Pathophys of Valvular Heart Disease, Pathology of Acquired Valvular Disease Flashcards
Other than changes of stenotic valve, obstruction leading to aortic stenosis can occur via
above (supravalvular)
below (HOCM)
aortic stenosis etiology 50-60 y/o
bicuspid
aortic stenosis etiology 60-70 y/o
rheumatic
aortic stenosis etiology >70
senile degenerative
wall stress=
Pressureradius/2wall thickness
physical findings of AS
- small/delayed carotid upstroke
- late peaking systolic aortic murmur
- absence of S2
AS tx
mechanical problem –> surgery
Esp if…
- severe stenosis and symptomatic (including isolated systolic dysfunc/dec EF)
- AS and undergoing CABG
baloon valvuloplasty is suboptimal
aortic regurg primary valve etiology
congenital, rheumatic, endocarditis, trauma
aortic regurg primary aortic root dilatation etiology
rheumatoid syndromes, CMN, Marfan’s, atherosclerotic
aortic regurgitation pathophys
huge RDV allows for ejection of large SV to maintain forward SV –> asymptomatic for years
but eventually wall stress inc, EF falls–> fatigue/DOE –> CHF –> death
aortic regurgitation physical exam
- long loud diastolic murmur, Austin-Flint murmur
- bounding pulses
- wide pulse pressure
AR tx
-afterload reduction (nifedipine, ACE inhib) may slow LV deterioration
aortic valve replacement in AR, when to do
- for symptomatic pts with severe AR
- asymptomatic pts with chronic severe AR and LV systolic dysfunction
mitral stenosis etiology in adults
always rheumatic –> inflammation –> deformity and fibrosis of leaflets –> fusion of commissures and chordae –> Ca and stiffening
mitral stenosis eventual outcome
inc LAP, LA dilation
inc RV and RA dilation and failure from pulm HTN
–> nutmeg liver
mitral stenosis sx
- none for years
- DOE, fatigue
- sx inc w/ onset of afib
- later, w/ RHF –> edema, venous congestion
- emboli
mitral stenosis PE
- loud S1, opening snap
- low diastolic rumble
- RV enlargement
mitral stenosis therapy
early: diuretics, beta blockers
later: MVR, balloon MVP
mitral regurgitation
- ejection of portion of SV into LA (low pressure)
- chronic volume-overload of the LV
chronic MR
- rheumatic
- non-rheumatic (MVP, papillary m. dysfunction, endocarditis, LV dilatation, Marfan’s)
MR physical exam
- loud, holosystolic murmur. Apex to axilla
- dec S1
- S3 rumble
chronic MR tx
- afterload reduction and diuretics
- surgical soon after sx develop (prevents irreversible changes in LV, LA, pulm vasculature)
tricuspid/pulmonic stenosis
usu congenital, early sx
P overload on chamber prod to valve
tx: balloon valvuloplasty
tricuspid/pulmonic stenosis in adults
carcinoid syndrome
tricuspid regurgitation etiology
usually secondary to RV/annular dilation
endocarditis in IVDA
RV and RA dilatation
large V waves on PE
systemic venous congestion
large V waves on PE
tricuspid regurgitation
most comm cause mitral stenosis
rheumatic heart disease
most comm cause aortic stenosis
calcification
most comm valve abnormalities
calcific AS
MVP
calcific AS
one of the most comm valvular abnormalities
myxoid degeneration
MVP
rheumatic fever
heart/joints/skin/brain effets
group A beta hemolytic strep pharyngitis
cross rxn w/ glycoproteins
major criteria of rheumatic fever
- migratory polyarthritis of lg joints
- carditis (PANcarditis)
- subcutaneous nodules
- sydenham’s chorea
Jones’ criteria
minor criteria of rheumatic fever
- fever
- arthralgia
- acute phase reactants
- antistreptolysin O
- ESR
to dx rheumatic fever, need
2 major or 1 major + 2 minor
histo findings of rheumatic fever
Aschoff nodule (fibrinoid necrosis, inflammatory cells, HISTIOCYTES (aschoff giant cells) Anitschkow cells (caterpillar))
Aschoff
giant cells (histiocytes
Anitschkow cell
specialized macrophage
looks like caterpillar
inside Aschoff nodule
fish mouth
mitral stenosis
most common organism in infective endocarditis
- alpha hemolytic strep (VIRIDANS)
^less virulent
most common organism in infective endocarditis w/ IV drug use
staph aureus
HACEK organisms
- hemophilus
- actinobacillus
- cardiobacterium
- eikenella
- kingells
complications of infective endocarditis
- valve destruction
- ring abscesses
- suppurative pericarditis (neutrophils)
- septic emboli forming abscesses (brain, heart, spleen, kidneys, lungs)
non-infected endocarditis vegetations
- nonbacterial thrombotic endocarditis (NBTE)
2. Libman-Sacks endocarditis (SLE)
nonbacterial thrombotic endocarditis (NBTE)
- hypercoaguable states
- other malignant
- debilitation, burns, sepsis, in-swelling venous catheter
Libman-Sacks endocarditis (SLE)
- 1-4mm single or multiple sterile verrucous vegetations (typically UNDERSURFACES aka inflow tract of mitral valve)
- fibrinoid material within and HEMATOXYPHIL bodies (macrophages or neutrophils which have phagocytksed nucleus of injured cell)
