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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
Dabigatran pharmacokinetics
Peaks at 1-2hrs, steady rate at 2-3 days, oral administration as prodrug, renal elimination, Category C in pregnancy
26
Dabigatran Uses
Atrial fibrillation, Venous thromboembolism
27
Dabigatran adverse rxns + treatment of overdose
Bleeding, gastritis. No antidote for overdose
28
Dabigatran drug-drug interactions
Decreased effect from P-glycoprotein inducers. Increased effect from P-glycoprotein inhibitors
29
Dabigatran advantages and disadvantages
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
Ravaroxaban and Apixaban MOA
Direct factor Xa inhibitor
31
Ravaroxaban and Apixaban monitoring lab test
Not routinely monitored
32
Ravaroxaban and Apixaban pharmacokinetics
Peak action in 2.5-4hrs, oral, hepatic metabolism ®, renal excretion, BID (A)
33
Ravaroxaban and Apixaban Uses
A fib, DVT-PE prevention after knee or hip replacement (R only)
34
Ravaroxaban and Apixaban adverse rxns + treatment of overdose
Bleeding (R ), Category C pregnancy
35
Ravaroxaban and Apixaban drug-drug interactions
P-glycoprotein inducers decrease effect, P-glycoprotein inhibitors increase effect
36
Ravaroxaban and Apixaban advantages and disadvantages
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
Aspirin MOA
Low dose selective inhibition of COX-1 (irreversible)
38
Aspirin pharmacokinetics
rapid onset, oral-once daily, hepatic elimination
39
Aspirin Uses
Acute MI/unstable angina, percutaneous coronary intervention, secondary prevention of MI-stroke
40
Aspirin adverse rxns + treatment of overdose
Bleeding, gastric upset, pregnancy category C/D
41
Aspirin drug-drug interactions
increased bleeding risk with anticoags
42
Ticagrelor, Clopidogrel, Prasugrel MOA
Inhibits platelet ADP (P2Y12) receptor. C+P are irreversible. T is reversible
43
Ticagrelor, Clopidogrel, Prasugrel pharmacokinetics
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
Ticagrelor, Clopidogrel, Prasugrel Uses
Acute MI, unstable angina, percutaneous coronary intervention
45
Ticagrelor, Clopidogrel, Prasugrel adverse rxns + treatment of overdose
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
Ticagrelor, Clopidogrel, Prasugrel drug-drug interactions
PPIs may block activation of C by CYP2C19
47
Dipyridamole MOA
Inhibits phosphodiesterase in platelets > increases cAMP > PGI2 > anti-aggregation effect
48
Dipyridamole pharmacokinetics
Oral, hepatic metabolism (phase I conjugation)
49
Dipyridamole Uses
secondary prevention of MI-stroke
50
Dipyridamole adverse rxns + treatment of overdose
Dizziness, HA, nausea, GI upset, Pregnancy category B
51
Dipyridamole drug-drug interactions
none
52
Abciximab, Eptifibatide, Tirofiban MOA
Blocks platelet GIIb/IIIa receptor preventing fibrinogen binding and platelet aggregation. A is monoclonal Ab, E is cyclic peptide, T is non peptide
53
Abciximab, Eptifibatide, Tirofiban pharmacokinetics
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
Abciximab, Eptifibatide, Tirofibane Uses
percutaneous coronary intervention
55
Abciximab, Eptifibatide, Tirofiban adverse rxns + treatment of overdose
bleeding
56
Abciximab, Eptifibatide, Tirofiban drug-drug interactions
none
57
Streptokinase MOA
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
Streptokinase Uses
acute MI, deep vein thrombosis, multiple pulmonary emboli
59
Streptokinase adverse rxns + treatment of overdose
Hemorrhage, allergic reactions
60
Tissue plasminogen MOA
tPA binds to fibrin and selectively activates bound plasminogen under physiological conditions (i.e., “clot-selective”)
61
Tissue plasminogen Uses
acute MI, deep vein thrombosis, multiple pulmonary emboli
62
Tissue plasminogen adverse rxns + treatment of overdose
Hemorrhage

CVPR II (25 decks)

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