Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Anti-thrombotic Agents > Flashcards

Anti-thrombotic Agents Flashcards

1
Q

What are venous and arterial thrombi composed of?

A

Venous: mainly fibrin and RBC w/ little platelets

arterial: mainly platelets with little fibrin holding it together

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

What are the main uses of anticoagulant agents?

A
  1. Prevention and tx of venous thrombus
  2. prevention of cardioembolic events w/ Afib
  3. arterial thrombus additive w/ antiplatelet agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the main uses of antiplatelet agents?

A
  1. prevention and tx of arterial thrombus (primary and secondary prevention of ACS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the drugs of choice for primary and secondary ACS prevention

A

Primary: ASA (M over 45, F over 65)

Secondary (ie. recent Mi or ischemic stroke): ASA +/- clopidogrel (or clopidogrel if ASA intolerant)

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

What are the drugs of choice for UA/NSTEMI

A

ASA
+/- clopidogrel or prasugrel or ticagrelor
+/- UFH or LMWH or fondaprinux
+/- GPIIb/IIIa inhibitors

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

What are the drugs of choice for acute MI/STEMI

A

ASA
+ clopidogrel or prasugrel or ticagrelor
+ UFH or LMWH or fondaprinux
+/- GPIIb/IIIa inhibitors

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

What are the drugs of choice for PCI

A

ASA
+ clopidogrel or prasugrel or ticagrelor
+ UFH or LMWH or bivalirudin
+/- GPIIb/IIIa inhibitors

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

What are the drugs of choice for Afib

A

Warfarin or dabigatran or rivaroxaban or apixaban

ASA for low risk pts

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

What are the drugs of choice for VTE treatment

A

LMWH or UFH or fondaparinux + warfarin

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

What are the drugs of choice for VTE prevention for:

pts hosptialized, general surgery, and orthopedic surgery

A

Hospitalized/ general surgery: ow dose UFH or LMWH or fondaparinux

ortho surg: Fondaparinux or rivaroxaban or dabigatran or LMWH or warfarin

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

What is the drug of choice for PAD

A

ASA (clopidogrel if ASA intolerant)

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

In patients with acute coronary syndrome (ACS), aspirin

reduces the incidence of myocardial infarction (MI) by __%

A

15-25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q 
A 70-year-old man taking clopidogrel for ACS has recently been diagnosed with erosive esophagitis and asks his physician which PPI he should take. Which of the following would be the most appropriate choice for this patient? 
A.  Esomeprazole 
B.  Lansoprazole 
C.  Omeprazole 
D.  Pantoprazole 
E.  Rabeprazole
A

B.  Lansoprazole
D.  Pantoprazole
E.  Rabeprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q 
The most common complication of  glycoprotein IIIa/IIb receptor antagonists is: 
A.  Bleeding at arterial access sites 
B.  Leukopenia 
C.  Intracranial hemorrhage 
D.  All of the above
A

A.  Bleeding at arterial access sites

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

Compared to unfractionated heparin (UFH), low-molecular weight heparin (LMWH):
A.  Is more likely to cause heparin-induced thrombocytopenia
B.  Has a more predictable anticoagulant response
C.  Is more completely neutralized by protamine
D.  May be safer in patients with renal impairment

A

B.  Has a more predictable anticoagulant response

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

Fondaparinux can be used for:

A
  1. Prophylaxis of deep vein thrombosis (DVT)
  2. Treatment of venous thromboembolism (VTE)
  3. UA/NSTEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A 55-year-old man with nonvalvular A-fib asks physician to recommend a treatment to reduce his risk of thromboembolic stroke. You could tell him that:
A.  Rivaroxaban is non-inferior to warfarin and does not require INR monitoring
B.  Apixaban is more effective than warfarin, but requires monitoring to keep the INR in the therapeutic range
C.  Dabigatran is more than warfarin and has an FDA approved antidote to reverse its anticoagulant effect
D.  All of the above

A

A.  Rivaroxaban is non-inferior to warfarin and does not require INR monitoring
C.  Dabigatran is more than warfarin and has an FDA approved antidote to reverse its anticoagulant effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
Which of the following anticoagulants would be an appropriate choice for a patient with A-fib associated with a mechanical valve 
A.  Apixaban 
B.  Dabigatran 
C.  Rivaroxaban 
D.  Warfarin
A

D. warfarin

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

What drugs accelerates the conversion of plasminogen to plasmin?

A

*Tissue plasminogen activators (fibrinolytics)
Reteplase
Alteplase

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

If a patient undergoes a PCI with placement of a stent in a coronary blood vessel, she may be given eptifibatide. Which of the following most accurately describes the antithrombotic mechanism of eptifibatide?
A.  Activation of antithrombin III
B.  Block of posttranslational modification of clotting factors
C.  Inhibition of thromboxane production
D.  Irreversible inhibition of platelet ADP receptors
E.  Reversible inhibition of platelet GPIIb/IIIa receptors

A

E.  Reversible inhibition of platelet GPIIb/IIIa receptors

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

Describe the mechanism of blood coagulation:

A
  1. damage to vessel exposes collagen of subendothelium
  2. vessels constrict to reduce blood loss
  3. adhesion and aggregation of platelets to damaged endothelium
  4. activation of platelets causes release of aggregating substances for more platelet adhesion and aggregation creating a thrombus plug
  5. aggregated platelets provide surface for fibrin deposition and coagulation
  6. Blood flow returns to normal when fibrinolysis occurs and clot is digested by enzymes from plasma (plasmin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Blood vessel constriction during the mechanism of blood coagulation is mediated by ___ released by___

A

Vasoactive substances released by platelets (5HT, TXA2)

*pro-aggregatory substanes that increase expression of GIIb/IIIa receptors

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

Adhesion of platelets to damaged endothelium. and Aggregate (with other platelets): Biochemical reaction involving ___ and ___ that activates platelets upon adhesion

A

collagen of endothelial wall and von Willebrand factor

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

Describe the coagulation cascade of the intrinsic and extrinsic pathways

A

Intrinsic TEN1021: surface contact–> 12–>11–> 9–> 10–> 2 (prothrombin)–> 1 (fibrinogen)
*In VIVO and formation of Xa w/in SECONDS

Extrinisic: Tissue factor–> 7–>10–>2–>1
*In VITRO and formation of Xa w/in MINUTES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

___ catalyzes prothrombin (II) –> thrombin (IIa)

___ catalyzes fibrinogen (I)–> fibrin (Ia)

A

Xa

thrombin (IIa)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How do you monitor lab values for the extrinsic and intrinsic clotting pathways

A

Intrinsic: aPTT

Extrinsic: PT/INR (1972 WEPT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MOA of warfarin

A
  1. inhibits liver synthesis of vitamin K dependent factors: 10, 9, 7, 2
    (1972 WEPT)
  2. inhibits synthesis of protein C

2= prothrombin

*delayed onset (hrs-todays)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

MOA of heparin/UFH

A

combines/binds w/ ATIII to inactivate IIa (thrombin) and Xa

*prevents prothrombin to thrombin and fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of LMWH/Fondaparinux

Enoxaparin/Dalteparin

A

combines/binds w/ ATIII to inactivate Xa

*prevents fibrinogen to fibrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

MOA of dabigatran

A

directly inactivates IIa (thrombin)

*prevents activity of thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

MOA of Rivaroxaban and Apixaban

A

Direly inactivates Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What anticoagulants can be administered PO

A

Warfarin, dabigatran, rivaroxaban, apixaban

*dabigatran is a prodrug

(the heparins are parental)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q 
What the brand names of:
Dabigatran
Rivaroxaban
Apixaban
Enoxaparin
A

Dabigatran: Pradaxa
Rivaroxaban: Xarelto
Apixaban: Eliquis
Enoxaparin: Lovenox

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What anticoagulants are eliminated renal vs hepatic metabolism (CYP)

A

Renal: LMWH, Enoxaparin, dabigatran (BID)

Hepatic: Warfarin, rivaroxaban, apixaban (BID)

*best to use warfarin in renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What monitoring lab tests are needed for:

  1. Heparin/UFH:
  2. LMWH/Enoxaparin:
  3. Warfarin:
  4. Dabigatran
  5. Rivaroxaban and Apixaban:
A
  1. Heparin/UFH: aPTT (activated partial thromboplastin time)
  2. LMWH/enoxaparin: NONE- action predictable
  3. Warfarin: PT/INR
  4. Dabigatran: no routine monitoring– could use DDT to assess management of bleeding episode or ECT (expensive)
  5. Rivaroxaban and Apixaban: no routine monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Adverse side effects of Heparin/UFH

A
  1. bleeding
  2. thrombocytopenia
  3. Osteoporosis w/ LT heparin use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Adverse side effects of LMWH/Enoxaparin

A
  1. bleeding
  2. thrombocytopenia (less than UFH)
  3. Osteoporosis w/ LT heparin use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Adverse side effects of Warfarin

A
  1. bleeding
  2. skin necrosis
  3. contraindicated in pregnancy
  4. osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Adverse side effects of Dabigatran

A
  1. bleeding

2. gastritis symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Adverse side effects of Rivaroxaban

A
  1. bleeding

2. hard to reverse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What anti-coagulants are safe in pregnancy?

A
  1. heparin/UFH
  2. LMWH/Enoxaparin

[D]-[R]-[A] are not studied yet and category C

**WARFARIN IS NOT SAFE! (X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

__ increase the risk of bleeding with all anticoagulants

43
Q

DDI of warfarin

A

Increase effect w/: CYP450 inhibitors, Abx

Decrease effect w/: CYP450 inducers, dietary Vit. K

44
Q

DDI of [D]-[R]-[A]

A

Increase effect w/: P-glycoprotein inhibitors
[R]: CYP3A4 inhibitors

Decrease effect w/: P-glycoprotein inducers (rifampin, dronedarone)

45
Q

DDI of haparin/UFH and LMWH

A

antiplatelet agents

46
Q

OD treatment of haparin/UFH and LMWH

47
Q

OD treatment of wafarin

A

Phytonadione (Vit. K) – FFP

48
Q

OD treatment of dabigatran

A

Idarucizumab– specific antidote for life threatening bleeding

49
Q

OD treatment of rivaroxaban and apixaban

A

No specific antidote–> hemostatic measures: FFP, RBCs

50
Q

Uses of haparin/UFH and LMWH

A
  1. ACS
  2. tx and prophylaxis of VTE +/- postop
  3. prevent cerebral thrombosis in evolving stroke
51
Q

Uses of Warfarin

A
  1. Afib

2. VTE prophylaxis w/ valvular heart dz or CKD

52
Q

Uses of Dabigatran

A
  1. Afib (FDA approved)

2. VTE (non-FDA approved)

53
Q

Uses of Rivaroxaban

A
  1. Afib

2. DVT-PE prevention after total hip or knee replacement

54
Q

Uses of Apixaban

55
Q

____ generally preferred over warfarin for nonvalvular A Fib

A

DOAC (direct oral anticoagulants)

Ie. dabigatran, rivaroxaban, apixaban

56
Q

___ and ___ reverse vasoconstriction and inhibit platelet aggregation

A

PGI2 (prostacyclin) and NO

57
Q

Activated protein C with cofactor S inactivates __ and ___ which results in

A

Va and VIIIa

diminishing rate of prothrombin and factor X activation

58
Q

___ proteolyzes ___ and limits thrombosis

A

plasmin proteolyzes fibrin

59
Q

the central process of fibrinolysis is activation of ____ by __

A

plasminogen to plasmin by tPA (tissue plasminogen activator)

60
Q

Contraindications of heparin (UFH and LMWH)

A
  1. hypersensitivity
  2. active bleeding/ ulcerative GI lesions
  3. hemophilia
  4. thrombocytopenia
  5. purpura
  6. severe hypertension
  7. bacterial endocarditis
  8. Threaten abortion
61
Q

Why is there a delay onset with warfarin

A

delayed as existing factors turn over (12-24 hrs)

62
Q

What is the management when the INR with warfarin is:

  1. Over therapeutic but less than 4.5 w/o bleeding:
  2. INR 4.5-10 w/o bleeding:
  3. over 10 w/o bleeding:
  4. major bleeding:
A
  1. Over therapeutic but less than 4.5 w/o bleeding: reduce or skip dose and monitor
  2. INR 4.5-10 w/o bleeding: hold 1-2 doses, check, restart at lower dose once therapeutic
  3. over 10 w/o bleeding: hold, administer Vit K po, resume at lower dose once therapeutic
  4. major bleeding: hold, Vit K IV, PCC over FFP or recombinant factor VIIa
63
Q

What are CYP450 inhibitors and what is there effect on Warfarin

A

increase warfarins effect:

  1. Amiodarone
  2. Cimetidine
  3. Fluconazole
  4. Fluoxetine
  5. Metronidazole
  6. Rosuvastatin
64
Q

What are CYP450 inducers and what is there effect on Warfarin

A

decrease warfarins effect:

  1. Barbiturates
  2. Carbamazepine
  3. Phenytoin
  4. Rifampin
  5. St. John’s Wort
  6. Cholestyramine
  7. Colestipol
    * *Decrease absorption
65
Q

Inhibitors of platelet thromboxane A2 synthesis

66
Q

Antagonists of platelet ADP receptor (P2Y12)

A
  1. Ticagrelor (Brilinta)
  2. Clopidogrel (Plavix)
  3. Prasugrel (Effient)
67
Q

MOA of ASA

A

low dose (81mg) “selective” inhibition of platelet COX-1 (irreversible)

68
Q

MOA of Ticagrelor, Clopidogrel, and Prasugrel (ADP antagonist)

A

inhibition of platelet ADP (P2Y12) receptor
[C]-[P]: irreversible, prodrugs activated by CYP2C19
[T]- reversible

69
Q

MOA of Dipyridamole (persantine)

A

inhibits phosphodiesterase in platelets–> increases cAMP–> increase PGI2 anti-aggregation effect

70
Q

MOA of Abciximab, Eptifibatide, and Tirofiban (GIIb/IIIa inhibitors)

A

blocks platelet GIIb and IIIa receptor preventing fibrinogen binding and platelet aggregation
[A]- monoclonal Ab
[E]- cyclic peptide
[T]- non-peptide

71
Q

Inhibitors of platelet GIIb/IIIa receptors

A
  1. Abciximab
  2. Eptifibatide
  3. Tirofiban
72
Q

Describe the administration of the antiplatelet drugs (ASA, ADP antagonists, GIIb/IIIa inhibitors, dipyridamole)

A
  1. ASA: PO, QD
  2. [C]-[P]: PO, QD
  4. [A], [E], T: parenteral
  5. D: PO
73
Q

What antiplatelets are eliminated renally vs hepatic (ASA, ADP antagonists, GIIb/IIIa inhibitors, dipyridamole)

A

Renal: all GIIb/IIIa inhibitor and [C]- activated by CYP2C19 then renal and fecal excretion

Hepatic: ASA, [P], [T], Dipyridamole

74
Q

Adverse effects of ASA

A
  1. Bleeding

2. Gastric upset

75
Q

Adverse effects of Clopidogrel

A
  1. Bleeding
  2. Dyspepsia
  3. Gastritis
  4. HA
76
Q

Adverse effects of Ticagrelor

A
  1. Bleeding
  2. dyspnea
  3. bradyarrhythmias
77
Q

Adverse effects of Dipyridamole

A
  1. Dizziness
  2. HA
  3. nausea
  4. GI upset
78
Q

Adverse effects of Abciximab, Eptifibatide, and Tirofiban (GIIb/IIIa inhibitors)

79
Q

Compare the efficacy of Ticagrelor, Clopidogrel, and Prasugrel (ADP antagonist)

A

P-T>C

*same pattern for bleeding risk

80
Q

What pregnancy category are the antiplatelet drugs?

ASA, ADP antagonists, GIIb/IIIa inhibitors, dipyridamole

A
  1. ASA: C/D (3rd)
  3. [P]-[T]: C
  4. Dipyridamole: B
  6. [E]-[T]: B
81
Q

DDI with ASA

A
  1. increased bleeding risk w/ anti-coagulants
82
Q

DDI with clopidogrel

A
  1. PPIs may block activation of prodrug by CYP2C19

* No DDI w/ [P] + PPIs

83
Q

Uses of ASA

A
  1. acute MI-unstable angina (ACS)

2. PCI/ secondary prevention MI-stroke

84
Q

Uses of Ticagrelor, Clopidogrel, and Prasugrel (ADP antagonist)

A
  1. acute MI-unstable angina

2. PCI

85
Q

Uses of Dipyridamole

A
  1. secondary prevention of MI-stroke
86
Q

Uses of Abciximab, Eptifibatide, and Tirofiban (GIIb/IIIa inhibitors)

87
Q

What are the drugs of choice for AMI/STEMI

A

ASA (chewed) + ADP antagonist

88
Q

What are the drugs of choice for unstable angina/NSTEMI

A

ASA +/- ADP antagonist

89
Q

What are the drugs of choice for PCI

A

ASA + ADP antagonist +/- GIIb/IIIa inhibitors

90
Q

What are the drugs of choice for secondary prevention of MI

A

ASA (enteric coated) +/- dipyridamole

91
Q

The risk of bleeding in patients receiving heparin is increased by aspirin because aspirin:
A.  Inhibits heparin anticoagulant activity
B.  Inhibits platelet function
C.  Displaces heparin from plasma protein-binding sites
D.  Inhibits prothrombin formation
E.  Causes thrombocytopenia

A

B.  Inhibits platelet function

92
Q

Examples of fibrinolytic drugs

A
  1. Tissue plasminogen activators (alteplase, reteplase, tenecteplase)
  2. Streptokinase
  3. Urokinase
93
Q

MOA of fibrinolytic drugs

A

rapid lysis of thrombi by increasing formation of plasmin from plasminogen –> generalized lytic state

94
Q

Streptokinase activates _____ while tPA (and variants) activate ___ limiting induction of a systemic lytic state

A

both circulating (free) and fibrin-bound plasminogen

bound plasminogen several hundredfold more rapidly than circulating plasminogen

95
Q

Human tPA from recombinant DNA technology: tPA binds to fibrin and selectively activates bound plasminogen under physiological conditions (i.e., “clot-selective”, but therapeutic levels are 100 times higher)

A

Alteplase tPA

96
Q

Newer, modified forms of tPA can be given as bolus and have prolonged duration of action.

A

Reteplase, Tenecteplase

  • Reteplase is less fibrin specific than tPA, while tenecteplase slightly more.
97
Q

Reteplase is ___ fibrin specific than tPA, while tenecteplase slightly ___.

98
Q

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.

A

Streptokinase

*no longer used in US

99
Q

Uses of fibrinolytic agents

A
  1. AMI/PCI
  2. DVT
  3. Multiple PE
100
Q
  • Emergency treatment of coronary artery thrombosis; prompt use [within 2 hours] associated with better clinical outcomes
  • Further reduction in mortality with use of adjunctive drugs (beta-blockers, ACE inhibitors, aspirin)
A

fibrinolytic agents

101
Q

Adverse effects of fibrinolytic agents

A
  1. Hemorrhage (intracranial hemorrhage is most serious)
102
Q

Fibrin-specificity: preferential activation of fibrin-bound vs circulating plasminogen

A

tPA over SK

103
Q

What fibrinolytic agent has the highest risk of systemic bleeding and ICH risks

104
Q

Contraindications of fibrinolytic agents

A
  1. Active PUD
  2. underlying bleeding disorder
  3. recent stroke
  4. recovering from recent surgery

Pharmacology (31 decks)

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