Heart Valve Disease Flashcards
Coaptation
When the heart valves come together.
Aortic valves ———– as you get older.
thicken. AKA fibrosis.
3 types of valvular heart disease.
1) Rheumatic Heart Disease
2) Infective Endocarditis
3) Non-infective Endocarditis
Saying about Rheumatic Fever
“RF licks the joints but bites the heart.”
How do you get RF (organism)?
You get infected with a beta-hemolytic (GAS) strep bacteria.
What are on the surface of the GAS strep bacteria?
An M protein and streptolysin (an exotoxin).
Why is the heart attacked in Rheumatic Fever?
Because the myosin and tropomyosin of the heart share the same M proteins as those found on the strep bacterial surface.
So the body’s antibodies attack the strep bacteria and also the heart muscle.
How does acute Rheumatic fever first present?
Pharyngitis then inflammation of the joints.
Clinical diagnosis of Rheumatic Heart Disease.
Jones criteria:
1) Rheumatic component.
2) Heart disease.
3) Recent GAS infection.
4) Polyarthritis
5) Skin lesions
Antibodies to the M protein on the strep bacteria ———— with M proteins on myosin and tropomyosin.
cross-react
Skin lesion associated with Rheumatic Fever/Heart Disease.
Erythema Marginatum
3 changes in the heart from Rheumatic heart disease.
(1) Vegetations
(2) Myocardial Aschoff bodies
(3) Fibrinous pericarditis
The look of the pericardium in rheumatic pericarditis.
Bread and butter appearance.
Aschoff Body
1) In acute Rheumatoid Fever.
2) Only in the heart.
3) Granuloma-like lesion.
4) Macrophages are present - called Anitschkow myocytes.
Caterpillar cell
AKA Anitschkow myocyte seen in Aschoff bodies.
Most important aspect of Acute Rheumatic Fever
Valvulitis.
Order of valves most to least affected
Mitral valve -> Aorta -> Tricuspid -> Pulmonary valves
Valvulitis of ARF
Verrucae (wart-like vegetations) seen on the valves.
Chronic rheumatic Valve Disease
Occurs years after having acute Rheumatic Fever. You get a deformed, thickened, fibrotic valve.
Signature lesion of Rheumatic Fever
Mitral stenosis
Difference between acute and subacute bacterial endocarditis.
In Acute, the valve was normal to begin with and gets damaged. In Subacute, the valve was already damaged, but can get damaged more.
Two types of bacterial endocarditis.
Acute and Subacute.
Who gets fungal endocarditis?
Drug users or immunocompromised hosts.
The organism that causes acute endocarditis.
Staph aureus.
The organism that causes subacute endocarditis.
Staph viridans.
What causes endocarditis?
Blood that is contaminated with bacteria gets to the heart and infects the valves, then the infected valves shed the bacteria to the body.
Sources of infection for endocarditis.
IV lines
Injection drug use
Dental procedures
Pathogenesis of endocarditis.
1) The endothelium is damaged.
2) Matrix and collagen is exposed.
3) Causes platelet aggregation and fibrin deposits on the valve.
Types of non-rheumatoid endocarditis
1) Infective
2) Non-Infective
Types of Infective endocarditis.
1) Acute
2) Sub-acute
Type of Non-infective endocarditis
1) Non-bacterial thrombotic endocarditis (marantic)
2) Atypical Verrucous endocarditis
Non-Bacterial Thrombotic Endocarditis (NBTE)
1) Often occurs in a hypercoagulable state.
2) Associated with malignant disease.
3) Often affects a normal valve.
4) Often spares (doesn’t damage) the valve.
5) Gives rise to emboli.
Marantic endocarditis AKA
NBTE
What doesn’t NBTE have?
NO INFLAMMATION OR BACTERIA. They’re STERILE deposits.
Vegetations are —— in NBTE.
Friable.
Most common need for valve replacement.
Aortic Stenosis.
Causes of aortic stenosis.
1) Rheumatic Fever
2) Aging
Aortic stenosis causes —– ——– hypertrophy.
left ventricular
_____ ______ is normal in aortic stenosis.
Serum calcium
Risk factor for arterial stenosis.
High LDL, males, smoking.
______ is related to stasis or endocardial injury.
Thrombosis.
Most common heart tumor in adults.
Cardiac myxoma.
Most common location of the cardiac myxoma.
Left atrium.
Cardiac myxomas can ________.
embolize
You’re not going to see these organisms in NBTE.
Neutrophils - because there’s no inflammation.
Blood culture in NBTE.
NEGATIVE BC THERE ARE NO BACTERIA!!!!!
Clinical features of infective endocarditis.
Fever Heart murmur \+ blood culture Known source of infection Evidence of emboli
Staph aureus causes.
Acute infective endocarditis. Affects normal valves.
Staph viridens causes.
Subacute infective endocarditis. Affects already-damaged valves.
Presentations of bacterial endocarditis.
Osler nodes
Janeway lesions
Splinter hemorrhages
conjunctival petechiae
Patients who are septic and have severe burns can become _________, thus making them predisposed to ________.
Hypercoagulable; NBTE
