28 Cardiovascular disease 1

Question 1

Define ischaemic heart disease.

Answer 1

Inadequate blood supply to the myocardium.

Question 2

Name the four ischaemic heart disease syndromes.

Answer 2

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

Question 3

How does the morphology of an MI change over time?

Answer 3

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

Question 4

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

Answer 4

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

Question 5

When are troponins detectable?

Which conditions raise them? (4)

Answer 5

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

MI, PE, heart failure, myocarditis.

Question 6

When is creatine kinase detectable after an MI?

Answer 6

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

Question 7

What are the three types of creatine kinase?

Answer 7

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

Question 8

What are the complications following an MI? (6)

Answer 8

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

Question 9

How may subendocardial MI occur?

Answer 9

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

Question 10

What are the causes of secondary hypertension?

Answer 10

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

Question 11

When is myoglobin detectable after an MI?

What else releases it?

Answer 11

2 hrs.

Damaged skeletal muscle.

Question 12

What is chronic ischaemic heart disease?

How does the heart change?

Answer 12

Relative ischaemia and angina on exertion.

Hypertrophy and dilation.

Question 13

Which genes are mutated in familial hypercholesterolaemia?

Rx of heterozygotes?

Answer 13

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

Question 14

Quick explanation of the RAA system.

Answer 14

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

Question 15

What is Conn’s syndrome?

What does it cause?

Answer 15

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

Question 16

What can systemic hypertension cause?

Answer 16

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

Question 17

What is a hypertensive crisis?

Sequelae? (3)

Answer 17

BP >180/120 mmHg.

Acute hypertensive encephalopathy, renal failure and retinal haemorrhages.

Question 18

What is pulmonary hypertension?

Answer 18

Higher than normal pressure in pulmonary artery.

Question 19

What is pulmonary hypertension caused by?

Answer 19

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

Question 20

What is the effect of pulmonary hypertension on the heart?

Answer 20

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

Question 21

What are the risk factors for cardiovascular disease?

Answer 21

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

Question 22

What is a phaechromocyoma?

Symptoms?

Answer 22

Tumour in adrenal medulla secreting adrenaline + NA.

Pallor, headache, sweating, nervous, hypertension.

Question 23

How does cushing’s disease cause hypertension?

Answer 23

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

Question 24

What are the causes of cushings disease?

Answer 24

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

Question 25

What does acute hypertensive encephalopathy cause?

Answer 25

Confusion.
Vomiting.
Convulsions.
Coma + death.