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Pharmacology Exam II > Hematologic Agents > Flashcards

Hematologic Agents Flashcards

1
Q

Hemostasis Systems (5)

A 
Vascular
Platelet
Coagulation
Anti-Coagulation
Fibrinolytic
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2
Q

Initial binding to begin platelet activation (receptor and binding ligand)

A

GpIb binds von Willebrand Factor

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3
Q

Platelets secrete 3 main things after being activated

A

ADP, TXA2, 5-HT

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4
Q

Linking of platelets together is due to activation of which receptor? What ligand stabilizes binding

A

GpIIb/IIIa

Fibrin

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5
Q

Intrinsic system

A

XII, XI, IX, VIII

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6
Q

Common Pathway

A

X, V, III, II

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7
Q

Extrinsic System

A

VII + Tissue Factor (III)

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8
Q

What factor stabilizes fibrin crosslinks?

A

XIIIa

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9
Q

What to factors inhibit the clotting cascade?

What factors do they inhibit/inactivate?

A

Protein C and S

Factor VIIIa and Va

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10
Q

What factor blocks Xa?

What speeds up its activity?

A

Antithrombin

Heparin

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11
Q

Where does fibrinogen bind to be converted to fibrin?

A

active site of thrombin

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12
Q

What is the E1 site on thrombin for?

A

binding fibrin

limits the diffusion of thrombin away from the clot

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13
Q

What is the significance of the thrombin already bound to fibrin?

A

It isn’t inhibited by antithrombin/heparin

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14
Q

What are the characteristics of venous thrombosis?

What is the significance for treatment?

A

platelet poor

often occur at valve cusps (slow moving/sluggish blood)

can lead to VTE or PE

Typically won’t use anti-platelet therapies

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15
Q

What are the characteristics of arterial thrombosis?

Most common cause of what?

A

often occur on top of ruptured atherosclerotic plauqes

rich in platelets

MI and Ischemic Strokes

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16
Q

Aspirin MOA

A

irreversibly blocks cyclooxygenase-1

reduces TXA2 synthesis - leads to decreased platelet activation

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17
Q

Dipyridamole MOA

A

elevated cAMP decreases Ca levels intracellularly

reduces activation of platelets

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18
Q

P2Y12 antagonists

A

Clopidogrel
Prasugrel
Ticagrelor
Cangrelor

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19
Q

Ticagrelor and Cangrelor don’t need what?

A

to be activated

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20
Q

Clopidogrel and Prasugrel need what?

A

to be activated through metabolism in the liver

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21
Q

P2Y12 antagonists Ultimate MOA

A

decrease activation of GpIIb/IIIa and decrease calcium mobilization

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22
Q

GpIIb/IIIa Antagonists General MOA

A

Inhibit cross linking of GpIIb/IIIa receptors

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23
Q

GpIIb/IIIa Antagonists

A

Abciximab
Eptifibatide
Tirofiban

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24
Q

Abciximab MOA

A

Fab fragment that binds to GpIIb/IIIa

also binds to receptor on leukocytes - may explain anti-inflammatory effects

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25
Q

Eptifibatide MOA

A

peptide that binds to GpIIb/IIIa

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26
Q

Tirofiban MOA

A

nonpeptide that binds and inhibits GpIIb/IIIa

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27
Q

Dual Antiplatelet Therapy

A

Aspirin + P2Y12 Antagonist

28
Q

Triple Antiplatelet Therapy

A

Aspirin, Warfarin, Clopidogrel

29
Q

Indirect Inhibitors of Thrombin or Factor Xa

A

Heparin
Enoxaparin
Fondaparinux

30
Q

Direct Thrombin Inhibitors

A

Lepirudin
Bivalirudin
Argatroban
Dabigatran

31
Q

Direct Xa Inhibitors

A

Rivaroxaban

Apixaban

32
Q

Vitamin K Antagonist

A

Warfarin

33
Q

Heparin MOA

A

specific sequence binds to antithrombin

changes conformation to increase affinity for factor Xa

can also increase AT-induced inhibition of thrombin (w/long enough molecules)

34
Q

Heparin administration

A

Intravenously most common

35
Q

Heparin characteristics

A

short half life

can bind to other plasma proteins and endothelium of vessels

Dosing is unpredictable because binding differs from person to person

36
Q

Heparin Pharmacokinetics Special Considerations

A

Cleared by 2 mechanisms

Clearance decreases as dose increases, therefore

half life increases as dose increases

37
Q

Heparin most common complication

Heparin overdose treatment

A

Bleeding

Protamine Sulfate

38
Q

Long term heparin use associated with?

A

osteoporosis

39
Q

Type 1 Heparin-Induced Thrombocytopenia

A

25% of patients develop thrombocytopenia within first 2-5 days fo tx

Not though to be caused by immune system

40
Q

Explain Type 2 Heparin-Induced Thrombocytopenia

A

Uncommon

Heparin can bind platelet factor 4

Antibodies are generated toward hep/PF4 complex

Can bind platelets and activate them

Leads to venous and arterial thrombosis

41
Q

Low molecular weight heparin (enoxaparin) MOA

Advantages

Disadvantage

A

primarily acts by inhibiting factor Xa

easier to dose, given subcutaneously, longer half life, predictable clearance, lower osteoporosis risk

Protamine only partially reverses

42
Q

Fondaparinux MOA

Cannot be inhibited by?

A

analog of AT-binding pentasaccharide sequence

inhibits factor Xa but CANNOT bind antithrombin

Protamine sulfate

43
Q

What test is used to monitor LMWH and Fondaparinux?

A

Anti-factor Xa assay

44
Q

LMWH and Fondaparinux contraindicated in?

A

patients with severe renal insufficiency

45
Q

Bivalirudin and Lepirudin MOA

A

bind to fibrin binding site and active site of thrombin

46
Q

Argatroban and Dabigatran MOA

A

bind only the active site of thrombin

47
Q

Parenteral Direct thrombin inhibitors

A

Bivalirudin, Lepirudin, Argatroban

48
Q

Oral direct thrombin inhibitor

A

Dabigatran

49
Q

Major advantage of DTI’s over Heparin?

A

DTI’s can inhibit thrombin bound to fibrin

50
Q

DTI’s used in (3)

A

heparin induced thrombocytopenia

percutaneous coronary intervention

Dabigatran also used in stroke prevention

51
Q

Warfarin MOA

A

competes with vitamin K for vitamin K reductase

reduces activation of factors 10, 9, 7, 2, Protein C, and Protein S

(coumadin)

52
Q

Warfarin Important Characteristics

A

close 100% bioavailability

small Vd

full effect takes about 3-5 days

53
Q

Warfarin is metabolized by

A

CYP2C9 and other CYP’s

54
Q

Drugs that potentiate Warfarins effect _____ INR

A

increase

55
Q

Drugs that inhibit warfarins effect _____ INR

A

decrease

56
Q

Drugs that increase Warfarins function

A

Broad-spectrum ABX
NSAID’s
Some SSRI’s
Some Statins

57
Q

Drugs that decrease Warfarins function

A

rifampin
barbiturates
carbamazepine

58
Q

Diseases that affect warfarin function

A

Hepatic function - increases INR - d/t decreased clearance

Intestinal diseases - increase INR - d/t decreased vit K absorption

Renal insufficiency - increases INR - d/t decreased albumin

59
Q

Warfarin Adverse Effects

A

Hemorrhage (stroke)
Placental Transfer
Birth defects
Necrosis (rare) - d/t protein C levels decrease

60
Q

Rivaroxaban MOA

A

direct factor Xa inhibitor

61
Q

Dabigatran MOA

Used for

Contraindicated in?

A

oral thrombin inhibitor

stroke prevention in a-fib and DVT/PE tx

patients with mechanical heart valves

62
Q

Main enzyme that breaks down fibrin?

A

plasmin

63
Q

Fibrinolytic Drugs (3)

A

Streptokinase
Urokinase plasminogen activator
Tissue plasminogen activator

64
Q

Alteplase MOA

A

activates plasminogen to form plasmin

65
Q

Main use of tPA’s

A

acute myocardial infarction, with ST segment elevation w/oin 12 hrs of onset

66
Q

Fibrinolysis Inhibitors

A

Aminocaproic acid

Tranexamic acid

67
Q

Fibrinolysis Inhibitors MOA

A

block interaction of plasmin with fibrin

Pharmacology Exam II (5 decks)

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