Cardiovascular Disease 3 Flashcards
(34 cards)
1
Q
What is endocarditis & its 2 main forms?
A
- Inflammation of the endocardium
- Prototypical lesion= vegetation on valves
- Infective & non-infective
2
Q
What are the 2 main types of non-infective endocarditis?
A
- Non bacterial thrombotic endocarditis
- Endocarditis of SLE (Libman-sacks disease)
3
Q
Describe infectious endocarditis
A
- Clinically serious
- Colonization/invasion of heart valves or chamber by a microbe
- Vegetations= mixture of thrombotic debris &organisms, destroy underlying cardiac tissue, aorta, aneurysmal sacs, blood vessels, prosthetic valves infected
- Mainly bacterial some fungi
4
Q
What are the types of infective endocarditis?
A
- Acute=nasty, infect healthy valve, caused by highly virulent organisms, necrotizing, ulcerative, destructive lesions, difficult to cure, death frequent
- Sub-acute= organisms of lower virulence, less destructive, insidious infection of deformed valves, cured with antibiotics
5
Q
How does infective endocarditis occur? Are there any risk factors?
A
- Normal heart
- Rheumatic disease
- RF: cardiac/valvular abnormalities, MV prolapse, artificial valves, valvular stenosis, bicuspid AV, congenital defects
6
Q
How does an infection get to the heart?
A
- Bacteria in bloodstream (IVDU, wounds, bowel cancer, dental abnormalitites)
- Strep viridans from mouth
- S. aureus from skin
7
Q
Which bacteria commonly infects prosthetic valves?
A
Coagulase-negative staph e.g s.epidermidis
8
Q
If Strep Bovis present in infectious endocarditis what is this a sign of?
A
Bowel malignancy
9
Q
What does the vegetation look like in acute infective endocarditis?
A
- Friable
- Bulky
- Potentially destructive
- Single/multiple more then one valve
- Can erode myocardium leading to abscess
- Emboli contain large no. virulent microbes= septic infarct
10
Q
What are the clinical features of infective endocarditis?
A
- Fever: rapidly developing
- Chills
- Weakness
- Loss of weight/flu-like symptoms
- Murmurs: left sided IE
11
Q
What are signs and complications of IE?
A
- C= immunologically mediated conditions (glomerulonephritis)
- S= Splinter haemorrhages, Janeway lesions (erythematous non-tender lesions on palms & soles), Osler’s nodes (Subcut nodules in digits), Roth spots (retinal haemorrhage)
12
Q
Describe non-infective endocarditis
A
- Occurs in debilitated patients (cancer/sepsis)
- Associated with hypercoagulable state (DVT, PE mutinous adenocarcinomas)
- Part of trousseau syndrome of migratory thrombophlebitis
- Endocardial trauma/ indwelling catheter
13
Q
What are the vegetations like in NBTE?
A
- small sterile thrombi on valve leaflets
- Single/multiple on line of closure of leaflet/cusp
- Not invasive, no inflame reaction, minimal local effect
- Systemic emboli: infarcts in brain, heart
14
Q
Describe Libman-Sacks endocarditis
A
- Associated e/systemic lupus erythematosis
- Mitral & tricuspid valves affected (small sterile pink warty vegetations, single/ multiple)
15
Q
What are Aschoff bodies?
A
- Distinctive cardiac lesions
- Foci of T-cells, plasma cells & macrophages
- Found in all 3 cardiac layers
- Diagnostic of rheumatic fever
16
Q
What are the pathological features of rheumatic fever?
A
- Vegetations=veruccae
- Classical mitral valve changes
- Mitral stenosis
- Leaflet thickening
- Always involved in chronic disease
- Fibrous bridging of valvular commissures & calcification (fish mouth stenosis)
17
Q
How is rheumatic fever diagnosed?
A
- Evidence of strep infection
- Major criteria: Carditis, chorea, polyarthritis, subcut nodules
- Minor criteria: fever, arthralgia, prolonged PR intervals, previous RF
- Right ventricular hypertrophy
- LA dilates–> mural thrombi form–> embolise
18
Q
What are the causes of pericarditis?
A
- Infections: viruses (coxsackie B), bacteria, fungi, TB, parasites
- Immunological: rheumatic fever, SLE, scleroderma, late post-MI=Dressler’s
- Other: Early post-MI, surgery, trauma, radiation, neoplasia
19
Q
What are the forms of pericarditis?
A
- Acute: serous, serofibrinous, fibrinous, purulent/suppurative, caseous, haemorrhagic
- Chronic: adhesive, constrictive, adhesive mediastinopericarditis
20
Q
Describe serous pericarditis
A
- Inflammation causes serous fluid accumulation
- Caused by non-infectious: inflamed adjacent structures, rarely viral, neoplasia, radiation, uraemia, SLE, scleroderma, RF
21
Q
Describe serofibrinous/fibrinous pericarditis
A
- Serous fluid &/or fibrinous exudate in pericardial sac
- Most common form
- Acute MI, Dressler’s, uraemia, radiation, RF, SLE, trauma, surgery
- Dry, granular roughened surface
- More intense inflammatory response
22
Q
Describe purulent/suppurative pericarditis
A
- Red, granular, exudate & pus
- Inflammation can extend causing mediastina-pericarditis
- Resolution is rare
- Organisation by scarring leads to restrictive pericarditis
23
Q
Describe haemorrhagic pericarditis
A
- Blood mixed with serous or suppurative effusion
- Neoplasia, infections (TB), cardiac surgery–> cardiac tamponade
24
Q
Describe the types of chronic pericarditis
A
- Adhesive: fibosis/stringy adhesion obliterates pericardial cavity
- Constrictive: heart encased in fibrous scar, limits cardiac function, removed by surgery
- Adhesive mediastino: follows infection, surgery, radiation, obliterates pericardial cavity with adherence to surrounding structures causes cardiac hypertrophy/dilation
25
What are clinical features&complications of pericarditis?
- Sharp central chest pain
- Pericardial friction rub
- Fever
- Leucocytosis
- Lymphocytosis
- Complications: pericardial effusion/cardiac tamponade
26
What is myocarditis?
- Infective process leading to myocardial injury
- Infections (coxsackie A&B, chagas disease)
- Heart failure, arrhythmia, sudden death, mimic acute MI, fatigue, dyspnoea, palpitations, precordial discomfort, fever
27
What are the causes of myocarditis?
- Viruses: Coxsackie A&B
- Bacteria: C.dip, N. meningococcus, Lyme disease
- Fungi: candida, histoplasma
- Protozoa: Chagas disease
- Helminths: trichonosis
- Chlamydiae
- SLE
- Post strep RF
- Transplant rejection
- Drugs
- Giant cell myocarditis
- Sarcoidosis
28
What is vasculitis?
- Inflammation of the vessel walls
| - Clinical features depend on vascular bed
29
Use Chapel Hill nomenclature to classify the types of vasculitis
- Large vessel V: aorta, arteries
- Medium vessel V: arteries
- Small vessel V: arterioles, capillaries, venuoles, veins
30
What is giant cell arteritis?
- Most common form
- Affects elderly
- Chronic granulomatous inflammation
- Large to medium sized arteries
- In the head (vertebral, ophthalmic, temporal)
- Opthalmic artery can lead to permanent blindness so medical emergency
31
Describe the morphology of giant cell arteritis
- Intimal thickening: reduces lumenal diametre
- Med. granulomatous inflammation: elastic lamina fragmentation
- Multinucleated giant cells
32
What are the clinical features of giant cell arteritis and how is it treated?
- Facial pain or headache
- Transient loss of vision
- Jaw claudication in STA
- STA painful to palpate
- Corticosteroids generally effective
- Anti-TNF therapy in refractory cases
33
What types of aneurysms are there?
- Atherosclerotic (most common, usually AAA, rupture= retroperitoneal haemorrhage, emboli= limb ischaemia)
- Dissecting (thoracic aorta secondary to hypertension, progressive vascular occlusion & haemopericardium)
- Berry (young hypertensives, rupture=subarachnoid haemorrhage)
- Microaneurysm (Charcot-bouchard aneurysm in intracerebral capillaries in hypertensive disease= stroke, retinal in diabetes= diabetic retinopathy)
- False (blood filled space around vessel, haematoma)
- Mycotic (weakening of arterial wall secondary to bacterial/fungal infection, organisms enter media from vasa vasorum, often cerebral)
- Syphilitic (ascending aorta aneurysms
34
What are the causes of acute arterial occlusion?
-Acute=Rupture/thrombosis of an atherosclerotic plaque, embolus from the heart or aorta, aortic dissection, acute compartment syndrome
