Mitral Valve Infective Endocarditis with Vegetations MCQ — NEET PG Practice Question | NEETPGAI
Mitral Valve Infective Endocarditis with Vegetations
medium
microscope Pathology
A 46-year-old intravenous drug user with rheumatic mitral valve disease presented with 3 weeks of fever, night sweats, and progressive dyspnea. Blood cultures grew Staphylococcus aureus. Transoesophageal echocardiography showed a 1.6 cm mobile vegetation on the mitral valve with severe regurgitation, and he underwent urgent valve replacement. On examination of the explanted valve specimen, the structure marked **A** is most characteristic of which pathological process in infective endocarditis?
A. Enzymatic degradation of collagen by neutrophil elastase leading to leaflet perforation
B. Deposition of fibrin, platelets, and bacterial colonies on the valve surface with minimal inflammatory response
C. Calcification and fibrosis of the valve leaflet secondary to chronic rheumatic disease
D. Immune complex deposition with granulomatous inflammation in the valve tissue
Explanation
Why "Deposition of fibrin, platelets, and bacterial colonies on the valve surface with minimal inflammatory response" is right
The structure marked A — large friable vegetations on the atrial surface of the leaflets — is the pathognomonic gross feature of infective endocarditis. According to Robbins and Cotran, these vegetations consist of fibrin, platelets, bacteria, and inflammatory cells deposited on the valve surface in a relatively non-inflammatory manner. The friable, bulky nature and atrial surface location (as opposed to the ventricular surface in rheumatic disease) are diagnostic hallmarks of bacterial endocarditis. The mobility seen on echocardiography reflects the loose, unorganized composition of these deposits. This patient's Staphylococcus aureus infection produced this classic vegetation morphology, which directly caused the flail segment and severe regurgitation necessitating valve replacement.
Why each distractor is wrong
Calcification and fibrosis of the valve leaflet secondary to chronic rheumatic disease: While this patient did have pre-existing rheumatic mitral disease, the acute vegetations seen at A are not calcified or fibrotic. Rheumatic changes are chronic and would not produce the mobile, friable appearance characteristic of acute bacterial endocarditis. The worsening regurgitation over 3 weeks is due to superimposed infection, not rheumatic progression.
Enzymatic degradation of collagen by neutrophil elastase leading to leaflet perforation: Although tissue destruction does occur in endocarditis (seen at B with chordal disruption), the primary composition of the vegetations at A is not enzymatic degradation. The vegetations are primarily sterile deposits of fibrin and platelets with embedded bacteria, not a primary inflammatory infiltrate. Perforation is a secondary consequence, not the defining feature of the vegetation itself.
Immune complex deposition with granulomatous inflammation in the valve tissue: Immune complex disease and granulomatous inflammation are features of chronic endocarditis or other valve pathologies (e.g., systemic lupus erythematosus), not acute bacterial endocarditis. The acute vegetations in this case show minimal organized inflammatory response and are primarily composed of fibrin-platelet-bacterial deposits, not immune complexes or granulomas.
High-YieldNEET PG
Infective endocarditis vegetations are friable, non-inflammatory fibrin-platelet-bacterial deposits on the atrial surface of valve leaflets; they differ fundamentally from rheumatic vegetations (which are verrucous, on the closure line) and from immune-mediated valve disease.
Robbins and Cotran Pathologic Basis of Disease, 10th Edition, Chapter on the Heart
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