All of the following are true about rheumatic fever/ rheumatic heart disease except -
Ans. is 'a' i.e., Mitral stenosis is evident in the early stage of the disease Rheumatic fever/ Rheumatic heart disease* Rheumatic fever (RF) is an acute, immunologically mediated, multisystem inflammatory disease classically occurring a few weeks after an episode of group A streptococcal pharyngitis; occasionally, RF can follow streptococcal infections at other sites, such as the skin.* Acute rheumatic carditis is a common manifestation of active RF and may progress over time to chronic rheumatic heart disease (RHD), mainly manifesting as valvular abnormalities. RHD is characterized principally by deforming fibrotic valvular disease, particularly involving the mitral valve.* Distinctive lesions occur in the heart, called Aschoffbodies, consisting of foci of T lymphocytes, occasional plasma cells, and plump activated macrophages called Anitschkow cells (pathognomonic for RF). These macrophages have abundant cytoplasm and central round-to-ovoid nuclei (occasionally binucleate) in which the chromatin condenses into a central, slender, wavy ribbon (hence the designation "caterpillar cells").* During acute RF, diffuse inflammation and Aschoff bodies may be found in any of the three layers of the heart, resulting in pericarditis, myocarditis, or endocarditis (pancarditis).* Inflammation of the endocardium and the left-sided valves typically results in fibrinoid necrosis within the cusps or tendinous cords. Overlying these necrotic foci and along the lines of closure are small (1 to 2 mm) vegetations, called verrucae.* Subendocardial lesions, perhaps exacerbated by regurgitant jets, can 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 short- ening, and thickening and fusion of the tendinous cords. In chronic disease the mitral valve is virtually always involved.* The mitral valve is affected in isolation in roughly two thirds of RHD, and along with the aortic valve in another 25% of cases. Tricuspid valve involvement is infrequent, and the pulmonary valve is only rarely affected.* Up to 60% of patients with ARF progress to RHD.* Valvular damage is the hallmark of rheumatic carditis. The mitral valve is almost always affected, sometimes together with the aortic valve; isolated aortic valve involvement is rare.* Early valvular damage leads to regurgitation. Over ensuing years, usually as a result of recurrent episodes, leaflet thickening, scarring, calcification, and valvular stenosis may develop.* Therefore the characteristic manifestation of carditis in previously unaffected individuals is mitral regurgitation, sometimes accompanied by aortic regurgitation.* Myocardial inflammation may affect electrical conduction pathways, leading to P-R interval prolongation (first- degree AV block or rarely higher-level block) and softening of the first heart sound.
Mitral stenosis is evident in the early stage of the disease
Mitral valve is most commonly affected
Presence of antischkow cells is pathognomic
MacCallum plaques are commonly seen in left atrium
C.V.S.