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Pharmacology Test #4 > Anticoagulation Drugs > Flashcards

Anticoagulation Drugs Flashcards

1
Q

Serine proteases

A

cleave down-stream factors to activate them or cleave factors Va and VIIIa

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2
Q

Examples of serine proteases that cleave down-stream factors

A

Factors XII, XI, X, IX, VII, II (procoagulants)

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3
Q

Examples of serine proteases that cleave factors Va and VIIIa

A

protein C (anticoagulant)

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4
Q

Glycoproteins

A

co-factors for activation of proteases and they bind to and inhibit thrombin

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5
Q

Cofactors for activation of proteases

A

Factors VIII, V, III (tissue factor), Protein S

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6
Q

Glycoproteins that bind to and inhibit thrombin

A

Anti-thrombin III

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7
Q

Ca2+

A

links certain factors to anionic lipids

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8
Q

Transglytaminase

A

cross-links fibrin fibers (Factor XIII)

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9
Q

Fibrinogen/Fibrin

A

ultimately, the substrate protein for factor IIa (thrombin) that polymerizes to form clot

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10
Q

Hemophilia A

A

deficiency in factor VIII (males)

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11
Q

Hemophilia B

A

deficiency in factor IX (males)

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12
Q

Factor V Leiden

A

resistance to activated protein C

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13
Q

Where are clotting factors produced?

A

all except for von Willebrand factor are made in the liver; vWF is produced in the endothelium, subendothelium, and megakaryocytes; Factor VIII is also produced in the endothelium

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14
Q

Extrinsic pathway

A

requires a factor (Tissue Factor) extrinsic to the blood; important when vessel is damaged and blood leaks out

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15
Q

Intrinsic pathway

A

triggered when collagen is exposed on the wall of the blood vessel

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16
Q

Intrinsic pathway is initiated by

A

contact with negatively charged collagen of diseased or injured vessels; blood in test tube clots by this mechanism

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17
Q

Extrinsic pathway relies on

A

factors outside bloodstream for activation; release of tissue thromboplastin initiates pathway

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18
Q

Describe the steps in the activation of the extrinsic pathway to coagulation

A
  1. TF is expressed on the surface of cells outside of but near blood vessels
  2. Factor VII normally resides in blood
  3. TF binding to factor VII activates it
  4. Factor VIIa binds and cleaves factor X
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19
Q

Describe the steps in the activation of the intrinsic pathway to coagulation

A
  1. Factor XIIa cleaves prekallikrein to kallikrein and Factor XI to XIa
  2. Kallikrein activates more Factor XII molecules to XIIa
  3. HMWK anchors kallikrein and Factor XIa to damaged surface
  4. Factor XIa cleaves HMWK, diffuses into circulation, and activates Factor IX
  5. Factor IXa binds Factor VIIIa on the surface of platelets and activates Factor X
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20
Q

What does thrombin do?

A

Thrombin converts fibrinogen into long strands of insoluble fibrin; activates factor XIII which then cross-links fibrin to form a stable clot incorporated into platelet plug

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21
Q

Prothrombin time (PT)

A

recalcified blood + thromboplastin - clots in 12-14 sec; used to monitor oral anticoagulant therapy

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22
Q

Activated partial thromboplastin time (aPTT)

A

recalcified blood + phospholipid - clots in 24-36 sec; used to monitor heparin therapy

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23
Q

Bleeding time

A

time taken for a standardized skin puncture to stop bleeding; measured in minutes (2-9 minutes); abnormal when defect in platelet numbers of function

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24
Q

Slow PT (prolonged time) means

A

defect in extrinsic or common coagulation pathways (oral coagulants)

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25
Q

Slow aPTT (prolonged time) means

A

defect in intrinsic or common coagulation pathways (heparin)

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26
Q

INR

A

standardization of PT - International Normalization Ratio

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27
Q

Equation for INR

A

(Patient PT/Control PT) ^C

C is the international sensitivity index (isi); corrects for different thromboplastin reagents

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28
Q

Therapeutic range for the INR

A

PT ratio of 1.35 - 1.6 = INR of 2-3

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29
Q

Why use anticoagulants?

A

prevent excessive clotting that can lead to occlusion of blood vessels: stroke, post MI, unstable angina, DVT, PE, artificial surfaces

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30
Q

Oral anticoagulant drugs

A

Warfarin (Coumadin) and Anisindione

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31
Q

Indandione anticoagulants

A

orally active; exhibit significant side effects; rarely used clinically

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32
Q

MOA of oral anticoagulants

A

inhibit reduction of vitamin K

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33
Q

Vitamin K is essential for

A

post-translation modification of clotting factors VII, IX, X, prothrombin (II) and anticoagulation proteins C and S

34
Q

Action of Vitamin K

A

Vitamin K carboxylase catalyzes the gamma-carboxylation of Glu in prothrombin; Vit K is oxidized in the process

35
Q

Coumarins inhibit

A

Vit K epoxide reductase, thus blocking reduction of Vit. K epoxide back to its active form

36
Q

Warfarin onset of action

A

delayed onset of action; must deplete the pool of circulating clotting factors; maximal anticoagulant effect is not observed until 3-5 days after initiation of therapy

37
Q

Loading/Maintenance dose of Warfarin

A

Loading dose: 5 mg/day

Maintenance dose: 2.5 or 5 mg/day

38
Q

What happens after discontinuing warfarin therapy

A

factors must be re-synthesized to return to normal PT (several days)

39
Q

Metabolism of warfarin

A

metabolized in liver by CYP2C9 (S-warfarin)

40
Q

Termination of action of warfarin is related to

A

termination of action is not correlated with plasma warfarin levels, but reestablishment of normal clotting factors

41
Q

Overdose of warfarin therapy

A

Iatrogenic hemorrhage; discontinue warfarin therapy; administer Vit K

42
Q

What can high levels of Vit K do?

A

can activate warfarin-inhibited reductase

43
Q

Warfarin use during pregnancy

A

contraindicated in women who are or may become pregnant; warfarin passes freely thru placenta; increased incidence of spontaneous abortions; fetal hemorrhage; birth defects

44
Q

Fetal warfarin syndrome

A

nasal hypoplasia and abnormal bone formation

45
Q

Vitamin K involved in the post-translation modification of

A

prothrombin, factors VII, IX, and X

46
Q

Uses of Vitamin K (Phytonadione)

A

individuals with abnormalities of fat absorption (vit K deficiency); all newborns receive an injection to prevent hemorrhagic disease; reverse anticoagulant effect of excess warfarin

47
Q

Parenteral anticoagulants

A

heparin (unfractionated heparin); low molecular weight heparins; non-heparinoids

48
Q

MOA of heparin

A

heparin binds to a positively charged region of antithrombin III; (AT) heparin binding greatly increases the rate at which AT interacts with plasma protease clotting factors; heparin then dissociates from complex and can interact with more AT

49
Q

What does binding of heparin do?

A

enhances the rate of inhibition of clotting factors

50
Q

Antithrombin III (AT) can inactivate

A

thrombin and factors Xa, VIIa, and IXa

51
Q

Administration of heparin

A

effective immediately; intermittent IV injection; continuous IV infusion - easiest to control SC injection

52
Q

When do you adjust heparin dosing based on

A

adjust dosing according to coagulation tests

53
Q

Adverse effects of heparin

A

Iatrogenic hemorrhage; thrombocytopenia; osteoporosis

54
Q

Risk factors for iatrogenic hemorrhage

A

patients over 50, ulcer patients, severe hypertension, antiplatelet drugs

55
Q

Treatment for iatrogenic hemorrhage due to heparin

A

stop heparin; protamine sulfate - binds tightly to heparin to neutralize the anticoagulant action

56
Q

Protamine sulfate

A

binds tightly to heparin to neutralize the anticoagulant aciton

57
Q

Thrombocytopenis and heparin

A

develops 7-12 days after starting therapy; antibodies develop to platelet (PF4) - heparin complex

58
Q

Osteoporosis and heparin

A

associated with extended therapy (3-6 months)

59
Q

Low molecular weight heparins

A

Dalteparin, Enoxaparin, Tinzaparin, Danaparoid

60
Q

Compare standard heparin to LMWH

A

equal efficacy; LMWH has increased bioavailability from SQ site of administration (only route); LMWH has less frequent dosing and a longer half life; no monitoring of clotting needed with LMWH

61
Q

MOA of LMW heparins

A

binding to AT is sufficient for Factor Xa inhibition; preferentially inhibit Factor Xa; only slightly affect thrombin activity; PT and aPTT are insenstivie measures of activity

62
Q

Advantages of LMWH

A

more predictable pharmacokinetic profile; good bioavailability fro SQ injection site; less protein binding/more uniform dosing; longer half life; lower incidence of thrombocytopenia and osteoporosis

63
Q

Fondaparinux sodium

A

Factor Xa inhibitor; synthetic sulfated pentasaccharide

64
Q

Fondaparinux sodium MOA

A

indireclty inhibits factor Xa by selectively binding AT

65
Q

Uses of Fondaparinux sodium

A

venous thromboembolism; acute DVT; PE; prophylaxis in patients undergoing hip fracture surgery, hip replacement, knee replacement or abdominal surgery

66
Q

Thrombocytopenia and fondaparinux sodium

A

low potential for thrombocytopenia; action not reversed by protamine sulfate!!

67
Q

Rivaroxaban (Xarelto)

A

Factor Xa inhibitor; treatment/prevention of VT and PE; prevention of thrombosis in NV atrial fibrillation

68
Q

Apixaban (Eliquis)

A

Factor Xa inhibitor; prevention of thrombosis in NV atrial fib

69
Q

Both Rivaroxaban and Apixaban need dose reduction in which patients?

A

dose reduction in patients with impaired renal function; increased risk of stroke upon discontinuation

70
Q

Edoxaban (Savaysa) used for

A

treatment of VT and PE after 5-10 days with parenteral anticoagulant; prevention of thrombosis in NV atrial fib

71
Q

Edoxaban is not used in patients with

A

impaired renal excretion; patients with creatinine clearance greater than 95 ml/min

72
Q

Risks with Edoxaban

A

increased risk of ischemic events upon premature discontinuation; risk of hematoma/paralysis in patients undergoing spinal puncture or epidural anesthesia

73
Q

Direct thrombin inhibitors/Non-heparinoid parenteral agents inhibit

A

free thrombin and fibrin-bound thrombin; do not act through AT-III

74
Q

Hirudin

A

peptide from saliva gland of medicinal leach

75
Q

Desirudin (Iprivask)

A

recombinant hirudin grown in yeast; highly specific direct irreversible inhibitor of thrombin; no effect on AT; aPTT values increase dose-dependently; can produce hypersensitivity reactions

76
Q

Bivalirudin (Angiomax)

A

direct thrombin inhibitor; reversible binding to catalytic site of thrombin; given IV during PCI; eliminated by renal excretion; low risk of bleeding doesn’t induce antibody formation

77
Q

Argatroban

A

direct thrombin inhibitor; binds reversibly to the active site of thrombin; doe snot require AT for activity; can inhibit free and clot-associated thrombin; metabolized in liver (CYP3A4/5)

78
Q

Argatroban is approved for

A

prophylaxis or treatment in patients with heparin-induced thrombocytopenia

79
Q

Dabigatran (Pradaxa)

A

orally adminstered direct thrombin inhibitor; indicated for prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation

80
Q

What is Dabigatran etexilate

A

the prodrug that gives rise to dabigatran upon ester hydrolysis

Pharmacology Test #4 (9 decks)

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