30 Cardiovascular disease 3

Question 1

What is endocarditis?

Answer 1

Inflammation of the endocardium in the heart.

Typically with vegetations on valves.

Question 2

What are the vegetations of acute infective endocarditis like?

Answer 2

Friable, bulky, destructive.
Often multiple.
May form abscess with large numbers of organisms.

Question 3

Differentiate between acute and subacute endocarditis.

Answer 3

Acute: highly virulent, in normal valve, necrotising + ulcerative lesions, require surgery. Death common.

Sub-acute: lower virulence, previous deformities, less destructive, curable with antiobics.

Question 4

What are the causative organisms of infective endocarditis? (4)

Answer 4

Step viridian’s from mouth.
Staph aureus from skin (IVDU).
Coagulase negative staphylococci (prosthetic valves).
Strep bovis - bowel cancer!

Question 5

What are the clinical features of infective endocarditis? (8)

Answer 5

Fever. Weight loss.
90% have murmur if L sided IE.
Glomerulonephritis.
Splinter haemorrhages.
Janeway lesions, Oslers nodes, Roth spots.

Question 6

Who gets non-bacterial thrombotic endocarditis and what is it associated with?

Answer 6

Debilitated patients: Ca/sepsis.
Hyper coagulable state.
Part of trousseau syndrome.

Question 7

What are the vegetations like in non-bacterial thrombotic endocarditis? (5)

Answer 7

Small and sterile.
On line of closure of leaflets.
Not invasive, minimal local effect.
May give off systemic emboli.

Question 8

What is Libman-Sacks endocarditis?

What type of vegetations does it cause?

Answer 8

Associated with SLE.
Usually asymptomatic. Affects Mitral and tricuspid valves.
Small and warty. On chordae or endocardium.

Question 9

What are the pathological features of rheumatic fever?

Answer 9

Aschoff bodies- cardiac lesion in all three layers with T cells, plasma cells and macrophages.
Vegetations = veruccae.
Mitral valve changes: leaflet thickening, fibrosis and calcification -> “fishmouth”/”buttonhole” stenoses.

Question 10

What is the aetiology and pathogenesis of rheumatic fever?

Answer 10

Immunological reaction following group A streptococcal pharyngitis.
Antibodies directed against M proteins cross react with heart. CD4 T cells specific for streptococcal peptides.

Question 11

What are the causes of pericarditis? (10)

Answer 11

Inflammation of pericardial sack caused by:
Infection: coxsackie B.
Immunological: rheumatic fever, SLE, dressler’s, post-cardiotomy.
Trauma, radiation, uraemia, neoplasia. Post MI.

Question 12

What is serous pericarditis?

Causes? (8)

Answer 12

Accumulation of serous fluid.
Generally non-infectious inflammatory causes. Coxsackie B, echovirus, rheumatic fever, SLE, scleroderma.
Uraemia, radiation, scleroderma.

Question 13

What is dressler’s syndrome?

When does it occur?

Answer 13

Secondary pericarditis weeks after MI.
Triad: fever, pleuritic chest pain, pericardial effusion.
Autoimmune reaction to antibodies released after an MI.

Question 14

What is suppurative/purulent pericarditis?
Cause?
Common outcome?

Answer 14

Red, granular exudate.
Infections.
May spread to cause mediation-pericarditis.
Heals by scarring - restrictive pericarditis.

Question 15

What is haemorrahgic pericarditis?

Common causes?

Answer 15

Blood mixed with serous or suppurative exudate.

Infections. Cancer. Follow cardiac surgery (cardiac tamponade).

Question 16

What are the three types of chronic pericarditis?

Answer 16

Adhesive.
Adhesive mediastinopericarditis - causes cardiac hypertrophy and dilation.
Constrictive pericarditis - heart encased by fibrous scar.

Question 17

What are the clinical features of pericarditis?

Answer 17

Sharp central chest pain exacerbated by movement, respiration and lying flat. Relieved by sitting forwards.
Pericardial friction rub loudest on the left sternal edge.
Fever, leucocytosis, lymphocytosis, pericardial effusion.

Question 18

What are the four types of cardiomyopathy? (4)

Answer 18

Dilated.
Restrictive.
Hypertrophic.
Arrythmogenic right ventricular.

Question 19

What is dilated cardiomyopathy?
What happens to the heart?
Causes?
Treatment?

Answer 19

Dilation of the heart leading to systolic dysfunction.
Hypertrophic cells with fibrosis.
Genetic (cytoskeletal proteins). Smoking.
5 yr survival 25%.
Transplant, long term ventricular assistance.

Question 20

What is hypertrophic cardiomyopathy?

Cause?

Answer 20

Hypertrophic cells - poorly compliant myocardium.
Diastolic dysfunction with preserved systole.
100% genetic - sarcomeric proteins.

Question 21

What are the clinical features of hypertrophic cardiomyopathy?

Answer 21

Reduced cardiac output.
25% have LV outflow obstruction (systolic ejection murmur).
Exertional dyspnoea.

Question 22

What are the complications of hypertrophic cardiomyopathy?

Answer 22

Mural thrombus formation - embolisation.
Atrial fibrillation. Cardiac failure. Ventricular arrhythmias.
Sudden death.

Question 23

Treatment of hypertrophic cardiomyopathy?

Answer 23

β-adrenergic blockers to decrease hr + contractility.

Septum tissue removal to reduce outflow obstruction.

Question 24

What are the causes and morphology of restrictive cardiomyopathy?

Answer 24

1o: decreased ventricular compliance.
2o: infiltration: tumour, fibrosis, amyloidosis, sarcoidosis.
Normal sized chambers with firm and noncompliant myocardium.

Question 25

What is arrythmogenic right ventricular cardiomyopathy?

Answer 25

Genetic disease: RV dilation, myocardial thinning.
Fibro-fatty replacement. Disorder of desmosomes.
Exercise leads to cell detachment and death.
Cause of sudden cardiac death in the young.

Question 26

What are the clinical features of myocarditis?

Answer 26

Asymptomatic.
Sudden heart failure, arrhythmias, death.
Non specifics: fatigue, dyspnoea etc.

Question 27

What are the causes of myocarditis?

Answer 27

Coxsackie A + B in West.
Chagas disease (trypanosoma cruzi) in S America. 
Infections, immune mediated, sarcoidosis, giant cell myocarditis.

Question 28

What is vasculitis?

How is it classified?

Answer 28

Inflammation of the vessel wall anywhere in the body.

Chapel-Hill nomenclature.

Question 29

What is the pathology of giant cell arteritis?

Answer 29

Chronic granulomatous inflammation in med-large arteries.

Ophthalmic may lead to permanent blindness..

Question 30

What are the morphological changes in giant cell arteritis?

Answer 30

Intimal thickening reducing lumen diameter.
Med granulomatous inflammation - elastic lamina fragmentation.
Multinucleate giant cells.

Question 31

How does giant cell arteritis present?
Diagnosis?
Treatment?

Answer 31

Facial pain, headache, jaw claudication.
Biopsy with histology.
Corticosteroids. Anti-TNF therapy if refractive.

Question 32

Describe the aetiology of atherosclerotic aneurysms:

Complications?

Answer 32

Elderly. Causes AAA. Rupture risk : size.
Rupture and retroperitoneal haemorrhage.
Embolisation and limb ischaemia.

Question 33

What is a dissecting aneurysm?

Classical symptoms?

Answer 33

Tear in blood vessel wall. Blood between intimatal and medial layers.
Usually in thoracic aorta 2o to hypertension. Causes occlusion and haemopericardium.
Tearing chest pain radiating to left shoulder.

Question 34

Where do Charcot-Bouchard aneurysms occur?

Answer 34

Intracerebrale capillaries due to hypertension. Cause of haemorrhage.

Question 35

What are mycotic aneurysms?

Associated risk?

Answer 35

Weakening of artery wall secondary to bacterial/fungal infection. Organisms enter media via vasa vasorum. Commonly subacute bacterial endocarditis.
Increases rupture risk.

Question 36

What is a false aneurysm?

When do they commonly occur?

Answer 36

Blood filled space around a vessel after trauma/perforation.

Femoral artery puncture during angioplasty/angiography.