pictures: endocarditis

Question 1

Answer 1

ballooning seen with mitral valve prolapse

Question 2

Answer 2

annular calcifications seen with normal age or “wear and tear” calcification of the valves. does not effect function of valve but can be a site for thrombus formation

Question 3

Answer 3

annular calcifications of the mitral valve seen in normal aging or wear-and-tear

Question 4

Answer 4

calcific aortic stenosis

1. Calcific aortic stenosis
   
   1. Most common valve abnormality
   2. Prevalence increases with age (usually manifest at 60-80 years)
   3. “wear and tear” associated with chronic HTN, hyperlipidemia, inflammation
   4. Bicuspid valves show an accelerated course
   5. Affected valves contain osteoblast-like cells, which deposit an
   6. osteoid-like substance → ossifies
   7. Mounded calcifications in cusps prevent complete opening of the valve
   8. Pressure overload hypertrophy, CHF

Question 5

Answer 5

1. Calcific aortic stenosis
   
   1. Most common valve abnormality
   2. Prevalence increases with age (usually manifest at 60-80 years)
   3. “wear and tear” associated with chronic HTN, hyperlipidemia, inflammation
   4. Bicuspid valves show an accelerated course
   5. Affected valves contain osteoblast-like cells, which deposit an
   6. osteoid-like substance → ossifies
   7. Mounded calcifications in cusps prevent complete opening of the valve
   8. Pressure overload hypertrophy, CHF

Question 7

Answer 7

1. Mitral valve prolapse: image shows where leaflets fling back and cause atrial endocardial disruption; harmless, but can become a site for infection or thrombus formation
   
   1. Valve leaflets prolapse back into LA during systole
   2. Affects 2-3% adults in US, with a 7:1 F:M, usually incidental (mid systolic click)
   3. Leaflets become thickened and rubbery, due to proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption
   4. May also occur as a complication of other causes of regurgitation (dilated hypertrophy)

Question 8

Answer 8

1. myxomatous degeneration
   
   1. ​elastic fiber disruption leading to Mitral valve prolapse
   2. Valve leaflets prolapse back into LA during systole
   3. Affects 2-3% adults in US, with a 7:1 F:M, usually incidental (mid systolic click)
   4. Leaflets become thickened and rubbery, due to proteoglycan deposits (myxomatous degeneration) and elastic fiber disruption
   5. May also occur as a complication of other causes of regurgitation (dilated hypertrophy)

Question 9

Answer 9

Aschoff bodies (RHD): arrows pointing to macrophages “caterpillar cells”

Question 10

Answer 10

1. Cardiac features of acute RF:
   
   1. Pancarditis, featuring Aschoff bodies
   2. Inflammation and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)
   3. Repeated streptococcal infections will cause these features to recur
   4. Chronic RHD: mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinous cords, resulting in mitral stenosis
   5. LA enlargement → atrial fib/thrombosis; pulmonary congestion/RHF

Question 11

Answer 11

1. “fish mouth” fusion of bicuspid, sequela of acute RHD during acute RF
2. Cardiac features of acute RF:
   
   1. Pancarditis, featuring Aschoff bodies
   2. Inflammation and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)
   3. Repeated streptococcal infections will cause these features to recur
   4. Chronic RHD: mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinous cords, resulting in mitral stenosis
   5. LA enlargement → atrial fib/thrombosis; pulmonary congestion/RHF

Question 12

Answer 12

1. Neovascularizarion of fused valves due to repeated inflammation and repair
2. Cardiac features of acute RF:
   
   1. Pancarditis, featuring Aschoff bodies
   2. Inflammation and fibrinoid necrosis of endocardium and left-sided valves, with verrucae (vegetations)
   3. Repeated streptococcal infections will cause these features to recur
   4. Chronic RHD: mitral leaflet thickening, fusion and shortening of commisures, fusion and thickening of tendinous cords, resulting in mitral stenosis
   5. LA enlargement → atrial fib/thrombosis; pulmonary congestion/RHF

Question 13

Answer 13

1. Infective endocarditis
   
   1. An infection of valves and endocardium
   2. characterized by vegetations consisting of microbes and debris, associated with underlying tissue destruction.
   3. Acute infective endocarditis is a rapidly progressing, destructive infection of a previously normal valve
   4. Requires surgery in addition to antibiotics
   5. Subacute infective endocarditis is a slower-progressing infection of
   6. a previously deformed valve (such as in chronic RHD)
   7. Can often be cured with antibiotics alone

Question 14

Answer 14

1. “ring abscesses” seen in infective endocarditis
2. Infective endocarditis
   
   1. An infection of valves and endocardium, characterized by vegetations consisting of microbes and debris, associated with underlying tissue destruction.
   2. Acute infective endocarditis is a rapidly progressing, destructive infection of a previously normal valve
   3. ◦ Requires surgery in addition to antibiotics
   4. Subacute infective endocarditis is a slower-progressing infection of
   5. a previously deformed valve (such as in chronic RHD) ◦ Can often be cured with antibiotics alone

Question 15

Answer 15

1. Nonbacterial thrombotic endocarditis
   
   1. Small, sterile thrombi on cardiac valve leaflets, along the line of closure
2. May be a source of emboli
3. Associated with
   
   1. malignancies
      
      1. especially mucinous adenocarcinomas
   2. sepsis, or catheter-induced endocardial trauma

Question 16

Answer 16

1. Nonbacterial thrombotic endocarditis
   
   1. Small, sterile thrombi on cardiac valve leaflets, along the line of closure
2. May be a source of emboli
3. Associated with malignancies (especially mucinous adenocarcinomas), sepsis, or catheter-induced endocardial trauma