Acute Coronary Syndromes Flashcards

1
Q

What is coronary artery disease (CAD)?

A

Narrowing of coronary arteries due to atherosclerosis

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2
Q

What characterizes chronic coronary syndrome?

A

Patients with stable angina or no symptoms managed in an outpatient setting

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3
Q

What is the main pathophysiology of chronic coronary syndrome?

A

Fixed narrowing

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4
Q

What conditions are included in acute coronary syndrome?

A

Myocardial infarction (STEMI or NSTEMI) and unstable angina

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5
Q

What is the main pathophysiology of acute coronary syndrome?

A

Sudden occlusion

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6
Q

What does the acronym DIABETES stand for in coronary artery disease risk factors?

A
  • D: Diabetes
  • I: Inactivity and obesity/metabolic syndromes
  • A: Age (older) and gender (men)
  • B: Blood pressure high (hypertension)
  • E: Elevated cholesterol (hypercholesterolemia)
  • T: Tobacco smoking
  • E: Ethnicity and family history
  • S: Stress
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7
Q

Which group has a significantly higher risk of coronary artery disease?

A

Postmenopausal women compared to premenopausal women

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8
Q

What is the QRISK2 Cardiovascular risk score used for?

A

Screening tool that measures risk of patient having a heart attack or stroke within the next 10 years

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9
Q

What are the risk categories for the QRISK2 score?

A
  • Low risk: Less than 10% (1 in 10 chance)
  • Moderate risk: Between 10-20% (1 in 2 in 10 chance)
  • High risk: More than 20% (over 1 in 5 chance)
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10
Q

What is the primary cause of coronary artery disease pathophysiology?

A

Mostly due to atherosclerosis affecting large and medium arteries, especially at branch points and bifurcations

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11
Q

What damages or dysfunctions the artery endothelium?

A

Due to tobacco or drug toxins, hyperlipidemia, hypertension, trauma

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12
Q

What happens to Low-density Lipoprotein (LDL) cholesterol in coronary artery disease?

A

Accumulates within dysfunctional tunica intima

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13
Q

What is fatty streak formation?

A

LDL accumulation causes monocyte recruitment, converting to macrophages and producing foam cells

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14
Q

What is atheroma formation?

A

Well-defined lipid core with macrophage debris and fibrous connective tissue

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15
Q

Describe atheroma morphology.

A

Raised lesion with soft yellow lipid core covered by white fibrous cap

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16
Q

What signals smooth muscle cell migration from tunica media during plaque progression?

A

Macrophage apoptosis

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17
Q

What are the effects of smooth muscle cell migration during plaque progression?

A
  • Secretion of elastin and collagen
  • Calcium deposition
  • Neovascularization signals
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18
Q

What condition does plaque progression cause?

A

Chronic coronary syndrome

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19
Q
A
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20
Q

What is plaque disruption and thrombus formation?

A

It is the process where clot formation occurs due to endothelial dysfunction, leading to artery occlusion.

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21
Q

What causes clot formation in arteries?

A

Endothelial dysfunction causes loss of antithrombotic properties and inappropriate vasoconstriction.

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22
Q

What are the consequences of weakened plaques in arteries?

A

They can lead to aneurysm formation and rupture.

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23
Q

What conditions are caused by artery occlusion?

A

Acute coronary syndromes.

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24
Q

What is angina?

A

Chest pain that occurs due to myocardial ischaemia.

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25
Q

What causes myocardial ischaemia in angina?

A

Atherosclerotic plaques partially block coronary arteries.

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26
Q

What are the four characteristics of angina?

A
  • Retrosternal pain that can spread to other areas
  • Feelings of crushing pressure and tightness
  • Precipitating factors (4 Es): Exertion, eating, emotional distress, extreme temperatures
  • Attacks last a few minutes
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27
Q

What is the typical location of pain in angina?

A

Retrosternal area, arms, neck, lower jaw, and upper abdomen.

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28
Q

What feelings are associated with angina?

A

Crushing pressure and tightness in the chest.

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29
Q

What are the relieving factors for angina?

A

Rest and/or nitrates provide relief within 2 minutes.

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30
Q

How long do attacks of angina typically last?

A

A few minutes.

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31
Q

What is Class I angina severity classification?

A

Ordinary activity doesn’t cause angina.

32
Q

What is Class II angina severity classification?

A

Slight limitation of ordinary activity.

33
Q

What is Class III angina severity classification?

A

Marked limitation of ordinary activity.

34
Q

What is Class IV angina severity classification?

A

Inability to carry on any physical activity without discomfort.

35
Q

What is stable angina?

A

Stable atherosclerotic plaque narrows lumen, causing angina when oxygen demand exceeds supply during exertion or stress.

36
Q

What are the two approaches to treating stable angina?

A

Symptomatic treatment and prognostic benefit.

37
Q

What does symptomatic treatment for stable angina include?

A

Lifestyle management: Regular exercise, smoking cessation, psychosocial stress management, diet.

38
Q

What are the medical management options for stable angina?

A
  1. Anti-anginals: Beta-blockers, calcium channel blockers, nitrates. 2. Vasculoprotective agents: Aspirin, statins, ACE inhibitors.
39
Q

What are first-line anti-anginals?

A

Beta-blockers and calcium channel blockers, which slow heart rate and increase coronary perfusion in diastole.

Examples: Diltiazem, amlodipine.

40
Q

What do nitrates do in the treatment of stable angina?

A

Reduce left ventricular end-diastolic pressure (LVEDP) and increase coronary vasodilation.

Example: Long-acting oral nitrates such as isosorbide mononitrate.

41
Q

What is surgical management for stable angina?

A

Revascularization with Percutaneous coronary intervention (PCI) or Coronary Artery Bypass Graft (CABG).

42
Q

When is PCI indicated?

A

If angina isn’t controlled on 2 anti-anginals, also used to treat NSTEMI MI urgently and emergency treatment of STEMI MI.

43
Q

When is CABG indicated?

A

If angina isn’t controlled on 2 drugs, indicated in left main stem, proximal 3 vessel diseases, and for more complicated disease and higher risk.

44
Q

What is unstable angina?

A

Atherosclerotic plaque becomes unstable and ruptures, causing partial occlusion of the artery due to bleeding and thrombosis.

45
Q

What are the symptoms of unstable angina?

A

Angina at rest or minimal exertion and is prolonged.

46
Q

What is variable/prinzmetal angina?

A

Coronary artery has intense vasospasm and suddenly narrows at night and during rest.

47
Q

What are the most significant acute coronary syndromes?

A

STEMI, NSTEMI, unstable angina

48
Q

What is STEMI?

A

Complete thrombus occlusion of artery, which causes myocardial infarction.

49
Q

What is NSTEMI?

A

Partial thrombus occlusion of artery, which causes myocardial infarction.

50
Q

What is unstable angina?

A

Athersclerotic plaque occlusion of artery becomes unstable and ruptures, causing partial occlusion of artery.

51
Q

What are common presentations of acute coronary syndromes?

A

Angina, nausea/stomach pain, shortness of breath (SOB).

52
Q

What is the first line investigation for acute coronary syndromes?

A

ECG findings.

53
Q

What is the second-line investigation for acute coronary syndromes?

A

Cardiac biomarkers in blood test.

54
Q

What does ST elevation indicate in ECG findings?

A

ST elevation, reciprocal ST depression in leads of other areas of heart.

55
Q

What are elevated cardiac biomarkers in NSTEMI?

A

Creatine kinase-myocardial band (CK-MB) and Troponin.

56
Q

What are the treatment components for acute coronary syndromes?

A

MONARCH BASIC.

57
Q

What does ‘M’ stand for in MONARCH BASIC?

58
Q

What does ‘O’ stand for in MONARCH BASIC?

59
Q

What does ‘N’ stand for in MONARCH BASIC?

A

Nitrates, e.g., Glyceryl trinitrate spray.

60
Q

What does ‘A’ stand for in MONARCH BASIC?

A

Aspirin, an antiplatelet drug.

61
Q

What does ‘R’ stand for in MONARCH BASIC?

A

Reperfusion with PCI or thrombolysis.

62
Q

What is primary percutaneous coronary intervention (PCI)?

A

Balloon is threaded through a blood vessel to the blockage site and inflated to compress the plaque.

63
Q

What is the first-line thrombolytic for thrombolysis?

A

Alteplase.

64
Q

What does ‘C’ stand for in MONARCH BASIC?

A

Clopidogrel, but prasugrel or ticagrelor is preferred.

65
Q

What does ‘H’ stand for in MONARCH BASIC?

66
Q

What is the first step in secondary prevention for a patient?

A

Start beta-blocker as soon as the patient is hemodynamically stable.

67
Q

When should beta-blockers be discontinued?

A

Beta-blockers can be discontinued after 12 months if LVEF is not reduced; otherwise, continue indefinitely.

68
Q

What anticoagulant therapy should be used in secondary prevention?

A

Use anticoagulant or dual antiplatelet therapy (aspirin with another antiplatelet).

69
Q

How long should aspirin be continued?

A

Aspirin should continue indefinitely.

70
Q

How long can dual antiplatelet therapy be continued?

A

Dual antiplatelet therapy can be continued up to 12 months.

71
Q

What is included in secondary prevention besides medications?

A

Statin and inhibitors (e.g., ACE inhibitor) should be started as soon as the patient is hemodynamically stable and continued indefinitely.

72
Q

What is the goal of correcting risk factors in secondary prevention?

A

Correction of risk factors has an effectiveness of 83%.

73
Q

What are some cardiac causes of chest pain?

A

Angina and pericarditis.

74
Q

What are some gastrointestinal causes of chest pain?

A

GERD, peptic ulcers, biliary coeliac, esophageal spasms.

75
Q

What are some musculoskeletal causes of chest pain?

A

Cervical radiculitis and costochondral syndrome.

76
Q

What are the further investigations for coronary artery disease?

A
  1. Stress tests (Exercise ECG, Myocardial perfusion imaging, Dobutamine stress echocardiography, Stress MRI)
  2. Echocardiogram
  3. Angiography (Non-invasive CT coronary angiogram or invasive coronary angiogram)
  4. FBC
77
Q

What does blue coloring indicate in myocardial perfusion imaging?

A

Blue coloring indicates extreme myocardial ischaemia on stress.