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CVPR II > Antithrombotic drugs details > Flashcards

Antithrombotic drugs details Flashcards

1
Q

Heparin MOA

A

Binds Antithrombin III and accelerates its activity> inactivates IIa and Xa of intrinsic pathway.

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2
Q

Heparin pharmacokinetics

A

rapid onset, parenteral (IV, SC) only, cleared by reticuloendothelial system

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3
Q

heparin monitoring lab tst

A

aPTT

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4
Q

Heparin Uses

A

Acute coronary syndrome, venous thromboembolism

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5
Q

Heparin adverse rxns + treatment of overdose

A

Bleeding, thrombocytopenia, narrow therapeutic index, safe in pregnancy. Overdose treated with protamine

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6
Q

Heparin drug-drug interactions

A

NSAIDS increase bleeding risk, antiplatelet agents

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7
Q

Heparin advantages and disadvantages

A

More rapid response than LMWH and completely reversed by protamine

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8
Q

LMWH examples

A

Enoxaparin-Dalteparin

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9
Q

LMWH MOA

A

Binds ATIII > inactivates Xa (but NOT IIa)

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10
Q

LMWH pharmacokinetics

A

3-5hr onset if SC, parenteral (IV or SC), renal clearance

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11
Q

LMWH monitoring lab test

A

Not needed, action is predictable

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12
Q

LMWH Uses

A

Acute coronary syndrome, venous thromboembolism

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13
Q

LMWH adverse rxns + treatment of overdose

A

Bleeding, thrombocytopenia, narrow therapeutic index, safe in pregnancy. Overdose treated with protamine (incomplete though)

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14
Q

LMWH drug-drug interactions

A

NSAIDS increase bleeding risk, antiplatelet agents also increase bleeding tendencies

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15
Q

LMWH advantages and disadvantages

A

Equal efficacy as heparin for VTE with less tendency for bleeding complications and less effect on platelets.

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16
Q

Warfarin MOA

A

Inhibits liver synthesis of Vit K-dep factors (II, VII, IX, and X)

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17
Q

Warfarin monitoring lab test

A

INR (PT)

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18
Q

Warfarin pharmacokinetics

A

Delayed onset(due to turnover of existing clotting factors), oral administration, hepatic metabolism, NOT safe in pregnancy

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19
Q

Warfarin Uses

A

Atrial fibrillation, Venous thromboembolism prophylaxis

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20
Q

Warfarin adverse rxns + treatment of overdose

A

Bleeding, skin necrosis, narrow therapeutic index. Overdose treated with Phytonadione (Vit K) FFP

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21
Q

Warfarin drug-drug interactions

A

CYP450 inhibitors and antibiotics increase effect. CYP450 inducers and dietary Vitamin K decrease effect

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22
Q

Warfarin advantages and disadvantages

A

In atrial fibrillation: advantages include once daily dosing, reversal of effects with vitamin K. Disadvantages include variability in dosage requirements, dietary attention to Vit K, INR monitoring, drug interactions

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23
Q

Dabigatran MOA

A

Direct thrombin (IIa) inhibitor

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24
Q

Dabigatran monitoring lab test

A

Not routinely monitored

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25
Q

Dabigatran pharmacokinetics

A

Peaks at 1-2hrs, steady rate at 2-3 days, oral administration as prodrug, renal elimination, Category C in pregnancy

26
Q

Dabigatran Uses

A

Atrial fibrillation, Venous thromboembolism

27
Q

Dabigatran adverse rxns + treatment of overdose

A

Bleeding, gastritis. No antidote for overdose

28
Q

Dabigatran drug-drug interactions

A

Decreased effect from P-glycoprotein inducers. Increased effect from P-glycoprotein inhibitors

29
Q

Dabigatran advantages and disadvantages

A

Advantages: lower rates of strokes, doesn’t require INR, no dietary restrictions (all compared to warfarin). Disadvantages: No monitoring lab, no antidote, twice daily dosing, shorter acting, renal clearance, must be stored in original container

30
Q

Ravaroxaban and Apixaban MOA

A

Direct factor Xa inhibitor

31
Q

Ravaroxaban and Apixaban monitoring lab test

A

Not routinely monitored

32
Q

Ravaroxaban and Apixaban pharmacokinetics

A

Peak action in 2.5-4hrs, oral, hepatic metabolism ®, renal excretion, BID (A)

33
Q

Ravaroxaban and Apixaban Uses

A

A fib, DVT-PE prevention after knee or hip replacement (R only)

34
Q

Ravaroxaban and Apixaban adverse rxns + treatment of overdose

A

Bleeding (R ), Category C pregnancy

35
Q

Ravaroxaban and Apixaban drug-drug interactions

A

P-glycoprotein inducers decrease effect, P-glycoprotein inhibitors increase effect

36
Q

Ravaroxaban and Apixaban advantages and disadvantages

A

Advantages (relative to warfarin): • Evidence for lower rates of strokes and fatal bleeding •Does not require INR monitoring • No dietary restrictions • Once-daily dosing for rivaroxaban. Disadvantages: • No method for determining extent of anticoagulation
• No specific antidote for reversal • Apixaban requires bid dosing • Dose adjustment in renally impaired patients

Advantages (relative to warfarin): • Evidence for lower rates of strokes and fatal bleeding •Does not require INR monitoring • No dietary restrictions • Once-daily dosing for rivaroxaban. Disadvantages: • No method for determining extent of anticoagulation
• No specific antidote for reversal • Apixaban requires bid dosing • Dose adjustment in renally impaired patients

37
Q

Aspirin MOA

A

Low dose selective inhibition of COX-1 (irreversible)

38
Q

Aspirin pharmacokinetics

A

rapid onset, oral-once daily, hepatic elimination

39
Q

Aspirin Uses

A

Acute MI/unstable angina, percutaneous coronary intervention, secondary prevention of MI-stroke

40
Q

Aspirin adverse rxns + treatment of overdose

A

Bleeding, gastric upset, pregnancy category C/D

41
Q

Aspirin drug-drug interactions

A

increased bleeding risk with anticoags

42
Q

Ticagrelor, Clopidogrel, Prasugrel MOA

A

Inhibits platelet ADP (P2Y12) receptor. C+P are irreversible. T is reversible

43
Q

Ticagrelor, Clopidogrel, Prasugrel pharmacokinetics

A

P+T are more efficacious than C. Onset 2 hrs, loading dose used, oral (C+P are once daily prodrugs, T is twice daily), C is activated by CYP2C19 then renal/fecal excretion, P is activated by CYP3A4, T is metabolized by CYP3A4 to active.

44
Q

Ticagrelor, Clopidogrel, Prasugrel Uses

A

Acute MI, unstable angina, percutaneous coronary intervention

45
Q

Ticagrelor, Clopidogrel, Prasugrel adverse rxns + treatment of overdose

A

Bleeding (P+T >C), C causes dyspepsia, gastritis, HA. T causes dyspnea, bradyarryhthmias. C is pregnancy category B. P and T are category C.

46
Q

Ticagrelor, Clopidogrel, Prasugrel drug-drug interactions

A

PPIs may block activation of C by CYP2C19

47
Q

Dipyridamole MOA

A

Inhibits phosphodiesterase in platelets > increases cAMP > PGI2 > anti-aggregation effect

48
Q

Dipyridamole pharmacokinetics

A

Oral, hepatic metabolism (phase I conjugation)

49
Q

Dipyridamole Uses

A

secondary prevention of MI-stroke

50
Q

Dipyridamole adverse rxns + treatment of overdose

A

Dizziness, HA, nausea, GI upset, Pregnancy category B

51
Q

Dipyridamole drug-drug interactions

A

none

52
Q

Abciximab, Eptifibatide, Tirofiban MOA

A

Blocks platelet GIIb/IIIa receptor preventing fibrinogen binding and platelet aggregation. A is monoclonal Ab, E is cyclic peptide, T is non peptide

53
Q

Abciximab, Eptifibatide, Tirofiban pharmacokinetics

A

rapid onset, parenteral infusion, renal elimination (half life is 30 min (A), 2.5hr (E) or 2 hr (T). Pregnancy categories C (A) and B (E+T)

54
Q

Abciximab, Eptifibatide, Tirofibane Uses

A

percutaneous coronary intervention

55
Q

Abciximab, Eptifibatide, Tirofiban adverse rxns + treatment of overdose

A

bleeding

56
Q

Abciximab, Eptifibatide, Tirofiban drug-drug interactions

A

none

57
Q

Streptokinase MOA

A

Inactive by itself, but forms 1:1 complex with plasminogen (proactivator above), this complex then converts uncomplexed plasminogen to active plasmin. Generally results in systemic activation of plasmin.

58
Q

Streptokinase Uses

A

acute MI, deep vein thrombosis, multiple pulmonary emboli

59
Q

Streptokinase adverse rxns + treatment of overdose

A

Hemorrhage, allergic reactions

60
Q

Tissue plasminogen MOA

A

tPA binds to fibrin and selectively activates bound plasminogen under physiological conditions (i.e., “clot-selective”)

61
Q

Tissue plasminogen Uses

A

acute MI, deep vein thrombosis, multiple pulmonary emboli

62
Q

Tissue plasminogen adverse rxns + treatment of overdose

A

Hemorrhage

CVPR II (25 decks)

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