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Clinical Pathology > Cardiovascular Disease 3 > Flashcards

Cardiovascular Disease 3 Flashcards

1
Q

What is endocarditis & its 2 main forms?

A
  • Inflammation of the endocardium
  • Prototypical lesion= vegetation on valves
  • Infective & non-infective
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2
Q

What are the 2 main types of non-infective endocarditis?

A
  • Non bacterial thrombotic endocarditis

- Endocarditis of SLE (Libman-sacks disease)

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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
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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
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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
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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
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7
Q

Which bacteria commonly infects prosthetic valves?

A

Coagulase-negative staph e.g s.epidermidis

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8
Q

If Strep Bovis present in infectious endocarditis what is this a sign of?

A

Bowel malignancy

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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
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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
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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)
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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
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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
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14
Q

Describe Libman-Sacks endocarditis

A
  • Associated e/systemic lupus erythematosis

- Mitral & tricuspid valves affected (small sterile pink warty vegetations, single/ multiple)

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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
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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
Q

What are clinical features&complications of pericarditis?

A
  • Sharp central chest pain
  • Pericardial friction rub
  • Fever
  • Leucocytosis
  • Lymphocytosis
  • Complications: pericardial effusion/cardiac tamponade
26
Q

What is myocarditis?

A
  • 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
Q

What are the causes of myocarditis?

A
  • 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
Q

What is vasculitis?

A
  • Inflammation of the vessel walls

- Clinical features depend on vascular bed

29
Q

Use Chapel Hill nomenclature to classify the types of vasculitis

A
  • Large vessel V: aorta, arteries
  • Medium vessel V: arteries
  • Small vessel V: arterioles, capillaries, venuoles, veins
30
Q

What is giant cell arteritis?

A
  • 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
Q

Describe the morphology of giant cell arteritis

A
  • Intimal thickening: reduces lumenal diametre
  • Med. granulomatous inflammation: elastic lamina fragmentation
  • Multinucleated giant cells
32
Q

What are the clinical features of giant cell arteritis and how is it treated?

A
  • 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
Q

What types of aneurysms are there?

A
  • 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
Q

What are the causes of acute arterial occlusion?

A

-Acute=Rupture/thrombosis of an atherosclerotic plaque, embolus from the heart or aorta, aortic dissection, acute compartment syndrome

Clinical Pathology (56 decks)

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