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

What is endocarditis?

A

Inflammation of the endocardium in the heart.

Typically with vegetations on valves.

2
Q

What are the vegetations of acute infective endocarditis like?

A

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

3
Q

Differentiate between acute and subacute endocarditis.

A

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
Q

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

A

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

5
Q

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

A
Fever. Weight loss.
90% have murmur if L sided IE.
Glomerulonephritis.
Splinter haemorrhages.
Janeway lesions, Oslers nodes, Roth spots.
6
Q

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

A

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

7
Q

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

A

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

8
Q

What is Libman-Sacks endocarditis?

What type of vegetations does it cause?

A

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

9
Q

What are the pathological features of rheumatic fever?

A

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
Q

What is the aetiology and pathogenesis of rheumatic fever?

A

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

11
Q

What are the causes of pericarditis? (10)

A

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

12
Q

What is serous pericarditis?

Causes? (8)

A

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

13
Q

What is dressler’s syndrome?

When does it occur?

A

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

14
Q

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

A

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

15
Q

What is haemorrahgic pericarditis?

Common causes?

A

Blood mixed with serous or suppurative exudate.

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

16
Q

What are the three types of chronic pericarditis?

A

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

17
Q

What are the clinical features of pericarditis?

A

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
Q

What are the four types of cardiomyopathy? (4)

A

Dilated.
Restrictive.
Hypertrophic.
Arrythmogenic right ventricular.

19
Q

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

A

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
Q

What is hypertrophic cardiomyopathy?

Cause?

A

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

21
Q

What are the clinical features of hypertrophic cardiomyopathy?

A

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

22
Q

What are the complications of hypertrophic cardiomyopathy?

A

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

23
Q

Treatment of hypertrophic cardiomyopathy?

A

β-adrenergic blockers to decrease hr + contractility.

Septum tissue removal to reduce outflow obstruction.

24
Q

What are the causes and morphology of restrictive cardiomyopathy?

A

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

25
Q

What is arrythmogenic right ventricular cardiomyopathy?

A

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
Q

What are the clinical features of myocarditis?

A

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

27
Q

What are the causes of myocarditis?

A
Coxsackie A + B in West.
Chagas disease (trypanosoma cruzi) in S America. 
Infections, immune mediated, sarcoidosis, giant cell myocarditis.
28
Q

What is vasculitis?

How is it classified?

A

Inflammation of the vessel wall anywhere in the body.

Chapel-Hill nomenclature.

29
Q

What is the pathology of giant cell arteritis?

A

Chronic granulomatous inflammation in med-large arteries.

Ophthalmic may lead to permanent blindness..

30
Q

What are the morphological changes in giant cell arteritis?

A

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

31
Q

How does giant cell arteritis present?
Diagnosis?
Treatment?

A

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

32
Q

Describe the aetiology of atherosclerotic aneurysms:

Complications?

A

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

33
Q

What is a dissecting aneurysm?

Classical symptoms?

A

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
Q

Where do Charcot-Bouchard aneurysms occur?

A

Intracerebrale capillaries due to hypertension. Cause of haemorrhage.

35
Q

What are mycotic aneurysms?

Associated risk?

A

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

36
Q

What is a false aneurysm?

When do they commonly occur?

A

Blood filled space around a vessel after trauma/perforation.

Femoral artery puncture during angioplasty/angiography.

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