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Pharm II Exam 3 > ACS Pharm and Therapeutics > Flashcards

ACS Pharm and Therapeutics Flashcards

1
Q

Thrombus type in STEMI-ACS?

A

Complete occlusion

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2
Q

Thrombus type in NSTEMI (Non ST elevation ACS)?

A

Non-fully occlusive, some patency w/ tissue damage or cardiac necrosis

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3
Q

Thrombus type in Unstable angina (Non ST elevation ACS)?

A

Non-fully occlusive, some patency

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4
Q

EKG for Unstable angina (Non ST elevation ACS)?

A

Non-specific EKG changes

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5
Q

EKG for NSTEMI (Non ST elevation ACS)?

A

ST-depression, T-wave inversions

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6
Q

EKG for STEMI-ACS?

A

ST-elevation, New LBBB

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7
Q

Enzymes for STEMI-ACS?

A

Troponin (Tn) positive

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8
Q

Enzymes for NSTEMI (Non ST elevation ACS)?

A

Troponin (Tn) positive

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9
Q

Enzymes for Unstable angina (Non ST elevation ACS)?

A

Within normal limits (WNL)

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10
Q

Thrombus formation?

A

-Glucose and fat will get stored along the lining of the lining of the lumen & create inflammation (endothelial injury) over time
-Fat plaque will build over endothelial matrix
-As plaque grows, artery gets more clogged
-Eventually increased BP from decreased area for blood to flow through lumen rips fat plaque from the wall

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11
Q

What does complete coronary occlusion cause?

A

Acute MI

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12
Q

What does spontaneous lysis, repair, and wall remodeling after occlusion cause?

A

Temporary resolution of instability, future high risk coronary lesion

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13
Q

What does incomplete coronary occlusion cause?

A

Unstable angina or non-Q-wave MI

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14
Q

How does a thrombus form?

A

Systemic thrombogenicity
Platelet activation, adhesion, aggregation
Coagulation pathway activation/thrombin formation
Fibrinogen conversion to fibrin w/ cross-linking of bands

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15
Q

Initial assessment for NSTEMI/STEMI?

A

12-lead EKG to differentiate, troponins, clinical presentation, TIMI risk score and GRACE scores

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16
Q

What do TIMI risk score and GRACE scores measure?

A

TIMI: risk of ischemic event/mortality in NSTEMI or unstable angina

GRACE: estimates in-hospital and 6 month to 3 year mortality risk of adverse events after ACS

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17
Q

Do all diabetics feel left arm pain?

A

No (due to neuropathies)
*can happen in T1DM and T2DM

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18
Q

What is the goal of ACS care?

A

Immediate relief of ischemia/prevention of further MI and death

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19
Q

Parmacotherapy plan for ACS care?

A

Early therapy –> Revascularization –> Long-term management
*appropriate therapies in all 3 areas minimizes morbidity & mortality

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20
Q

What happens if patients do not receive therapy for ACS management?

A

Increased chance of CV event in the next year

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21
Q

What should all ACS patients receive early in hospital care?

A

Anti-ischemic and analgesic medication
*MONA plus B-Blocker

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22
Q

What is MONA therapy?

A

Morphine
O2
Nitroglycerin
Aspirin (ASA)

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23
Q

Why is morphine given in MONA therapy? How often is it given?

A

To relieve stress, pain, provide vasodilation
Administer every 5-30 min

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24
Q

When should O2 be given in MONA therapy?

A

If SaO2 <90% (oxygen saturation of arterial blood), if pt in respiratory stress or has features of hypoxia

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25
Q

How can Nitroglycerin be administered for MONA therapy?

A

NTG spray under tongue, Sublingual tablet, or IV

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26
Q

Does nitroglycerin improve mortality in ACS?

A

No

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27
Q

Limitations in nitroglycerin therapy for ACS?

A

Vitals: SBP<90 mmHg, arrhythmias (ex. Severe bradycardia/tachycardia)

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28
Q

Should Nitroglycerine prevent other mortality reducing therapies?

A

No, should not prevent/preclude
(Ex. Alteplase, heparin)

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29
Q

How does aspirin benefit ACS in MONA therapy?

A

Helps stabilize plaque/clot
*inflammatory markers can promote clot expansion –> Aspirin helps regulate/reduce inflammation/prevent expansion

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30
Q

What does DAPT stand for?

A

Dual anti-platelet therapy

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31
Q

What is used for DAPT?

A

Aspirin PLUS a P2Y12 receptor inhibitor (clopidogrel, ticagrelor, or prasugrel)

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32
Q

How long is ASA taken after ACS?

A

For life

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33
Q

What can be taken in place of Aspirin if a patient is allergic?

A

Clopidogrel

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34
Q

How should B-Blocker be administered for ACS?

A

IV initially and then transition to PO

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35
Q

What does B-Blocker therapy improve in ACS patients?

A

Reduced mortality, re-infarction rate, and frequency of arrhythmias

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36
Q

Use caution with B-blocker therapy in which conditions?

A

New HFrEF or acute decompensated HF

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37
Q

Which B-Blocker is the most popular in early hospital care for ACS?

A

Metoprolol

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38
Q

Contraindications for B-blockers?

A

Pulmonary disease: carvedilol not ideal (Beta-2 R activity in the lungs)
Low HR/bradycardia
Hypoglycemia

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39
Q

What is indicated in treatment for a STEMI (completely blocked coronary artery)?

A

Urgent revascularization (either PCI or fibrinolytics)

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40
Q

Is PCI or fibrinolytic treatment preferred for revascularization of STEMI/complete blockage?

A

PCI

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41
Q

What kind of PCI is usually used for revascularization of STEMI/complete blockage?

A

Usually re-profusion w/ stent

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42
Q

When would fibrinolytics be indicated for revascularization of STEMI/complete blockage?

A

When PCI is unavailable/cannot be performed within 120 minutes of onset

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43
Q

What is indicated for early hospital care for NSTE-ACS (UA or NSTEMI)?

A

Early invasive strategy usually done over ischemia guided strategy

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44
Q

Define the difference between early invasive strategy and ischemia guided strategy for NSTE-ACS (UA or NSTEMI)?

A

Early invasive strategy: stent/evaluation for cabg ASAP
Ischemia guided: med therapy w angiography only if pt has recurrent of refractory ischemic sx
*depends on severity/stability of patient, availability for procedure, etc.

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45
Q

Which treatments are antiplatelet agents?

A

DAPT (aspirin and P2Y12 inhibitor) and GPIIb/IIIa inhibitors

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46
Q

Which meds are GPIIb/IIIa inhibitors?

A

Abciximab (Repro), Eptifibatide (Integrilin), Tirofiban (Aggrastat)

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47
Q

What are the anticoagulation strategies for ACS?

A

UFH, Enoxaparin, Bivalirudin, Fondaparinux

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48
Q

Mechanism of action for clopidogrel (P2Y12 inhibitor)?

A

Blocks ADP from platelet by binding to P2Y12 R’s

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49
Q

Mechanism of action for aspirin?

A

Blocks arachidonic acid from platelet by inhibiting Cox-1

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50
Q

Mechanism of action for fibrinolytics?

A

Blocks fibrin from linking platelets
Converts plasminogen to plasmin that degrades fibrin

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51
Q

Mechanism of action for GPIIb/IIIa inhibitors?

A

Block IIb/IIIa receptors on platelet, inhibit fibrinogen binding

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52
Q

Mechanism of action for Heparin, LMWH, Fondaparinux, Direct thrombin inhibitors?

A

Block thrombin from platelet

53
Q

Which anticoagulants are less commonly used due to cost ($$$)?

A

Fondaparinux, Direct thrombin inhibitors

54
Q

When would fondaparinux or direct thrombin inhibitors be indicated over heparin?

A

Incidences of HIT (Heparin induced thrombocytopenia)

55
Q

Which stent may be more prone to atherosclerosis/clogging?

A

Bare metal stent

56
Q

Which stent can prevent atherosclerotic build-up/remains more open over time?

A

Drug eluting stent (releases meds)

57
Q

What is extremely important for those undergoing drug eluting stent PCI?

A

Need to be compliant with DPT, if not death risk is increased 10 fold due to plaque formation

58
Q

Which antiplatelet therapy is indicated before PCI revascularization procedure in a patient with STEMI?

A

Aspirin, all 3 P2Y12i’s (clopidogrel, prasugrel, ticagrelor), ?? check

59
Q

Which antiplatelet therapy is indicated before PCI revascularization procedure in a patient with STEMI + fribinolytic administered?

A

Aspirin, Clopidogrel

60
Q

Which antiplatelet therapy is indicated before PCI revascularization procedure in a patient with NSTEMI early invasive intervention?

A

Aspirin, all 3 P2Y12i’s (clopidogrel, prasugrel, ticagrelor)

61
Q

Which antiplatelet therapy is indicated before PCI revascularization procedure in a patient with NSTEMI ischemia guided intervention?

A

Aspirin, Copidogrel or Ticagrelor

62
Q

Peak platelet inhibition for Clopidogrel (Plavix)?

A

600mg load 2 hours

63
Q

Peak platelet inhibition for Prasugrel (Effient)?

A

60mg load 1-1.5 hours

64
Q

Peak platelet inhibition for Ticagrelor (Brilinta)?

A

180mg load <1 hour

65
Q

Contraindications of Clopidogrel (Plavix)?

A

Active bleeding
(however no one will use these meds, or any anticoagulants if there is a major active bleed)

66
Q

Contraindications of Prasugrel (Effient)?

A

History of stroke/TIA

67
Q

Contraindications of Ticagrelor (Brilinta)?

A

Intracerebral hemorrhage (ICH), hepatic disease

68
Q

Metabolism of Clopidogrel (Plavix)?

A

Pro-drug, 2 step process by CYP2C19 enzymes

69
Q

Metabolism of Prasugrel (Effient)?

A

Pro-drug, several CYP pathways

70
Q

Metabolism of Ticagrelor (Brilinta)?

A

Not a pro-drug

71
Q

Half-life of Clopidogrel (Plavix)?

A

8 hours

72
Q

Half-life of Prasugrel (Effient)?

A

3.5 hours

73
Q

Half-life of Ticagrelor (Brilinta)?

A

8 hours

74
Q

What might cause someone to have no response to Clopidogrel (Plavix)?

A

CYP2C19 polymorphisms/varients

75
Q

Are there any incidences where there would be no response to Prasugrel (Effient) or Ticagrelor (Brilinta)?

A

No known issues that would cause lack of response

76
Q

Drug-drug interactions of Clopidogrel (Plavix)?

A

PPI’s (omeprazole and esomeprazole)

77
Q

Drug-drug interactions of Prasugrel (Effient)?

A

Limited data

78
Q

Drug-drug interactions of Ticagrelor (Brilinta)?

A

3A4 substrates, avoid Simvastatin (competes for same substrate, increases concentration)

79
Q

Bleeding risk of Clopidogrel (Plavix)?

A

Lower risk

80
Q

Bleeding risk of Prasugrel (Effient)?

A

Higher risk

81
Q

Bleeding risk of Ticagrelor (Brilinta)?

A

Higher risk

82
Q

GP IIb/IIIa inhibition has the greatest benefit in which patients?

A

Those with highest risk features for DM2, high troponins, or recent ACS

83
Q

Addition of IIb/IIIai reduces what?

A

Composite endpoint of MI, hospitalization, or death

84
Q

Addition of IIb/IIIai increases risk of what?

A

Bleeding

85
Q

In addition to DAPT, all patients with ACS should be administered what?

A

An anticoagulant (to reduce risk of intracoronary & catheter thrombus formation)

86
Q

Class I recommendation for STEMI (PCI) anticoagulant treatment?

A

UFH

87
Q

Class I recommendation for STEMI w/ fibrinolytic therapy anticoagulant treatment?

A

UFH or enoxaparin

88
Q

Class I recommendation for NSTE-ACS w/ early invasive strategy anticoagulant treatment?

A

UFH, enoxaparin, bivalirudin, or fondaparinux

89
Q

Class I recommendation for NSTE-ACS w/ ischemia guided strategy anticoagulant treatment?

A

UFH or enoxaparin

90
Q

If a patient is considered high risk for poor outcomes, and GP IIb/IIIa inhibitors are used, what is the preferred anticoagulant?

A

UFH

91
Q

If a patients is considered high risk for poor outcomes, and has a risk of bleeding then what medication is recommended?

A

Bivalirudin (instead of UFH and GP IIb/IIIai)

92
Q

When is Fondaparinux most commonly used for anticoagulation?

A

Allergy to UFH or enoxaparin (ex. HIT)

93
Q

Is anticoagulation treatment continued or discontinues after PCI is completed?

A

Discontinued

94
Q

What is Enoxaparin (Lovenox) classified as?

A

LMWH

95
Q

What is Fondaparinux (Arixtra) classified as?

A

Factor Xa inhibitor

96
Q

What is Bivalirudin (Angiomax) classified as?

A

Direct thrombin inhibitor

97
Q

What are the dose adjustments for UFH in renal failure?

A

None

98
Q

What are the dose adjustments for Enoxaparin (Lovenox) in renal failure?

A

If CrCl <30ml/min reduce dose by 50%

99
Q

What are the dose adjustments for Fondaparinux (Arixtra) in renal failure?

A

CONTRAINDICATED if CrCl <30ml/min

100
Q

What are the dose adjustments for Bivalirudin (Angiomax) in renal failure?

A

If CrCl <30ml/min: infusion must be reduced (see clinical protocol)

101
Q

What should be monitored in UFH therapy?

A

aPTT to about 50-70 seconds

102
Q

When should UFH be avoided?

A

If history of HIT

103
Q

When should fibrinolytics be given to patients?

A

If the patient has STEMI (symptoms w/in 12 hours) and PCI cannot be performed within 120 min of first medical contact

104
Q

What some commonly used fibrinolytic agents?

A

Alteplase, Reteplase, Tenecteplase

105
Q

Which fibrinoltic out of Alteplase, Reteplase, & Tenecteplase has the most efficacy?

A

They all have similar efficacy

106
Q

What should be administered along with fibrinolytics and for how long?

A

Anticoagulant therapy for minimum 48hrs (preferable for the duration of hospitalization)

107
Q

What are the relative contraindications of fibrinolytic therapy?

A

BP>180/110
Hx of ischemic stroke w/in last 3 months
Dementia
Oral anticoagulant therapy (ex. Warfarin)

108
Q

Absolute contraindications of fibrinolytic therapy?

A

Prior hemorrhagic stroke
Ischemic stroke w/in last 3 months
Cranial or spinal surgery w/in last 2 months
Severe uncontrolled HTN (unresponsive to emergency therapy)

109
Q

How long is ASA taken for long term management post-ACS?

A

Indefinitely (Baby aspirin)

110
Q

How long is P2Y12 inhibitor therapy administered along with ASA (DAPT) for long term management after ACS?

A

P2Y12 inhibitors minimum of 12 months

111
Q

What is the harm in stopping anticoagulation early/patient non compliance with a bare metal stent?

A

Lowest risk if non-compliant, Re-stenosis or buildup of atherosclerosis

112
Q

What is the harm in stopping anticoagulation early/patient non compliance with a drug eluting stent?

A

High risk of death if non-compliant/stopped early, Re-thrombosis/clotting

113
Q

30 day mortality rates of drug therapy compliant patients post ACS vs. non-compliant?

A

Compliant: 0.7%
Non-complient: 7%

114
Q

Which is more expensive: clopidogrel or ticagrelor?

A

Ticagrelor

115
Q

Which has better efficacy: clopidogrel or ticagrelor?

A

Ticagrelor

116
Q

When is early discontinuation of post-ACS therapy reasonable?

A

When risk of morbidity exceeds the benefits of therapy

117
Q

What medication is indicated for all post-ACS patients?

A

Beta blocker unless contraindicated

118
Q

When should beta blocker therapy be started for post-ACS patients?

A

ASAP

119
Q

Which beta blockers can be used for post-ACS patients?

A

Metoprolol, Atenolol, Carvedilol, or Bisoprolol

120
Q

If EF<40% which beta blocker should be used (HFrEF)?

A

Metoprolol, Carvedilol, Bisoprolol preferred

121
Q

When are ACEi’s appropriate for post-ACS patients?

A

In HTN, CKD, DM, or EF<40% (Entresto)

122
Q

If post-ACS patients have a cough while taking ACEi’s, what can be used instead?

A

ARB

123
Q

When are aldosterone receptor blockers indicated in post-ACS patients?

A

If patients already on BB and ACEi who have EF<40%

124
Q

Contraindications of aldosterone receptor blocker therapy?

A

Elevated K+, impaired renal function

125
Q

What pain relievers should be avoided in post-ACS patients? Why?

A

NSAIDs (ibuprofen, naproxen, celecoxib)
**Increase risk of recurrent ACS

126
Q

What pain relievers should be considered for post-ACS patients?

A

Tramadol or Acetaminophen

127
Q

Which 2 lipid management drugs are appropriate for post-ACS patients?

A

Atorvastatin (higher doses 40-80mg/day) and Rosuvastatin (40mg/day)
*Dose specific

128
Q

Worst place to get atherosclerosis/complete blockage?

A

Left coronary artery (The widow maker)

Pharm II Exam 3 (6 decks)

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