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Therapeutics > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

How is angina clinically characterized?

A

Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or arm.

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2
Q

What typically aggravates angina?

A

Angina is typically aggravated by exertion or emotional stress.

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3
Q

How is angina usually relieved?

A

Angina is usually relieved by rest.

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4
Q

How long does angina usually last?

A

Angina usually lasts less than 20 minutes.

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5
Q

What is the most common cause of angina?

A

The most common cause of angina is atherosclerosis.

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6
Q

What is the trend in the incidence of angina?

A

The incidence of angina is increasing in all population groups.

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7
Q

In which demographic is there a large increase in the number of angina cases?

A

There is a large increase in the number of young women experiencing angina.

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8
Q

What factors are contributing to the increased incidence of angina?

A

The Western diet and lifestyle are contributing factors to the increased incidence of angina.

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9
Q

What is a key initial event in the pathophysiology of angina?

A

Endothelial damage is a key initial event in the pathophysiology of angina.

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10
Q

What does endothelial damage lead to in the context of angina?

A

Endothelial damage leads to inflammation with plaque deposition, including cholesterol and fibrin.

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11
Q

What determines the likelihood of plaque rupture in angina?

A

The stability of the fibrous cap determines the likelihood of plaque rupture, not the size of the plaque.

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12
Q

What initiates the process of atherothrombosis?

A

Endothelial injury initiates the process of atherothrombosis.

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13
Q

What factors can cause endothelial injury in atherothrombosis?

A

Factors like hypertension, high cholesterol, smoking, and diabetes can cause endothelial injury

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14
Q

What happens during the lipid accumulation stage of atherothrombosis?

A

During lipid accumulation, LDL cholesterol penetrates the endothelium, oxidizes, and attracts monocytes.

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15
Q

How does the inflammatory response contribute to atherothrombosis?

A

Monocytes transform into macrophages, ingest oxidized LDL, and become foam cells during the inflammatory response.

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16
Q

What is formed during the plaque formation stage of atherothrombosis?

A

Foam cells aggregate into fatty streaks, smooth muscle cells migrate and produce extracellular matrix, forming a fibrous cap over the plaque during plaque formation.

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17
Q

What happens during the plaque progression stage of atherothrombosis?

A

Chronic inflammation causes plaque growth and complexity during the plaque progression stage.

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18
Q

What causes plaque destabilization in atherothrombosis?

A

Inflammation thins the fibrous cap, making it prone to rupture, which causes plaque destabilization.

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19
Q

What occurs during the thrombosis stage of atherothrombosis?

A

Rupture exposes the plaque’s contents, activating platelets and the coagulation cascade, forming a blood clot during thrombosis.

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20
Q

What are the potential clinical manifestations of thrombosis in atherothrombosis?

A

Thrombosis can block arteries, leading to conditions like heart attack, stroke, or peripheral arterial disease.

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21
Q

The end stages of atherothrombosis

A
  1. myocardial infarction
  2. ischemic stroke
  3. critical leg ischemia
  4. cardiovascular death
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22
Q

What factors increase oxygen demand in angina pectoris?

A

Factors that increase oxygen demand in angina pectoris include increased heart rate, increased systolic blood pressure (SBP), and increased wall stress.

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23
Q

What factors increase oxygen supply in angina pectoris?

A

Factors that increase oxygen supply in angina pectoris include increased coronary flow, increased hemoglobin (Hb), and increased oxygen (O2) levels.

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24
Q

What is angina pectoris?

A

Angina pectoris is a clinical syndrome characterized by chest pain or discomfort resulting from myocardial ischemia, typically due to atherosclerotic disease of the coronary arteries.

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25
Q

What are the typical locations of chest pain or discomfort in angina pectoris?

A

The chest pain or discomfort is typically located behind the sternum but can also occur in the neck, jaw, shoulders, arms, or epigastrium.

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26
Q

How is the chest pain in angina pectoris usually described?

A

The chest pain is usually described as a squeezing, pressing, burning, or tightness sensation.

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27
Q

What are the common provoking factors for angina pectoris?

A

Common provoking factors include physical exertion, cold weather, large meals, and emotional stress.

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28
Q

How is angina pectoris typically relieved?

A

Angina pectoris is typically relieved by rest and sublingual nitroglycerin.

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29
Q

What is the usual duration of angina pectoris symptoms?

A

The symptoms usually last between 1 to 15 minutes.

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30
Q

What are some associated symptoms of angina pectoris?

A

Associated symptoms include dyspnea (shortness of breath), sweating, and nausea.

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31
Q

What are the different types of angina?

A

The different types of angina are stable angina, unstable angina, and variant (Prinzmetal’s) angina.

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32
Q

What characterizes stable angina?

A

Stable angina is predictable, occurs with exertion or stress, and is relieved by rest or nitroglycerin.

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33
Q

What characterizes unstable angina?

A

Unstable angina is characterized by new onset, increasing frequency, duration, or severity of symptoms, or occurring at rest, indicating a higher risk of myocardial infarction.

34
Q

What characterizes variant (Prinzmetal’s) angina?

A

Variant (Prinzmetal’s) angina is caused by coronary artery spasm, typically occurring at rest and often in cycles.

35
Q

What is the prognosis of angina?

A

Angina generally has a good prognosis.

36
Q

What type of disease is angina considered to be?

A

Angina is considered a primary care disease.

37
Q

What lifestyle changes are essential for managing angina?

A

Essential lifestyle changes for managing angina include diet, exercise, and maintaining an ideal body weight.

38
Q

What factors influence the prognosis of angina?

A

The prognosis of angina is influenced by left ventricular function, the number of coronary arteries with significant stenosis, and the extent of jeopardized myocardium.

39
Q

How does left ventricular function affect the prognosis of angina?

A

Left ventricular function affects the prognosis of angina as impaired function can indicate more severe disease and a poorer prognosis.

40
Q

How does the number of coronary arteries with significant stenosis impact prognosis?

A

The prognosis worsens with an increasing number of coronary arteries affected by significant stenosis, as this indicates more extensive coronary artery disease.

41
Q

What does the extent of jeopardized myocardium indicate about prognosis?

A

The extent of jeopardized myocardium indicates the severity of myocardial ischemia and damage, which can impact the overall prognosis.

42
Q

What are the typical findings on physical examination for angina?

A

Physical examination for angina often reveals little specific findings.

43
Q

What should be assessed to diagnose macrovascular disease in angina?

A

To diagnose macrovascular disease in angina, assess for diminished peripheral pulses, bruits, and other signs of vascular disease.

44
Q

Why is it important to consider risk factors in the diagnosis of angina?

A

Considering risk factors is important in diagnosing angina as they contribute to the likelihood of coronary artery disease and help guide diagnostic and management strategies.

45
Q

What are some precipitating factors for angina?

A

Precipitating factors for angina include anemia, thyrotoxicosis, and tachyarrhythmias.

46
Q

What evidence might indicate ischemic changes to the heart in angina?

A

Evidence of ischemic changes to the heart includes an enlarged heart, signs of heart failure, and the presence of S3/S4 heart sounds.

47
Q

Investigations

A
  • Resting ECG (NB)
  • Stress ECG if indicated
  • CXR
  • Blood
    – Cholesterol
    – Glucose
    – Renal function if required
48
Q

Risk factors for angina

A
  • HPT
  • Diabetes
  • Smoking
  • Obesity
  • Age: male greater than 40, Postmeno female.
  • +ve family Hx Previous - - MI
49
Q

What clinical factors are used for risk stratification in angina?

A

Clinical factors for risk stratification include hypertension (HPT) and diabetes

50
Q

How does an abnormal resting ECG contribute to risk stratification in angina?

A

An abnormal resting ECG contributes to risk stratification by indicating potential ischemic changes or arrhythmias that may increase risk.

51
Q

What role does left ventricular (LV) dysfunction play in risk stratification for angina?

A

Left ventricular (LV) dysfunction plays a role in risk stratification as it signifies impaired cardiac function, which can indicate more severe disease and higher risk.

52
Q

What are the primary objectives of managing angina?

A
  1. To prevent MI
  2. Reduce symptoms in order to improve quality of life.
53
Q

Management of angina by ABCDEF

A
  • Aspirin and Anti-anginals
  • Beta blockers and BP
  • Cholesterol and Cigarettes
  • Diet and Diabetes
  • Education and Exercise
  • Follow up
54
Q

What is the typical dosage range for aspirin in angina management?

A

The typical dosage range for aspirin in angina management is 75-150 mg/day.

55
Q

What is the mechanism of action of aspirin in managing angina?

A

Aspirin is a COX inhibitor that prevents platelet thromboxane formation and inhibits platelet aggregation.

56
Q

Why is aspirin important in the prevention of atherosclerotic plaque formation?

A

Aspirin is important in preventing atherosclerotic plaque formation because it inhibits platelet aggregation, which helps reduce the risk of plaque rupture and subsequent thrombosis.

57
Q

How does aspirin help preserve endothelial function?

A

Aspirin helps preserve endothelial function by reducing platelet aggregation and preventing thromboxane A2 formation, which contributes to maintaining healthy endothelial cells.

58
Q

What do controlled studies suggest about the use of aspirin in patients with stable angina?

A

Controlled studies suggest that aspirin should be used in all patients with stable angina, provided there are no contraindications, such as gastrointestinal issues.

59
Q

What is the primary action of nitrates in angina management?

A

Nitrates are potent vasodilators that venodilate, decreasing preload and venous return, which reduces myocardial oxygen requirements.

60
Q

What is the preferred form of nitrate administration for acute angina?

A

Sublingual (S/L) nitrates are preferred for acute angina due to their rapid onset of action.

61
Q

Can nitrates be used prophylactically?

A

Yes, nitrates can be used prophylactically to prevent angina attacks.

62
Q

What should be remembered about the use of nitrates regarding side effects?

A

Postural hypotension is a common side effect of nitrates. Additionally, headaches are common; patients should spit out the tablet when the pain subsides.

63
Q

How can headaches from nitrate use be managed?

A

Paracetamol can be used to manage headaches in some patients caused by nitrate use.

64
Q

What are common adverse effects of nitrates?

A

Common adverse effects of nitrates include postural hypotension, headache, and flushing.

65
Q

What should be considered to avoid dangerous interactions when using nitrates?

A

Be cautious with the use of nitrates in combination with Viagra and other similar medications due to the risk of severe hypotension.

66
Q

What are some contraindications for using nitrates?

A

Contraindications for using nitrates include hypotension, fixed output states, and recent use of Viagra or similar medications.

67
Q

How do beta blockers help manage angina?

A

Beta blockers decrease heart rate and myocardial contraction, which in turn decreases myocardial oxygen requirements. This helps delay or avoid the onset of angina.

68
Q

What is the target resting heart rate for patients on beta blockers for angina?

A

The target resting heart rate for patients on beta blockers is 55-60 beats per minute.

69
Q

Can the heart rate be adjusted in patients with symptomatic angina?

A

Yes, the heart rate can be further decreased in symptomatic patients, provided there are no symptoms of bradycardia.

70
Q

When should beta blockers be used in the management of angina?

A

Beta blockers should be used as a first-line treatment for angina if there are no contraindications.

71
Q

Contraindications of beta blockers

A
  • Asthma
  • COPD with reversibility
  • CCF??
  • Heart block
  • Bradycardia (<50)
72
Q

Adverse effects of beta blockers

A
  • Impotence.
  • Bronchospasm.
  • Lethargy/ decreased exercise ability
  • Bradycardia/heart block.
  • Cold peripheries.
73
Q

Risk modification for angina

A

1, lipid lowering
2. smoking cessation
3. hypertension
4. diabetes
5. obesity
6. exercise

74
Q

lipid lowering

A
  1. Highly beneficial role for statins.
  2. Reduces risk of MI and the need for revascularisation.
  3. Diet must not be overlooked!
75
Q

Smoking cessation

A
  1. Few randomised trials.
  2. However in primary prevention setting, smoking cessation decreases risk of cardiac event by 45%.
  3. Use other healthcare workers to increase rate of cessation
76
Q

Hypertension

A
  1. Beneficial effects on cardiac mortality confirmed in many trials.
  2. Poorly controlled HPT aggravates angina.
  3. Rational prescribing (B blocker) facilitates control of both.
77
Q

Diabetes

A

Strict control prevents microvascular complications as well as accelerated atherosclerosis.

78
Q

Obesity

A
  1. Commonly associated with angina.
  2. Contributes to other risk factors e.g. HPT, Diabetes, hypercholesterolaemia.
  3. Wt reduction improves these risks and reduces O2 demand.
79
Q

Exercise

A

Good trial data to support exercise.
BP lowering, lipid improvement occur as bonus!

80
Q

Follow Up

A
  • Has patient’s activity decreased?
  • Have anginal symptoms changed?
  • Is therapy tolerated?
  • Are modifiable risks treated?
  • Has co-morbid illness developed?
81
Q

Refer

A
  • Failure of medical therapy.
  • ? Diagnosis.
  • UAP/MI
  • CCF symptoms or signs. - Dizziness or syncopal signs.
  • Poor quality of life.
  • Very +ve stress test.

Therapeutics (15 decks)

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