Acute Coronary Syndrome Flashcards

1
Q

Acute Coronary Syndrome (ACS)

A
  • Really an Acute MI from atherosclerosis, plaque etc.
  • Consists of STEMI’s, Non-STEMI’s and unstable angina
  • Life-threatening
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2
Q

DDx for ACS

A
  • ACS
  • Pulmonary Embolism
  • Non- STEMI
  • Aortic Dissection
  • Gastroesophageal reflux
  • STEMI
  • Unstable angina

**Difficult!!! esp. cause you have to act fast to treat MI!

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3
Q

What do you give a STEMI (or new LBBB) or a Non-STEMI after taken history, physical exam and ECG?

A

ONAM!!!

  1. ) Oxygen
  2. ) Nitroglycerin
  3. ) Aspirin
  4. ) Morphine (controversy, possible increased mortality?)
  • Others: Beta-blocker, Anithrombin
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4
Q

After meds for STEMI, what next?

A

Either:
- Emergent PCI, use with Glycoprotein IIb/IIIa inhibitors
OR
- Fibrinolytic Therapy

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5
Q

After meds for non- STEMI, what next?

A

Either:
- Early Intervention, use Glycoprotein IIb/IIIa inhibitors or bivalirudin with PCI
OR
- Medical management; consider Glycoprotein IIb/IIIa inhibitors or bivalirudin for high-risk patients

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6
Q

UNSTABLE ANGINA

A
  • Secondary to reduced myocardial perfusion
  • Three principle types:
    1. Rest angina
    2. New-onset severe angina
    3. Crescendo angina (had it but getting worse and more frequent)

–> treat symptomatically

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7
Q

NSTEMI

A

Defined by ACC and ECC as:

  • Rise and fall of serum troponin levels
  • Fall of CK-MB levels
  • Ischemic symptoms
  • Development of pathologic waves on the ECG
  • ST-segment changes indicative of ischemia

Intermediate risk (not fully occlusive, could progress quickly

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8
Q

STEMI

A
  • Most lethal form of acute coronary syndrome
  • Completely occlusive thrombus results in total cessation of coronary blood flow
  • Accurate diagnosis vital because Immediate consideration of reperfusion by mechanical or drug methods
    - Thrombolytics have potentially fatal outcomes so use has guidelines
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9
Q

Antiplatelets?

A

Aspirin

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10
Q

How aspirin works?

A

Affects Thromboxane A2 (on platelets) –> it suppresses it so platelets don’t stick well together –> stop/slow clots

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11
Q

Indications for Aspirin?

A

o Treatment of mild-to-moderate pain, inflammation, and fever
o Prevention and treatment of acute coronary syndromes (ST-elevation MI, non-ST-elevation MI, unstable angina)
o Acute ischemic stroke, and transient ischemic episodes
o Management of rheumatoid arthritis, rheumatic fever and osteoarthritis
o Adjunctive therapy in revascularization procedures (coronary artery bypass graft, percutaneous transluminal coronary angioplasty, carotid endarterectomy), stent implantation

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12
Q

Does aspirin work?

A

YES!!! 50% reduction in death of MI

  • Shown to be effective (in combination) in reducing recurrent ischemic events in patients undergoing intracoronary stent placement
  • CABG –> 50% reduction in early thrombotic graft occlusion

*** So take on regular basis to prevent MI!

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13
Q

ADR of aspirin

A

• Aspirin sensitivity
o Respiratory sensitivity
o Cutaneous sensitivity
o Systemic sensitivity

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14
Q

Aspirin maintenance dose prescription

A

81 mg

One tablet daily

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15
Q

Aspirin dose with ER presentation

A

160-325 mg

Must take chewable tablets and chew

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16
Q

Prescription for Clopidogrel maintenance dose

A

75 mg
One tablet daily
• Maintenance Dose, get effect in 10-11 days

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17
Q

Prescription for Clopidogrel for use with PCI

A

Load 300 mg and maintain at 75 mg once daily

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18
Q

How do the oral Antiplatelets (Clopidogrel) work?

A

o Stop ADP from binding to receptor (P2Y12)
o So the P2Y12 receptor can’t activate the Glycoproteins IIb/IIIa receptors to be made
 Glycoproteins IIb/IIIa receptors normally link up platelets  clot
• They can’t do this with this drug

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19
Q

Clopidogrel Metabolism

A

Prodrug- two step including 2C19, 3A4, 2B6, 1A2

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20
Q

Clopidogrel Indications

A
  • Acute coronary syndrome (UA, NSTEMI, STEMI)

- Recent myocardial infarction, recent stroke or established peripheral vascular disease

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21
Q

What are the other antiplatelets beside Clopidogrel?

A
  • Ticlopidine
  • Prasugrel
  • Ticagrelor
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22
Q

Clopidogrel resistance

A

Genetic basis affected by CYP2C19

  • Metabolize too fast –> don’t get therapeutic effect
  • Not enough, so don’t metabolize fast enough –> toxic levels
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23
Q

Drug interactions of Clopidogrel ?

A
  • Genetic basis affected by CYP2C19
  • The Great Debate- Clopidogrel and the Use of Proton Pump Inhibitors (PPIs)
  • PPIs suppress CYP2C19, and Clopidogrel levels too low –> clot possibility
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24
Q

Clopidogrel Works?

A
  • CURE/COMMIT- relative risk reduction primary outcome was 20% and 7%
  • CHARISMA- “failed to demonstrate a reduction…of the primary endpoint
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25
Q

ADR of Clopidogrel

A
o	Bleeding
    - Wide variances seen in studies
    - All significantly lower than 5%
•	Labeled at 4% major and 5% minor
o	Rash, pruritus
o	Gastrointestinal hemorrhage
o	Thrombotic thrombocytopenic purpura
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26
Q

• Ticlopidine (Ticlid™)

A

o Life-threatening hematologic reactions

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27
Q

• Prasugrel (Effient™)

A

o Similar action to clopidogrel but reduced number of biotransformation steps
o Not intended for use in:
 Patients 75 years of age or older
 Patients who weigh less than 60 kg

28
Q

• Ticagrelor (Brilinta™)

A

o Faster onset compared to clopidogrel

o Load and then twice a day dosing

29
Q

What are the IV antiplatelets

A
  • Abciximab
  • Eptifibatide
  • Tirofiban
30
Q

Indication for Abciximab

A
  • Prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention
  • Prevention of cardiac ischemic complications in patients with unstable angina/non-ST-elevation myocardial infarction unresponsive to conventional therapy when PCI is scheduled within 24 hours
31
Q

Indication for Eptifibatide?

A

Treatment of patients with acute coronary syndrome including patients who are to be managed medically and those undergoing percutaneous coronary intervention

32
Q

Indication for Tirofiban?

A

Treatment of acute coronary syndrome (ie, unstable angina/non-ST-elevation myocardial infarction ) in combination with heparin

33
Q

How the IV antiplatelets work?

A

o Block binding of fibrinogen and von Wilebrand factor to glycoproteins IIb/IIIa on platelets

34
Q

ADR of IV antiplatelets

A
o	Bleeding
	Major bleeding at 10%
	Thrombocytopenia 0.5 to 1%
o	Abciximab’s problem
	Acute profound thrombocytopenia
•	Due to long activity, reversal may be needed by administering platelets
o
35
Q

Prescription for Eptifibatide

A

 Integrilin
180 mcg/kg IV bolus over 1-2 minutes then infuse
2 mcg/kg/min intravenously
 PA’s can’t write for

36
Q

How Nitrates work

A

o ↑ nitric oxide levels

 Potent vasodilator

37
Q

Differences between nitrates

A
  • *Dosage forms and kinetics
    1. ) Rapid onset and short duration
  • Nitroglycerin sublingual
  • Isosorbide dinitrate sublingual
    2. ) Slower onset and sustained duration
  • Nitroglycerin transdermal patch
  • Isosorbide mononitrate tablets
38
Q

Uses for Nitrates

A

o Useful in reducing vasospasm and myocardial oxygen demand in acute situations
 Intravenous administration quick and safe
o Relief of ischemic pain
 Does the use of a nitrate reduce mortality rates?
o

39
Q

• Route of Administration for Nitrates

A

o Emergent use requires sublingual administration
 Peak plasma concentrations in 4 minutes
 Sublingual spray faster than sublingual tablets
o Oral and cutaneous for prophylaxis

40
Q

• Tolerance of nitrates (aka The “drug-free” zone)

A

cells become refractory to it and don’t respond to nitric oxide, so need drug free zone for maintenance doses (patch on in 8 am, off at 8pm, don’t put new 1 on)
 Drug free for 12 hours

41
Q

ADR of Nitrates

A

o Headache

o Dizziness, weakness, effects of postural hypotension

42
Q

Nitroglycerin prescription

A

0.4 mg sublingually
One tablet under the tongue every 5 minutes for 3 doses
• Don’s Rule: If 1st dose doesn’t work  call 911

43
Q

Nitroglycerin patch prescription

A

0.4 mg/hour

Apply patch in the morning, remove at 8 PM and repeat each day

44
Q

Nitrites

A

Amyl Nitrite

45
Q

Amyl Nitrite administration

A
  • Inhalation only

- Same mechanism of action as the nitrates

46
Q

Amyl Nitrite as a Combination drug?

A
  • With cocaine or ecstasy euphoric state intensified and prolonged
  • “poppers”
    Once actually considered to be the genesis of AIDS in the gay community
47
Q

Beta Blocker for ACS?

A

Metoprolol

48
Q

Metoprolol acute dose?

A

Acutely 5 IV mg every 2 minutes for three doses then

49
Q

Metoprolol dose after acute dose?

A

50 mg orally every 6 hours starting 15 minutes after the last IV dose

50
Q

Metoprolol maintenance dose

A

100 mg twice a day

51
Q

Anticoagulants

A
  • Heparin (unfractionated heparin and Low Molecular weight heparin)
  • Enoxaparin
  • Fondaparinux
  • Bivalirudin
52
Q

How do the Anticoagulants work?

A

o Inactivates factor Xa and inhibits conversion of prothrombin to thrombin

53
Q

• Enoxaparin (Lovenox™) info and dose

A

o Low Molecular weight heparin –> adjust for renal function
o NSTEMI- 1 mg/kg SC every 12 hours
o STEMI- 30 mg IV bolus and then 1 mg/kg every 12 hours

54
Q

• Fondaparinux (Arixtra™) info and dose

A

o Factor Xa Inhibitor –>adjust for renal function
o NSTEMI- 2.5 mg SC once daily for 8 days or discharge
o STEMI- 2.5 mg IV once then 2.5 mg once daily for 8 days or discharge

55
Q

• Bivalirudin (Angiomax™) info and dose

A

o Direct Thrombin Inhibitor  PCI only
o NSTEMI*- 0.1 mg/kg IV bolus then 0.25 mg/kg/hour
o STEMI**- 0.75 mg/kg bolus then 1.75 mg/kg/hour
o

56
Q

• Heparin (unfractionated heparin) info

A

o Monitor the aPTTs constantly

 q. 4-6 hours  1.5-2 times the controlled value

57
Q

ADR of Anticoagulants

A

Bleeding

58
Q

Heparin Prescription

A

 Heparin sodium
Give X units IV push now and start an infusion of heparin at X units/hour
 Units driven by weight

59
Q

Fibrionlytics

A
  • Altepase (Activase)
  • Reteplase (Retevase)
  • Tenecteplase (TNKase)
60
Q

How the Fibrionlytics work

A

o Activate Plasmin to break down the Fibrin clot –> clot busters

61
Q

Contraindications for Fibrionlytics

A

o Any prior intracranial hemorrhage
o Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
o Known malignant intracranial neoplasm (primary or metastatic)
o Ischemic stroke within 3 months except acute ischemic stroke within 3 hours
o Suspected aortic dissection
o Active bleeding or bleeding diathesis (excluding menses)
o Significant closed-head or facial trauma within 3 months

62
Q

Altepase other indications

A
  • Management of acute ischemic stroke
  • Management of acute pulmonary embolism
  • Different dosing schemes
63
Q

Fibrinolytics reversal agent?

A

• No specific reversal agent

o Unlabeled- will tranexamic acid work?

64
Q

ADRs of Fibrinolytics

A

o Bleeding
o Rapid lysis causing reperfusion-related atrial or ventricular arrhythmias
o Cardiovascular events reported
o

65
Q

Alteplase Prescription

A

15 mg IV bolus over 1-2 minutes then infuse 50 mg over 30 minutes and then 35 mg over one hour

66
Q

Post ACS/MI care

A

• Aspirin
o Clopidogrel option (only if aspiring sensitivity or contraindicated)
• Beta blocker: ↓ post MI mortality
• ACE Inhibitor
o If history of known coronary heart disease
• Lipid-lowering
o HMGCoA reductase inhibitors (Statins aka Lipitor)
 Help stabilize plaques so don’t rupture and get MI
 Target LDL less than 100 mg/dL, HDl greater than 40 mg/dL and triglycerides less than 200 mg/dL