L21- CVS Pathology III Flashcards
Valvular disease can be (1) or (2) in nature / development. Valvular disease results in either (3) or (4).
1/2- congenital, acquired
3- stenosis: failure to open completely, impeding forward flow
4- incompetence, regurgitation, insufficiency: failure of valve to close completely, allows reverse flow
acquired valve stenosis is the consequence of (1) and leads to (2) then (3)
1- chronic injury
2- fibrosis
3- calcification
acquired valve regurgitation is the consequence of (1) or (2) and can exist in a(n) (3) or (4) duration
1- intrinsic valve disease
2- damage to supporting structures
3/4- acute or chronic
list the signs and symptoms of mitral stenosis
Sxs: dyspnea (pulmonary edema), fatigue, hemoptysis (blood in sputum)
Signs: late low pitch diastolic murmur, crepitations in lung
list the signs and symptoms of mitral regurgitation
Sxs: dyspnea (pulmonary edema), palpitations, fatigue
Signs: pansystolic murmur radiating to axilla
list the signs and symptoms of aortic stenosis
Sxs: angina, syncope, CHF
Signs: ejection systolic murmur loudest at base and radiates to neck after S1
list the signs and symptoms of aortic regurgitation
Sxs: volume overload LHF
Signs: bounding pulses, early diastolic murmur, displaced apex beat
list the 5 common acquired valvular diseases
- rheumatic heart disease
- calcific aortic stenosis
- mitral valve disease
- endocarditis
- prosthetic valve disease
Rheumatic fever occurs as a result of (1) and mostly in (2) countries.
1- GAS infection (pharyngitis), about 3 wks after (3% of strep patients)
2- developing countries, economically depressed areas
In rheumatic fever, Igs are produced against (1) which will cross react with (2) areas in the body leading to (3) in those areas.
-(4) list the evidence that supports this hypothesis
1- M proteins (on GAS)
2- heart, joints, other tissues
3- inflammation
4- elevated ASO, anti-DNAase titers, Strep absent from lesions, Sxs develop 2-3 wks post-infection
list the 3 morphologies of acute rheumatic fever in the heart
Pancarditis: inflammation in all three layers of the heart
1) myocarditis
2) endocarditis (verrucous)
3) pericarditis (fibrinous pericarditis)
myocarditis is mostly evident by the presence of the following histologically….
- Paravascular Aschoff Bodies (in all 3 layers of heart): central zone of eosinophilic matrix infiltrated by T-cells, plasma cells, activated macrophages w/in CT of heart
- Anitschkow cells: wavy ribbon like chromatin (caterpillar cells)
endocarditis is mostly evident by the presence of the following histologically….
(verrucous)
- edematous and thickened valves with foci of fibrinoid necrosis
- multiple tiny 1-2 mm wart-like vegetations along lines of mitral valve closure (no effect on function)
describe acute rheumatic fever morphology in other places besides the heart
-Joints: chronic inflammatory infiltrate, edema in joints and periarticular soft tissues
-Erythema Marginatum: maculopapular rash
-Skin Nodules
(chorea)
(JONES: joints, ocular, nodules (skin), erythema marginatum, Sydenham chorea)
chronic rheumatoid fever usually involves (1) valves more than (2) valves
1- mitral, aortic
2- tricuspid, pulmonary
chronic mitral valvulitis is mostly evident by the presence of the following histologically….
(more frequent)
- irregular fibrous thickening and calcification of leaflets
- fusion of commissures and shortening of chordae tendinae => fixed narrow opening
- mitral stenosis and regurgitation
chronic aortic valvulitis is mostly evident by the presence of the following histologically….
- thickened, firm cusps adherent to each other
- valve orifice is reduced to rigid, triangular channel
describe the clinical features of acute rheumatic fever (besides timing of onset with GAS pharyngitis)
- Arthritis: migratory, large joints
- Carditis, pericardial friction rub, weak heart sounds, CHF
- Chorea: involuntary, purposeless, rapid movements
- Skin Changes
describe the clinical features of chronic rheumatic fever
Chronic Rheumatic Carditis:
- valvulitis, M > A > T > P murmurs
- cardiac hypertrophy and dilation
- CHF
- arrhythmias
- infective endocarditis
Jones Criteria for Rheumatic Fever diagnosis
(2 major OR 1 major, 2 minor)
Major: i) pancarditis, ii) subcutaneous nodules, iii) sydenham chorea, iv) migratory polyarthritis, v) erythema marginatum
Minor: fever, arthralgia, elevated ESR
AND preceding Strep, infection
Ca deposition will affect the (1) valve by depositing in the (2) of the valve, causing (3). It usually occurs in one of the following three situations: (4), (5), (6)
1- aortic
2- cusps, valve ring
3- stenosis / narrowing of aortic valve lumen
4- elderly, degenerative process (90% > 65 y/o)
5- congenital bicuspid aortic valve (1% of population, 40-50 y/o)
6- scarred result from rheumatic fever
Calcific aortic stenosis is the result of (dystrophic/metastatic) calcification. The leaflets will appear (2). The deposits are evident behind (3) and extending to (4). There is sometimes (5), a predisposition, but (6) is also usually evident as a result.
1- dystrophic
2- rigid, deformed (irregular calcified masses)
3- valve cusps
4- into sinus of Valslava –> coronary ischemia
5- congenital bicuspid aortic valve
6- marked LVH
describe the clinical features of calcific aortic stenosis
- Angina pectoris: inc requirements of hypertrophic myocardium
- Syncope: poor cerebral perfusion
- Death via CHF or arrhythmia
Mitral valve prolapse is usually discovered in (1) age group and is more common in (males/females).
There exists an intrinsic defect in (3) and can arise from as a complication from (4) hereditary disorder.
1- 20-40 y/o
2- females (7x)
3- connective tissue
4- Marfan Syndrome
In mitral valve prolapse the cusps will appear (1) and the valve leaflet will (2). The (3) are usually elongated and fragile, leaving (4) as a possibility. (5) may be dilated allowing (6). The tricuspid valve is involved in (7)% of cases.
1- soft, puffed up, rubbery 2- balloon into LA during systole 3- chordae tendinae 4- rupturing (severe cases) 5- mitral annulus 6- regurgitation 7- 20-40%
describe histological appearance of mitral valve prolapse
- thinning of fibrosa layer of valve + expansion of spongiosa layer
- excessive loose, edematous, faintly basophilic ground substance w/in middle layer of valve leaflets and chordae (myxomatous degeneration)
describe the clinical presentation of mitral valve prolapse
- most are asymptomatic
- palpitations, fatigue / atypical chest pain
- midsystolic click (abrupt tension on leaflets and chordae as valve closes)
- Severe complications (3%): mitral regurgitation, CHF, infective endocarditis, ventricular arrhythmia (=> SCD), thromboemboli => stroke
- Rarely scoliosis, high arched palate
Endocarditis in an infection of (1) or (2) resulting in formation of (3) termed (4) that will (5) the underlying cardiac tissue.
1- cardiac valves 2- mural surface 3- adherent, bulky mass of thrombotic debris and organisms 4- vegetations 5- destroy
Acute Endocarditis:
(1) original valve status
(2) extent of destruction
(3) causational organisms
(4) mortality
1- normal valve
2- highly destructive, fulminent (severe, sudden)
3- highly virulent organisms
4- high mortality even with antibiotics or surgery
Subacute Endocarditis:
(1) original valve status
(2) extent of destruction
(3) causational organisms
(4) mortality
1- abnormal valve
2- low destruction
3- low virulent organisms
4- most recover with appropriate therapy
list the predisposing factors for infective endocarditis
- pre-existing cardiac abnormality: rhematic valvular disease, mitral prolapse, congenital defects, degeneratice calcific aortic stenosis
- prosthetic heart valves (10-20% of cases)
- IV drug abuse (tricuspid valve)
- transient bacteremia (dental procedures, urinary cath., endoscopy
(1) is the most common causative organism of endocarditis
(2) is seen IV drug abuse
(3) is associated with colon cancer
(4) is another popular group
1- Strep. Viridans
2- S. aureus
3- Strep. Bovis
4- HACEK (hemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
list the Hemodynamic factors and Adherence properties of organisms involved in infective endocarditis
Hemo: abnormal blood flow across damaged valve –> endothelial injury –> focal deposition of platelets, fibrin
Adherence: fibronectin, adhesion factors like polysaccharides
Infective endocarditis usually affects (1) valves, and (2) valves in IV drug abuse.
1- mitral, aortic
2- tricuspid
(1) are the hallmarks of infective endocarditis, they are described as (2) lesions containing (3). (1) are prone to (4), which can lead to (5).
1- vegetations
2- friable, bulky, potentially destructive lesions
3- fibrin, inflammatory cells, bacteria
4- embolization
5- septic infarcts, abscesses, mycontic aneurysms
describe the gross and microscopic appearance of subacute endocarditis
Gross: vegetations are less friable, less valve destruction, ring abscesses are uncommon
Micro: granulation tissue, fibrosis, calcification, chronic inflammatory infiltrate
describe the clinical appearance of infective endocarditis
- fever (PUO- pyrexia of unknown origin)
- clubbing of fingers, splinter hemorrhages under nail beds
- Osler nodes: tender subcutaneous nodules
- Janeway lesions: nontender maculae on palms/soles
- Roth spots: retinal hemorrhages w/ clear center
-systemic embolism: stroke, distal organ infarcts
compare acute and subacute bacterial endocarditis
Acute:
- high grade fever, chills
- new cardiac murmur
- features of septicemia
Subacute:
- low grade fever, malaise
- changing cardiac murmur
- weight loss
- splenomegaly
diagnostic requirements for infective endocarditis
- duke criteria
- repeated blood cultures (aerobic, anaerobic organisms)
- echocardiography
describe treatment for infective endocarditis
difficult because valves are avascular, but longterm, IV antibacterial therapy is required
(1) endocarditis occurs in SLE patients and is characterized by (2) that result from (3). (4) and (5) are other special features.
1- Libman-Sacks
2- sterile vegetations
3- IC (immune complex) deposition
4- special predilection for lines of valve closure
5- able to extend towards ostia (opening) of coronary arteries
(1) endocarditis occurs in debilitated patients, and has (2) as an alternate name. It is characterized by (3) and is associated with (4). It will present as (5) and (6) are the possible complications.
1- nonbacterial thrombotic endocarditis (NBTE)
2- marantic endocarditis
3- sterile thrombi on leaflets (previously normal valves)
4- endothelial abnormalities, hypercoagulable states, adenocarcinomas
5- asymptomatic
6- embolism, infective endocarditis
describe the gross and microscopic appearance of NBTE
(nonbacterial thrombotic endocarditis)
Gross: multiple 1-5 mm nodules along closure line, non-invasive and destructive vegetations, commonly Mitral Valve
Micro: eosinophilic (fibrin) nodules with delicate layer of aggregated plateletsloosely attached to the cusp, no inflammation, no fibrosis
Describe the complications of prosthetic valve disease
Mechanical valve: thrombo-embolism, life long anticoagulation / bleeding, infective endocarditis, hemolysis, inadequate healing (paravalvular leak)
Tissue valve / Bioprostheses (porcine, bovine, human; no anticoagulation needed): less durable => matrix deterioration, rigidity, calcification –> stenosis; infective endocarditis, inadequate healing
