Valve Heart Disease Flashcards
Atrioventricular Valves
Tricuspid (r)
Mitral (l)
Semilunar outflow valves
pulmonary (r)
aortic (l)
Valve Function
Maintain unidirectional blood flow
Stenosis
Regurgitation
impaired forward flow
=incompetence
Allowing reversed flow
Can be pure or mixed
Common heart valve pathologies
mitral stenosis/regurg
Aortic stenosis/regurg
Ventricular abnormalities
Pathologies involving artificial valves
What can detect signs of valve pathologies
auscltation
Draw murmurs
…
Common pathogenic mechanisms in valvular heart disease
1) Developmental defects in CT (eg; marfans syndrome)
2) Calcification
3) Infection
4) Post-infection
5) Hypercoagulable states
6) Carcinoid tumours
Developmental Defects in the CT
Stenosis of pulmonary or aortic valve
Leaflet abnormalities (eg) bicuspid aortic valve)
Myxomatous degeneration of mitral valve
-may affect upto 4% adults (idiopathic)
-Occurs in Marfans and other CT disorders.
-Often symptomatic
-May increase risk of infective edocarditis &mitral insufficiency
Often leads to secondary damage
Developmental defects in CT: myxomatous mitral valve degeneration
“floppy” mitral valves
Mitral valve prolapse
Dystrophic calcification
- Can occur in local areas after extensive cell injury
- cumulative damage
- Initiates when dead/dying cells accumulate calcium (in mitochondria/ membrane-bound vesicles)
- propagates
Most common
1) annular calcification of mitral valve (‘ring’)
2) stenosis of aortic valve
sometimes secondary to developmental defects
Infection: “infective endocarditis”
Colonisation or invasion of heart valves by a microbe
-often after seeding blood with
microbes (surgery or IVDA)
Lesion = vegetations build up
Pathogens: bacteria, fungi, chlamydiae (a range)
“infective endocarditis” is divided into two types
- Acute: high virulence organisms, often previously normal valve, destructive, high mortality
- Sub-acute: Low-virulence organism, often previously abnormal valve. insidious
Post-infective: Rhuematic fever
- multi-system inflammation occurring week after nasopharyngeal infection by strp. pyogenes (grp A strep)
- Type II hypersensitivity reaction
- Immune response against strep may cross-react with heart antigens.
Symptoms and what it leads to: post -Infective rhuematic fever
-Can cause scaring and fibrosis of heart: valve veges, aschoff bodies and pericarditis
leads to ‘chronic valve deformities’ especially mitral stenosis
Predisposes infective endocarditis
Aschoff bodies
foci of oedematous CT surrounded by lymphocytes, plasma cells and macrophages.
In the myocardium, pale areas
Valve damage from rhuematic fever predisposes
Infective endocarditis
Hypercoagulable states
Thrombosis on a heart vavle, eg; NBTE, prosthetic valves
NBTE
Non-bacterial thrombotic endocarditis
- deposition of fibrin/platelets on heart valves
- No pathogens (so sterile) involved
- May occur if patient in hypercoagulable state due to an underlying cause (cancer/sepsis)
Can predispose to I.E
Carcinoid tumours
Range of neoplasms arising from neuroendocrine cells hormone producing) or their precursors
- secrete variety of bioactive substances > plaque-like thickenings (made of SM) on R heart
- Affect tricuspid and pulmonary
