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Anti-Coagulants (LOOK AT TABLES IN PPT) Flashcards

1
Q

Aspirin MOA

A

Irreversibly inhibits cox-1

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2
Q

Which is the only irreversible NSAID?

A

Aspirin

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3
Q

What is a low does of aspirin used for?

A

MI and TIA

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4
Q

What is a high dose of aspirin used for?

A

Anti-inflammatory

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5
Q

Side effects of aspirin

A

Increases GI bleeding

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6
Q

Dipyridamole MOA

A

Phosphodiesterase inhibitor
Inhibits adenosine uptake in the RBC, thereby increasing adenosine levels in the blood
Adenosine binds to platelet adenosine A2 receptor, activating adenylyl cyclase –> increasing cAMP
Increased cAMP reduces platelet aggregation
Dipyridamole also inhibits cGMP phosphodiesterase activity, increasing cGMP and causing vasodilation

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7
Q

What must dipyridamole be used in combination with?

A

Aspirin
For treatment of TIA
Alone, it has no effect

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8
Q

Cilostazol

A

cAMP phosphodiesterase III (PDEIII) inhibitor

Increased cAMP leads to inhibition of platelet aggregation and increased vasodilation

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9
Q

What is cilostazol used for?

A

Intermittent claudication (Leriche syndrome)

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10
Q

ADP receptor blockers MOA

A

Ticlopidine, clopidogrel

Irreversibly inhibits the binding of ADP to its receptors on platelets (no platelet activation)

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11
Q

Side effects of ADP receptor blockers

A

Bleeding
Leukopenia
Thrombocytopenic purpura

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12
Q

What are ADP receptor blockers used for?

A

Alternatives to ASA in TIAs, post MI and unstable angina

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13
Q

How is clopidogrel activated?

A

It is a prodrug and must be activated by p450 CYP2C19.

Patients with polymorphism of this ensue have decreased effectiveness of clopidogrel

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14
Q

Why is clopidogrel preferred over ticlopidine?

A

Ticlopidine has an increased chance of causing thrombotic thrombocytopenia purpura and requires a high dose

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15
Q

GP IIb/IIIa receptor blockers MOA

A

Inhibit the final common pathway of platelet aggregation

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16
Q

Which are the most effective anti platelet drugs

A

GP IIb/IIIa receptor blockers

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17
Q

Which drugs are GP IIb/IIIa receptor blockers?

A

Monoclonal antibody: Eg. Abciximab

Fibrinogen analog: Eptifibatide and Tirofiban

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18
Q

What are GP IIb/IIIa receptor blockers used for?

A

Only in acute coronary syndromes (MI) and angioplasty and postangioplasty

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19
Q

Heparin MOA

A

Biological

Heparin increases antithrombin III activity to degrade XIIa, XIa, Xa, IXa, IIa, by 1000x

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20
Q

LMWH and Fondaparinaux act on:

A

Xa

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21
Q

Does heparin cross the BBB? What about the placenta?

A

No and no –> safe to use in pregnancy

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22
Q

How are heparins metabolized?

A

Highly acidic –> can be neutralized by protamine
Metabolized in macrophages and endothelial cells; high doses are also cleared by the kidneys
Half life = 2h

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23
Q

When are heparins used?

A

Used for rapid anticoagulation for thrombosis, emboli, unstable angina, DIC and open heart surgery

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24
Q

Pathogenesis of heparin induced thrombocytopenia

A

1-5% incidence
Body produces antibodies against platelet factor 4 bound with heparin
IgG+antibody+heparin+PF4 binds to the Fc receptor of platelets, activating them –> platelet microparticles form and a blood clot develops

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25
Q

Signs of HIT

A

New thrombosis
Platelet count drops >30%
Occurs 5-10 days after beginning heparin therapy

26
Q

How do you treat HIT

A

Monitor platelet count frequently

Discontinue heparin and switch to DTI or fondaparinux

27
Q

Side effects of heparin

A

HIT
Increases bleeding –> hemorrhagic stroke
Hematoma formation
Reversible alopecia
Osteoporosis (use for 5-8 months - incidence 2-5%. May be due to inhibit cytokine-related osteoblast maturation)

28
Q

What is the antidote for hemorrhagic stroke?

29
Q

When is heparin contraindicated?

A 
Heparin allergy 
Bleeding disorders (hemophilia, thrombocytopenia, ulcerative lesions of the GIT) 
Brain, eye or spinal cord surgery
Intracranial hemorrhage 
Infective endocarditis 
Severe HTN
Active TB
30
Q

How does protamine sulphate affect LMWH

A

Protamine sulfate is only partially effective in reversing it’s anticoagulant effect

31
Q

Which are the LMWH drugs?

A

Enoxaparin, dalteparin, tinzaparin

32
Q

Why is LMWH better than heparin?

A 
LMWH has higher bioavailability and longer duration of action (Enoxaparin T1/2 4.5h)
Relatively safe, subcutaneous injection, lower dose, less frequently, do not need aPTT monitoring.
Less HIT (0.8% by LMWH vs 1-5% by heparin)
LMWH more effective than heparin in high risk setting (eg. Trauma, orthopedic surgeries).
33
Q

When is LMWH unsafe to use?

A

LMWH unsafe in pts. with renal insufficiency due to mainly cleared by renal

34
Q

Fondaparinux MOA

A

Synthetic
Inactivates Xa by binding to antithrombin III
Half life = 15h

35
Q

How does protamine affect fondaparinux?

A

It will not reverse it’s action

36
Q

Does fondaparinux have heparin structure?

37
Q

What does excess protamine cause?

A

Bleeding (protamine-heparin complex may damage platelet function)

38
Q

Which are the oral direct Xa inhibitors?

A

Rivaroxaban, apixaban, edoxaban

39
Q

What are direct Xa inhibitors used for?

A

Non-valvular a-fib, DVT and PE
They are preferred over warfarin
Do not require monitoring

40
Q

When are direct Xa inhibitors contraindicated?

A

Liver and renal dysfunction

41
Q

Direct thrombin inhibitors MOA

A

Directly bind to and irreversibly inhibit thrombin

Monitored by aPTT (oral dabigatran is not monitored routinely)

42
Q

When are DITs used?

A

In patients with HIT

43
Q

Hirudin

A

Specific irreversible thrombin inhibitor from leech saliva

44
Q

Which are the DTIs?

A

Lepirudin, bivalirudin, argatroban, dabigatran

45
Q

What is warfarin used to treat?

A 
Used to maintain anticoagulation therapy over long term
To prevent thrombosis in patients with: 
valvular a-fib 
mechanical heart valves 
kidney dysfunction 
liver dysfunction
46
Q

What is dicoumarol?

A

Drug similar to warfarin, but not as effective

47
Q

Warfarin MOA

A

Inhibits vit k epoxide reductase, reducing the conversion of vit k epoxide (KO) to hydroquinone (KH2), which is the active form.
Therefore, warfarin inhibits synthesis of new clotting factors II, VII, IX, X, protein C and protein S. It has no effect on old clotting factors already synthesized.

48
Q

How can effects of warfarin be reversed?

A

Vitamin K, but it takes time. So immediate remedy is through transfusion of fresh frozen plasma.

49
Q

Can warfarin be used in pregnancy?

A

NO. Crosses the placenta and produces fetal toxicity because fetal proteins with carboxyglutamate residue in bone may be affected and can cause abnormal bone formation. LMWH are a better alternative.

50
Q

What is the half life and Vd of warfarin?

A

Half life: 2-5 days
Vd: low because it is 99% protein bound
Onset is 6-8h
Bioavailability is 100%

51
Q

Side effects of warfarin

A

Bleeding (monitor INR)
Skin necrosis due to low protein C (Because of the delay in thrombin suppression, heparin is administered concurrently with warfarin for 4-5 days to prevent thrombus propagation)

52
Q

Which drugs cause increased action of warfarin?

A 
Cephalosporins
Cimetidine
Macrolide antibiotics 
Ketoconazole 
Fluconazole
Metronidazole
Amiodarone
Sulfa drugs
53
Q

Which drugs cause decreased action of warfarin?

A 
Barbiturates
Phenytoin
Rifampin
Vitamin K
Cholestyramine
St Johns wort
54
Q

When should fibrinolytic therapy be started?

A

ASAP to reestablish blood flow
After MI –> within 12h
After ischemic stroke –> within 3h
Prevention of further clot formation starts with heparin for a week to achieve immediate action, followed by warfarin for 6 months maintenance therapy. Antiplatelet drugs are added to therapy

55
Q

Which are the fibrinolytic drugs?

A 
Streptokinase
Urokinase
Anistreplase 
Alteplase 
Reteplase 
Tenecteplase
56
Q

MOA of fibrinolytics

A

Rapidly lyse the thrombi by catalyzing the formation of plasmin from plasminogen

57
Q

Which fibrinolytic is binds to fibrin more tightly and is approved for treatment of ischemic stroke?

58
Q

When is thrombolytic therapy for ischemic stroke contraindicated?

A

Use of heparin in the previous 48 hours
A platelet count less than 100 000/mm3
Another stroke or a serious head injury in the previous 3 months
Major surgery within the preceding 14 days
SBP >185mm Hg, DBP > 110 mm Hg
Rapidly improving neurological signs
Prior intracranial hemorrhage
Blood glucose less than 50 mg/dL or greater than 400 mg/dL
Seizure at the onset of stroke
GI or urinary bleeding within the preceding 21d
Recent MI

59
Q

What are the antidotes for tPA?

A

Epsilon amino caproic acid, tranexamic acid

60
Q

Tranexamic acid MOA

A

Binds to plasminogen and inhibits plasminogen activation

Used in the treatment of fibrinolytic overdose, hemophilia, postoperative bleeding, etc.

61
Q

Agents used in excessive bleeding:

A 
Blood transfusion 
Fresh frozen plasma
Clotting factors and Platelets
Protamine sulphate 
Vitamin K 
Antifibrinolytics
Idarucizumab

Pharm (7 decks)

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