Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Heparin pharmacokinetics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

heparin monitoring lab tst

A

aPTT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Heparin Uses

A

Acute coronary syndrome, venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Heparin adverse rxns + treatment of overdose

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Heparin drug-drug interactions

A

NSAIDS increase bleeding risk, antiplatelet agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Heparin advantages and disadvantages

A

More rapid response than LMWH and completely reversed by protamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LMWH examples

A

Enoxaparin-Dalteparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

LMWH MOA

A

Binds ATIII > inactivates Xa (but NOT IIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LMWH pharmacokinetics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

LMWH monitoring lab test

A

Not needed, action is predictable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

LMWH Uses

A

Acute coronary syndrome, venous thromboembolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

LMWH adverse rxns + treatment of overdose

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

LMWH drug-drug interactions

A

NSAIDS increase bleeding risk, antiplatelet agents also increase bleeding tendencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

LMWH advantages and disadvantages

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Warfarin MOA

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Warfarin monitoring lab test

A

INR (PT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Warfarin pharmacokinetics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Warfarin Uses

A

Atrial fibrillation, Venous thromboembolism prophylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Warfarin adverse rxns + treatment of overdose

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Warfarin drug-drug interactions

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Dabigatran MOA

A

Direct thrombin (IIa) inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Dabigatran monitoring lab test

A

Not routinely monitored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

56
Q

Abciximab, Eptifibatide, Tirofiban drug-drug interactions

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions