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M2 - Pharm > FA Anticoagulants > Flashcards

FA Anticoagulants Flashcards

1
Q

COX inhibitor

A

Aspirin

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2
Q

Aspirin MOA

A

Covalently acetylates platelet and endothelial COX 1 and 2 –> decreases TXA2 and PGI2 synthesis, respectively
No effect on PT or PTT

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3
Q

Aspirin low dose

A

more specific for COX 1

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4
Q

Aspirin Clinical Use

A

Antipyretic, Analgesic, Anti-Inflammatory, Anti-Platelet (aggregation)

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5
Q

4 Types of Antiplatelet Drugs

A

COX inhibitors; ADP antagonists; PDE III inhibitors; GpIIb/IIIa inhibitors

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6
Q

Aspirin Toxicity

A 
Gastric ulceration (dose-dependent); tinnitus ("salicylism" -- CN8 -- very high doses)
Chronic use: acute renal failure, interstitial nephritis, GI bleeding
Reye syndrome in children w/viral infxns
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7
Q

Aspirin Overdose

A

Initially causes hyperventilation and respiratory alkalosis, then transitions to mixed metabolic acidosis and respiratory alkalosis (HCO3 does not change)

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8
Q

ADP Receptor Antagonist Drugs

A

Clopidogrel, Prasugrel, Ticlopidine, Ticagrelor (reversible)

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9
Q

ADP Receptor Antagonist MOA

A

Irreversibly block ADP receptors –> indirectly inhibit GpIIb/IIIa expression –> inhibit aggregation

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10
Q

ADP Receptor Antagonist Clinical Use

A

Acute coronary syndrome, coronary stenting, decrease incidence or recurrence of thrombotic stroke

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11
Q

ADP Receptor Antagonist Toxicity

A

Neutropenia, TTP (Ticlopidine)

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12
Q

This ADP Receptor Antagonist is NOT a prodrug

A

Ticagrelor

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13
Q

This ADP Receptor Antagonist is reversible

A

Ticagrelor

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14
Q

This ADP Receptor Antagonist is metabolized by CYP 3A4

A

Prasugrel

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15
Q

This ADP Receptor Antagonist is metabolized by CYP 2C19

A

Clopidogrel

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16
Q

This This ADP Receptor Antagonist is more likely to vary in effectiveness among individuals

A

Clopidogrel – more polymorphisms for CYP 2C19

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17
Q

PDE III Inhibitor Drugs

A

Cliostazol, Dipyridamole

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18
Q

PDE III Inhibitor MOA

A

inhibits Phosphodiesterase III –> increases cAMP in platelets –> inhibits platelet aggregation, causes vasodilation

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19
Q

PDE III Inhibitor Clinical Use

A

intermittent claudication, coronary vasodilation, angina prophylaxis, stroke/TIA prophylaxis (+aspirin)

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20
Q

PDE III Inhibitor Toxicity

A

HypOtension, abdominal pain, facial flushing, nausea, headache

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21
Q

GpIIb/IIIa Inhibitor Drugs

A

TEA: Tirofiban, Eptifibatide, Abciximab

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22
Q

GpIIb/IIIa Inhibitor MOA

A

binds GpIIb/IIIa, preventing aggregation and fibrinogen cross-linking of platelets

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23
Q

GpIIb/IIIa Inhibitor Clinical Use

A

Unstable angina, PTCA

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24
Q

GpIIb/IIIa Inhibitor Toxicity

A

Thrombocytopenia, bleeding

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25
Q

Heparin MOA

A

Activate ATIII –> decrease F10 and F2

Short half-life

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26
Q

Heparin Clinical Use

A

Immediate anticoag for PE, acute coronary syndrome, MI, DVT
Okay for pregnancy
Monitor PTT

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27
Q

Heparin Toxicity

A

HIT (IgG Ab’s to Heparin-PF4 complex –> thrombosis and thrombocytopenia), osteoporosis, bleeding, drug interaxns

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28
Q

Heparin Reversal

A

protamine sulfate

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29
Q

Low Molecular Weight Heparin (LMWH) Drugs

A

Enoxaparin, Dalteparin, Fondeparinux

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30
Q

LMWH Activity

A

more specific to F10, better bioavailability, longer half-life, less incidence of HIT, can be administered subcutaneously and w/o lab monitoring, not easily reversible

31
Q

LMWH Reversal

A

not easily reversible

32
Q

These drugs are alternatives to Heparin for pts w/HIT

A

Direct Thrombin Inhibitors (Bivalirudin, Argatroban, Dabigatran)

33
Q

Direct Thrombin Inhibitor Drugs

A

Bivalirudin, Argatroban, Dabigatran

34
Q

This GpIIb/IIIa inhibitor can cause allergic rxns w/readministration

A

Abciximab

35
Q

Heparin Bridge

A

Warfarin rapidly depletes Proteins C + S, leaving pt hypercoaguable in 1st few days –> use Heparin/LMWH as “bridge” for not less than 4 days when starting warfarin for the first time or restarting it after a hospitalization or procedure to prevent clotting –> check INR

36
Q

Warfarin (Coumarin) MOA

A

inhibits Vit K epoxide reductase –> interferes w/gamma-carboxylation of F2, 7, 9, 10, Proteins C + S
Metabolism affected by polymorphisms in VKORC1 gene
Long half-life (war lasts a long time!)
Monitor PT-INR

37
Q

Warfarin Clinical Use

A

Chronic anticoagulation: DVT prophylaxis, prevention of stroke in afib
C/I in pregnancy – crosses placenta (don’t wage war on baby)

38
Q

Warfarin Toxicity

A

Skin necrosis (small vessel microthromboses), teratogen, bleeding, drug-drug interaxns

39
Q

Warfarin Reversal

A

FFP (immediate); Vitamin K

40
Q

How does Rifampin affect Warfarin metabolism?

A

Rifampin is a 2C9 inducer –> need to increase Warfarin dose to get same effect

41
Q

Which drugs can displace Warfarin from albumin?

A

Phenytoin, High Dose Aspirin

42
Q

Which drugs are 2C19 inhibitors, and how do they affect Warfarin?

A

azoles, amiodarone, SSRIs, metronidazole, sulfonamides, omeprazole –> need to decrease Warfarin dose b/c not metabolized as quickly

43
Q

how do herbals affect Warfarin?

A

ginger, garlic, ginko, and feverfew can increase Warfarin effect

44
Q

how can long-term antibiotic therapy affect Warfarin?

A

long-term antibiotics decrease gut flora –> decrease Vit K –> increase Warfarin effect

45
Q

how can cholestyramine affect Warfarin?

A

reduced absorption –> reduce Warfarin effect

46
Q

Which LMWH is most specific for F10?

A

Fondaparinux

47
Q

Factor 10 Inhibitor Drugs

A

Rivaroxaban, Apixaban

48
Q

Heparin structure

A

Large, anionic, acidic polymer

49
Q

Warfarin structure

A

Small, amphipathic molecule

50
Q

Heparin ROA

A

Parenteral

51
Q

Warfarin ROA

A

Oral

52
Q

Heparin site of action

A

Blood

53
Q

Warfarin site of action

A

Liver

54
Q

Heparin onset of action

A

Rapid

55
Q

Warfarin onset of action

A

Slow – limited by half-lives of clotting factors

56
Q

Heparin duration of action

A

Acute (hours)

57
Q

Warfarin duration of action

A

Chronic (days)

58
Q

Factor 10 Inhibitor MOA

A

Bind to and directly inhibit F10

59
Q

Factor 10 Inhibitor Clinical Use

A

Rx + Prophylaxis for DVT, PE; stroke prophylaxis for afib

Oral agents = usually no monitoring

60
Q

Factor 10 Inhibitor Toxicity

A

Bleeding (no reversal)

61
Q

Factor 10 Inhibitor Reversal

A

None

62
Q

Thrombolytic Drugs

A

-Plase: Alteplase, Reteplase, Tenecteplase, Streptokinase

63
Q

Thrombolytic MOA

A

Directly or indirectly aid conversion of plasminogen to plasmin (like tPA) –> cleave fibrin and thrombin clots
Increases PT + PTT
No change in platelet count

64
Q

Thrombolytic Clinical Use

A

Early MI + Ischemic Stroke (w/i 4.5h of onset); direct thrombolysis of severe PE

65
Q

Thrombolytic Toxicity

A

Bleeding.

C/I in pts w/active bleeding, Hx intracranial bleed, recent Sx, known bleeding diatheses, severe HTN

66
Q

Thrombolytic Reversal

A

Aminocaproic Acid; FFP and Cryoprecipitate can also be used to correct Factor deficiencies

67
Q

This thrombolytic has the most side effects

A

Streptokinase – from B-hemolytic Streptococcus; immune rxns, fibrinogen depletion

68
Q

Another name for ADP receptor antagonists

A

Thienopyridines

69
Q

Treat arterial thrombi with what kind of drugs?

A

antiplatelet

70
Q

Treat venous thrombi with what kind of drugs?

A

anticoagulant

71
Q

Post-MI anticoagulation

A

Aspirin + Clopidogrel + Warfarin

72
Q

What is INR and why would you monitor it?

A

A mathematical “correction” of PT for differences in sensitivity of thromboplastin reagents – use to monitor Warfarin

73
Q

Conditions that increase bleeding risk w/Warfarin?

A

HAS BLED: HTN, Abnl liver/renal fcn, Stroke, Bleeding Hx, Labile INR, Elderly (65+), Drug/alcohol use

M2 - Pharm (10 decks)

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