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Therapeutics I > CAD/ACS > Flashcards

CAD/ACS Flashcards

1
Q

Who qualifies as Chronic coronary disease

A
  1. Post ACS events
  2. LVSD
  3. Stable angino or symtpoms
  4. CCD diagnosis
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2
Q

What are the types of ischemic heart disease?

A
  1. Stable
  2. Acute coronary syndrome
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3
Q

How many heart attacks are silent?

A

1 in 5

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4
Q

What are the types of IHD?

A

Stable and ACS

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5
Q

What are the types of SIHD?

A
  1. Chronic stable exertional angina
  2. Silent ischemia
  3. Microvascular angina
  4. Coronary vasospasm
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6
Q

What are the types of acute coronary syndrome?

A
  1. Unstable angina
  2. Non-ST-segment myocardial infarction (NSTEMI)
  3. ST-segement elevation MI (STEMI)
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7
Q

What population with prevalent CAD?

A

Black and Men

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8
Q

What is the leading cause of ischemic heart disease? Caused by?

A

CAD caused by atherosclerotic plaque in epicardial vessels

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9
Q

What is known as the vulnerable plaque?

A

ASCVD

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10
Q

How do 2/3 of ACS events occur in the morning?

A

Catecholamine release due to circadian rhythm

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11
Q

Describe the thrombus formation process?

A

Rupture of thin fibrous plaque → Initial platelet adhesion → Rolling → Firm adhesion → Platelet aggregation → formation of fibrin network → Recruitment of leukocytes → Net formation of the necrotic core

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12
Q

What is the foundational etiology of CAD?

A

Decrease in myocardial oxygen supply

Increase in oxygen demand

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13
Q

What factors contribute to myocardial oxygen demand?

A
  1. HR
  2. Myocardial contractility
  3. Intramyocardial wall tension
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14
Q

What is intramyocardial wall tension?

A

Increased MVO2 and is directly related to the radius or size of the ventricular cavity and BP

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15
Q

How do you calculate rate pressure product?

A

Rate-pressure product = HR x Systolic BP

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16
Q

What factors contribute to myocardial oxygen supply?

A
  1. Coronary blood flow
  2. HR and systole
  3. Oxygen extraction and Oxygen carrying capacity
  4. Coronary collateral circulation Angiogenesis
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17
Q

What increases coronary Collateral Circulation

A

Angiogenesis

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18
Q

What increases Oxygen Extraction and Oxygen Carrying Capacity?

A

Hemoglobin concentration and O2 sat

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19
Q

What state does the heart perfuse in?

A

Diastole

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20
Q

What are the factors that contribute to MI?

A
  1. Rupture of AC plaque
  2. Thrombus formation impairing blood flow
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21
Q

What are the MI types?

A
  1. Due to atherosclerosis
  2. Due to coronary vasospasm, coronary embolism, coronary artery dissection, a concomitant condition that acutely increases oxygen demand
  3. Cardiac death
  4. Mi associated with PCI related myocardial injury
  5. MI associated with CABG surgery
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22
Q

What factors contribute to MI-induced injury?

A

Decreased CO
Increased SNS and RAAS

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23
Q

How should you treat patients with or without IHD?

A
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24
Q

What are the CAD non-modifiable risk factors?

A
  1. Age
  2. Sex
  3. Family hx of ASCVD
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25
Q

What are modifiable CAD risk factors?

A
  1. HTN
  2. DM
  3. Dyslipidemia
  4. Cigarette smoking
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26
Q

What are the sensations of cardiac chest pain?

A
  1. Squeezing
  2. Crushing
  3. Heaviness
  4. Tightness
  5. Numbness
  6. Burning
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27
Q

Where are the locations of cardiac chest pain?

A
  1. Substernal
  2. Radiate to the right or left shoulder, right or left arm, neck, back, or abdomen
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28
Q

What is PQRST?

A
  1. Precipitating factors
  2. Palliative measures
  3. Quality of pain
  4. Region
  5. Radiation
  6. Severity
  7. Temporal pattern
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29
Q

What are the typical angina symptoms?

A
  1. Substernal chest discomfort with a characteristic quality and duration
  2. Provoked by exertion or emotional stress
  3. Relieved by rest or NTG
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30
Q

What are the atypical angina symptoms?

A
  1. Two of three typical criteria
  2. Mid epigastric discomfort, effort intolerance, dyspnea, and excessive fatigue
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31
Q

How experiences atypical angina symptoms?

A

Women and elderly

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32
Q

What is Class I of angina?

A

Ordinary physical activity doesn’t cause angina

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33
Q

What is Class II of angina?

A

Slight limitation or ordinary activity

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34
Q

What is Class III of angina?

A

Marked limitations of ordinary physical activity

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35
Q

What is Class IV of angina?

A

Inability to carry on any physical activity without discomfort

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36
Q

How do you diagnose SIHD or ACS?

A

12 leadECG
1. ST segment elevation
2. ST segment depression
3. T wave inversion
4. Normal

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37
Q

How do you diagnose SIHD?

A

Stress test
1. Excersise
2. Pharmacologic
Coronary angiography
Myocardial perfusion imaging
Cardiac magnetic resonancy
CAC

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38
Q

How do you diagnose ACS?

A
  1. Troponin
  2. Myocardial injury is considered acute if there is a dynamic rise and/or fall by 20% or more in serial cTn values
39
Q

Why is troponin used as a biomarker? How do you draw it?

A
  1. Peak levels correlate with severity of MI and cell injury/death
  2. Normal levels at early stages of disease
  3. Draw in sets of 2-3 spaced out every 3-6 hr
40
Q

What are the risk scoring tools used for CAD?

A
  1. Thrombolysis in Myocardial Infarction (TIMI) risk score for NSTE-ACS
  2. Global Registry of Acute Coronary Events (GRACE) score
  3. History, ECG, Age, Risk factors, and Troponin (HEART) score
41
Q

What are the features of hMACE?

A
  1. Socioeconomic status/Demographic
    2.Health conditions
  2. Ancillary cardiac testin or imaging
  3. Biomarkers
42
Q

What are STEMIs scored?

A

TIMI risk score

43
Q

How should you incorporate shared-decision making using patients and clinical care team?

44
Q

What factors increase risk of MACE?

A
  1. Elevated BMI
  2. Previous MI, PCI, CABG
  3. Abnormal ECG
  4. Abnormal ECHO
  5. High BNP
  6. Demographics
45
Q

What the features of CCD guideline directed management and therapy?

A
  1. Fix underlying conditions
  2. Exercise and weigh management
  3. Smoking cessastion
  4. Avoid alcohol
  5. Nutrition
46
Q

Algorithm to treat DLD?

47
Q

What are the types of revscularization?

A
  1. Coronary artery bypass grafting surgery (CABG)
  2. Percutaneous coronary intervention (PCI) with or without stent placement
48
Q

What is the difference between PCI?

A

Drug eluting stent: stent contains drug
Bare metal stent: Just metal

49
Q

What is the mechanism of aspirin?

A

Irreversibly blocks cyclooxygenase-1 (COX-1) activity → Inhibits thromboxane A2 production → reduced platelet activation and aggregation

50
Q

What happens if you give a high dose of aspirin?

A

Impair endothelial secretion of prostacyclin

51
Q

What do you do when you give both an NSAID and ASA?

A

Give ASA first

52
Q

Used to prevent MI and death in patients unable to take aspirin?

A

Clopidogrel

53
Q

How is clopidogrel metabolized? How does this affect dosing?

A

CYP2C19

Responses are highly variable

54
Q

Prasurgrel CI?

A
  1. Hx of stroke or TIA
  2. Over 75 yo
  3. Reduce in pts <60kg
55
Q

What are ADRs of ticagrelor?

A
  1. Dyspnea
  2. Increase in asymptomatic ventricular pauses
  3. Increases in uric acid
  4. Small increase in serum creatinine
56
Q

How should you not dose Cangrelor?

A

The loading dose of a thienopyridine should not given until the cangrelor infusion has been D/C

57
Q

What are the P2Y12i? How are they metabolized on of them metabolized?

A
  1. Prasurgrel (Effient)
  2. Ticagrelor (Brillinta)
  3. Cangrelor (Kengreal)

2C19 Plavix

58
Q

What are the GPIIB/IIIA inhibitors?

A
  1. Eptifibatide (Integrilin)
  2. Tirofiban (Aggrastat)
59
Q

What do you need to coadminister with GP IIb/IIIa inhibitor?

60
Q

When would you see the most benefit using GP IIb/IIIa inhibitor?

A
  1. PCI for NSTE-ACS
  2. STEMI not preloaded with a P2Y12 inhibitor and bivalirudin
61
Q

What are the CIs of GP IIb/IIIa inhibitor?

A
  1. Ischemia → no benefit
  2. STEMI treated with fibrinolytic → Increased risk for major bleeding and ICH
62
Q

How are ACEis used for CAD?

A
  1. Stabilize coronary plaque
  2. Provide restoration or improvement in endothelial fucntion
  3. Inhibit vascular smooth muscle cell growth
  4. Inhibiting platelet aggregation and augmenting the endogenous fibrinolytic system
63
Q

What CCBs are safe for HFrEF?

A

Amlodipine and felodipine

64
Q

What are metabolizing enzymes of Non-DHP CCB?

A

CYP3A4

Verapamil inhibits PGP

65
Q

How can CCBs used for CAD?

A

All CCBs reduce myocardial oxygen demand

Impacts on myocardial Ca2+ channels

66
Q

What CCBs have the most to least impact on myocardial Ca2+ channels

A

Verapamil > diltiazem > DHP

67
Q

What are the ADRs of Non DHP?

A
  1. Bradycardia
  2. Hypotension
  3. AV block
  4. LV depression symptoms
68
Q

What are the ADRs of DHP?

A
  1. Reflex tachycardia
  2. Hypotension
  3. HA
  4. Gingival hyperplasia
  5. Peripheral edema
69
Q

What are the effects of venous vasodilation?

A

Reduces preload, Myocardial wall tension, myocardial oxygen demand

70
Q

ADRs of nitrates?

A
  1. HA
  2. flushing
  3. Nausea
  4. Postural hypotension
  5. Syncope
71
Q

CI of nitrates?

72
Q

What are the types of nitrates?

A
  1. Nitroglycerin
  2. Isosorbide dinitrate
  3. Isosorbide mononitrate
73
Q

How should you dose nitrates?

A

7 hrs apart (BID)

74
Q

How do you prevent nitrate tolerance?

A

10-14 hr nitrate free interval QD

75
Q

What are SL NTG with CAD?

A
  1. Treats acute episodes of angina
  2. Onset: 5 minutes
  3. Take 2-5 minutes before activities
76
Q

What are some counseling points with SL NTG?

A
  1. Do not store with child-resistant safety cap
  2. Keep SL NTG close by at all times
  3. Sit down with taking
  4. Tablets need to be refilled every 6 months and spray every 3 years
  5. May be taken in advance
  6. Contact 911 if first SL NTG does not relieve angina
77
Q

What are beta blockers for in CAD?

A
  1. Beta selectivity does not matter, however, refrain from using agents with intrinsic sympathomimetic activity
  2. Reduce both symptomatic and silent episodes of myocardial ischemia
  3. Beta-1 receptors in the heart and kidneys
78
Q

What are the ADRs of beta blockers?

A
  1. Bradycardia
  2. Hypotension
  3. Heart block
  4. Impaired glucose metabolism
  5. Altered serum lipids
  6. Fatigue
  7. Depression
  8. Insomnia
  9. Malaise
79
Q

CIs of beta blockers?

A
  1. Bradycardia
  2. Asthma
  3. HFrEF
  4. Hypoglycemia
80
Q

How should you DC beta blockers?

A

taper over 2-3 weeks to prevent withdrawl

81
Q

What is ranolazine used for in regards to CAD?

A

Reduces ischemic episodes by selective inhibition of late sodium current

Reduction in intracellular Na+

82
Q

Dosing of ranolazine?

A

500 mg twice daily for 7-14 days, then 1000 mg twice daily

83
Q

What are the DDIs of ranolazine?

A
  1. CYP3A4
  2. CYP2D6
  3. PGP

Digoxin doses should be reduced

Metformin should be reduced to 850mg BID when using ranolazine 1000mg BID

84
Q

What are the ADRs of ranolazine?

A
  1. Constipation
  2. Nausea
  3. DZ
  4. HA
  5. QTc Prolongation
85
Q

What are the anticoagulations used for ACS?

A
  1. Rivaroxaban
  2. Heparin
  3. LMW heparins
  4. Bivalirudin
86
Q

What anticoagulant has evidence to support it’s use in atherosclerotic related cardiovascular disease?

A

Rivaroxaban

87
Q

CI of Rivaroxaban?

88
Q

What is the heparin goal?

A

aPTT goal of 1.5-2 times the institution’s control value

89
Q

What is bivalirudin MOA?

A

Direct thrombin inhibitor → does not have to first bind to AT to provide its anticoagulant effect

90
Q

When should bivalirudin be used?

A

PCI monitored with an ACT in the cath lab

91
Q

What are the benefits of using Low-Molecular-Weight Heparins?

A

No need for routine therapeutic monitoring

Anti-Xa monitoring may be helpful

92
Q

What is the target peak anti-Xa level?

A

0.3 to 0.7 IU/mL (kIU/L) drawn 4 hours after the third dose

93
Q

When should a single anticoagulant be used for?

A

ACS patients and the duration is abbreviated

Therapeutics I (32 decks)

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