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Pharmacology > Antiplatelet drugs and thrombolytics > Flashcards

Antiplatelet drugs and thrombolytics Flashcards

1
Q

What are Heparin and Warfrin?

A

Anticoagulants that prevent arterial and venous thrombosis

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2
Q

What are the anti-platelet drugs particularly good @

A

Most effective at preventing arterial thrombosis and generally less effective at preventing venous thrombosis.

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3
Q

What do Thrombolytics (Fibrinolytics) do?

A

Lyse both arterial and venous thrombi

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4
Q

How does asprin exert its effects?

A

By non selectively inhibiting COX1 and COX2

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5
Q

Inhibition of which cyclo-oxygenase prevents the synthesis of the pro-aggregarory prostaglandin ThromboxaneA2?

A

COX1

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6
Q

What is the biological halflife of the asprin effect (acetylating)

A

4-7 days (the time needed to generate new platelets

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7
Q

What effects does asprin have in COX2 inhibition?

A

Prevents synthesis of antiaggregatory PGI2 in endothelial cells

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8
Q

Where is the effect of Asprin stronger?

A

On Thromboxane

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9
Q

What is the daily dosing range for anti-platelet therapy

A

81-325mg

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10
Q

What are the adverse side effects of Asprin?

A
  1. G.I bleeding
  2. Hemmorrhagic stroke
  3. Asthma (more production of leukotrienes)
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11
Q

What are the contraindications for asprin therapy?

A
  1. Coumarin anticoagulants (inceased risk of bleeding)
  2. Peptic Ulcer disease
  3. Asprin hypersensitivity (asthma)
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12
Q

Do NSAID have same effeect as asprin?

A

Also inhibit COX1 and 2 but their effect is reversible and temporary

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13
Q

Do NSAIDS replace the anti-platelet effect of asprin?

A

No they compete for COX1 binding sites and prevent acetylation

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14
Q

Should NSAID be taken the same time as asprin?

A

NO

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15
Q

How does acetaminaophen exert its antipyretic effect?

A

It inhibits brain COX but has little anti-inflammatory and antiplatelet effects

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16
Q

What is the ideal analgesic/antipyretic for patients on anticoagulats?

A

Tylenol aka Acetaminophen

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17
Q

What is Celecoxib aka Celebrex?

A

Selective COX2 inhibitor

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18
Q

How does it exert its effect?

A

Inhibits PGI2

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19
Q

What is a side effect of Celebrex?

A

CVD stemming from increaded BP and unopposed TXA2

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20
Q

What does celebrex not inhibit?

A

COX-1

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21
Q

What are the only 2 drugs that should be used for anti-platelet function?

A

Asprin and Clopidogrel

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22
Q

How do phosphodiesterase exert their effect?

A

Inhibits the enzyme that degrades cAMP . Increased platelet cAMP inhibits aggregation
2.Also activates platelet adenylate cyclase by inhibiting adenosine uptake

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23
Q

Dipyridamole has?

A
  1. Weak antiplatelet effect used alone
  2. Benefit of (extended relief prep) in combination with asprin in patients with cerebrovascular disease.
  3. When combined with Warfarin reduces thromboembolitic events in patients with artificial heart valves
  4. Also a potent Vasodilator used IV to induce coronary steal in cardiac studies
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24
Q

What is Cilostazol

A

A PDE IIB inhibitor, vasodilator used for intermittent claudication in peripheral artery disease.
2.Is also a reversible platelet inhibitor

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25
Q

The combination therap of Asprin and Dipyridamole is used for

A

Stroke patients

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26
Q

What receptor mediates platelt activation?

A

P2Y12 ADP receptor

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27
Q

What drugs inhibit the ADP receptor mediated activation of platelets?

A

Thienopyridines

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28
Q

How do the Thienpyridines exert their anti-platelet effect?

A

They block the ADP receptor P2Y12 preventing the ADP-induced activation of GP IIb/IIIa receptor

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29
Q

How long does the effect of the Thienpyridines last?

A

Takes 5-7 days for recovery of platelet function

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30
Q

What was the first Drug of the thienopyridines?

A

Ticlopidine

31
Q

What side effects are associated with Ticlopidine?

A

Neutropenia, thrombotic thrombocytopenic purpura and aplastic anemia

32
Q

What is the preffered agent of the Thienopyridines?

A

Clopidogrel (lower incidence of TTP & neutropenia)

33
Q

Which cytochrome metabolizes Clopidogrel?

A

CYP2C19 (metabolizes the pro-drug to make it active)

34
Q

What is needed in the 2-14% of patients who are slow metabolizers of Clopidogrel (PLAVIX)

A

A higher dose

35
Q

What drugs may interfere with formation of active Clopidogrel metabolite formation?

A

Omeprazole

36
Q

What is the risk in Prasugrel not as elevated in Clopidogrel?

A

Bleeding Risk

37
Q

Which CYP metabolises and activates Prasugrel?

A

CYP3A4 & CYP2B6

38
Q

When would one consider Prasugrel?

A

In patients with CYPC19 polymorphisms

39
Q

Is Clopidogrel + Asprin more effective than Asprin alone?

A

Marginally

40
Q

Is clopidorel and asprin combined

A

1.Increases risk of bleeding

41
Q

What is Eptifibidate?

A
  1. Inhibitor of GPIIa/IIIb
  2. Inhibits platelet aggregation
  3. Prevents platelet binding to Fibrinogen and VWF
42
Q

How is Eptifibidate administered?

A

Paraenteral IV

43
Q

What is Abciximab

A

Monoclonal antibody 7E3

44
Q

How does Abciximab exert its effect?

A

Blocks GPIIb/IIIa, and vitronectin receptor

45
Q

Where is the effect/benefit of Abciximab greatest?

A

In patients with High Troponin levels

46
Q

What do Eptifibidate and Abciximab have in common?

A

Other than both blocking GpIIb/IIIa the are both administered IV prior to cardiac catherization and angioplasty to prevent in stent thrombosis / stenosis

47
Q

What is the role od Warfrin in coronary heart disease?

A
  1. Reduced cardivascular events more than asprin alone

2. Warfrin not routinely recommended in CHD prevention

48
Q

What is Warfrin the drug of choice for?

A

DVT and pulmonary embolism prophylaxis, and preventing thromboembolism in atrial fibrillation

49
Q

How do thrombolytic drugs work?

A

Promote Fibrinolysis by conversion of plamingen to its active form plasmin

50
Q

What are some of the therapeutic used of fibrinolytics?

A

MI
DVT
PE
Thrombotic stroke

51
Q

What is concomittantly administered with warfrin and why?

A

Asprin and Heparin to prevent re-thrombosis

52
Q

How effect is the IV administration of thrombolytic after acute MI?

A

Results in lysis of coronary thrombosis 60-70% o

53
Q

What are the toxicities of Thrombolytics?

A
  1. Systemic lytic state

2. MOST SERIOUS SIDE EFFECT IS INTRACRANIAL HEMORRHAGE

54
Q

What are the contraindications for throbolytics i.e Warfarin?

A
  1. Recent surgery, organ biopsy or puncture of noncompressible vessel
  2. Recent G.I bleeding
  3. Uncontrolled hypertension (180/110)
  4. Active intracranial process or recent cerebrovascular accident
  5. Active bleeding or Hemorrhagic disorder
  6. Aortic dissection
  7. Acute pericarditis
  8. Age >75
55
Q

What is Streptokinase?

A

First Gen thrombolytic isolated from hemolytic streptococci

56
Q

How does Streptokinase exert its effect?

A

Forms activator complex with plasminogen (has nointristic protease activity)
2.Indiscriminately activates circulating and fibrin bound plasminogen producing a systemic lytic state

57
Q

What are some coplications associated with Streptokinase?

A

1.Strongly immunogenic; formation of antistreptokinase antibodies

58
Q

What is the presentation of anti-streptokinase antibodies?

A
  1. Serum sickness
  2. Hypotension
  3. bronchospasm
  4. angioedema
59
Q

How many times can one administer Streptokinase?

A

ONCE. Antibodies inactivate it from previous administration and even from prior streptococcal infection

60
Q

What is the major advantage of using Streptokinase?

A

Cost

61
Q

What is Urokinase?

A

Trypsin like serine protease produced from cultures of human fetal kidneys

62
Q

How does Urokinase exert its effect?

A

Directly cleaves plasminogen to plasmin

63
Q

What is a major benefit of Urokinase?

A

Not antigenic, no allergic reactions

64
Q

Does Urokinase produce a systemic lytic state?

A

Yes

65
Q

When is Urokinase indicated?

A

Treatment of massive or hemodynamically instable PE

66
Q

What is Tissue type plasminogen activator?

A

Maturally occurring protein released by vascular endothelial cells (a serine protease)

67
Q

How is therapeutic t-PA produced?

A

Via recombinant technology

68
Q

What is different about t-PA?

A

Is relatively fibrin specific localizes plasminogen activation to the fibrin clot

69
Q

When is t-PA indicated?

A

For MI, PE, and acute ischemic stroke less than 3 hours with no hemorrhage on CT

70
Q

What is r-PA?

A

Deletion variant of t-PA

71
Q

What are benefits of r-PA

A

Longer half life

72
Q

What is Aminocaproic Acid?

A

Antifibrinolytic

73
Q

How does Aminocaproic Acid exert its effect?

A

Analogue of lysine that inhibits plasmin

74
Q

Whaen is Aminocaproic acid indicated?

A

In treatment of excessive bleeding from systemic hyperfibrinolysis and urinary fibrinolysis

  1. For Haemophiliac after dental procedures
  2. Haematuria
  3. Bleeding associated with Cardia surgery

Pharmacology (2 decks)

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