Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

CVPR > CVPR Week 4: CAD > Flashcards

CVPR Week 4: CAD Flashcards

1
Q

Objectives

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Case 1 ECG

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Case 1 ECG

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does this indicate and why?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Identify

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Question 2 of ECG 1

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ck levels

A

came in almost normal around 300 then rose massively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Temporary occlusion with reperfusion

A

the earlier the reperfusion the better

still viable until around 20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Atherosclerosis onset

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Atherosclerotic plaque cartoon

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fibrous cap

A

composed of collagen and smooth muscle cells

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Atherosis & sclerosis

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Factors that predispose a plaque to stability

3 listed

A
  • Dense fibrous cap
  • Smooth muscle cell hyperplasia
  • Laminar flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Factors that predispose a plaque to instability

4 listed

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Segments of coronary artery in different stages of CAD

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atherosis features

4 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Sclerosis features

3 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Factors predisposing a plaque to stability

3 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Factors predisposing a plaque to instability

3 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Instability of a plaque results in?

A

Acute coronary syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Acute coronary syndrome Features

3 listed

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Acute coronary syndrome symptoms

3 listed

A
  • can be subclinical/assymptomatic
  • can result in unstable angina and NSTEMI
  • can result in complete thrombotic occlusion STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Acute coronary syndrome types

4 listed

A
  • Asymptomatic/subclinical
  • Unstable angina (NSTEACS)
  • NSTEMI (NSTEACS)
  • STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Stable ischemic heart disease possibilities

2 listed

A
  • chronic stable angina
  • asymptomatic CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Acute coronary syndromes vs stable ischemic heart disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Segments of CAD

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

troponin is a biomarker for?

A

myocardial injury indicating MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Case #2

What is the diagnosis?

A. Unstable Angina

B. NSTEMI

C. STEMI

D. Aortic Dissection

E. Anxiety

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Case #3

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

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How is typical angina diagnosed?

3 listed

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

A sudden onset and peak intensity immediately is most likely?

A

Not typical angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How is atypical angina diagnosed?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is non-cardiac chest pain diagnosed?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Clinical features of Acute MI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Chances of having CAD table

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is CAD clinically classified?

3 listed

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Anti-anginal therapy

6 listed

A

top 3 the most important Rxs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Angina basic pathophysiology

A

myocardial O2 demand > supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Non-cardioselective β-blockers: effect on vascular tone

A

↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Non-cardioselective β-blockers: intramyocardial diastolic tension

48
Q

Non-cardioselective β-blockers: coronary collateral circulation

49
Q

Non-cardioselective β-blockers: duration of diastole

50
Q

Non-cardioselective β-blockers: preload

51
Q

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

52
Q

Non-cardioselective β-blockers: contractility

53
Q

Non-cardioselective β-blockers: HR

54
Q

Cardioselective β-blockers: effect on vascular tone

55
Q

Cardioselective β-blockers: intramyocardial diastolic tension

56
Q

Cardioselective β-blockers: coronary collateral circulation

57
Q

Cardioselective β-blockers: duration of diastole

58
Q

Cardioselective β-blockers: intramyocardial systolic tension

59
Q

Cardioselective β-blockers: preload

60
Q

Cardioselective β-blockers: afterload (peripheral vascular resistance)

61
Q

Cardioselective β-blockers: contractility

62
Q

Cardioselective β-blockers: HR

63
Q

Major antianginal effects of β-blockers

3 listed

A
  • Duration of diastole ↑↑↑
  • contractility ↓↓↓
  • HR ↓↓↓
64
Q

Atenolol vs placebo for angina

3 listdd

A
  • weekly angina attack rate goes down and weekly consumption of Nitroglycerine goes down
  • exercise ability increases
  • ST depression degree of ST-segment depression decreases
65
Q

Nifedipine for treating angina: vascular tone

66
Q

Nifedipine for treating angina: intramyocardial diastolic tension

67
Q

Nifedipine for treating angina: coronary collateral circulation

68
Q

Nifedipine for treating angina: duration of diastole

A

0↑ (↓↓)

69
Q

Nifedipine for treating angina: Intramyocardial systolic tension

70
Q

Nifedipine for treating angina: Preload

71
Q

Nifedipine for treating angina: afterload (peripheral vascular resistance)

72
Q

Nifedipine for treating angina: contractility

A

↓(↑↑)*

73
Q

Nifedipine for treating angina: HR

74
Q

Verapamil for treating angina: vascular tone

75
Q

Verapamil for treating angina: intramyocardial diastolic tension

76
Q

Verapamil for treating angina: coronary collateral circulation

77
Q

Verapamil for treating angina: duration of diastole

A

↑↑↑(↓)

78
Q

Verapamil for treating angina: intramyocardial systolic tension

79
Q

Verapamil for treating angina: preload

80
Q

Verapamil for treating angina: afterload

81
Q

Verapamil for treating angina: contractility

A

↓↓(↑)*

82
Q

Verapamil for treating angina: HR

A

↓↓(↑)

83
Q

Diltiazem for treating angina: vascular tone

84
Q

Diltiazem for treating angina: intramyocardial diastolic tension

85
Q

Diltiazem for treating angina: coronary collateral circulation

86
Q

Diltiazem for treating angina: duration of diastole

A

↑↑(↓)

87
Q

Diltiazem for treating angina: intramyocardial systolic tension

88
Q

Diltiazem for treating angina: preload

89
Q

Diltiazem for treating angina: Afterload (peripheral vascular resistance)

90
Q

Diltiazem for treating angina: contractility

91
Q

Diltiazem for treating angina: HR

A

↓↓(↑)

92
Q

Major Ca2+ effects for Tx of angina

4 listed

A
  • vascular tone ↓↓↓
  • duration of diastole 0 or (↑↑↑) or (↑↑) but can (↓↓) or (↓)
  • contractility ↓ or ↓↓ but can (↑) or (↑↑)
  • HR 0 or ↓↓(↑)
93
Q

Treadmill time on Ca2+ blockers

94
Q

Nitrates: vascular tone

95
Q

Nitrates: intramyocardial diastole tension

96
Q

Nitrates: coronary collateral circulation

97
Q

Nitrates: duration of diastole

98
Q

Nitrates: preload

99
Q

Nitrates: afterload (peripheral vascular resistance)

100
Q

Nitrates: contractility

101
Q

Nitrates: HR

102
Q

Major effects of nitrates for angina

2 listed

A

Intramyocardial diastolic tension ↓↓↓

preload ↓↓↓

103
Q

Exercise duration on nitrates

104
Q

Case #4

105
Q

Case #4

106
Q

Complications after AMI

6 listed

107
Q

lab levels hours after MI

108
Q

Lab value typically used to Dx MI

A

Troponin i

109
Q

Identify

110
Q

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

A

All of the above

111
Q

Question

112
Q

What are the major players in MI?

A

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

113
Q

Platelets in MI

5 listed

A
  • 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
114
Q

Statins and pleitropism

A

statins do a lot

  • reduced lipid levels
  • lower oxidized LDL
  • lower macrophages
  • lower T cell count
  • lower apoptotic cells (TUNEL)
  • Increased Smooth muscle cells
115
Q

Lipid levels and CVA

A

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

116
Q

Targeting therapy for a beneficial balance

117
Q

Conclusion

CVPR (93 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions