28 Cardiovascular disease 1 Flashcards Preview

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Flashcards in 28 Cardiovascular disease 1 Deck (25):
1

Define ischaemic heart disease.

Inadequate blood supply to the myocardium.

2

Name the four ischaemic heart disease syndromes.

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

3

How does the morphology of an MI change over time?

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

4

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

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

5

When are troponins detectable?
Which conditions raise them? (4)

2 hrs, peak @ 12hrs, until 7days.
MI, PE, heart failure, myocarditis.

6

When is creatine kinase detectable after an MI?

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

7

What are the three types of creatine kinase?

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

8

What are the complications following an MI? (6)

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

9

How may subendocardial MI occur?

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

10

What are the causes of secondary hypertension?

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

11

When is myoglobin detectable after an MI?
What else releases it?

2 hrs.
Damaged skeletal muscle.

12

What is chronic ischaemic heart disease?
How does the heart change?

Relative ischaemia and angina on exertion.
Hypertrophy and dilation.

13

Which genes are mutated in familial hypercholesterolaemia?
Rx of heterozygotes?

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

14

Quick explanation of the RAA system.

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

15

What is Conn's syndrome?
What does it cause?

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

16

What can systemic hypertension cause?

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

17

What is a hypertensive crisis?
Sequelae? (3)

BP >180/120 mmHg.
Acute hypertensive encephalopathy, renal failure and retinal haemorrhages.

18

What is pulmonary hypertension?

Higher than normal pressure in pulmonary artery.

19

What is pulmonary hypertension caused by?

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

20

What is the effect of pulmonary hypertension on the heart?

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

21

What are the risk factors for cardiovascular disease?

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

22

What is a phaechromocyoma?
Symptoms?

Tumour in adrenal medulla secreting adrenaline + NA.
Pallor, headache, sweating, nervous, hypertension.

23

How does cushing's disease cause hypertension?

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

24

What are the causes of cushings disease?

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

25

What does acute hypertensive encephalopathy cause?

Confusion.
Vomiting.
Convulsions.
Coma + death.

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