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Week 126 - Chronic Stable Angina Flashcards

1
Q

What are some of the differential diagnoses for angina?

A
  • MI
  • PE
  • Reflux Oesophagitis
  • Pneumothorax
  • Aortic Dissection
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2
Q

What investigations should be performed for a suspected case of angina?

A

ECG, Blood profile, Exercise Stress Test, Angiography

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3
Q

What are some of the lifestyle management options for chronic stable angina?

A
  • Smoking Cessation
  • Diet
  • Exercise
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4
Q

What are the medical treatment options for chronic stable angina?

A

• Drugs-

  • Antiplatelets
  • Beta-blockers
  • Statins
  • Nitrates
  • Calcium channel blockers
  • *• Treat related conditons-**
  • Anaemia
  • Diabetes
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5
Q

What are the revascularisation options for chronic stable angina?

A
  • Percutaneous coronary intervention - Plain old balloon angioplasty, bare metal stents, drug eluting stents.
  • Coronary Artery Bypass Surgery
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6
Q

Coronary Artery Bypass Surgery for Chronic Stable Angina: What are the indications, risks and benefits?

A

Indications -
- 3VD, 2VD with LV impairment or LMS.

Risks -
- Risk stratification, unit results, individual results.

Benefits -
- Symptoms and prognosis.

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7
Q

What is a the definition of Hypoxia?

A

A lack of oxygen resulting in a decrease in oxidative respiration leading to tissue damage.

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8
Q

What is the definition of ischaemia?

A
  • A lack of blood supply from a stenotic/occluded artery or reduced venous drainage causes ischaemia.
  • This causes a lack in oxygen **and **metabolites, causes cell injury more rapidly than hypoxia.
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9
Q

What is the definition of infarction?

A

Irreversible cell death due to hypoxia or ischaemia.

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10
Q

What are the four main pathophysiological outcomes of cell injury?

A
  • Decreased ATP
  • Membrane damage
  • Increased intracellular calcium
  • Increased oxygen derived from free radicals
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11
Q

What is the impact of decreased ATP during cell injury?

A

• Decreased activity of Na/K pump leads to;

  • Influx of Ca, H2O, Na
  • Eflux of K leading to cell swelling, loss of microvilli.

• Increased anaerobic glycolysis leading to;
- Decreased pH and Glycogen

• Detachment of ribosomes;
- Decreased protein synthesis.

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12
Q

What occurs to the membrane during cell damage?

A
  • Decreased ATP leads to decreased production of phospholipids.
  • Influx of Ca activates phospholipases and proteases leading to destruction of cytoskeleton.
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13
Q

During cell damage their is an influc of Ca, what effect does this have on the cell?

A
  • ATPase causing decrease in ATP.
  • Increase in phospholipases, causes a decrease in phospholipids.
  • Increase in proteases, causes destruction of membrane and cytoskeleton.
  • Increase in endonucleases, leading to chromatin breakdown.
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14
Q

What is iscahemia-reperfusion injury? What are the hypothesis for its mechanism?

A
  • Some cells which are reversibly damaged for ischaemia may then die when blood flow returns.
  • Oxygen free radicals, Mitochondrial permeability transition, inflammation associated injury, Complement.
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15
Q

What is atheroscleorsis?

A
  • Atheroma is the accumulation of lipid and fibrous tissue within the antima of the artery.
  • These localised collections are called ‘plaques’.
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16
Q

What is the difference between a stable and unstable plaque?

A

• **Stable **-
- Concentric, rish in firbous stroma, rich in smooth muscle.

  • *• Unstable - **
  • Eccentric, rich in lipid, Macrophages, Inflammation, endothelial cell injury.
17
Q

What are the risk factors for atherosclerosis?

A
  • Age, Gender, Family history
  • Smoking, Hypertension, Hyperlipidaemia, Diabetes Melitus.
18
Q

What are the four life-threatening causes of chest pain that you should **never **miss?

A
  • MI
  • PE
  • Tension pneumothorax
  • Dissecting aortic aneurism
19
Q

What is the definition of stable angina?

A

• Reversible ischaemia to myocardiam brought about due to increased stress and relieved by rest.

20
Q

What are the four classifications of stable angina?

A
  • Class I - Strenuous or protracted exercise.
  • Class II - Slight limitation with vigorous exercise.
  • Class III - Marked limitation with activities of everyday living.
  • Class IV - Inability to perform daily activites.
21
Q

What initial investogations should be performed for stable angina?

A
  • ECG
  • Bloods
  • CXR - For determining causes of chest pain.
22
Q

What is the drug-therapy for chronic stable angina?

A
  • Nitrates
  • Beta-Blockers
  • Calcium Channel Blockers
  • Longer-acting nitrates
  • Potassium channel activators
  • Ivabradine
  • Ranolazine
23
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Nitrates?

A
  • 1st line choice for rapid relievement of symptoms, can also be used as prophylaxis.
  • Release of NO to activate cAMP which causes smooth muscle relaxation and subsequent vasodilation.
  • Sideffects - Hypotension, Headache, Flushing.
  • Contraindications - Hypotension, Aortic and mitral stenosis, Hypertrophic cardiomyopathy.
24
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Beta-blockers?

A
  • 1st line treatment.
  • Causes reduction in sympathetic stimulation to cause a reduction in heart rateand myocardial contractability.
  • Side-effects - Bronchospasm, bradycardia, cold extremities, numbness, sleep disturbance, fatigue, sexual dysfunction.
  • Contra-indications - Asthma, bradycardia, uncontrolled heart failure, 2˚ and 3˚ heart block, severe peripheral artery disease.
25
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Calcium Channel Blockers (dihydropyridines)?

A
  • Amlodipine, Nifedipine, Felodipine.
  • 2nd-line addition to Beta-blockers.
  • Smooth muscle relaxation by inhibiting influx of calcium ions.
  • Side-effects: Flushing, headaches, dizziness, ankle oedema, hypotension.
  • Contraindications: Uncontrolled heart failure, MI in past month, significant aortic stenosis.
26
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Calcium channel blockers (Non-dihydropyridines)?

A
  • Verapamil, Diltiazem.
  • Option for patiens where beta-blockers are contraindicated.
  • Conduction of AV node, has rate limiting mechanism.
  • Side-effects - SA/AV block, constipation.
  • Contraindications - 2˚/3˚ heart block, uncontrolled heart failure.
27
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of **Longer-acting nitrates? **

A
  • Added into beta-blocker for symptom control.
  • Release of NO to activate cAMP to cause smooth muscle relaxation and subsequent vasodilation.
  • Side-effects: Hypotension, headache, flushing.
  • Contra-indications: Hypotension, aortic and mitral stenosis, hypertrophic cardiomyopathy.
28
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Potassium-channel activator?

A
  • Nicorandil
  • 3rd-line added in drug.
  • NO donor to activate cAMP, smooth muscle relaxation, vasodilation.
  • Opens K+ channels resulting in decreased Ca influx.
  • Side-effects: Headache, Hypotension, GI irritation.
  • Contra-indications: Left ventricular failure, hypotension.
29
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Ivabradine?

A
  • 3rd line treatment.
  • Blocks a pacemaker or ‘funny’ current channel in SA node.
  • Side-effects: Visual disturbances, Bradycardia, 1˚ heart block, Headache and dizziness.
  • Contraindications: Bradycardia, 2˚/3˚ heart block, Acute MI.
30
Q

Chronic Angina Medical Therapy: What is the role in treatment, mechanism, side-effects and contraindications of Ranolazine?

A
  • Add-on for symptomatic control if no relief from previous medical therapy.
  • Inhibits ‘late’ sodium channels - resulting in decreased influx of Ca resulting in relaxation of smooth muscle.
  • Side-effects: Constipation, Nausea and Vomitting, Dizziness and headache.
  • Contradindications - Moderate to severe hepatic impairment.

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