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Pharm > Hematological agents I > Flashcards

Hematological agents I Flashcards

1
Q

What are the three chemokines released from platelets at the site of injury, that cause vasoconstriction?

A

Thromboxane A2
5HT
ADP

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2
Q

Thrombin causes endothelial cells to secrete what chemokine? What does this do?

A

endothelin 1

Vasoconstricts

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3
Q

What is the protein on blood vessels that is exposed and allows for the attachment of GP Ib?

A

von Willebrand factor

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4
Q

What is the protein on platelets that attachs to vWF?

A

GP Ib

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5
Q

What are the proteins on platelets that interact with ADP?

A

P2Y1 and P2Y12 GPCRs

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6
Q

What does the glycoprotein GPIIb/IIIa on platelets bind to?

A

fibrinogen in the plasma, which binds other platelets

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7
Q

What does the coagulation cascade utimately produce? What does that cause?

A

thrombin, which activates fibrinogen into fibrin

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8
Q

Thrombin activates protease-coupled receptors (PARs). What is the function of this?

A

further activation of platelets

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9
Q

What mineral increases with platelet activation, and activates phospholipase A2?

A

Ca

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10
Q

What is the role of phospholipase A2, after activation by Ca?

A

cleaves phospholipids to create arachiodonic acid

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11
Q

What is the MOA by which ASA decreases platelet activation?

A

Prevents formation of thromboxane A2 by inhibiting cox enzymes

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12
Q

What organ synthesizes most of the coagulation factors?

A

Liver

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13
Q

What are the components of the prothrombin activator complex?

A

Xa, Va, Ca2+

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14
Q

What activates factor 12 in the intrinsic pathway?

A

negative surface of a damaged blood vessel

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15
Q

What is the order of the intrinsic pathway?

A

12, 11, 9, 10

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16
Q

What are the components of the tenase complex? What is the role of the tenase complex?

A

factors 8 and 9significantly accelerates the catalytic activity of IXa

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17
Q

What is the cause of hemophilia A?

A

reduced levels of factor VIII

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18
Q

What allows the initial small amounts of thrombin to lead to an explosive burst of thrombin production?

A

Positive feedback of thrombin mediated Factor VIII and V activation

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19
Q

What factor is an intregral membrane protein, that binds to , and proteolytcally activates facot VII?

A

Factor 3

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20
Q

What is the order of the extrinsic pathway of coagulation

A

3, 7, 10

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21
Q

What does the factor 3 and 7 complex do?

A

activates factor X

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22
Q

What is the protein that initially tethers platelets to the site of injury?

A

GP 1b

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23
Q

What are the two mechanisms by which the anticoagulation system prevent aberrent clot formation?

A

Prevent thrombin mediated fibrin clot formationDestroying thrombin

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24
Q

What is thrombomodulin?

A

integral membrane protein on vasculature endothelial cells that can bind thrombin and protein C

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25
Q

What is protein C? What role does it play in it’s complexed form?

A

Protein that is activated by thrombomodulin, and activates protsin SProteolytically activates factors V and VIII

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26
Q

What is the role of tissue factor pathway inhibitor?

A

Circulating protein that inhibits tissue factor/ VII complex and factor X

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27
Q

What is the role of antithrombin?

A

Circulating protease inhibitor that inactivates thrombin when bound to heparin

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28
Q

What is the key protein involved in the fibrinolytic system?

A

Plasminogen / plasmin

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29
Q

What activates plasminogen, and turns it into plasmin? What cells express this activator?

A

tPA which is expressed by endothelial cells

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30
Q

How is it that not all clots are dissolved if tPA is expressed by endothelial tissue?

A

tPA removed by plasminogen activator inhibitorthrombin-activatable fibrinolysis inhibitor

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31
Q

What is the role of alpha2 antiplasmin?

A

Inhibits unbound plasmin

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32
Q

What is the role of factor XIII?

A

Stabilizes the fibrin clot

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33
Q

What organ produces antithrombin?

A

Liver

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34
Q

What is the complex that activates protein C?

A

Thrombin+ thrombomodulin

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35
Q

What does the E1 site on thrombin bind?

A

Fibrin

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36
Q

How is thrombin prevented from forming clots throughout the body? What stops antithrombin from stopping it?

A

Has to bind to fibrinBinding site is not exposed to antithrombin

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37
Q

True or false: the antithrombin/heparin complex does not inhibit thrombin bound to fibrin

A

True

38
Q

Why are venous thromboses referred to as “red clots”?

A

Platelet poor, filled with RBCs

39
Q

Why are arterial thrombi white?

A

Full of platelets

40
Q

Where do venous thrombi usually form?

A

Vavle cusps

41
Q

Why aren’t antiplatelet therapies not very useful for veinous thromboses?

A

Not a lot of platelets in the clot

42
Q

Prothrombitic or antithrombic: factor V leidin

A

Prothrombotic

43
Q

Prothrombitic or antithrombic: Protein C mutation

A

Prothrombotic

44
Q

What is the MOA of ASA?

A

Irreversibly blocks COX-1 in plateletsReduces thromboxane A2 production

45
Q

Why don’t other NSAIDs reduce platelet aggregation?

A

Do not irreversibly bind cox enzyme

46
Q

What are the adverse effects of ASA?

A

Gastric bleeding and inducing bronchospasms

47
Q

What activates phospholipase A2? What does it produce?

A

Ca levelsProduces arachiodonic acid

48
Q

Why is blocking of the Cox enzyme so effective in antiplatelet therapy?

A

Platelets do not have the machienery to make more

49
Q

What is the MOA of dipyridamole?

A

Phosphodiesterase inhibitor that prevents conversion of cAMP to AMP, which lowers Ca levelsAlso increases cAMP uptake

50
Q

True or false: dipyramidole has little effect without ASA

A

True

51
Q

What is the role of P2Y12?

A

Protein on platelets that increases clotting when bound by Ca

52
Q

What is the MOA of clopidogrel?

A

Prevents P2Y12 activation, which decreases {Ca] within platlets

53
Q

True or false: clopidogrel is administered orally in the active form

A

False-prodrug form

54
Q

What is one major issue that decreases the effectivness of clopidogrel?

A

Some pts have polymorphims that detract from effectiveness

55
Q

What is the MOA of prasugrel?

A

Irreversible P2Y12 inhibitor

56
Q

What is the major difference between clopidegreal and prasugrel?

A

Prasugrel is more activated, but higher rates of bleeding

57
Q

What is the MOA of ticagrelor?

A

Reversible P2Y12 inhibitor

58
Q

True or false: ticagrelor is administered as a prodrug

A

False

59
Q

Why is it that ticagrelor’s effect are more easily reversed than clopidogrel or prasugrel?

A

Others are irreversible inhibitors of P2Y12

60
Q

What is the MOA of cangrelor?

A

Reversible P2Y12 inhibitor

61
Q

What is the major difference between cangrelor and other P2Y12 antagonists like clopidogrel or prasugrel?

A

Administered IV

62
Q

Why is ticagrelor more potent than other P2Y12 inhibitors?

A

Administered in the active state

63
Q

What is the enzyme that clopidogrel needs to be activated? What drugs inhibit this enzyme?

A

CYP2C19Omeprazole

64
Q

What is the major contraindication to using prasugrel or ticagrelor? Why?

A

h/o intracrainal bleeding because causes bleeding

65
Q

What is the MOA of abciximab?

A

Glycoprotein IIb/IIIa receptor antagonist, preventing crosslinking of platelets

66
Q

How is abciximab administered?

A

IV bolus

67
Q

What are the major adverse effects of abciximab?

A

Bleeding and thrombocytopenia

68
Q

What is the MOA of Eptifbatide?

A

Peptide that prevents GP IIb/IIIa from binding other platelets

69
Q

What is the major difference between abciximab and Eptifbatide?

A

Eptifbatide has a longer half life, with lower adverse effects

70
Q

What is the MOA or tirofiban?

A

Inhibitor of GP IIa/IIIb

71
Q

What is the MOA of vorapaxar?

A

Protease activated receptor (PAR) antagonist

72
Q

What are the indications for vorapaxar use?

A

Reduction in thrombotic cardiovascular events in pts with a h/o MI

73
Q

What do protease activated receptors do?

A

Thrombin binds to PARs and cause an increase in platelet activation

74
Q

What are the adverse effects of Vorapaxar?

A

Intracrainal bleeding

75
Q

True or false: antiplatelet therapy usually involves multiple drugs being used at once

A

True

76
Q

What are the three drugs that are indirect inhibitors of thrombin and/or factor X?

A

HeparinEnoxaparinFondaparinux

77
Q

What are the four direct thrombin inhibitors?

A

LepirudinBivalirudinArgatrobanDabigatran

78
Q

What are the direct factor X inhibitors?

A

RivaroxabanApixaban

79
Q

What is the vit K antagonist?

A

Warfarin

80
Q

What are the diseases that anticoagulants are generally used?

A

Treatment/prevention of venous thromboses

81
Q

What exactly is heparin?

A

family of sulfated polysaccharides found on mast cells

82
Q

Is heparin usually found in the plasma?

A

No

83
Q

What does it mean when heparin is unfractionated?

A

contains many different sizes of polysaccharide chains

84
Q

What is the MOA of heparine?

A

binds to antithrombin, which inactivates coagulation factor Xa

85
Q

How must heparin be administered?

A

IV or SQ (but must be parenterally)

86
Q

What are the two ways that heparin is cleared?

A

Kidneys and liverEndothelial cells take it up

87
Q

Why is it that uptake of heparin by endothelial cells is saturatable?

A

Limited space on endothelial cells

88
Q

What is the equation for half life?

A

0.693 x Vd/CL

89
Q

What is the lab test that is used to monitor heparin?

A

aPTT

90
Q

Heparin clear is so variable, that it is often given in amounts greater than therapeutic range, causing bleeding. Why is this not such a big deal?

A

Short half life, so just tone back

91
Q

What is the drug that can be given to inhibit heparin? MOA?

A

Protaminebinds and inactivates larger heparin molecules

92
Q

What disease can be caused by long term heparin use?

A

Osteoporosis

Pharm (73 decks)

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