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Semester 2 Year 1 > Drugs Affecting Haemostasis and Thrombosis > Flashcards

Drugs Affecting Haemostasis and Thrombosis Flashcards

1
Q

What are the main constituents of coagulation?

A
  • Vessel wall lined by endothelium
  • Platelets- derived from megakaryocytes in marrow
  • Coagulation factors in un-activated state
  • Inhibitors of coagulation
  • Fibrinolytic system and inhibitors
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2
Q

Describe platelet-vessel wall interaction

A
  • Adhere to vessel wall via Von Willibrand’s factor and Glycoprotein Ib
  • Adhere to each other via Glycoprotein IIb-IIIa and fibrinogen
  • Granule release
  • Fibrin formation
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3
Q

What is the coagulation cascade?

A

• Factors present in inactive state- activated by “intrinsic or extrinsic” pathway

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4
Q

What are some pathways that activate the coagulation cascade?

A 
Tissue factor (extrinsic) pathway
Contact activation (intrinsic) pathway
Common pathway
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5
Q

What blood products can be used as drugs to help blood clot/prevent bleeding

A

• Blood products

  • Platelets-derivedfromblooddonation
  • Fresh frozen plasma- 200ml plasma from blood donation- contains coag factors in normal proportions. Dose 15 ml/Kg
  • Cryoprecipitate- pools of 5 donations using precipitate at 4C- concentrated fibrinogen, Von Willebrand factor and VIII
  • Specific coag factors eg IX VIII fibrinogen
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6
Q

What is tranexamic acid?

A
  • Anti-fibrinolytic drug
  • Oral or IV
  • Inhibits activation of plasminogen to plasmin
  • Uses in trauma/GI bleeding/post op or delivery
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7
Q

Describe the results of the CRASH 2 trial

A
  • 20,000 trauma patients

given bolus plus one more dose of tranexamic acid or placebo.

Effective only if given in first 3-4 hours. No increase in thrombotic events.

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8
Q

What vitamin is required to activate certain clotting factors?

A

Vitamin K

Vitamin K dependent clotting factors

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9
Q

What part of the vitamin K cycle is inhibited by warfarin?

A

Vitamin K ecocide and Vitamin K reductase

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10
Q

What is Warfarin?

A
  • 1920’s- Cattle dying of haemorrhage after eating mouldy clover
  • Coumarin isolated at Wisconsin Alumni Research Federation warfarin
  • Inhibits production of vitamin K in reduced form
  • Standard oral anticoagulant 1940’s-2010
  • Effect measured by prothrombin time ( expressed as INR)- venous or capillary sample
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11
Q

What are the positive aspects of warfarin?

A
  • Established for decades
  • Cheap
  • Easily measurable effect
  • Can be reversed with vitamin K or factor concentrate
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12
Q

What are the negative aspects of warfarin?

A
  • Lots of drug interactions to enhance or inhibit effect
  • Slow onset- several days
  • Unpredictable dose need
  • Needs regular blood testing
  • Risk of bleeding
  • Narrow “therapeutic window”
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13
Q

What drugs increase the effect of warfarin?

A
  • Amoxycillin- reduce gut vit K
  • Erythromycin, statins, acute alcohol intake- enzyme inhibition
  • Aspirin, clopidogrel, NSAIDs- increase bleeding risk- platelet function and GI mucosal damage
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14
Q

What drugs decrease the effect of warfarin?

A

• Rifampicin, carbamazepine, phenytoin, chronic alcohol intake- enzyme induction

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15
Q

What are the indications of warfarin?

A
  • Deep vein thrombosis (DVT) and pulmonary embolism (PE)- short or long term depending on whether recurrent and/or provoked
  • Prosthetic heart valve replacement
  • Atrial fibrillation to reduce stroke risk
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16
Q

What can be done to reduce stroke risk in atrial fibrillation

A

• Be aware of -absolute and relative risk reduction -balance of risks and benefits
-scoring risk of thrombosis (CHA2DS2-VASc) and bleeding (HAS-BLED)

17
Q

What are the different aspects of CHA2DS2-VASc scoring system

A

Hooo boy, really rolls of the tongue eh?
Right:

C - congestive heart failure (or left ventricular systolic dysfunction)
1 point

H - Hypertension - BP consistently above 140/90 mmHg (or treated on medication)
1 point

A2 - Age =/> 75 years
2 points

D - Diabetes mellitus
1 point

S2 - Prior stroke or transient ischaemic attack or thromboembolism
2 points

V - Vascular disease
1 point

A - Age 65 - 74 years
1 point

Sc - sex category (ie female)
1 point

18
Q

What is the stroke risk in % compared to CHA2DS2-VASc score?

A 
0 - Around 1% chance 
1 - 1.3%
2 - 2.2%
3 - 3.2%
4 - 4.0%
5 - 6.7%
6 - 9.8%
7 - 9.6%
8 - 12.5%
9 - 15.2%
19
Q

Is warfarin effective at reducing strokes?

A

Between CHA2DS2-VASc 3-8 Yes absolutely

20
Q

What are Direct OralAnticoagulants (DOACs)?

A
  • Xa inhibitors eg apixaban, rivaroxaban, edoxaban

* Direct thrombin inhibitors eg dabigatran

21
Q

What are the factors that favour warfarin in the warfarin vs DOACs debate?

A
  • Established drug
  • Cheap- but needs monitoring
  • Can be reversed
  • Effect can be easily measured
  • Can be used with poor renal function
22
Q

What are the factors that favour DOACs in the warfarin vs DOACs debate?

A
  • Good trial evidence
  • No monitoring needed
  • Lower bleeding risk
  • As effective for stroke prevention
  • Reversal agents recently availablebut ££££!
  • Short half life
23
Q

What is heparin?

A

• Naturally occurring anticoagulant- discovered 1916- 2nd year student
• Can be extracted from lung and liver
• Given as IV – unfractionated- half life <1 hour
or s/c – low molecular weight (LMWH)- half life approx. 12 hours
• Binds to and activates anti-thrombin so reducing Xa and thrombin generation

24
Q

What monitoring occurs in heparin administration?

A

• IV heparin is monitored by APPT plasma testing and dose adjusted • S/c LMWH eg dalteparin

  • used as fixed dose for prophylaxis and weight adjusted dose for treatment
  • no routine monitoring unless poor renal function, extreme body weightorpregnancy. Anti-Xalevelsgivemeasureoflevelof anticoagulation
  • Both used for treatment and prevention of DVT/PE
  • All patients on admission assessed for thromboembolism risk (VTE)
25
Q

What are the adverse effects of heparin?

A
  • Pain at site of injection
  • Increased bleeding risk
  • Osteoporosis with prolonged use
  • Heparin-induced thrombocytopenia- antibody mediated, 5-10 days into treatment
26
Q

What drugs are used to modify platelet function?

A

Aspirin

Clopidogrel

27
Q

Describe the use of aspirin

A
  • Aspirin- low doses eg 75-150mg/day cause irreversible inhibition COX-1 so less thromboxane A2 production- less aggregation of platelets
  • Typically used after transient ischaemic attack (TIA) or myocardial infarction
  • Some effect in stroke prevention in AF but not as effective as warfarin/DOAC
  • Increase in GI bleeding risk, dyspepsia
28
Q

Describe the use of clopidogrel

A

• Inhibit ADP induced platelet aggregation
• Used with aspirin to prevent recurrent myocardial infarction
• Used in ischaemic stroke and TIAs
• Increased risk of dyspepsia and GI bleeding
No reversal agents for aspirin and clopidogrel so effect will last the duration of platelet lifespan- 5-10 days

29
Q

What are thrombolytic drugs?

A
  • Drugs to increase activation of plasminogen to plasmin
  • Tissue plasminogen activators (tPA) eg streptokinase and alteplase- used for thrombolysis brain/heart/occluded venous catheters
  • Cause breakdown of fibrin and fibrinogen
  • Increased bleeding risk in hours after dose
  • Stenting and clot removal are alternative treatments

Semester 2 Year 1 (82 decks)

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