CVPR Week 4: CAD

Question 1

Objectives

Answer 1

Question 2

Case 1 ECG

Answer 2

Question 3

Case 1 ECG

Answer 3

Question 4

What does this indicate and why?

Answer 4

Question 5

Identify

Answer 5

Question 6

Identify

Answer 6

Question 7

Identify

Answer 7

Question 8

Identify

Answer 8

Question 9

Identify

Answer 9

Question 10

Identify

Answer 10

Question 11

Question 2 of ECG 1

Answer 11

Question 12

Ck levels

Answer 12

came in almost normal around 300 then rose massively

Question 13

Temporary occlusion with reperfusion

Answer 13

the earlier the reperfusion the better

still viable until around 20 minutes

Question 14

Atherosclerosis onset

Answer 14

Question 15

Atherosclerotic plaque cartoon

Answer 15

Question 16

fibrous cap

Answer 16

composed of collagen and smooth muscle cells

the goal of the fibrous plaque is to wall off the lipid pool from the circulating blood

Question 17

Atherosis & sclerosis

Question 18

Factors that predispose a plaque to stability

3 listed

Answer 18

• Dense fibrous cap
• Smooth muscle cell hyperplasia
• Laminar flow

Question 19

Factors that predispose a plaque to instability

4 listed

Answer 19

• Production of inflammatory cytokines, proteases, vasoactive molecules (breakdown of collagen and causes instability)
• Activated macrophages, mast cells, T cells (inflammatory plaque)
• LArge lipid core/oxidized LDL
• Low levels of NO

blood becomes exposed if the fibrous capsule breaks open and blood meets with the lipids and a clot forms

Question 20

Segments of coronary artery in different stages of CAD

Answer 20

Question 22

Atherosis features

4 listed

Answer 22

Question 23

Sclerosis features

3 listed

Answer 23

Question 24

Factors predisposing a plaque to stability

3 listed

Answer 24

Question 25

Factors predisposing a plaque to instability 3 listed

Answer 25

Question 26

Instability of a plaque results in?

Answer 26

Acute coronary syndrome

Question 27

Acute coronary syndrome Features 3 listed

Answer 27

Question 28

Acute coronary syndrome symptoms 3 listed

Answer 28

* can be subclinical/assymptomatic * can result in unstable angina and NSTEMI * can result in complete thrombotic occlusion STEMI

Question 29

Acute coronary syndrome types 4 listed

Answer 29

* Asymptomatic/subclinical * Unstable angina (NSTEACS) * NSTEMI (NSTEACS) * STEMI

Question 30

Stable ischemic heart disease possibilities 2 listed

Answer 30

* chronic stable angina * asymptomatic CAD

Question 31

Acute coronary syndromes vs stable ischemic heart disease

Answer 31

Question 32

Segments of CAD

Answer 32

in the vulnerable stage - although there is a large atherosclerotic plaque however it doesn't impinge upon the lumen of the coronary artery (this would be asymptomatic) When ruptured thrombosis occurs due to tissue factors and thrombogenic factors in the lipid plaque obstructive is stenosis (could be stable angina or stable ischemic heart disease) This would be considered a stable atherosclerotic plaque)

Question 33

troponin is a biomarker for?

Answer 33

myocardial injury indicating MI

Question 34

Case #2 What is the diagnosis? A. Unstable Angina B. NSTEMI C. STEMI D. Aortic Dissection E. Anxiety

Answer 34

Correct answer is NSTEMI because the troponin is indicative of myocardial damage and it isn't a STEMI because there is no ST elevation on the EKG

Question 35

Case #3 exercise induced chest tightness, stop and rests it goes away, primary care orders stress test

Question 36

How is typical angina diagnosed? 3 listed

Answer 36

* Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief * provoked by exertion or emotional stress * relieved by rest or NTG

Question 37

A sudden onset and peak intensity immediately is most likely?

Answer 37

Not typical angina

Question 38

How is atypical angina diagnosed?

Answer 38

* Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief * provoked by exertion or emotional stress * relieved by rest or NTG Meets 2 of the above characteristics

Question 39

How is non-cardiac chest pain diagnosed?

Answer 39

Meets one or none of the typical angina characteristics shown below * Sub-sternal chest discomfort with a characteristic quality and duration: gradual onset and gradual relief * provoked by exertion or emotional stress * relieved by rest or NTG

Question 40

Clinical features of Acute MI

Answer 40

Question 41

Chances of having CAD table

Answer 41

Question 42

How is CAD clinically classified? 3 listed

Answer 42

* ischemic heart disease * vs * STEMI (unstable angina, NSTEMI, STEMI) may not occur with exertion or emotional stress and may not resolve with NO or rest

Question 43

Case #3 Stress test Which of the following would not be useful to reduce this patient's angina burden? A. Start metoprolol 25 mg BID B. increased Nifedipine 30 to 60 mg C. start isosorbide mononitrate 30 mg daily D. increase aspirin from 81 to 325 mg daily E. All of the above would be useful

Answer 43

metoprolo will help his angina by reducing HR and contractility nifedipine Ca blocker will reduce contractility isosorbide yes by dilation aspirin no Statin no doesn't decrease the burden of angina, howerver would help prevent future events

Question 44

Anti-anginal therapy 6 listed

Answer 44

top 3 the most important Rxs

Question 45

Angina basic pathophysiology

Answer 45

myocardial O₂ demand \> supply

Question 46

Non-cardioselective β-blockers: effect on vascular tone

Answer 46

↑

Question 47

Non-cardioselective β-blockers: intramyocardial diastolic tension

Answer 47

↑

Question 48

Non-cardioselective β-blockers: coronary collateral circulation

Answer 48

0

Question 49

Non-cardioselective β-blockers: duration of diastole

Answer 49

↑↑↑

Question 50

Non-cardioselective β-blockers: preload

Answer 50

↑

Question 51

Non-cardioselective β-blockers: afterload (peripheral vascular resistance)

Answer 51

↑↑

Question 52

Non-cardioselective β-blockers: contractility

Answer 52

↓↓↓

Question 53

Non-cardioselective β-blockers: HR

Answer 53

↓↓↓

Question 54

Cardioselective β-blockers: effect on vascular tone

Answer 54

0↑

Question 55

Cardioselective β-blockers: intramyocardial diastolic tension

Answer 55

↑

Question 56

Cardioselective β-blockers: coronary collateral circulation

Answer 56

0

Question 57

Cardioselective β-blockers: duration of diastole

Answer 57

↑↑↑

Question 58

Cardioselective β-blockers: intramyocardial systolic tension

Answer 58

IDK

Question 59

Cardioselective β-blockers: preload

Answer 59

↑

Question 60

Cardioselective β-blockers: afterload (peripheral vascular resistance)

Answer 60

↑

Question 61

Cardioselective β-blockers: contractility

Answer 61

↓↓↓

Question 62

Cardioselective β-blockers: HR

Answer 62

↓↓↓

Question 63

Major antianginal effects of β-blockers 3 listed

Answer 63

* Duration of diastole ↑↑↑ * contractility ↓↓↓ * HR ↓↓↓

Question 64

Atenolol vs placebo for angina 3 listdd

Answer 64

* weekly angina attack rate goes down and weekly consumption of Nitroglycerine goes down * exercise ability increases * ST depression degree of ST-segment depression decreases

Question 65

Nifedipine for treating angina: vascular tone

Answer 65

↓↓↓

Question 66

Nifedipine for treating angina: intramyocardial diastolic tension

Answer 66

↓↓

Question 67

Nifedipine for treating angina: coronary collateral circulation

Answer 67

↑

Question 68

Nifedipine for treating angina: duration of diastole

Answer 68

0↑ (↓↓)

Question 69

Nifedipine for treating angina: Intramyocardial systolic tension

Answer 69

IDK

Question 70

Nifedipine for treating angina: Preload

Answer 70

↓0

Question 71

Nifedipine for treating angina: afterload (peripheral vascular resistance)

Answer 71

↓↓

Question 72

Nifedipine for treating angina: contractility

Answer 72

↓(↑↑)\*

Question 73

Nifedipine for treating angina: HR

Answer 73

0(↑↑)

Question 74

Verapamil for treating angina: vascular tone

Answer 74

↓↓↓

Question 75

Verapamil for treating angina: intramyocardial diastolic tension

Answer 75

0

Question 76

Verapamil for treating angina: coronary collateral circulation

Answer 76

0

Question 77

Verapamil for treating angina: duration of diastole

Answer 77

↑↑↑(↓)

Question 78

Verapamil for treating angina: intramyocardial systolic tension

Answer 78

IDK

Question 79

Verapamil for treating angina: preload

Answer 79

↑0↓

Question 80

Verapamil for treating angina: afterload

Answer 80

↓

Question 81

Verapamil for treating angina: contractility

Answer 81

↓↓(↑)\*

Question 82

Verapamil for treating angina: HR

Answer 82

↓↓(↑)

Question 83

Diltiazem for treating angina: vascular tone

Answer 83

↓↓↓

Question 84

Diltiazem for treating angina: intramyocardial diastolic tension

Answer 84

0

Question 85

Diltiazem for treating angina: coronary collateral circulation

Answer 85

↑

Question 86

Diltiazem for treating angina: duration of diastole

Answer 86

↑↑(↓)

Question 87

Diltiazem for treating angina: intramyocardial systolic tension

Answer 87

IDK

Question 88

Diltiazem for treating angina: preload

Answer 88

0↓

Question 89

Diltiazem for treating angina: Afterload (peripheral vascular resistance)

Answer 89

↓

Question 90

Diltiazem for treating angina: contractility

Answer 90

↓(↑)\*

Question 91

Diltiazem for treating angina: HR

Answer 91

↓↓(↑)

Question 92

Major Ca²⁺ effects for Tx of angina 4 listed

Answer 92

* vascular tone ↓↓↓ * duration of diastole 0 or (↑↑↑) or (↑↑) but can (↓↓) or (↓) * contractility ↓ or ↓↓ but can (↑) or (↑↑) * HR 0 or ↓↓(↑)

Question 93

Treadmill time on Ca²⁺ blockers

Answer 93

Question 94

Nitrates: vascular tone

Answer 94

↓↓

Question 95

Nitrates: intramyocardial diastole tension

Answer 95

↓↓↓

Question 96

Nitrates: coronary collateral circulation

Answer 96

↑

Question 97

Nitrates: duration of diastole

Answer 97

0(↓)

Question 98

Nitrates: preload

Answer 98

↓↓↓

Question 99

Nitrates: afterload (peripheral vascular resistance)

Answer 99

↓

Question 100

Nitrates: contractility

Answer 100

0(↑)

Question 101

Nitrates: HR

Answer 101

0(↑)

Question 102

Major effects of nitrates for angina 2 listed

Answer 102

Intramyocardial diastolic tension ↓↓↓ preload ↓↓↓

Question 103

Exercise duration on nitrates

Answer 103

Question 104

Case #4

Question 105

Case #4

Answer 105

Question 106

Complications after AMI 6 listed

Answer 106

Question 107

lab levels hours after MI

Answer 107

Question 108

Lab value typically used to Dx MI

Answer 108

Troponin i

Question 109

Identify

Answer 109

Question 110

Case #5 Which of the following has been shown to reduce future CV events? A. Aspirin 81mg/day B. Atorvastatin 80mg/daily C. Regular aerobic exercise D. Smoking Cessation E. All of the above

Answer 110

All of the above

Question 111

Question

Answer 111

Question 112

What are the major players in MI?

Answer 112

platelets stick to the lipid core after a rupture and promote thrombus formation

Question 113

Platelets in MI 5 listed

Answer 113

* platelets stick * Expression of adhesions molecules result in the ability to "stick" * As a consequence of adherence, platelets become activated and aggregate * Release of cytokines and growth factors consequent to platelet activation (along with thrombin) * Platelet membrane facilitates thrombin activation and propagation of thrombosis

Question 114

Statins and pleitropism

Answer 114

statins do a lot * reduced lipid levels * lower oxidized LDL * lower macrophages * lower T cell count * lower apoptotic cells (TUNEL) * Increased Smooth muscle cells

Question 115

Lipid levels and CVA

Answer 115

lower LDL or closer to 70 the lower the clinical event rate

Question 116

Targeting therapy for a beneficial balance

Answer 116

Question 117

Conclusion

Answer 117