Aschoff nodules are characteristically seen in: (Repeat)

Ans: A (Rheumatic carditis) Ref: Robbins Pathologic Basis of Disease, 8th edition, Pg: 529Explanation:Rheumatic Fever (RF)MorphologyDuring acute RF, local inflammatory lesions are found in various tissues.Distinctive lesions occur in the heart, called Aschoff bodies, which consist of foci of lymphocytes (primarily T cells), occasional plasma cells, andPlump activated macrophages called Anitschkow cells (pathognomonic for RF) with abundant cytoplasm and multiple central round-to ovoid nuclei in which the chromatin is disposed in a central, slender, wavy ribbon (Hence, also known as "caterpillar cells").During acute RF. diffuse inflammation and Aschoff bodies may be found in any of the three layers of the heart, causing pericarditis, myocarditis, or endocarditis (pancarditis).Inflammation of the endocardium and the leftsided valves typically results in fibrinoid necrosis within the cusps or along the tendinous cords.Overlying these necrotic foci are small (l - to 2- mm) vegetations, called verrucae. along the lines of closure.These vegetations place RHD within a small group of disorders that are associated with vegetative valve disease, each with its own characteristic morphologic features.Subendocardial lesions, perhaps exacerbated by regurgitant jets, may induce irregular thickenings called MacCallum plaques, usually in the left atrium.The cardinal anatomic changes of the mitral valve in chronic RHD are leaflet thickening, commissural fusion and shortening, and thickening and fusion of the tendinous cords.In chronic disease the mitral valve is virtually always involved.The mitral valve is affected alone in 65% to 70% of cases, and along with the aortic valve in another 25% of cases.Tricuspid valve involvement is infrequent, and the pulmonary valve is only rarely affected. Because of the increase in calcific aortic stenosis and the reduced frequency of RHD. rheumatic aortic stenosis now accounts for less than 10% of cases of acquired aortic stenosis.Fibrous bridging across the valvular commissures and calcification create "fish mouth" or "buttonhole" stenoses.With tight mitral stenosis, the left atrium progressively dilates and may harbor mural thrombi in the appendage or along the wall, either of which can embolize.Microscopically, in the mitral leaflets there is organization of the acute inflammation and 'subsequent diffuse fibrosis and neovascularization that obliterate the originally layered and avascular leaflet architecture.