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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
What are modifiable CAD risk factors?
1. HTN 2. DM 3. Dyslipidemia 4. Cigarette smoking
26
What are the sensations of cardiac chest pain?
1. Squeezing 2. Crushing 3. Heaviness 4. Tightness 5. Numbness 6. Burning
27
Where are the locations of cardiac chest pain?
1. Substernal 2. Radiate to the right or left shoulder, right or left arm, neck, back, or abdomen
28
What is PQRST?
1. Precipitating factors 2. Palliative measures 3. Quality of pain 4. Region 5. Radiation 6. Severity 7. Temporal pattern
29
What are the typical angina symptoms?
1. Substernal chest discomfort with a characteristic quality and duration 2. Provoked by exertion or emotional stress 3. Relieved by rest or NTG
30
What are the atypical angina symptoms?
1. Two of three typical criteria 2. Mid epigastric discomfort, effort intolerance, dyspnea, and excessive fatigue
31
How experiences atypical angina symptoms?
Women and elderly
32
What is Class I of angina?
Ordinary physical activity doesn't cause angina
33
What is Class II of angina?
Slight limitation or ordinary activity
34
What is Class III of angina?
Marked limitations of ordinary physical activity
35
What is Class IV of angina?
Inability to carry on any physical activity without discomfort
36
How do you diagnose SIHD or ACS?
**12 leadECG** 1. ST segment elevation 2. ST segment depression 3. T wave inversion 4. Normal
37
How do you diagnose SIHD?
**Stress test** 1. Excersise 2. Pharmacologic **Coronary angiography** **Myocardial perfusion imaging** **Cardiac magnetic resonancy** **CAC**
38
How do you diagnose ACS?
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
Why is troponin used as a biomarker? How do you draw it?
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
What are the risk scoring tools used for CAD?
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
What are the features of hMACE?
1. Socioeconomic status/Demographic 2.Health conditions 3. Ancillary cardiac testin or imaging 4. Biomarkers
42
What are STEMIs scored?
TIMI risk score
43
How should you incorporate shared-decision making using patients and clinical care team?
44
What factors increase risk of MACE?
1. Elevated BMI 2. Previous MI, PCI, CABG 3. Abnormal ECG 4. Abnormal ECHO 5. High BNP 6. Demographics
45
What the features of CCD guideline directed management and therapy?
1. Fix underlying conditions 2. Exercise and weigh management 3. Smoking cessastion 4. Avoid alcohol 5. Nutrition
46
Algorithm to treat DLD?
47
What are the types of revscularization?
1. Coronary artery bypass grafting surgery (CABG) 2. Percutaneous coronary intervention (PCI) with or without stent placement
48
What is the difference between PCI?
Drug eluting stent: stent contains drug Bare metal stent: Just metal
49
What is the mechanism of aspirin?
Irreversibly blocks cyclooxygenase-1 (COX-1) activity → Inhibits thromboxane A2 production → reduced platelet activation and aggregation
50
What happens if you give a high dose of aspirin?
Impair endothelial secretion of prostacyclin
51
What do you do when you give both an NSAID and ASA?
Give ASA first
52
Used to prevent MI and death in patients unable to take aspirin?
Clopidogrel
53
How is clopidogrel metabolized? How does this affect dosing?
CYP2C19 Responses are highly variable
54
Prasurgrel CI?
1. Hx of stroke or TIA 2. Over 75 yo 3. Reduce in pts <60kg
55
What are ADRs of ticagrelor?
1. Dyspnea 2. Increase in asymptomatic ventricular pauses 3. Increases in uric acid 4. Small increase in serum creatinine
56
How should you not dose Cangrelor?
The loading dose of a thienopyridine should not given until the cangrelor infusion has been D/C
57
What are the P2Y12i? How are they metabolized on of them metabolized?
1. Prasurgrel (Effient) 2. Ticagrelor (Brillinta) 3. Cangrelor (Kengreal) 2C19 Plavix
58
What are the GPIIB/IIIA inhibitors?
1. Eptifibatide (Integrilin) 2. Tirofiban (Aggrastat)
59
What do you need to coadminister with GP IIb/IIIa inhibitor?
Heparin
60
When would you see the most benefit using GP IIb/IIIa inhibitor?
1. PCI for NSTE-ACS 2. STEMI not preloaded with a P2Y12 inhibitor and bivalirudin
61
What are the CIs of GP IIb/IIIa inhibitor?
1. Ischemia → no benefit 2. STEMI treated with fibrinolytic → Increased risk for major bleeding and ICH
62
How are ACEis used for CAD?
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
What CCBs are safe for HFrEF?
Amlodipine and felodipine
64
What are metabolizing enzymes of Non-DHP CCB?
CYP3A4 Verapamil inhibits PGP
65
How can CCBs used for CAD?
All CCBs reduce myocardial oxygen demand Impacts on myocardial Ca2+ channels
66
What CCBs have the most to least impact on myocardial Ca2+ channels
Verapamil > diltiazem > DHP
67
What are the ADRs of Non DHP?
1. Bradycardia 2. Hypotension 3. AV block 4. LV depression symptoms
68
What are the ADRs of DHP?
1. Reflex tachycardia 2. Hypotension 3. HA 4. Gingival hyperplasia 5. Peripheral edema
69
What are the effects of venous vasodilation?
Reduces preload, Myocardial wall tension, myocardial oxygen demand
70
ADRs of nitrates?
1. HA 2. flushing 3. Nausea 4. Postural hypotension 5. Syncope
71
CI of nitrates?
PDE5i
72
What are the types of nitrates?
1. Nitroglycerin 2. Isosorbide dinitrate 3. Isosorbide mononitrate
73
How should you dose nitrates?
7 hrs apart (BID)
74
How do you prevent nitrate tolerance?
10-14 hr nitrate free interval QD
75
What are SL NTG with CAD?
1. Treats acute episodes of angina 2. Onset: 5 minutes 3. Take 2-5 minutes before activities
76
What are some counseling points with SL NTG?
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
What are beta blockers for in CAD?
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
What are the ADRs of beta blockers?
1. Bradycardia 2. Hypotension 3. Heart block 4. Impaired glucose metabolism 5. Altered serum lipids 6. Fatigue 7. Depression 8. Insomnia 9. Malaise
79
CIs of beta blockers?
1. Bradycardia 2. Asthma 3. HFrEF 4. Hypoglycemia
80
How should you DC beta blockers?
taper over 2-3 weeks to prevent withdrawl
81
What is ranolazine used for in regards to CAD?
Reduces ischemic episodes by selective inhibition of late sodium current Reduction in intracellular Na+ 
82
Dosing of ranolazine?
500 mg twice daily for 7-14 days, then 1000 mg twice daily
83
What are the DDIs of ranolazine?
1. CYP3A4 2. CYP2D6 3. PGP Digoxin doses should be reduced Metformin should be reduced to 850mg BID when using ranolazine 1000mg BID
84
What are the ADRs of ranolazine?
1. Constipation 2. Nausea 3. DZ 4. HA 5. QTc Prolongation
85
What are the anticoagulations used for ACS?
1. Rivaroxaban 2. Heparin 3. LMW heparins 4. Bivalirudin
86
What anticoagulant has evidence to support it’s use in atherosclerotic related cardiovascular disease?
Rivaroxaban
87
CI of Rivaroxaban?
CrCl <15
88
What is the heparin goal?
aPTT goal of 1.5-2 times the institution’s control value
89
What is bivalirudin MOA?
Direct thrombin inhibitor → does not have to first bind to AT to provide its anticoagulant effect
90
When should bivalirudin be used?
PCI monitored with an ACT in the cath lab
91
What are the benefits of using Low-Molecular-Weight Heparins?
No need for routine therapeutic monitoring Anti-Xa monitoring may be helpful
92
What is the target peak anti-Xa level?
0.3 to 0.7 IU/mL (kIU/L) drawn 4 hours after the third dose
93
When should a single anticoagulant be used for?
ACS patients and the duration is abbreviated

Therapeutics I (32 decks)

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