Flashcards in Pathology of Valve Disease Deck (38):
3 layers of valve leaflets?
Fibrosa - on back (downstream) surface of valve, continuous with annulus fibrosa.
Spongiosa - central loose connective tissue.
Ventricularis - upstream side, rich in elastic fibers.
Are normal valves vascularized?
What's the "most important" etiology of aortic stenosis?
dystrophic calcification (wear and tear from old age)
What's the most important etiology of mitral stenosis?
chronic rheumatic heart disease
What is the most important etiology of aortic regurgitation?
dilation of the aortic root (old age, HTN, atherosclerosis, Marfan syndrome)
What are the 2 most important etiologies of mitral regurgitation?
Dilation of the mitral valve ring due to LV dilation from LV failure.
What increases rates of dystrophic calcification?
Turbulent blood flow... shares some risk factors with atherosclerosis, such as HTN.
Does dystrophic calcification cause valve leaflet fusion?
No, that's more a thing with chronic rheumatic heart disease.
Where do the nodules of dystrophic calcification of the aortic valve often protrude?
Into the sinus of Valsalva.... meaning... into the aorta.
What age range does dystrophic calcification usually become symptomatic, if the valve was previously normal? If the valve is congenitally deformed?
eighth to ninth decade.
Congenital deformations -> more wear and tear -> early symptomatic dystrophic calcification.
What's the deal with calcification of the mitral valve annulus?
Ususually in older women, associated with myxomatous degeneration.
It causes regurgitation.
When does chronic rheumatic heart disease have its onset, compared to the instance of acute rheumatic fever?
Occurs years to decades after acute rheumatic fever.
What changes happen to the valves in chronic rheumatic heart disease?
To the chordae tendinae?
Valves thicken, commissures fuse, and they become vascularized.
Chordae tendinae shorten, thicken, and fuse.
(and scarred valves are predisposed to infection)
Does chronic rheumatic heart disease produce stenosis or regurgitation?
It can cause either or both.
What does mitral stenosis from chronic rheumatic heart disease look like?
A fish mouth.
Complications of mitral regurgitation?
Increased pressure -> dilated LA.
Stasis in LA -> left atrial appendage thrombus.
What does chronic rheumatic heart disease look like histologically?
Bland fibrosis in the valves - the distinction between the 3 layers of the valve is lost.
What kind of remodeling of the LV does aortic regurgitation cause?
Eccentric (dilated) hypertrophy
4 causes of aortic regurgitation?
Dilation of the aortic root.
Perforation or tear of leaflet - (infectious endocarditis)
Retracted leaflet (chronic rheum. heart dis.)
Fixed leaflets (dystrophic calcification, or chronic rheum heart dis.)
Which valve does myxomatous degeneration usually affect?
Is it usually symptomatic?
The mitral valve, causing regurgitation.
It's usually asymptomatic
What does "myxomatous degeneration" mean?
Mucopolysaccharide deposition in spongiosa, attenuation of fibrosa.
Leaflets become floppy and "billow" i.e. prolapse into prior chamber (the LA).
4 "clinical lesions" of myxomatous degeneration? What are the outcomes of 2 these "lesions"?
(this is the vaguest use of the word "lesion" I have yet seen)
Asymptomatic "systolic click."
Mitral regurgitation - gradual from annulus dilation, or sudden from snapped chordae tendinae.
Thrombus formation -> embolus or endocarditis.
Dysrhythmia -> syncope or sudden death (unclear why).
Underlying myxomatous degeneration....
may be a genetic defect in connective tissue similar to that in Marfan's syndrome.
What does mitral regurgitation do to the lungs?
increased pressure backs up... -> venous congestion, alveolar edema, SOB, orthopnea
(can also then mess up the right heart)
What are 2 sequelae of chronic mitral regurgitation?
Fibrosis in pulmonary veins.
Changes in pulmonary arteries that increase resistance (concentric intimal thickening)...
leading to fixed pulmonary hypertension.
How does bacterial endocarditis happen?
Fibrin on a valve leaflet gives bacteria (or whatever else) a place to anchor, where they grow.
What's a non-cardiovascular complication of bacterial endocarditis?
Immune complex deposition.
Contrast acute from subacute bacterial endocarditis. (what causes it, who gets it, etc.)
Acute endocarditis: more aggressive bacteria (eg. S. aureus), can attack healthy heart valves, untreated is lethal within 6 weeks.
Subacute endocarditis: less aggressive bacteria (eg. Strep. viridians), usu. on previously damaged valves, untreated usu. isn't lethal before 6 weeks.
Valve-related conditions that predispose to bacterial endocarditis?
All the stuff we've talked about (dystrophic calcifcation, chronic rheumatic heart disease, myxomatous degeneration, congenital defects)... and artificial valves.
4 non-valve-related factors that predispose to bacterial endocarditis?
IV foreign bodies (e.g. catheters)
IV drug use (esp. right sided endocarditis)
3 sequelae of bacterial endocarditis?
Regurgitation from valve damage.
Emboli -> infarct. Or septic emboli -> abscess elsewhere.
How can endocarditis cause heart block?
If it damages / causes fibrosis of the conducting tracts that pierce the fibrous skeleton of the heart.
Why are immune complexes from endocarditis bad?
They can cause acute necrotizing glomerulonephritis.
Which bacteria really like prosthetic valves?
Which pathogens commonly cause endocarditis in IV drug users?
S. aureus, Candida, Aspergillus
What causes non-bacterial thrombotic endocarditis (NBTE)? (hint: it's not bacteria)
Valve damage in the setting of hypercoaguability (Virchow's triad met, e.g.)
Not caused by a pathogen - there are no bugs when you look at the histology of this stuff.
Examples of conditions that predispose to NBTE?
Mild disseminated intravascular coagulation (DIC), sepsis, burns, malignancies (esp. mucinous adenocarcinomas of the pancreas)