28 Cardiovascular disease 1 Flashcards

1
Q

Define ischaemic heart disease.

A

Inadequate blood supply to the myocardium.

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2
Q

Name the four ischaemic heart disease syndromes.

A

Angina pectoris: typical/ variant/ crescendo.
Acute coronary syndrome: MI/ crescendo AP.
Sudden cardiac death.
Chronic ischaemic heart disease.

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3
Q

How does the morphology of an MI change over time?

A
Under 24hrs: normal gross, necrosis + neutrophils.
1-2d: yellow.
3-7d: hyperaemic border, macrophages.
1-3wks: red/grey, granulation
3-6wks: scar, collagen
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4
Q

Which blood markers can be used to detect myocyte damage? (5)

A
Troponin's.
Creatinine kinase.
Myoglobin.
Lactate dehydrogenase isoenzyme 1.
Aspartate transaminase.
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5
Q

When are troponins detectable?

Which conditions raise them? (4)

A

2 hrs, peak @ 12hrs, until 7days.

MI, PE, heart failure, myocarditis.

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6
Q

When is creatine kinase detectable after an MI?

A

2hrs, peaks 10-24hrs, until 3 days.

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7
Q

What are the three types of creatine kinase?

A

MM - muscle (cardiac+skeletal).
BB - brain and lung.
MB - mainly cardiac (+skeletal).

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8
Q

What are the complications following an MI? (6)

A
Contractile dysfunction and chronic failure.
Infarct extension.
Myocardial rupture.
Pericarditis - Dressler's syndrome.
Mural thrombus. 
Ventricular aneurysm.
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9
Q

How may subendocardial MI occur?

A

Relatively poorly perfused, so stable atheromatous occlusion or acute hypotension may infarct subendocardium without occlusion.

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10
Q

What are the causes of secondary hypertension?

A

Renal.
Endocrine: cushings, primary aldosteronism, phaechromocytoma
CV: aorta coarctation, increased IV vol/ cardiac output.
Neurological.

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11
Q

When is myoglobin detectable after an MI?

What else releases it?

A

2 hrs.

Damaged skeletal muscle.

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12
Q

What is chronic ischaemic heart disease?

How does the heart change?

A

Relative ischaemia and angina on exertion.

Hypertrophy and dilation.

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13
Q

Which genes are mutated in familial hypercholesterolaemia?

Rx of heterozygotes?

A

LDL receptor gene.
Lipoprotein B.
Statins: hydroxymethylglutaryl CoA reductase inhibitors.

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14
Q

Quick explanation of the RAA system.

A

Renin from kidney, cleaves angiotensinogen to angiotensin I, converted to ang II. Vasoconstrictor, stim adrenal cortex to produce aldosterone. Sodium and water retention.

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15
Q

What is Conn’s syndrome?

What does it cause?

A

Adrenocortical adenoma causing XS aldosterone secretion. Na and water retention, K loss.
Hypertension, muscle weakness, arrhythmia, metabolic alkylosis.

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16
Q

What can systemic hypertension cause?

A

Heart disease: hypertrophy + dilation.
Chronic renal failure: arterial intimal fibroelastosis, hyaline arteriosclerosis.
Cerebrovascular: encephalopathy, haemorrhage, aneurysm.

17
Q

What is a hypertensive crisis?

Sequelae? (3)

A

BP >180/120 mmHg.

Acute hypertensive encephalopathy, renal failure and retinal haemorrhages.

18
Q

What is pulmonary hypertension?

A

Higher than normal pressure in pulmonary artery.

19
Q

What is pulmonary hypertension caused by?

A

Loss of pulmonary vasculature.
L ventricular failure.
Systemic to pulm art shunt. Idiopathic.

20
Q

What is the effect of pulmonary hypertension on the heart?

A

Increased R ventricular work.
Hypertrophy.
Later dilation and failure -> systemic venous congestion.

21
Q

What are the risk factors for cardiovascular disease?

A

Gender, hypertension, smoking, high cholesterol, low LDL, diabetes, sedentary, obesity, high alcohol use, south Asian ethnicity.

22
Q

What is a phaechromocyoma?

Symptoms?

A

Tumour in adrenal medulla secreting adrenaline + NA.

Pallor, headache, sweating, nervous, hypertension.

23
Q

How does cushing’s disease cause hypertension?

A

Cortisol overproduction leads to more sympathetic NS activity.
Also an aldosterone like action on kidney.

24
Q

What are the causes of cushings disease?

A

Adrenocortical neoplasm.
Pituitary adenoma.
Paraneoplastic effect - particularly SCLC.

25
Q

What does acute hypertensive encephalopathy cause?

A

Confusion.
Vomiting.
Convulsions.
Coma + death.