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CVPR: CV Unit II > Anticoagulant & Antiplatet Drugs > Flashcards

Anticoagulant & Antiplatet Drugs Flashcards

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1
Q

General characteristics of normal thrombus formation

A
  1. exposure of circulating blood elements to thrombogenic material (e.g. unmasked sub-endothelial collagen after plaque rupture)
  2. activation and aggregation of platelets
  3. triggering of the coagulation cascade –> fibrin clot formation
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2
Q

Intrinsic pathway summary and common drug targets

A
  • Factor XIIa -> XIa -> IXa + VIII -> Xa.
  • Heparin inactivates: XIIa, XIa, IXa, Xa
  • Warfarin inhibits synthesis: IX, X
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3
Q

Extrinsic pathway summary and common drug targets

A
  • tissue factor + VIIa -> Xa.
  • Heparin inactivates: VIIa
  • Warfarin inhibits synthesis: VII
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4
Q

Common pathway summary and common drug targets

A

Common: Xa + Va –> IIa (Thrombin) -> Ia (Fibrin) + XIII -> clot.

  • Heparin inactivates: Xa, Thrombin (IIa)
  • Warfarin inhibits synthesis: X, Prothrombin (II)
  • Rivaroxaban & LMWH-ATIII/Fondaparinux inhibit: Xa
  • Dabigatran & Hirudin/Bivalirudin inhibit: Thrombin
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5
Q

Thrombin inhibitors

A
  • Dabigatran
  • Hirudin/Bivalirudin
  • Warfarin
  • Heparin
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6
Q

Factor Xa inhibitors

A
  • Rivaroxaban
  • LMWH-ATIII/Fondaparinux
  • Warfarin
  • Heparin
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7
Q

Coagulation cascade summary/drug targets (diagram)

A

[picture}

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8
Q

Examples of anticoagulant drugs

A
  • Heparin
  • low MW heparins [enoxaparin]
  • warfarin
  • dabigatran
  • rivaroxaban
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9
Q

Examples of thrombolytic agents

A
  • streptokinase

- tissue plasminogen activator and variants

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10
Q

Examples of antiplatet agents

A
  • Aspirin
  • clopidrogel
  • dipyridamole
  • abciximab/epifibatide/tirofiban
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11
Q

Venous vs. aterial thrombi

A
  • venous = composed mainly of fibrin and trapped red blood cells with relatively few platelets
  • arterial = composed mainly of platelet aggregates held together by small amounts of fibrin
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12
Q

Anticoagulant agents general characteristics

A
  • prevention and treatment of venous thromboembolism
  • prevention of cardioembolic events in patients with atrial fibrillation
  • also effective for arterial thrombosis and their effects can be additive with antiplatelet agents
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13
Q

Antiplatet agents general characteristics

A
  • primarily for prevention and treatment of arterial thrombosis
  • primary and secondary prevention and treatment of acute coronary syndrome
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14
Q

General mechanisms of blood coagulation

A
  1. emerging blood increases mechanical pressure and helps limit blood loss; vessel damage exposes collagen of subendothelium
  2. vessels constrict
  3. platelets adhere
  4. platelets activate
  5. blood coagulates via coagulation cascade
  6. blood flow returns to normal
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15
Q

Warfarin inhibits:

A
  • vit K factors:
  • II
  • VII
  • IX
  • X
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16
Q

Heparin inactivates:

A
  • w/antithrombin III (ATIII):
  • IIa
  • IXa
  • Xa
  • XIa
  • XIIa
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17
Q

Low molecular weight heaparins (LMWH)/Fondaparinux inactivates

A
  • w/ATIII:

- Xa

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18
Q

Hirudin, Dabigatran inactivates

A

-directly inactivates IIa (thrombin)

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19
Q

Rivaroban inactivates:

A

-directly inactivates Xa

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20
Q

PT test

A
  • tests extrinsic pathway –> prolonged = defect @ extrinsic
  • used to monitor oral (warfarin) anticoag therapy
  • INR=patient PT/mean normal PT –> allows comparison between labs
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21
Q

aPTT test characteristics

A
  • tests intrinsic pathway –> prolonged = defect @ intrinsic
  • used to monitor heparin therapy
  • not significantly affected by LMWH
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22
Q

Ecarin Clotting Time (ECT)

A

-monitors therapy w/direct thrombin (IIa) inhibitors = hirudin & dabigatran

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23
Q

Factors that normally limit clot formation

A
  • prostacyclin (PGI2) and nitrous oxide=vasodilate and inhibit platelet agg.
  • Antithrombin III & Protein C/Protein S
  • fibrinolysis via plasmin
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24
Q

Fibrin inhibition mechanisms

A

-Antithrombin: protease inhibitor that inactivates IIa, IXa, Xa, XIIa less activated of X

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25
Heparin: MOA
- inhibits activated clotting factors - accelerates ATIII activity --> inhibits clotting factors - inhibits: IIa (thrombin), IXa, Xa, XIa, XIIa, XIIIa
26
Heparin: Pharmacokinetics
- IV or SC - loading dose needed for anticoagulant effect - continuous infusion preferred for heparin - renal elimination - safe in pregnancy
27
Heparin: Uses
- treatment of coronary occlusion in unstable angina/acute MI - prophylaxis tx of venous thromboembolism (VTE) - prevent cerebral thrombosis in stroke - prophylaxis tx for post-op thromboembolism
28
Heparin: Adverse Rxns
- bleeding risk - hypersensitivity - thrombocytopenia: mild or severe (immune-mediated) - osteoporosis
29
Parenteral anticoagulants
-heparin -LMWH (Enoxapirin) -Fondaparinux Direct thrombin (IIa) inhibitors
30
LMWH: drug example
-Enoxapirin
31
LMWH: MOA
-Binds to ATIII to inactivate factor Xa, but not IIa (thrombin)
32
LMWH: Pharmacokinetics
- IV or SC - longer t1/2 - first-order renal elimination - safe in pregnancy
33
LMWH: Uses
- equal efficacy as regular heparin for VTE - less bleeding complications & thrombocytopenia - PTT not affected --> no monitoring needed
34
LMWH: Overdose sx/signs and tx
- bleeding is chief sign nosebleed, hematuria, bruising | - tx: protamine --> neutralizes hepearin w/in 5 min
35
Warfarin: MOA
* Acts in liver to prevent synthesis of clotting factors * Blocks vit-K dependent factors (II, VII, IX, X) * Increases prothrombin time
36
Warfarin: Pharmacokinetics
* Oral * Onset delayed until turnover of existing clotting factors * Reaches max effect @ 3-5 days * Metabolized by CYP2C9 * Genetic polymorphisms
37
Warfarin:Uses
* Afib: prevent thromboembolic complications | * Prophylaxis/treatment of vneous thromboembolism
38
Warfarin: Adverse Rxns
* Hemorrhage * GI upset * Contraindicated in pregnancy
39
Warfarin: overdose signs/sx & management
* Sx: Hematuria, gum bleed, excessive menstrual bleeding * INR < 4.5: reduce or skip dose * INR 4.5-10: hold 1-2 doses * INR > 10 w/out bleed: hold, administer vit K * Major bleed: hold, slow vit K infusion + Prothrombin complex concentrate (better than fresh frozen plasmin) or recombinant factor VIIa
40
Dabigatran: MOA
• Acts in plasma to directly inhibit the activity of thrombin (IIa)
41
Dabigatran : Pharmacokinetics
* Oral = rapidly absorbed as prodrug * Renal excretion * Requires frequent monitoring and dosage adjustments
42
Dabigatran :Uses
• Reduce risk of systemic embolism w/non-valvular afib (not VTE)
43
Dabigatran : Adverse Rxns
* Bleeding * GI complaints * Fewer drug interactions
44
Warfarin vs. Dabigatram in aFib
* Warfarin=long history of use, once-daily dosing, reversal w/vitK, but requires INR monitoring, drug interactions * Dabigatran=lower rates of strokes/intracranial complications, no INR monitoring or diet restrictions, fewer drug rxns, but no good monitoring tool, no specific antidote, twice-daily dowing, storage challenges, and renal adjustment
45
Rivaroxavan/Apixaban: MOA
• Acts in the plasma to directly inhibit the activity of factor Xa
46
Rivaroxavan/Apixaban : Pharmacokinetics
* Oral | * Hepatic metabolism and renal excetrion
47
Rivaroxavan/Apixaban :Uses
* Reduce risk of systemic embolism in patients w/non-valvular aFib * Approved for prevention and tx of DVT/VTE
48
Rivaroxavan/Apixaban : Adverse Rxns
* Bleeding | * No antidote for rapid reversal
49
Warfarin vs. Rivaroxavan/Apixaban in aFib
* Adv of Riv/Apix: lower rates of stroke/bleeding, no INR, no dietary restrictions, once-daily dosing (Riv) * Disadv: no monitoring tool, no specific antidote, bid dosing (Apix), renal dosing
50
Main antiplatelet agents
* Aspirin * Clopidogrel * Dipyridamole * Abciximab, Eptifibatide, Tirofibanm
51
Aspirin: MOA
• Inhibition of COX-1 synthesis of thombroxane (COX-1 inhibit > COX-2 @ endothelial cells)
52
Aspirin : Pharmacokinetics
* Oral | * Low-dose daily dosing
53
Aspirin :Uses
* Acute MI (STEMI) (w/ADP antagonist) * Unstable angina/NSTEMI * Percutaneous coronary interventions (w/ADP antagonist) * Secondary prevention of MI/ischemic stroke
54
Aspirin : Adverse Rxns
* Rare w/low-dose therapy | * GI complaints or bleeding
55
Clopidogrel (Plavix): MOA
* ADP receptor antagonists → interferes w/ADP-induced platelet aggregation via irreversible inhibition * Synergistic actions w/aspirin
56
Clopidogrel (Plavix): Pharmacokinetics
• Once-daily dosing w/loading dose
57
Clopidogrel (Plavix):Uses
* Acute MI (STEMI) (w/aspirin) * Sometimes: Unstable angina/NSTEMI * Percutaneous coronary interventions (w/asprin)
58
Clopidogrel (Plavix)/Other ADP antagonists: Adverse Rxns
* Clopidogrel: GI upset, headache, dizziness, URI, bleeding * Prasugrel: bleeding * Tricagrelor: bleeding
59
Dipyridamole: MOA
• Blocks phosphodiesterase breakdown of cAMP → prostacyclin anti-aggregatory effect
60
Dipyridamole : Pharmacokinetics
* Oral | * 3-4x before meals
61
Dipyridamole :Uses
• ischemic stroke: dipyridamole + aspirin
62
Dipyridamole : Adverse Rxns
• minimal and transient
63
Abciximab: MOA
• blocks IIb/IIIa receptors on platelet → prevents integrin and fibrinogen binding
64
Abciximab : Pharmacokinetics
• continuous IV infusion
65
Abciximab :Uses
• Percutaneous coronary interventions (PCI): aspirin + ADP antagonists + GIIb/IIa inhibitors
66
Abciximab : Adverse Rxns
• Bleeding
67
Thrombolytics: MOA
* Increased formation of plasmin from plasminogen * Streptokinase = activates free and fibrin-bound plasminogen * tPA = activates bound plasminogen
68
Streptokinase characteristics
• systemic activation of plasmin
69
Tissue Plasminogen Activator (tPA) characteristics
• recombinant tPA → binds to fibrin and activates bound plasminogen
70
Reteplase/Tenecteplase characteristics
* given bolus w/prolonged duration of action | * less fibrin-specific than tPA
71
Thrombolytics: Uses
* Acute MI → coronary artery thrombosis * DVT * Multiple PE
72
Thrombolytics: Adverse Effects
• hemorrhage

CVPR: CV Unit II (17 decks)

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