anticoagulations and antiplatelets Flashcards

1
Q

what do you need to consider before starting a patient on anticoagulation

A

are there any contraindications to anticoagulation?
- active bleeding, surgeries, bleeding disorders ect

what is the indication for anticoagulation and is there more than 1?
some require specific types of drug eg warfarin

whats the patients likely bleeding risk?
has-bled

are there any patient related factors that dictate choice of anticoagulant

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2
Q

what drugs require warfarin?

A

metallic valves
valvar AF
rheumatic mitral stenosis
antiphospholipid syndrome

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3
Q

warfarin

A

vitamin K reductase inhibitor

decreases activity of vitamin K dependant clotting factors:
- factor II
- factor VII
- factor IX
- factor X

decreases protein C and S

only fully anticoagulated when prothrombin and factor 10 drop - can take a few days

prolongues PT and APTT

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4
Q

what factors does vitamin K act on - therefore warfarin decreases?

A

2
7
9
10

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5
Q

contraindications warfarin

A

pregnancy
malignancy
many drug-drug interactions

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6
Q

when is warfarin used

A
  • VTE
  • AF
  • metallic heart valves
  • mitral stebnosis
  • thrombosis and renal imparement
  • thrombosis and need for extra monitoring
  • antiphospholipid syndrome
  • recurrent thromboses on current anticoagulations
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7
Q

warfarin half life

A

36 hours

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8
Q

Heparins how they work and their classes

A

Boosts the activity of anti-thrombin

  • Inhibits thrombin and Xa
  • Can’t be orally absorbed
  • Derived from porcine intestine
  • Be aware of religious objections

Two classes:
- Unfractionated heparin (UFH) inhibits FXa + thrombin
- Low molecular weight heparin (LMWH) - only inhibits FAx

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9
Q

which pathways does heparin act on and whats its effect on the APTT and PT?

A

Impacts on
-common pathway
UFH - Prolongs PT AND APTT, APTT >PT
LMWH – PT and APTT may be normal or prolonged

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10
Q

which pathways does warfarin act on and whats its effect on the APTT and PT?

A

Impacts on
-extrinsic
-intrinsic
-common pathways
PROLONGS PT AND APTT, PT first (due to FVII)

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11
Q

when is UH and LMWH used?

A

UH:
- VTE
- need for anticoag but high bleed risk or severe renal imparement
- bridging pateints on warfarin
- pre-post surgery

LMWH:
- VTE prophylaxis
- VTE treatment
- malignancy or pregnancy
- anticoag w concerns about bleed risk
- patients establishing on warfarin
- pre-post surgery

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12
Q

contraindications of UH + LMWH

A

UH:
- risk of heparin induced thrombocytopaenia
- drop in platelet count

LMWH:
- lower risk of heparin induced thrombocytopaenia

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13
Q

dosage of heparins

A

UH - based of APTT ratio
LMWH - based of weight

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14
Q

heparins monitoring

A

UH - APTT ratio at least once daily

LMWH - not routinely

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15
Q

warfarin monitoring

A

INR - usual target range 2-3 X higher

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16
Q

DOACS examples and the pathways they act on and PT APTT results

A

direct oral anticoagulants

Factor Xa inhibitors
Apixaban, rivaroxaban, edoxaban

Direct thrombin inhibitors
Dabigatran

Impacts on
-common pathway
Variable impact on PT and APTT
-may be completely normal!

17
Q

when are Xa inhibitors (DOACS) used

A

VTE prophylaxis after orthopaedic surgery
VTE treatment
Non valvular AF

18
Q

Xa inhibitor contraindications

A

Contra-indicated - CrCl <15, pregnancy
Be aware of drug interactions
Apixaban - lowest risk GI bleeding
Edoxaban - best evidence in low body weight

19
Q

monitoring DOACS

20
Q

whens thrombin inhibitors (DOAC) used?

A

VTE prophylaxis after orthopaedic surgery
VTE treatment
Non-valvular AF

21
Q

thrombin inhibitors (DOAC) contraindications

A

Contra-indicated - CrCl <30, pregnancy
Be aware of drug interactions

22
Q

how antiplatelets work and common examples

A

Typically prevent platelet activation or aggregation with other platelets

May be used in combination after acute event

Most commonly used
Aspirin
Clopidogrel
Ticagrelor
Prasugrel

23
Q

aspirin mechanism

A

Mechanism
Cyclo-oxygenase inhibitor
-blocks production of thromboxane (TXA2)
-TXA2 facilitates aggregation and stimulates further platelet activation and vasoconstriction

-binds irreversibly for platelet lifespan

24
Q

p2y12 inhibitors

A

Inhibit ADP binding to P2Y12
P2Y12 binding stimulates aggregation via GPIIb/IIIa receptors and granule release for further platelet activation

Clopidogrel and prasugrel are prodrugs – converted by liver CYP450 into active form
Clopidogrel and prasugrel bind irreversibly for platelet lifespan, ticagrelor reversible binding

25
whens aspirin used
Primary and secondary prevention of cardiovascular disease TIA/ischaemic stroke
26
whens p2y12 used
In combination with aspirin after MI TIA/ischaemic stroke – clopidogrel Peripheral vascular disease - clopidogrel
27
antiplatelet monitoring?
nah