Brainscape's Knowledge GenomeTM

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


See full index

Pharm Exam 2 > List: Anticoagulants and Thrombolytic Drugs > Flashcards

List: Anticoagulants and Thrombolytic Drugs Flashcards

1
Q

Hemostasis:

A

Hemostasis: process that maintains the integrity of the circulatory systems after vascular damage

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

Primary hemostasis:

A

Primary hemostasis: platelet plug formation (platelets adhere to damaged endothelium to form plug)

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

Secondary hemostasis:

A

Secondary hemostasis: blood coagulation (clot forms upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug) –> Formation of a thrombus

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

Thrombus Formation:

A

Thrombus Formation: extrinsic and intrinsic pathways merge into common pathway, leading to factor X activation

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

Factor X to fibrin:

A

Factor X cleaves prothrombin –> thrombin

Thrombin cleaves fibronigen –> fibrin

Fibrin incorporated into thrombus

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

Thrombolysis/Fibronolysis:

In response to injury, endothelial cells synthesize and release:

t-PA converts plasminogen:

Plasmin cleaves:

A

Thrombolysis/Fibronolysis: process of fibrin digestion by plasmin (protease)

  • In response to injury, endothelial cells synthesize and release tissue plasminogen activator (t-PA)
  • t-PA converts plasminogen  plasmin
  • Plasmin cleaves fibrin and dissolves the clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Endogenous Inhibitors of this Process

PAI-1/PAI-2:
α2-antiplasmin:

A

PAI-1/PAI-2: inhibit t-PA

α2-antiplasmin: inhibitor of plasmin

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

3 Major Classes of Anticoagulant Drugs:

A

Indirect Thrombin Inhibitors

Parenteral Direct Thrombin Inhibitors

Oral Anticoagulants

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

Indirect Thrombin Inhibitors:
Parenteral Direct Thrombin Inhibitors:
Oral Anticoagulants:

A

Indirect Thrombin Inhibitors: Heparin, Fodaparinux

Parenteral Direct Thrombin Inhibitors: Hirudin, Bivalirudin, Argatroban

Oral Anticoagulants: Warfarin, next generation drugs (Apixaban, Pradaxa, Rivaroxaban)

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

Indirect Thrombin Activators

General MOA:

A

General MOA: antithrombotic effect due to interaction with antithrombin III (ATIII) and factor Xa

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

Indirect Thrombin Activators

Preparations: (3)

A

o Unfractionated heparin
o Low-molecular weight heparin
o Fondaparinux (synthetic polysaccharide)

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

Heparin

General:

A

General: heterogeneous mixture of sulfated mucopolysaccharides

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

Heparin Targets: (3)

A
  • Thrombin
  • Factor Xa
  • Factor IXa
    .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Heparin

MOA:

A

MOA: activated ATIII binds heparin and efficiently degrades thrombin and factor X

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

Heparin

Therapeutic Use: (6)

A
  • Venous thrombosis (initial treatment)
  • Pulmonary embolism (initial treatment)
  • Acute MI (initial treatment)
  • Surgery requiring cardiopulmonary bypass
  • Patients with DIC
  • Unstable angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Heparin
Pharmacokinetics:
LMW can be given ____ and without ______

A

Pharmacokinetics: LMW heparin preparations have more predictable pharmacokinetics than HMW heparin
- LMW can be given subQ and without laboratory monitoring

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

Management of Heparin Treatment

Full-dose heparin therapy:
subQ heparin:

A

Full-dose heparin therapy by continuous IV infusion needs to be monitored by activated partial thromboplastin time (aPTT)

Can give subQ heparin for long-term anticoagulant therapy in patients with contraindications for warfarin use (ie. pregnancy)

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

Heparin
Toxicity

Bleeding:
Protamine Sulfate:
Heparin-induced thrombocytopenia:

A

Bleeding: incidence somewhat less in patients treated with LMW form
- Protamine Sulfate: can be given in cases of life-threatening hemorrhage to reverse the effects of heparin (binds tightly and neutralizes it)

Heparin-induced thrombocytopenia: decreased platelet count; lower incidence with LMW form

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

Fondaparinux

Use:

A

Use: approved for thromboprophylaxis of patients undergoing hip or knee surgery
- To prevent pulmonary embolism and deep vein thrombosis

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

Fondaparinux

Management:

A

Management: similar to LMW heparin

  • Can be used with daily subQ administration
  • Does not require monitoring
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Parenteral Direct Thrombin Inhibitors

Drugs in this Class: (3)

A

Hirduin
Bivalirudin
Argatroban

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hirduin:
Bivalirudin:
Argatroban:

A

Hirduin: bivalent specific, irreversible thrombin inhibitor (leech saliva)
Bivalirudin: bivalent inhibitor of thrombin
Argatroban: small molecule thrombin inhibitor

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

Parenteral Direct Thrombin Inhibitors

Drug Targets:

A

Thrombin

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

Therapeutic Use/Management
Hirudin

Treatment of patients with:
Administered by:
Dose adjusted to maintain:

A
  • Treatment of patients with heparin-induced thrombocytopenia
  • Administered by IV
  • Dose adjusted to maintain aPTT at 1.5-2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Therapeutic Use/Management
Bivalirudin

Alternative to:
Administered by:

A
  • Alternative to heparin in patients undergoing coronary angioplasty
  • Administered by IV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Therapeutic Use/Management
Argatroban

Alternative to:

A

Alternative to hirudin for prophylaxis treatment of patients with or at risk of developing heparin-induced thrombocytopenia

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

Parenteral Direct Thrombin Inhibitors
Toxicity

Use with caution in renal failure:
Development of anti-hirudin Abs:

A

Use with caution in renal failure: can accumulate and cause bleeding

Development of anti-hirudin Abs: can cause paradoxical increase in aPTT (daily monitoring of aPTT recommended)

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

Warfarin

General:

A

General: synthetic derivative of coumarin

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

Warfarin

Administered as:
bioavailability:
T½:
vs heparin:

A
  • Administered as a sodium salt
  • Has 100% bioavailability
  • Long T½ in plasma (36 hours)
  • Slower acting than heparin (for long term management, NOT for an acute event)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Warfarin

MOA:
Blocks ______ of glutamate residues in coagulation factors

A

MOA: inhibits the vitamin-K dependent synthesis of biologically active forms of the Ca++-dependent clotting factors (prothrombin, VII, IX, X) and protein C (regulatory factor)
- Blocks gamma-carboxylation of glutamate residues in coagulation factors

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

Warfarin
Therapeutic Use

Prevent progression or recurrence of:
Prevention of ____________ in patients undergoing orthopedic or gynecological surgery

A

Prevent progression or recurrence of acute DVTs or pulmonary embolism (follows initial course of heparin)

Prevention of venous thromboembolism in patients undergoing orthopedic or gynecological surgery

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

Warfarin

Preventing systemic emboli in patients with: (3)

A

Preventing systemic emboli in patients with:

  • Acute MI
  • Prosthetic heart valves
  • Chronic atrial fibrillation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Warfarin
International Normalized Ration (INR)

Therapeutic range for:
Defined as:
Prothrombin time determined from:

A

International Normalized Ration (INR): therapeutic range for oral anticoagulant therapy

Defined as patient prothombin time/mean of normal prothrombin time for the lab

Prothrombin time determined from a fasting blood sample obtained 8-14 hours after the last dose of an oral anticoagulant

34
Q

Warfarin

Use with caution in patients with: (3)

A

Patients with congenital coagulation deficiency

Patients with thrombocytopenia

Patients with hepatic or renal insufficiency

35
Q

Warfarin

Never use:

A

Patients who are pregnant (readily crosses the placenta and causes hemorrhagic disorder in the fetus/serious birth defects)

36
Q

Warfarin resistance:

Difficult to manage because:

A

Warfarin resistance: can develop in some patients (most common in those with advanced cancer); progression/recurrence of the thrombotic event
- Difficult to manage because raising INR in these patients also increases risk of bleeding

37
Q

Warfarin
DDIs

Decrease anticoagulant effect:

A

Decrease anticoagulant effect: barbiturates and rifampin

38
Q

Warfarin
DDIs

Increase anticoagulant effect:

A

Increased anticoagulant effect: aspirin and cephalosporins

39
Q

Oral Direct Thrombin Inhibitors

Main advantage to these new ones is:
New Drugs: (3)

A

New Drugs: main advantage to these new ones is that they do not require drug monitoring
o Pradaxa: targets thrombin only (already FDA approved)
o Rivaroxiban: targets factor Xa
o Apixaban: targets factor Xa

40
Q

Oral Direct Thrombin Inhibitors (apart from warfarin)

Pradaxa:
Rivaroxiban:
Apixaban:

A

Pradaxa: targets thrombin only (already FDA approved)

Rivaroxiban: targets factor Xa

Apixaban: targets factor Xa

41
Q

Fibrinolytic Drugs

General MOA:

A

General MOA: cause rapid lysis of thrombi by catalyzing the activation of plasmin

42
Q

Fibrinolytic Drugs
Tissue Plasminogen Activator (tPA)

General:

A

General: endogenous serine protease that is a poor plasminogen activator in the absence of fibrin

43
Q

Fibrinolytic Drugs
Tissue Plasminogen Activator (tPA)

MOA:
Presence of fibrin _____ the speed of activation
Clearance:
Half Life:

A

MOA: binds to fibrin via lysine binding sites at amino terminus and activates bound plasminogen
- Presence of fibrin increases the speed of activation several hundredfold

Clearance: occurs by hepatic metabolism
- Half Life: 5-10 minutes

44
Q

Fibrinolytic Drugs
Tissue Plasminogen Activator (tPA)
Use: (3)

A

Use: lyses thrombi during the treatment of

  • Acute MI
  • Pulmonary embolism
  • Severe DVT
45
Q

Recombinant tPA: (2)

Effect on half lives:

A

Recombinant tPA: Reteplase and Tenecteplase

Increased half lives (allow for convenient bolus dosing)

46
Q

Fibrinolytic Drugs
Streptokinase

General:

A

General: produced by beta-hemolytic streptococci

47
Q

Fibrinolytic Drugs
Streptokinase

MOA:

A

MOA: no intrinsic enzymatic activity, but forms a stable complex with plasminogen, producing a conformational change that exposes the active site on plasminogen –> plasmin

48
Q

Fibrinolytic Drugs
Streptokinase

Use:

A

Use: decreased due to advent of newer agents

49
Q

Fibrinolytic Drugs

Recent Studies:

A

Recent Studies: suggest that angioplasty without stent placement is superior to thrombolytic therapy, when it is feasible

50
Q

Fibrinolytic Drugs
Hemorrhage:
_____ at sites of vascular injury

A

Hemorrhage: major toxicity of all thrombolytic agents; results from 2 factors

Lysis of fibrin in physiological thrombi at sites of vascular injury

51
Q

Fibrinolytic Drugs
Hemorrhage

A systemic lytic state that results from systemic formation of plasmin, causing: (2)

A
  • Fibrinogenolysis

- Destruction of other coagulation factors (V and VIII especially)

52
Q

Fibrinolytic Drugs
Toxicity

Aminocaproic acid:

A

Aminocaproic acid: potent inhibitor of fibrinolysis (blocks interaction of fibrin and plasmi) and can reverse excessive fibrinolysis

53
Q

Contraindications to Thrombolytic Therapy

Any of the following within 10 days: (4)

A
  • Surgery (including organ biopsy)
  • Puncture of noncompressible vessels
  • Serious trauma
  • Cardiopulmonary resuscitation
54
Q

Contraindications to Thrombolytic Therapy

Within 3 months:
History of :
Active ____ or _____ disorder

A

o Within 3 months: serious GI bleeding
o History of HTN (diastolic >110 mmHg)
o Active bleeding or hemorrhagic disorder

55
Q

Contraindications to Thrombolytic Therapy

CV:
Aorta;
Pericardium:

A

o Previous cerebrovascular accident or active intracranial process
o Aortic dissection
o Acute pericarditis

56
Q

Antiplatelet Drugs: (4)

A
  • Aspirin
  • Dipyridamole
  • Clopidogrel (Plavix)
  • Ticlopidine
57
Q

Aspirin

MOA:
Acetylates ______ near the active site of ______
Effects last for:

A

MOA: blocks platelet aggregation and vasoconstriction by inhibiting synthesis of thromboxane A2

Acetylates a serine residue near the active site of COX-1 (responsible for production of precursor of TXA2)

Effects last for the life of the platelet (7-10 days)

58
Q

Aspirin

Low dose immediately after a heart attack to :
Low dose long-term for prevention of: (3)

A

Low dose immediately after a heart attack to reduce the risk of another or to prevent the death of cardiac tissue

Low dose long-term for prevention of:

  • Heart attacks
  • Strokes
  • Blood clot formation
59
Q

Aspirin
Toxicity

At higher doses:
Use in combination with _______ increases risk of upper GI bleeding

A

Increased at higher doses (especially bleeding)

Use in combination with clopidogrel or warfarin increases risk of upper GI bleeding

60
Q

Dipyridamole

MOA:

A

MOA: vasodilator

61
Q

Dipyridamole

Use:

A

Use: only recommended for postoperative prophylaxis of thromboemboli in patients with prosthetic heart valves, in combination with warfarin

62
Q

Dipyridamole
Toxicity

most common:
most severe:

A

N/V/D most common

Leukopenia is most severe

63
Q

Clopidogrel (Plavix)

MOA:

A

MOA: platelet ADP receptor antagonist (inhibits platelet activation)

64
Q

Clopidogrel (Plavix)

Use: (4)

A

Used with aspiring after angioplasty (continued for at least 1 year)

Reduce stroke and MI in patients with recent strokes and MIs

Treatment of peripheral arterial disease

Treatment of acute coronary syndrome

65
Q

Clopidogrel (Plavix)
Toxicity

Vs dipyridamole and ticlopidine:
Less frequent cases of:

A

Toxicity: more favorable side effect profile that dipyridamole and ticlopidine

Less frequent cases of thrombocytopenia and leukopenia

66
Q

Ticlopidine

MOA:

A

MOA: platelet ADP receptor antagonist (inhibits platelet activation)

67
Q

Ticlopidine

Use:

A

Reduce the risk of thrombotic stroke in patients who have experience stroke precursors and/or in patients who have had a completed thrombotic stroke

68
Q

Ticlopidine
Toxicity

most common:
most severe:

A

N/V/D most common

Leukopenia is most severe

69
Q

Glycoprotein IIb/IIIa Inhibitors

Inhibit platelet aggregation by blocking: (2)

A

Glycoprotein IIb/IIIa Inhibitors: inhibit platelet aggregation by blocking the binding of these platelet-surface integrins to fibrinogen and von Willebrand factor (block cross-linking of platelets)

70
Q

Glycoprotein IIb/IIIa Inhibitors: (3)

A

o Abciximab
o Eptifibatide
o Tirofiban

71
Q

Abciximab

MOA:

A

MOA: Fab fragment of a humanized mAb against the AlphaIIbBeta3 receptor

72
Q

Abciximab
Use

In conjunction with ______ for coronary thromboses

Use along with aspirin and heparin effective in preventing: (3)

A

In conjunction with percutaneous angioplasty for coronary thromboses

Use along with aspirin and heparin effective in preventing restenosis, recurrent MI and death

73
Q

Abciximab

Major side effect:
If severe:

A

Toxicity: major side effect is bleeding

If severe: platelet transfusions can reverse aggregation defect

74
Q

Eptifibatide

MOA:

A

MOA: cyclic peptide inhibitor of the fibrongen binding site on AlphaIIbBeta3 integrin

75
Q

Eptifibatide
Use

Treatment of:
What have reduced MI and death by ~20%?

A

Treatment of acute coronary syndrome (IV)

Angioplastic coronary interventions (IV)- have reduced MI and death by ~20%

76
Q

Eptifibatide

Major side effect:
If severe:

A

Toxicity: major side effect is bleeding

If severe: platelet transfusions can reverse aggregation defect

77
Q

Tirofiban

MOA:

A

MOA: nonpeptide, small-molecule inhibitor of AlphaIIbBeta3 integrin

78
Q

Tirofiban

Use in conjunction with:
For: (2)

A

Use: in conjunction with heparin

  • Non-Q wave MI
  • Unstable angina
79
Q

Tirofiban

Toxicity:
What is possible?
Transfusions required to:

A

Toxicity: bleeding on local sites of clinical intervention and systemically

Major bleeding possible

Transfusions required to terminate bleeding

80
Q

Example of Treatment Regimen for Acute MI

Prehospital: (4)

A

o Aspirin
o Oxygen (CPR if necessary)
o Analgesia/ECG/Antiarryhtmics
o Defibrillation

81
Q

Example of Treatment Regimen for Acute MI

Hospital: (5)

A

o Antiarrhythmics an same supportive care as above
o Fibrinolytic therapy (up to 12 hours after onset), OR
o Coronary angioplasty, OR
o Coronary artery bypass graft surgery
o Anticoagulant (aspirin, heparin, start on warfarin)

82
Q

Example of Treatment Regimen for Acute MI

Outpatient: (3)

A

o Antiarrhythmics as necessary
o Anticoagulant (aspirin or warfarin)
o Antiplatelet drug

Pharm Exam 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions