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Pharm block 4 hemostasis and cardiac > antiplatelet drugs > Flashcards

antiplatelet drugs Flashcards

1
Q

antiplatelet drugs inhibit what functions

A

primary hemostatic plug formation, aggregation, activation and release mechanisms.

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2
Q

Platelet Aggregation Assay

A
  1. prepare PRP
  2. activate platelets (PRP+ ADP, TRAP, epinephrine,
    5-HT, collagen, ristocetin, AA)
  3. measure Light transmittance (low= no aggregration, high = aggregation)
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3
Q

Light (alpha) granule release products:

A

a. Platelet factor 4 (aka heparin co-factor)
b. Beta-thromboglobulin
c. Platelet-derived growth factor (PDGF)

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4
Q

Dark (beta) granule release products:

A

a. Ca+2
b. Serotonin
c. ATP/ADP

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5
Q

Products formed during platelet activation and endothelial interaction:

A

prostaglandin derivatives, endoperoxides, thromboxanes.

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6
Q

advantages of antiplatelet drugs vs heparins and anticoagulants

A

These drugs are effective in the arterial circulation, where anticoagulants such as heparin and oral anticoagulants have relatively little effect.

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7
Q

types of antiplatelet drugs

A
  1. Aspirin
  2. Cyclooxygenase (COX) inhibitors (COX1 and COX2 inhibitors)
  3. Propionic acid derivatives (NSAIDs)
  4. ADP Receptor inhibitors
  5. Dipyridamole (Persantine®) a coronary vasodilator
  6. Cilostazol (Pletal®) – used for the management of intermittent claudication
  7. GPIIb/IIIa Inhibitors
  8. Prostacyclin analogue (Iloprost®)
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8
Q

what drugs belong to the ADP Receptor inhibitors group

A 
Ticlopidine (Ticlid), 
Clopidogrel (Plavix), 
Prasugrel (Effient),
Ticagrelor (Brilinta) and 
Cangrelor (Kengreal)
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9
Q

which drugs belong to GPIIb/IIIa Inhibitors group

A

abciximab, ReoPro®;
tirofiban, Aggrastat®, and
eptifabatide, Integrilin®

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10
Q

Dipyridamole (Persantine®) MOA

A

coronary artery dilator (used for coronary artery surgeries)

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11
Q

Aspirins MOA

A

COX-1 and COX-2 inhibitor

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12
Q

aspirins dosing for antiplatelet effects

A

Aspirin is used as a single low dose 81 mg/daily for antiplatelet actions

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13
Q

aspirin resistance

A

many pts do no respond to the normal daily dose of 81 mg per day leading to theurapeutic failure. Increasing the dose can restore the antiplatelet effect.

may be the cause of recurrent ischemic vascular events in patients taking asprin.

may be due to COX polymorphism

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14
Q

clopidogrens MOA

A

selectively inhibits ADP binding to its platelet receptor, preventing subsequent platelet aggregation

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15
Q

clopidogrel vs. Prasugrel

A

both inhibit platelet aggreation.
clopidogrel has a large amount of variation in responses within the population while prasurgrel has less variation and is therefore effective for a larger % of people.

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16
Q

Dual Antiplatelet Therapy

A

Aspirin/ADP receptor inhibitors
Aspirin/GP IIb/IIIa inhibitor
Aspirin/Dipyridamol

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17
Q

Triple Antiplatelet Therapy

A

Aspirin/ADP receptor inhibitor/ Cilostazol

not commonly used

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18
Q

GP IIb-IIIa inhibitors MOA

A

after platelets are activated they express GP IIb/IIIa, the GP IIb/IIIa inhibitor binds to the active site preventing fibrinogen from binding

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19
Q

clinical uses for antiplatelet drugs

A
  1. Cerebrovascular disease:
    a. Transient ischemic attack (TIA)
    b. Complete stroke
  2. Coronary artery disease:
    a. Acute myocardial infarction
    b. Unstable Angina
  3. Saphenous vein coronary artery bypass grafts:
  4. Peripheral vascular disease:
    a. Venous thrombosis
    b. Peripheral arterial disease (PAOD, intermittent claudication)
  5. Small vessel disease
    a. **Thrombotic thrombocytopenic purpura
  6. Prevention of thrombus formation on artificial surfaces
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20
Q

Drug Interactions with Antiplatelet Agents

A

Thrombolytic agents (urokinase, streptokinase and tissue plasminogen activator).

  1. Heparin/LMW Heparin/oral anticoagulants
  2. Warfarin
  3. Antithrombin agents (hirudin, bivalirudin and argatroban).

all increase the antiplatelet effect and risk of bleeding

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21
Q

Arachidonic Acid is released from

A

membrane phospolipids

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22
Q

Arachidonic Acid is used to make

A

Leukotrienes, Thromboxanes, Prostacyclins, Prostaglandins

aspirin and NSAIDs block thromboxanes, prostacyclins, and prostaglandins

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23
Q

arachidonic acid is metabolized by which 2 pathways

A

Cyclooxygenase pathway
-Prostaglandins, thromboxanes, prostacyclins

Lipoxygenase pathway
- Leukotrienes

24
Q

Cyclooxygenase Pathway

A

Cycloxygenase represents constitutive (COX-1) and inducible (COX-2) enzymes.

Aspirin inhibits both COX-1 and COX-2 thereby limiting the production of prostaglandins.

In particular, thromboxane formation in platelets is inhibited.

This is the main mechanism by which aspirin mediates its therapeutic effects.

25
Q

what participates in the Regulation of Prostacyclin and Thromboxane Synthesis

A 
A.	* Endothelial lining
B.	* Lipoproteins and other blood components
C.	Diet
D.	Drugs
E.	Hemodynamic factors
26
Q

Lipoxygenase Pathway

A

A. Leukotrienes (SRSA)
Inhibitors of lipoxygenase
Zileuton (ZYFLO) –used in maintenance treatment of asthma
Leukotriene antagonists
- Montelkast (Singulair)- used in treatment of asthma and seasonal allergies
- Zarirlukast (Accolate, Accoleit and Vanticon) used in the treatment of asthma

this is the anti-inflammatory pathway. Drugs that affect this pathway are used for respiratory disease

27
Q

prostacyclin effects

A

vasodilation, inhibits platelet aggregation

not affected by aspirin as much bc aspirin does not penetrate the endothelial cells

28
Q

thromboxanes effects

A

vasoconstriction, promotes platelet aggregation

inhibited by aspirin

29
Q

active ingredients in fish oil

A

A. α-linolenic acid
B. eicosapentaenoic acid
C. docosahexaenoic acid

30
Q

Mechanism of antiplatelet action of fish oil

A

A. Membrane effects
B. Thromboxane A3 (inactive) formation - the acids compete with arachidonic acid in the prostaglandin pathway and are converted to thromboxane A3

31
Q

clopidogrel MOA

A

ADP receptor inhibitor

32
Q

Prasugrel MOA

A

ADP receptor inhibitor

33
Q

Ticagrelor MOA

A

ADP receptor inhibitor

34
Q

NSAIDs MOA

A

COX inhibitor

35
Q

Dipyridamole MOA

A

Phosphodiesterase inhibitor

36
Q

Cilostazol MOA

A

phosphodiesterase inhibitor

37
Q

Abciximab MOA

A

GP IIb/IIIa inhibitor

38
Q

Eptifibatide MOA

A

GP IIb/IIIa inhibitor

39
Q

Tirofiban MOA

A

GP IIb/IIIa inhibitor

40
Q

Aspirin indications

A

ACS, stroke, arterial thrombosis

41
Q

clopidogrel indication

A

ACS, stroke, arterial thrombosis

42
Q

prasugrel and ticagrelor indications

A

ACS, stroke, arterial thrombosis

43
Q

dipyridamole indications

A

arterial thrombosis, stroke

44
Q

cilostazol indications

A

intermittent claudication

45
Q

Abciximab indications

A

ACS/PCI

46
Q

Eptifibatide indications

A

ACS/PCI

47
Q

Tirofiban indication

A

ACS/PCI

48
Q

cilostazol side affects

A

hypotension

49
Q

side effects of all antiplatelet drugs

A

bleeding

50
Q

Monteleukast, zafirleukast, Zieuton MOA

A

inhibit leukotrienes

51
Q

Monteleukast, zafirleukast, Zieuton indications and side effects

A 
allergic rxn (monteleukast)
Asthma

side effects : hypotension

52
Q

Which enzyme is responsible for the formation of arachidonic acid?

A

Phospholipase A2

53
Q

Celebrex® MOA

A

COX-2 inhibitor

54
Q

Vioxx MOX

A

COX-2 inhibitor

55
Q

Bextra

A

COX-2 inhibitor

Pharm block 4 hemostasis and cardiac (12 decks)

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