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CV Unit 2 Pharm > Anti-Coagulants & Anti-Platelets > Flashcards

Anti-Coagulants & Anti-Platelets Flashcards

1
Q

Heparin: MoA

A

Paraenteral anti-coagulant Binds to and accelerates activity of AT III in plasma to inhibit activated clotting factors. (IIa, IXa, Xa, XIa, XIIa, XIIa). Prevents conversion of prothrombin and fibrinogen.

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2
Q

Heparin: Clinical Use

A

Prevent state of hypercoagulability following vascular injury/venous stasis. Adjunct in treatment of coronary occlusion in UA/acute MI. Prophylaxis/treatment of VTE. Prevention of cerebral thrombosis in evolving stroke. Low dose prophylaxis of post-op thromboembolism (SC).

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3
Q

Heparin: Side Effects/Toxicity

A
  • Side effects: Hemorrhage (esp. elderly women), hypersensitivity (obtained from beef/pork), osteoporosis, thrombocytopenia more likely than with LMWH.
  • Contraindicated: Hypersensitivity rxn in the past, active bleeding, hemophilia, thrombocytopenia, purpura, severe HTN, bacterial endocarditis, ulcerative GI lesions, threatened abortion.
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4
Q

Heparin: DDI

A

Increased bleeding tendencies w/ drugs that interfere with platelet aggregation:

  • aspirin
  • indomethacin
  • ibuprofen
  • dextran
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5
Q

Heparin: Overdose

A

Protamine (strongly basic protein with + charge) complexes and neutralizes heparin in 5 min.

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6
Q

Enoxapirin (& Dalteparin): MoA

A

Low-molecular weight heparin (LMWH)

  • Binds to AT III and inactivates factor Xa, but NOT IIa (thrombin). Longer durations of activity (once-twice daily dosing). First-order renal elimination.
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7
Q

Enoxapirin (& Dalteparin): Clinical use

A

Low-molecular weight heparin (LMWH)

  • Prevent state of hypercoagulability following vascular injury/venous stasis. Adjunct in treatment of coronary occlusion in UA/acute MI.
  • Prophylaxis/treatment of VTE. Prevention of cerebral thrombosis in evolving stroke. Low dose prophylaxis of post-op thromboembolism (SC).
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8
Q

Enoxapirin (& Dalteparin): Side Effects / Toxicity

A

Low-molecular weight heparin (LMWH) Thrombocytopenia less likely than with heparin.

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9
Q

Enoxapirin (& Dalteparin): DDI

A

Increased bleeding tendencies w/ drugs that interfere with platelet aggregation: aspirin, indomethacin, ibuprofen, dextran.

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10
Q

Enoxapirin (& Dalteparin): Overdose

A

Protamine – incomplete reversal

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11
Q

Enoxaprin (& Dalteparin): Advantages

A

Less tendency for bleeding and thrombocytopenia than heparin. No effect on aPTT (routine monitoring not required). More bioavailability

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12
Q

Fondaparinux (anti-coagulant): MoA

A

Paraenteral Pentasaccharide activator of AT III - inactivates factor Xa only

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13
Q

Fondaparinux (anti-coagulant): Clinical Use

A
  • Prevent state of hypercoagulability following vascular injury/venous stasis. Adjunct in treatment of coronary occlusion in UA/acute MI.
  • Prophylaxis/treatment of VTE. Prevention of cerebral thrombosis in evolving stroke. Low dose prophylaxis of post-op thromboembolism (SC).
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14
Q

Fondaparinux (anti-coagulant): Side Effects/Toxicity

A

Hemorrhage (esp. elderly women). Hypersensitivity (obtained from beef/pork). Osteoporosis. No thrombocytopenia risk.

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15
Q

Fondaparinux (anti-coagulant): DDI

A

Increased bleeding tendencies w/ drugs that interfere with platelet aggregation:

  • aspirin
  • indomethacin
  • ibuprofen
  • dextran.
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16
Q

Argatroban: MoA

A

Parenteral anti-coagulation Direct thrombin (IIa) inhibitor No combination with AT III needed.

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17
Q

Bivalirudin: MoA

A

Parenteral anti-coagulation Direct thrombin (IIa) inhibitor No combination with AT III needed.

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18
Q

Lepirudin: MoA

A

Parenteral anti-coagulation Direct thrombin (IIa) inhibitor No combination with AT III needed.

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19
Q

Desirudin: MoA

A

Parenteral anti-coagulation Direct thrombin (IIa) inhibitor No combination with AT III needed.

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20
Q

Warfarin: MoA

A
  • Oral anti-coagulant
  • Blocks liver synthesis of vit K-dep. clotting factors (II, VII, IX, X, Ca++-dep. factors) via preventing reactivation of vit K. Also inhibits protein C synthesis (can result in early procoagulant effect).
  • 100% oral absorption. 99% bound to plasma proteins. Onset of anticoag effect delayed (allows turnover of existing clotting factors). Increased PT in 8-12 hrs (max effect in 3-5 days). Metabolized by CYP2C9 to inactive metabolites.
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21
Q

Warfarin: Clinical Uses

A

A fib (assoc. w/ mechanical valve, bioprosthetic valve, prior mitral repair, mitral stenosis) – prevention of thromboembolic complications. Prophylaxis (for pt’s with prosthetic heart valves only) & treatment of VTE.

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22
Q

Warfarin: Side Effect/Toxicity

A
  • Hemorrhage. Necrosis of fatty soft tissue (esp females). GI upset. Osteoporosis.
  • Contraindicated: Pregnancy (crosses placenta).
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23
Q

Warfarin: DDI

A
  • Increased effect (inc PT/INR) via inhibiting metabolism (amiodarone, cimetidine fluconazole, fuoxetine, metronidazole, rosuvastatin) or interfering with platelet/vit K function (aspirin, oral antibiotics).
  • Decreased effect (dec. PT/INR) via increased metabolism (barbiturates, carbamazepine, phenytoin, rifampin, St. John’s Wort), dec. absorption (cholestyramine, colestipol), or antagonizing warfarin action (vit K via diet).
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24
Q

Warfarin: Overdose

A

Manage high INR and/or bleeding (during major bleeding: slow IV infusion of vit K and use of PCC and recombinant factor VIIa).

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25
Q

Warfarin: Advantages/Disadvantages

A
  • Advantages: Patients who are already comfortable with INR monitoring. Patients with chronic kidney disease. Patients unlikely to comply with BID dosing. Warfarin is low cost.
  • Disadvantages: Vit K epoxide reductase complex 1 (VKORC1) displays genetic polymorphisms – can result in differential sensitivity to warfarin. Variability in dosage requirements. Dietary restrictions related to Vit K. Need for close monitoring of INR. Many drug interactions.
26
Q

Dabigatran: MoA

A

Newer oral anti-coag, direct thrombin inhibitor

Directly inhibits both free and clot-bound thrombin in the plasma. Highly polar drug w/ poor oral bioavailability. Prodrug (exilate) is rapidly absorbed from GI tract and coverted to active form via plasma & liver esterases. More rapid onset of action than warfarin. BID dosing. Steady state levels in 2-3 days. Renal elimination.

27
Q

Dabigatran: Clinical Uses

A

Reduction of stroke & systemic embolism risk in pt’s with non-valvular A Fib.

28
Q

Dabigatran: Side Effects/Toxicity

A

May cause bleeding. GI complaints in 1/3 of pt’s. Irreversible anti-coagulant effect. Not yet approved for VTE.

29
Q

Dabigatran: Overdose

A

Hemostatic measures – FFP, then PCC or rVIIa.

30
Q

Dabigatran: Advantages/Disadvantages

A
  • Advantages: Does not require INR monitoring & dosage adjustments as with warfarin. Dec rates of strokes/intracranial bleeding compared to warfarin. No dietary restrictions (no CYP450 metabolism).
  • Disadvantages: Dosage adjustment if renally impaired. No method for determining extent of anticoagulation. No antidote for reversal. Shorter-acting (missed doses could increase thrombosis risk). Must be kept in original container. If need to assess bleeding risk of pt, measurement of ECT is expensive and not currently widely available.
31
Q

Rivaroxaban: MoA

A

New oral anti-coag, direclty inhibits factor Xa in plasma. Oral. QD dosing. CYP3A4 and renal elimination.

32
Q

Rivaroxaban: Clinical Uses

A

Reduction of stroke & systemic embolism risk in pt’s with non-valvular A Fib. Prevention of DVT in pt’s following hip-knee replacement surgery. **Approved for prevention VTE & treatment of DVT/PE.

33
Q

Rivaroxaban: Side effect/ Toxicity

A

Bleeding is most common side effect. Difficult to reverse anticoagulant effect.

Contraindicated: Patients with CrCl>95ml/min.

34
Q

Rivaroxaban: Advantages/Disadvantages

A
  • Advantages: Does not require INR monitoring. Lower rates of strokes/fatal bleeding. No dietary restrictions.
  • Disadvantages: Dose adjustment if renally impaired. No method for determining extent of anticoagulation. No antidote for reversal. Shorter acting (missed doses could increase thrombosis risk).
35
Q

Apixaban: MoA

A

New oral anti-coag, Direclty inhibits factor Xa in plasma. Oral. BID dosing. CYP3A4 and renal elimination.

36
Q

Apixaban: Clinical Uses

A

Reduction of stroke & systemic embolism risk in pt’s with non-valvular A Fib. Prevention of DVT in pt’s following hip-knee replacement surgery.

37
Q

Apixaban: Side effect /Toxicity

A

Bleeding is most common effect. Difficult to reverse anticoagulant effect.

Contraindicated: Patients with CrCl>95ml/min.

38
Q

Apixaban: Advantages/Disadvantages

A
  • Advantages: Does not require INR monitoring. Lower rates of strokes/fatal bleeding. No dietary restrictions.
  • Disadvantages: Dose adjustment if renally impaired. No method for determining extent of anticoagulation. No antidote for reversal. Shorter acting (missed doses could increase thrombosis risk).
39
Q

Edoxaban: MoA

A

New oral anti-coag, direclty inhibits factor Xa in plasma. Oral. High renal elimination (minimal metabolism).

40
Q

Edoxaban: Clinical Uses

A

Reduction of stroke & systemic embolism risk in pt’s with non-valvular A Fib. Prevention of DVT in pt’s following hip-knee replacement surgery.

41
Q

Edoxaban: Side effects/ Toxicity

A

Bleeding is most common effect. Difficult to reverse anticoagulant effect.

Contraindicated: Patients with CrCl>95ml/min.

42
Q

Edoxaban: Advantages/Disadvantages

A
  • Advantages: Does not require INR monitoring. Lower rates of strokes/fatal bleeding. No dietary restrictions.
  • Disadvantages: Dose adjustment if renally impaired. No method for determining extent of anticoagulation. No antidote for reversal. Shorter acting (missed doses could increase thrombosis risk).
43
Q

Asprin: MoA

A

Irreversibly inhibits COX-1 synthesis of thromboxane in platelets.

Single dose inhibits platelet aggreg. up to 8 days. Largest conc. in portal vein, thus greater effect on circulating platelet COX-1 relative to tissue endothelial cell COX-2 – decreased tendency for clotting.

44
Q

Asprin: Clinical Uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

45
Q

Asprin: Side Effect/Toxicity

A

Side effects are rare w/ low dose therapy. Dyspepsia, nausea, vomiting can occur. GI bleeding can occur.

46
Q

Clopidogrel: MoA

A

Anti-platelet agent

ADP (purinergic-P2Y12) receptor antagonists

Interferes with ADP-induced platelet aggregation.

Oral QD. Prodrug converted to active metabolite by CYP450.

47
Q

Clopidogrel: Clinical Uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

48
Q

Clopidogrel: Side Effects/Toxicity

A

Bleeding. GI upset. Headache. Dizziness. URI.

49
Q

Colpidogrel: DDI

A

Synergistic w/ aspirin. Proton pump inhibitors (PPIs) may inhibit activation via CYP2C19.

50
Q

Prasugrel: MoA

A

Anti-platelet agent

ADP (purinergic-P2Y12) receptor antagonists

Interferes with ADP-induced platelet aggregation.

Oral QD. Prodrug converted to active metabolite by CYP450.

51
Q

Prasugrel: Side Effects/Toxicity

A

Bleeding (>clopidogrel).

52
Q

Prasugrel: Clinical uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

53
Q

Ticagrelor: MoA

A

Anti-platelet agent

ADP (purinergic-P2Y12) receptor antagonists

Interferes with ADP-induced platelet aggregation.

Oral BID w/ meals. Reversible inhibitor. Does not require activation by CYP450.

54
Q

Ticagrelor: Clinical Uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

55
Q

Ticagrelor: Side Efects/Toxicity

A

Bleeding, dyspnea, bradyarrythmias

56
Q

Abciximab, Eptifibatide, Tirofiban: MoA

A

Blocks IIb/IIIa receptors on platelet – prevents integrin and fibrinogen binding that facilitates aggregation.

Given as a continuous IV infusion.

57
Q

Abciximab, Eptifibatide, Tirofiban: Clinical Uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

58
Q

Abciximab, Eptifibatide, Tirofiban: Side Effects/Toxicity

A

Bleeding

59
Q

Abciximab, Eptifibatide, Tirofiban: Advantages/Disadvantages

A

Advantage: Blocks all pathways of platelet activation.

60
Q

Dipyridamole: MoA

A

Blocks phosphodiesterase breakdown of cAMP, elevating cAMP levels and potentiating prostacyclin’s anti-aggregatory action.

Oral BID/QID before meals (or BID as Aggrenox).

61
Q

Dipyridamole: Side Effect/Toxicity

A

Side effects are minimal & transient. Some dizziness and GI distress.

62
Q

Dipyridamole: Clinical Uses

A

Acute MI (STEMI): aspirin + ADP antagonist. UA/UNSTEMI: aspirin +/- ADP antagonist. Percutaenous coronary interventions (PCI): aspirin + ADP antagonists +/- GIIb/IIIa inhibitors. Secondary prevention of MI: aspirin +/- dipyridamole.

Little or no apparent benefit as antithrombotic agent

CV Unit 2 Pharm (2 decks)

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