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PR3154 > IC3 Anticoagulants, Antiplatelet, Fibrinolytics, Blood disorders > Flashcards

IC3 Anticoagulants, Antiplatelet, Fibrinolytics, Blood disorders Flashcards

1
Q

What are the 4 stages of clotting?

A
  1. Vasoconstriction
  2. Primary haemostasis
  3. Secondary haemostasis
  4. Clot stabilization

Primary haemostasis - platelets bind to collagen via VWF. Thrombin not activated yet

Secondary haemostasis - activation of thrombin and formation of fibrin

Clot stabilization - Cross-linking of platelets

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2
Q

What are the general MOA of antiplatelet drugs?

A

Antiplatelet drugs target primary haemostasis.

  1. Prevention of platelet adhesion
  2. Platelet inactivation
  3. Platelet aggregation inhibitor
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3
Q

What are the 4 main antiplatelets that you must know?

A
  1. Dipyridamole
  2. Aspirin
  3. Clopidogrel
  4. Ticagrelor
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4
Q

What is dipyridamole’s MOA?

A

Dipyridamole inhibits:
1. Adenosine reuptake
2. PDE3

Platelets require a decrease in cAMP to become activated.
By inhibiting adenosine reuptake & PDE3, it will cause cAMP concentration to increase, preventing the activation of platelets

The inhibition of cAMP and PDE3 will also cause vasodilation

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5
Q

Why is dipyridamole only used as an adjunctive therapy?

A

Due to its vasodilation property which can lead to ADR.

There is a certain dose limit of dipyridamole that we can give to avoid ADR.

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6
Q

What ADRs are associated with dipyridamole?
(think of vasodilation)

A
  1. Hypotension
  2. Dizziness
  3. N&V
  4. Headache
  5. Diarrhoea
  6. GI disturbances
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7
Q

What is the MOA of aspirin?

A

Aspirin is an irreversible COX inhibitor.
- Inhibits COX 1 and 2

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8
Q

What happens when COX-1 is inhibited by aspirin?

A

tXA2 will not be produced. This results in decreased platelet aggregation and reduced vasoconstriction.

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9
Q

Why is aspirin more effective at low dose?

A

At low dose, aspirin primarily inhibits COX-1. At higher doses, it will bind to more COX-2 enzymes.

The inhibition of COX 1 inhibits platelet aggregation, while the inhibition of COX 2 promotes platelet aggregation.

As we mainly want an antiplatelet effect, aspirin at a low dose will reduce COX-2 inhibition and will have the strongest inhibition of platelet aggregation effect .

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10
Q

What is the ADR of aspirin?

A

Upper GI events - e.g gastric ulcers, bleeding

COX-1 primarily produces prostaglandins in the GI tract to protect the stomach.
Inhibition of COX-1 will increase risk of gastric ulcers.

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11
Q

What is the MOA of clopidogrel and ticagrelor?

A

They are ADP P2Y12 inhibitors.

ADP is released by platelets, which binds to ADP P2Y12 receptor to recruit more platelets for aggregation.

Inhibition of the ADP P2Y12 receptors will prevent the recruitment of more platelets and their aggregation.

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12
Q

What is the difference between Clopidogrel and Ticagrelor?

  1. Prodrug / active drug
  2. Reversible / irreversible binding
  3. Duration of effect
  4. Potency
  5. Metabolism affected by CYP2C19 variability?
A

Clopidogrel: Prodrug w an active metabolite
Ticagrelor: Active drug

Clopidogrel: Irreversible binding to ADP P2Y12 receptor
Ticagrelor: Reversible binding to ADP P2Y12 receptor

Clopidogrel: Last for 7-10days
Ticagrelor: Last for 2-3 days

Clopidogrel: Less potent
Ticagrelor: More potent

Clopidogrel: Affected by CYP2C19 variability
Ticagrelor: Not affected by CYP2C19 variability

Summary:
Clopidogrel:
- Prodrug w an active metabolite
- Irreversible binding to ADP P2Y12 receptor
- Last for 7-10days
- Less potent
- Affected by CYP2C19 variability

Ticagrelor:
- Active drug
- Reversible binding to ADP P2Y12 receptor
- Last for 2-3 days
- More potent
- Not affected by CYP2C19 variability

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13
Q

What is the general MOA of anticoagulants?

A

Anticoagulants target secondary haemostasis.

They prevent the activation of fibrin polymerization.

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14
Q

What are the 2 route of administration for anticoagulants?

A
  1. Oral
  2. Parenteral
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15
Q

What are the 2 main types of oral anticoagulants (OAC)?

A
  1. Vitamin K antagonist - warfarin
  2. Non-vitamin K antagonist - DOACs
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16
Q

What are the 2 main types of parenteral anticoagulants?

A
  1. Heparin
  2. Low molecular weight heparin (LMWH)
17
Q

What is the MOA of warfarin?

A

Warfarin is a vitamin K reductase inhibitor.

It prevents the conversion of inactive oxidised vitamin K to active reduced vitamin K.

18
Q

How is warfarin metabolised?

A

Warfarin is metabolised hepatically, via CYP2C9.

Half-life of warfarin is highly variable due to gene variability of CYP2C9 and VKORC1

19
Q

What are some DDIs, drug-food interactions of warfarin?

A

DDIs:
1. Long term Paracetamol at high doses
2. Allopurinol
3. NSAIDs
4. Salicylates
5. PPIs
6. Metronidazole

Drug-food interactions:
1. Food high in vitamin K
2. Traditional medications - e.g. Gingko, ginseng
3. Green tea

20
Q

What is Darbigatran MOA?

A

It is a competitive reversible antagonist of thrombin.

21
Q

What is the reversal agent for darbigatran?

A

Idarucizumab

22
Q

What is rivaroxaban’s MOA?

A

It is a competitive reversible antagonist of activated factor Xa.

23
Q

What is the MOA of heparin and LMWHs?

A

They bind to antithrombin III, forming complexes that inactivate thrombin and factor Xa.

LMWH are more selective for factor Xa.

Heparin acts on both thrombin and factor Xa.

24
Q

Why is LMWH favoured over heparin?

A

LMWH have longer half-life and higher bioavailability

25
Q

What is the reversal agent for heparin?

A

Protamine sulfate

26
Q

What is the reversal agent for LMWH?

A

Andexanet alfa.

Andexanet alfa can also be used to reverse other selective factor Xa inhibitors - apixaban, rivaroxaban, edoxaban.

27
Q

What are the 2 main types of thrombolytics we need to know?

A
  1. rTPAs - Alteplase, tenecteplase
  2. Streptokinase
28
Q

What is the reversal agent for alteplase?

A
  1. Tranexamic acid
  2. Aminocaproic acid
29
Q

What are the 4 main types of blood disorders?

A
  1. Aplastic anaemia
  2. Immune thrombocytopenia
  3. Agranulocytosis
  4. Haemolytic anaemia
30
Q

What are the causes of the 4 blood disorders & how to treat them?
1. Aplastic anaemia
2. Immune thrombocytopenia
3. Agranulocytosis
4. Haemolytic anaemia

A
  1. Aplastic anaemia
    - Caused by cancer, chemotherapy, carbamazepine, phenytoin, chloramphenicol, etc.
    - Treat w immunosuppresants, GM-CSF, G-CSF, IL-14
  2. Immune thrombocytopenia
    - Caused by heparin (impt)***, sulfonamides, carbamazepine, phenytoin GPIIb/IIIa inhibitors
    - Treated w immunosuppresants
  3. Agranulocytosis
    - Caused by clozapine, thiomides, b-lactams abx, etc
    - Treat w GM-CSF, G-CSF
  4. Haemolytic anaemia
    - Induced by methyldopa, quinidine, penicillin, cephalosporins, streptomycin, cisplatin, oxaliplatin, beta-lactamase inhibitors
    - Treat w steroids, immunoglobulins, rituximab
31
Q

What is cytopenia?

A

Cell deficiency.

Anaemia - RBC
Neutropenia - WBC
Thrombocytopenia - platelets.

32
Q

What are the 4 drugs we can use for anaemia?

A
  1. Iron
  2. Vitamin B12
  3. Folic acid
  4. Erythropoiesis stimulating agents
33
Q

What are the 2 main classes of drugs for neutropenia?

A
  1. Granulocyte colony-stimulating factor (G-CSF)
    E.g. Filgrastim, pegfilgrastim
  2. Granulocyte-macrophage colony stimulating factor
    E.g. Sargramostim
34
Q

What is the main class of drug for treatment of thrombocytopenia?

A

Megakaryocyte growth factors / platelet stimulating agents (PSAs)

E.g of PSAs:
1. Recombinant IL-11
2. Fc-fusion protein thrombopoietin receptor agonist
3. Oral non-peptide thrombopoietin receptor agonists

35
Q

What are the 2 causes that lead to abnormally large RBCs that cannot function properly?

A
  1. Vit B12 deficiency
  2. Folate deficiency
36
Q

What causes RBC to be smaller and fewer in amount?

A

Iron deficiency

PR3154 (19 decks)

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