VTE and anti-coagulant meds Flashcards

1
Q

VTE prophylaxis

A

LMWH- enoxaparin
(contraindicated if active bleeding, warfarin or NOAC)

anti embolic stockings (contraindicated if significant peripheral arterial disease)

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2
Q

DVT presentation

A
unilateral calf or leg swelling
dilated superficial veins
tenderness to the calf
oedema
colour changes to the leg

measure the circumference of the calf 10cm below the tibial tuberosity
>3cm difference is signficiant

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3
Q

Diagnosis of DVT

A
  • D dimer
  • Ultrasound (repeat -ve USS after 6-8 days if there was a positive D dimer score)

PE: CTPA or V/Q scan

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4
Q

D- dimer specificity

A

95% sensitive but not specific for VTE

other causes of raised D dimer:
Pneumonia
Malignancy
Heart failure
Surgery
Pregnancy
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5
Q

management of DVT

A

LMWH- immediately before confirming the diagnosis where DVT or PE is suspected and delay in scanning.

e.g enoxaparin, dalteparin.

long term anticoauglation

  • warfarin (INR 2-3)
  • NOAC
  • LMWH
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6
Q

switching from LMWH to warfarin

A

continue LMWH for 5 days or until the INR is 2-3 for 24 hours (the longer option)

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7
Q

NOACs and DOACs

A

oral anticoagulants that are not warfarin
the alternative option does not require monitoring

‘direct acting oral anticoauglants’
e.g. apixaban, dabigatran, rivaroxaban

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8
Q

NOACs and DOACs

A

oral anticoagulants that are not warfarin
the alternative option does not require monitoring

‘direct acting oral anticoauglants’
e.g. apixaban, dabigatran, rivaroxaban

LMWH is first line VTE for pregnancy or cancer

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9
Q

VTE anticoauglation

A

3 months if there is an obvious reversible cause (then review)
Beyond 3 months if the cause is unclear, there is recurrent VTE or there is an irreversible underlying cause such as thrombophilia. This is often 6 months in practice.
6 months in active cancer (then review)

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10
Q

IVC filter

A
  • devices inserted into the inferior vena cava
  • filter the blood and catch any blood clots travelling from the venous system towards the heart and lungs.
  • act like sieve, allowing blood to flow through whilst stopping larger blood clots.
  • used in unusual cases of patients with recurrent PEs or those that are unsuitable for anticoagulation to prevent emboli traveling to the lungs.
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11
Q

investigating an unprovoked DVT

A
History and examination
Chest X-ray
Bloods (FBC, calcium and LFTs)
Urine dipstick
CT abdomen and pelvis in patients over 40
Mammogram in women over 40

test for antiphospholipid syndrome (antiphospholipid antibodies)

In patients with an unprovoked VTE with a family history of VTE they recommend testing for hereditary thrombophilias:

Factor V Leiden (most common hereditary thrombophilia)
Prothrombin G20210A
Protein C
Protein S
Antithrombin
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12
Q

What is a VTE?

A

common and fatal condition
thrombosis (clot) develops in circulation

  1. stagnation of blood
  2. hypercoagulable. state

DVT can mobilise to the right side of the heart > lungs > PE

if a patient has an ASD the blood clot can pass into the left side > brain > stroke

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13
Q

Virchow’s triad

A

stasis of blood flow
endothelial injury
hypercoagulability

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14
Q

types of clots

A

arterial thrombosis (platelt rich clot)

venous thrombosis (venous rich clot)

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15
Q

risk factors for arterial thrombosis

A
Smoking
Hypertension
Hypercholesterolaemia
Diabetes Mellitus
Obesity
Family History
Personal History
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16
Q

therapeutic targets

antiplatelts

A

TxA2 – COX1 antagonist – Aspirin

ADP receptor (P2Y12) – Clopidogrel, Prasugrel, Ticagrelor

Phophodiesterase inihibitor - dipyridamole

GPIIb/IIIa antagonist – abciximab

17
Q

aspirin

A

Irreversibly inhibits cyclo-oxygenase (COX-1) by acetylation
Causes reduction in Thromboxane A2 – reducing platelet aggregation & vascular constriction
Used for secondary prevention of arterial thrombosis ( ACS, CVA, Post CABG)
Effect persists for 7-10 days, until platelets replaced
Major side effects: gastric ulcers and bleeding - may be life-threatening
Should not be used for primary prevention – Address risk factors

18
Q

anti platelet P2Y12 antagonist (clopidogrel)

A

P2Y12 receptors = ADP sensitive
ADP receptor inhibitor (thienopyridine)
Reduce intra-platelet Ca, reduce aggregation, reduce platelet secretion, reduce GP IIbIIIa expression
Inter-individual variability
Inhibiting arteriolar thrombus: MI, CVA, PVD, Coronary stents

19
Q

coagulation cascade

A

extrinsic pathway VII (vessel injury)

intrinsic pathway XII

common pathway Xa

prothrombin to thrombin
fibrinogen to fibrin

20
Q

anti coagulants

A

vitamin K antagonist
ODI’s?
novel anticoagulants

21
Q

example of NOACs

A

Dabigatran: Direct oral Thrombin inhibitor
Rivaroxaban, Apixaban, Edoxaban: Direct oral Xa inhibitors
Very predictable pharmacokinetics - no monitoring required
Wide therapeutic window
Limited drug/food interactions
Relatively short half lives
Reversal agents in place for dabigatran, coming for others

22
Q

warfarin

A
50 years experience with use
Many patients have stable INR & reassured
Proven efficacy as an anticoagulant
Broad range of application
Half-life = about 50 hours
Rapidly reversed (Vit K +/- PCC)
NPSA: top 5 drug for litigation
NPSA: top 5 drug for  mortality (25% ICH)
Longest list of interactions in BNF!
23
Q

LMWH

A

dalteparin

enoxaparin