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Flashcards in 30 Cardiovascular disease 3 Deck (36):
1

What is endocarditis?

Inflammation of the endocardium in the heart.
Typically with vegetations on valves.

2

What are the vegetations of acute infective endocarditis like?

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

3

Differentiate between acute and subacute endocarditis.

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

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

4

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

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

5

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

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

6

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

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

7

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

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

8

What is Libman-Sacks endocarditis?
What type of vegetations does it cause?

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

9

What are the pathological features of rheumatic fever?

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.

10

What is the aetiology and pathogenesis of rheumatic fever?

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

11

What are the causes of pericarditis? (10)

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

12

What is serous pericarditis?
Causes? (8)

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

13

What is dressler's syndrome?
When does it occur?

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

14

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

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

15

What is haemorrahgic pericarditis?
Common causes?

Blood mixed with serous or suppurative exudate.
Infections. Cancer. Follow cardiac surgery (cardiac tamponade).

16

What are the three types of chronic pericarditis?

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

17

What are the clinical features of pericarditis?

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.

18

What are the four types of cardiomyopathy? (4)

Dilated.
Restrictive.
Hypertrophic.
Arrythmogenic right ventricular.

19

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

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.

20

What is hypertrophic cardiomyopathy?
Cause?

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

21

What are the clinical features of hypertrophic cardiomyopathy?

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

22

What are the complications of hypertrophic cardiomyopathy?

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

23

Treatment of hypertrophic cardiomyopathy?

β-adrenergic blockers to decrease hr + contractility.
Septum tissue removal to reduce outflow obstruction.

24

What are the causes and morphology of restrictive cardiomyopathy?

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

25

What is arrythmogenic right ventricular cardiomyopathy?

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.

26

What are the clinical features of myocarditis?

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

27

What are the causes of myocarditis?

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

28

What is vasculitis?
How is it classified?

Inflammation of the vessel wall anywhere in the body.
Chapel-Hill nomenclature.

29

What is the pathology of giant cell arteritis?

Chronic granulomatous inflammation in med-large arteries.
Ophthalmic may lead to permanent blindness..

30

What are the morphological changes in giant cell arteritis?

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

31

How does giant cell arteritis present?
Diagnosis?
Treatment?

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

32

Describe the aetiology of atherosclerotic aneurysms:
Complications?

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

33

What is a dissecting aneurysm?
Classical symptoms?

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.

34

Where do Charcot-Bouchard aneurysms occur?

Intracerebrale capillaries due to hypertension. Cause of haemorrhage.

35

What are mycotic aneurysms?
Associated risk?

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

36

What is a false aneurysm?
When do they commonly occur?

Blood filled space around a vessel after trauma/perforation.
Femoral artery puncture during angioplasty/angiography.

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