (DVT)
Pulmonary embolus (PE)
Cerebral, mesenteric, axillary, splanchnic, splenic

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15
Q

What are the clinical features of lower limb DVT?

A
  • Pain, swelling, increased temperature of limb, dilation of superficial veins
  • Usually unilateral= may be bilateral if thrombosis sited in inferior vena cava, differential diagnosis: calf haematoma, ruptured Baker’s cyst, cellulitis
  • Clinical probability score Well’s score
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16
Q

What is the Clinical Model to standardise Clinical Assessment?

A

Well’s pre-test probability (clinical likelihood) of DVT

Stratify patients into low, intermediate or high probability categories

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17
Q

What are examples of objective testing of lower limb DVT?

A

Contrast venography; reference standard for diagnosis of DVT

Compression USS and D-dimer

18
Q

What is Venous ultrasonography?

USS

A

Non-compressibility of the common femoral vein or popliteal vein diagnostic of DVT
Compression B-mode ultrasonography +/- colour duplex imaging: sensitivity 95%, specificity 96% for diagnosis of symptomatic proximal DVT
Sensitivity and specificity of 60-70% for isolated calf vein thrombosis

19
Q

What are the clinical features of pulmonary embolism?

A
  • Depends on number, size and distribution of emboli
  • Collapse, faintness, crushing central chest pain
  • Pleuritic chest pain
  • Difficulty breathing
  • Haemoptysis
  • Exertional dyspnoea
20
Q

What tests are required for diagnosis of PE?

A
  • Chest X-ray (to exclude other pathology)
  • Electrocardiogram (ECG)
  • Arterial blood gases
  • D-dimer
  • Ventilation Perfusion (V/Q) scan
  • CT-pulmonary angiogram
  • Echocardiogram
21
Q

What are the two principles of anticoagulant therapy?

A

Rapid initial anticoagulation

Extended therapy

22
Q

Describe rapid initial anticoagulation

A

-Parenteral anticoagulation: heparin, low molecular weight heparin, fondaparinux, OR
-Direct oral anticoagulant
Aim: to reduce the risk of thrombus extension and fatal pulmonary embolism

23
Q

Describe extended therapy

A

-Orally active anticoagulant: vitamin K antagonist
-OR direct oral anticoagulant
Aim: to prevent recurrent thrombosis and chronic complications such as post-phlebitic syndrome

24
Q

Describe management of VTE- the “traditional way”

A
  • Give LMWH or UFH for a minimum of 5 das if uncomplicated thrombosis, 7 days or longer if extensive disease
  • Start warfarin therapy on day 1
  • Overlap with LMWH or UFH until INR (International Normalised Ratio) is 2.0 for 2 days
25
Q

What are Direct Oral Anticoagulants (DOACs)?

A
  • Used for VTE over past few years
  • Dabigatran, Rivaroxaban, Edoxaban and Apixaban licensed in UK for treatment of acute DVT
  • Enables rapid initial coagulation orally
  • Then continue a maintenance dose for 6 months or longer for secondary prevention of VTE
  • Apixaban and Rivaroxaban do not need any overlap with heparin- big advantage in outpatient setting
26
Q

What is involved in investigation of a procoagulant tendency?

A
  • Full blood count
  • Antithrombin
  • Protein C
  • Free protein S
  • Antiphospholipid antibodies and lupus anticoagulant
  • Thrombin time/ reptilase time (to investigate fibrinogen function)
  • Factor V Leiden, Prothrombin 20210A (genetic tests)
  • JAK-2 mutation (to investigate myeloproliferative conditions)
  • PNH screen (if patient has cytopenia, for splanchnic bed thrombosis)
27
Q

Who do we test for thrombophilia?

A
  • Venous thrombosis less than 45 years
  • Recurrent venous thrombosis
  • Family history of unprovoked thrombosis
  • Combined arterial and venous thrombosis
  • Venous thrombosis at an unusual site (cerebral vein thrombosis/ Budd-Chiari syndrome/ portal vein and splanchnic vein thromboses)
28
Q

Where are the sites of action of blood coagulation inhibitors?

A
  • Draculin= active site blocked f1Xa, monoclonal Ab, Vs f1X/ 1Xa
  • Tick Anticoagulant Peptide= Rivaroxaban, Apixaban, Edoxaban
  • Pentasaccharide, Heparin+ LMWH
  • Hirudin, Argatroban, Dabigatran
29
Q

What are the types of Heparin?

A

Unfractionated

Low-molecular weight heparin

30
Q

What is Heparin?

A

Sulphated glycosaminoglycan
Biological product derived from porcine intestine
Binds to unique Pentasaccharide on antithrombin and potentiates its inhibitory action towards fXa and thrombin

31
Q

Describe unfractionated heparin (UFH)

A

Heterogeneous group of molecules with a range in MW from 3000 to 30,000D
Unpredictable anticoagulant response fur to binding to plasma proteins
Monitoring required by activated partial thromboplastin time (APTT)

32
Q

Describe Low Molecular Weight Heparin

A

Produced by enzymatic/ chemical depolymerisation of UFH with mean MW of 5000 (reduction in chain length- reduced capacity to inhibit thrombin vs UFH)
-Better bioavailability, more predictable anticoagulant response and dose-dependent renal clearance/ no lab monitoring usually necessary (if required LMWH-antiXa level can be performed, monitor levels in renal impairment obesity and pregnancy)

33
Q

What are the different properties of UFH and LMWH?

A 
UFH= used when high risk of bleeding/ binds to plasma proteins so monitoring using APTT/ continuous IV infusion or twice daily sc administration/ risk of osteoporosis, heparin-induced thrombocytopenia/ reverse by d/c infusion also protamine
LMWH= not reversible partial by protamine, nearly 100% bioavailability means reliable dose dependent effect/ no monitoring unless renal impairment and extreme body weight/ once daily/ reduced risk of osteoporosis and HIT
34
Q

What are Coumarins?

A
  • Inhibit vit K dependent carboxylation of factors 11, V11, 1X and X in the liver (warfarin)
  • Causes a relative deficiency of these coagulation factors= monitored by INR derived from prothrombin time/ takes around 5 days to establish maintenance dosing/ loading regimes assist early dosing/ individual dose from each patient (racial differences reflect natural occurring polymorphisms in CYP2C9 and VKORC1 genes)/ Dietary intake of vit K also affects warfarin dose
35
Q

What are the problems with coumarins?

A

Many drug interactions
Requires monitoring at least monthly or more
Most serious common side effect= bleeding
Major bleeding occurs in 1% of patients each year, risk of fatal intracranial haemorrhage 0.25% per annum

36
Q

Describe the reversal of warfarin

A
  • Management depends on whether the patient is bleeding or not
  • National reversal policies
  • Vitamin K- oral or intravenous routes
  • Reverse by administering the deficient clotting factors
  • Tendency to use factor concentrate (factor 11, 1x and X) in place of fresh frozen plasma (prothrombin complex concentrate PCC)
37
Q

What are the indications of DOACs?

A

Treatment of DVT and pulmonary embolism/ prevention of cardioembolic events in patients with atrial fibrillation

38
Q

What benefits does DOACs have over warfarin?

A
  • More predictable anticoagulant profile
  • Fewer drug and food interactions
  • Wider therapeutic window
  • Oral administration
  • No need for monitoring
  • Simple dosing
39
Q

Describe the reversal of DOACs

A
  • Antidotes being developed- new now in use for dabigatran
  • For Xa inhibitors= basic measures
  • Determine how long since last dose
  • Start standard resuscitation measures
  • Moderate to severe bleeding= local measures, fluid replacement, consider fresh frozen plasma or platelets, antifibrinolytic inhibitors, consider use of factor concentrates if extreme bleeding
40
Q

What are the methods to prevent venous thrombosis?

A 
Mechanical= mechanical foot pumps, graduate compression stockings
Pharmacological= LMWH, UFH, Fondaparinux, Dabigatran, Rivaroxaban, Warfarin

Cardiovascular (52 decks)

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