PATHOLOGY SDL

A)Rheumatic Heart Disease:

Pathogenesis: Rheumatic heart disease results from
immune response to group A streptococci, which
happen to cross-react with host tissues. Antibodies
detected against the M proteins of streptococci have
been seen to cross-react with self antigens in the heart.
In addition, CD4+ T cells specific for streptococcal
peptides also react with self proteins in the heart, and
produce cytokines that activate macrophages. Damage
to heart tissue thus be caused by a combination of
antibody- and T cell-mediated reactions.
Morphology of Heart:
1) Distinctive lesions occur in the heart, called as
Aschoff bodies, consisting, foci of lymphocytes,
occasional plasma cells, and plump activated
macrophages called Antischkow cells. These
macrophages have abundant cytoplasm and
central round-to-ovoid nuclei in which the
chromatin is disposed, in a central, slender, wavy
ribbon, hence called as caterpillar cells.
2) Inflammation of the endocardium and the left
sided valves typically results in fibrinoid necrosis
within the cusps or along the tendinous cords.
 Overlying these necrotic foci are small
vegetations, called verrucae.
3) Subendocardial lesions, perhaps exacerbated by
regurgitant jets, may induce irregular thickenings,
called MacCallum Plaques, usually in left atrium.
B) Emphysema:
Types of emphysema:
There are four types of emphysema; centriacinar,
panacinar, paraseptal and irregular. Centriacinar
emphysema affects the alveoli and airways in the
central acinus, destroying the alveoli in the walls of
the respiratory bronchioles and alveolar ducts.
Panacinar emphysema affects the whole acinus.
Paraseptal emphysema is believed to be the basic
lesion of pulmonary bullous disease. Irregular
emphysema, so named because the acinus is
irregularly involved, is almost invariably associated
with scarring.
Pathogenesis: