Coronary Heart Disease Flashcards

1
Q

Pathogenesis of CAD

A

-Atherosclerosis
-Rare
=Aortitis
=Vasculitis
=Autoimmune connective tissue diseases

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2
Q

Describe atherosclerosis

A

-Progressive inflammatory disorder of arterial wall characterised by focal lipid-rich deposits of atheroma
=Clinically silent until large enough to impair tissue perfusion/ ulceration/ disruption of lesion resulting in thrombotic occlusion or distal embolisation of vessel

-Deposits of lipids in vessel wall (sites of altered arterial shear stress like bifurcations and abnormalities of endothelial function)
=Monocytes and inflammatory cells bind to receptors expressed by endothelial cells
=Migrate into intima, take up oxidised LDL by phagocytosis to become foam cells

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3
Q

Clinical manifestations of CAD

A

-Stable angina
-Unstable angina
-MI
HF
-Arrhythmia
-Sudden death

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4
Q

What is stable angina?

A

Ischaemia due to fixed atheromatous stenosis of one or more coronary arteries

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5
Q

What is unstable angina?

A

Ischaemia caused by dynamic complete or partial obstruction of a coronary artery due to plaque rupture or erosion with superimposed thrombosis

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6
Q

What causes MI?

A

-Myocardial necrosis caused by acute occlusion of a coronary artery due to plaque rupture or erosion with superimposed thrombosis
-Supply demand imbalance where blood flow cannot meet the needs of the myocardium. This may be caused by fixed atheromatous obstruction with high myocardial demand for blood

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7
Q

Risk factors for atherosclerosis

A

-Age and sex (sex difference disappears after menopause)
-Genetics (hypertension, hyperlipidaemia, DM, early onset disease)
-Smoking
-Hypertension
-Hypercholesterolaemia
-DM (especially T2)
-Obesity
-Inactivity
-Platelet activation and high plasma fibrinogen concentrations
-Alcohol
-Diet
-Social deprivation

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8
Q

Primary prevention of CAD

A

-Lifestyle changes/ therapeutic interventions

=Do not smoke
=Take regular exercise (minimum 20 minutes, three times a week)
=Maintain an ideal body weight
=Eat a mixed diet rich in fresh fruit and vegetables
=Aim to get no more than 10% energy intake from saturated fat

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9
Q

Pathogenesis of Angina

A

-Coronary atherosclerosis
-Aortic valve disease and hypertrophic cardiomyopathy
-Coronary artery spasm (transient ST elevation)

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10
Q

Characteristic features of angina

A
  1. Constricting discomfort in the centre of the chest, or in the neck, shoulders, jaw or arms
  2. Precipitated by physical exertion
  3. Relieved by rest (or GTN) within 5 minutes
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11
Q

Classification of angina

A

-Typical angina : All three features
-Atypical angina : Two features
-Non-anginal chest pain : One or no features

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12
Q

Investigations of angina

A

-Blood tests, 12-lead ECG, CXR, ECHO
-Exercise ECG?= down-sloping ST segment depression 1mm or more indicative of ischaemia

-CT coronary angiography
-Stress testing

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13
Q

Advice to patients with stable angina

A

-Do not smoke
-Aim for an ideal body weight
-Take regular exercise (exercise up to, but not beyond, the point of chest discomfort is beneficial and may promote collateral vessels)
-Avoid severe unaccustomed exertion, and vigorous exercise after a heavy meal or in very cold weather
-Take sublingual nitrate before undertaking exertion that may induce angina

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14
Q

Medications for stable angina

A

-Low-dose 75mg aspirin/ clopidogrel 75mg
-Statin

-GTN
-Beta-blocker
-CCB and long-acting nitrate if needed

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15
Q

Non-pharmacological treatments for angina

A

-Percutaneous coronary intervention
=dilated balloon, coronary stent

-Coronary artery bypass grafting
=radial and internal mammary arteries, saphenous vein

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16
Q

Wellen’s syndrome

A

Wellen’s syndrome is an ECG pattern that is typically caused by high-grade stenosis in the left anterior descending coronary artery.

The patient’s pain may have resolved at the time of presentation and cardiac enzymes may be normal/minimally elevated.

ECG features
biphasic or deep T wave inversion in V2-3
minimal ST elevation
no Q waves