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Haematology BL > Anticoagulant Drugs - BB > Flashcards

Anticoagulant Drugs - BB Flashcards

(43 cards)

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1
Q

Heparin - general

A

Polymer - glycosaminoglycan structure
- Molecules of varying chain lengths

Activates anti-thrombin III (ATIII) - a naturally occurring anticoagulant

Occurs naturally (found in mast cells)

Used as medication in 2 forms:
1 - Unfractioned - widely varying polymer chains
2 - Low molecular weight - smaller polymers only

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2
Q

Clotting factors that unfractioned heparin (UFH) inhibits:

A

VIA ATIII

  • thrombin (II)
  • XII (12)
  • XI (11)
  • IX (9)
  • Xa (10)
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3
Q

Administration of UFH

A

IV/ SC - acute onset

Highly variable response to a dose:

  • Because of binding to plasma proteins/ cells
  • Dose must be adjusted to reach target PTT
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4
Q

Clotting tests in UFH:

A
  1. Increased PTT (intrinsic pathway) - because affects many components of this pathway
  2. Increased Thrombin Time
  3. Can increase PT at high doses
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5
Q

Reversal agent for heparin (UFH)

A

Protamine

UFH - not as effective with LMWH

Binds heparin and neutralises the drug

Used in:

  1. heparin overdose
  2. Cardiac surgery - where very high dose is needed for heart-lung bypass
    - Quick reversal is needed at end of surgery
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6
Q

Uses of UFH:

A

Acute management:

- DVT/PE
- MI
- Stroke

Prophylaxis:
- For DVT in hospitalised patients (SC)

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7
Q

Side effects of UFH:

A
  • Bleeding/ thrombocytopenia (rare)
  • Osteoporosis (in long term use)
  • Elevated AST/ALT (mild)
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8
Q

Heparin and thrombocytopenia:

A

2 Types:

  1. Non-immune thrombocytopenia
    • mild 10-20% reduction in platelets
    • Due to direct suppressive effect on platelet production
  2. HIT - Heparin-Induced Thrombocytopenia
    - Immune mediated reaction
    - Immune complexes bind to PF4-Heparin complex
    - TII hypersensitivity reaction
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9
Q

HIT:

A

Heparin induced thrombocytopenia

Type II hypersensitivity

Immune complexes bind to PF4-Heparin complex and these can cause:

- Removal by splenic macrophages (reduced platelets)
- Platelet aggregation/activation (THROMBOSIS)
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10
Q

Presentation of HIT:

A

5-10 days after exposure to heparin (in 0.2-5% of heparin patients)

  1. Abrupt fall in platelets (>50%)
  2. Arterial/venus thrombosis (can develop ischaemic limb/DVT)
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11
Q

Diagnosis and management of HIT:

A

Presumptive Diagnosis: - in ptx on heparin with:

  • Significan drop in platelet count
  • Thrombosis formation

Definitive diagnosis:
- HIT antibody testing - (takes days to come back and you dont want to wait)

Management:

  • Give alternative drug treatment
    - Lepirudin or Bivalirudin (Direct thrombin inhibitors)
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12
Q

LMWH - effects

A

Only inhibits factor Xa (indirectly through activation of ATIII)
- Limited compared to UFH

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13
Q

LMWH - administration

A

(Enoxaparin)

Predictable dosing - no need to titrate (based on weight)
- Because of reduced binding to plasma proteins and cells

Given subcutaneously (SQ)

Lower incidence of HIT

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14
Q

Clotting tests in LMWH:

A
  • Will not affect thrombin time (unlike UFH)
  • PTT is not sensitive to changes in LMWH-dose-induced changes
    - Response curve is shallow - UFH’s is steep
  • Monitoring of LMWH done using Anti Xa Levels
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15
Q

Monitoring of LMWH:

A

Anti Xa levels used (not PTT like in UFH)

Ususally no monitoring is needed - EXCEPT in:

  • Obestiy
  • Renal failure
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16
Q

Anti-Xa Level:

A

Xa substrate linked to chromophore (which illuminates when substrate is split) is mixed with patient sample

  • Low Xa activity - small amount of substrate splitting and therefore small amount of illuminaiton
  • High Xa activity - lots of substrate splitting - therefore greater illumination

Illumination is converted into a number - called ANTI-Xa ACTIVITY

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17
Q

Factor Xa inhibitors:

A

Indirect:

  • LMWH
  • UFH

Direct:

  • Rivaroxaban
  • Apixaban
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18
Q

Direct factor Xa inhibitors:

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A

Rivaroxaban

Apixaban

19
Q

Uses of Rivaroxaban and Apixaban

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A

Used in AF as alternatives to warfarin

20
Q

Direct Factor Xa inhibitors (Rivaroxaban and Apixaban) - general

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A
  • ORAL DRUGS (DOACs)
  • Do not require monitoring of PT/INR
  • Standard dosing
21
Q

Direct Factor Xa inhibitors (Rivaroxaban and Apixaban) - test changes

Study These Flashcards
A

Can increase PT and PTT (factor Xa in both pathways)

Will not affect thrombin time

22
Q

Direct thrombin Inhibitors: (DTIs) - Name the drugs

Study These Flashcards
A

Hirudin

Lepirudin

Bivalirudin

Desirudin

Argatroban

Dabigatran - Only oral (DOAC)

23
Q

Test changes in DTIs:

Study These Flashcards
A

Prolonged PT, PTT, and thrombin time

- Thrombin activity common to all these tests

24
Q

What can cause prolonged thrombin times?

Study These Flashcards
A
  1. Unfractionated heparin (ATIII)

2. Direct thrombin inhibitors (DTIs)

25
Uses of DTIs:
1. Patients with HIT - (stop heparin start DTI) - Hirudin, lepirudin, bivalirudin, desirudin, argatroban - PTT often monitored whilst being administered 2. ACS/ Coronary interventions - Bivalirudin 3. Atrial Fibrillation: - (Dabigatran) - Oral (alternative to warfarin) - Standard dosing doesn't require PT/INR monitor
26
Warfarin Mechanism of Action:
Antagonist to vitamin K (epoxide reductase inhibitor) - Epoxide reductase reduces vitamin K so that it can be used to activate clotting factors Reduces levels of vitamin K dependent clotting factors (II, VII, IX, X)
27
Vitamin K in Clotting cascade:
Reduced vitamin K Forms Gla residues in clotting factors (Gamma-carboxylation) - Then becomes oxidated - Epoxidase Reductase - reduces vitamin K back to usable form
28
Dietary sources of Vitamin K
Green leafy vegetables (K1 form) - Cabbage, kale, spinach - Egg yolk - Liver
29
K2 form of vitamin K
Synthesised by GI bacteria
30
Administration of warfarin:
Takes days to achieve effects - because time required for clotting factors to fall Dose adjusted to reach target PT/INR (once a month check needed) - Because drugs effect varies with diet (vitamin K) - Antibiotics may also kill GI bacteria - dec vit K - Increasing INR - Some drugs interfere with the metabolism of warfarin
31
Warfarin Blood tests:
PT/INR used to measure effect because: - factor VII - has shortest half-life and will fall the fastest - therefore extrinsic pathway is most sensitive PTT will also be increased - but less sensitive to warfarin Thrombin time will be normal
32
Prothrombotic effects of warfarin:
Protein C is vitamin K dependent with a short half-life - is an anti-clotting factor Initial warfarin treatment leads to a transient protein C deficiency (pro-thrombotic) - Brief - as other factors will fall shortly after
33
Mitigating prothrombotic effects of warfarin:
Other drugs such as heparin are given anytime warfarin is started in clot disorders (DVT/PE) - however this is less relevant as often heparin is used for acute onset anyway before prophylaxis is started (because of its immediate effect) ATRIAL FIBRILLATION - EXCEPTION: - No active clots, just a risk of clots - warfarin is often started without heparin - brief increase in risk of clot is very low
34
Anticoagulants in pregnancy:
Warfarin - crosses placenta (avoided in pregnancy) - especially in 1st trimester - can cause Fetal Warfarin Syndrome - abnormal foetal development Unfractionated heparin is often used in pregnancy as it does not cross the placenta
35
Warfarin skin necrosis:
Rare complication of warfarin therapy 1. Occurs in ptx with protein C defiiency 2. Can also occur at high doses Initial exposure to warfarin causes decreased protein C - resulting in skin thromboses Large dark, purple skin lesions
36
Warfarin uses:
Stroke prevention in ptx with atrial fibrillation Mechanical heart valves DVT/PE - treated with warfarin for at least a few months
37
Chronic oral coagulation:
Indications are: - AF - Mechanical heart valve - Prior DVT/PE Drugs used: - Warfarin: - Pros: oral drug, cheap - Cons: Monthly INR monitoring - NOACs/DOACs: - Rivaroxaban/ apixaban and Dabigatran - Pros: Consistant dosing - no INR monitoring - Cons: Expensive, cannot be used in certain patients
38
DOACs:
2x direct factor Xa inhibitors: - Rivaroxaban - Apixaban 1x Direct thrombin inhibitor: - Dabigatran CANNOT BE USED IN PTX with: - Dialysis - Mechanical heart valves
39
Reversal agents for rivaroxaban and apixaban
Andexanet alpha - inactive decoy that binds the drug
40
Reversal agent for Dabigatran:
Idarucizumab - anti-dabigatran monoclonal antibody
41
3 Thrombolytic drugs:
tPA Streptokinase Urokinase (all 3 increase conversion of plasminogen into plasmin)
42
Risks of thrombolytic agents:
MAJOR bleeding risk as they break down clotting factors as well as fibrin
43
Reversal of warfarin:
1. Fresh Frozen Plasma (FFP) - Corrects deficiencies in any clotting factor - PT/PTT will normalise after infusion - Used if severe bleeding and increased INR 2. Vitamin K (oral or IV) - IV can cause anaphylaxis - Used if raised INR and no bleeding INR 3-5 - hold warfarin INR 5-9 - Hold warfarin, oral vitamin K INR >9 - Consider IV vitamin K, FFP Raised INR + Severe Bleeding - > Administed FFP

Haematology BL (14 decks)

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