. The elements of pathological histology with special reference to practical methods . ctivechanges in the valve not so considerable. For this reason the issueof this form of the disease is either not fatal at all or only at alate stage, when the bacteria may be already dead. When minute particles are torn from the thrombotic deposits by theblood-current, they commonly give rise, if caught in terminal arteries,to infarctions, which are of the simple hccmorrhagic or antemic A^arietyonly when the particles are free from bacteria, but otherwise {, ifthe particles torn off contained pyococci)
. The elements of pathological histology with special reference to practical methods . ctivechanges in the valve not so considerable. For this reason the issueof this form of the disease is either not fatal at all or only at alate stage, when the bacteria may be already dead. When minute particles are torn from the thrombotic deposits by theblood-current, they commonly give rise, if caught in terminal arteries,to infarctions, which are of the simple hccmorrhagic or antemic A^arietyonly when the particles are free from bacteria, but otherwise {, ifthe particles torn off contained pyococci) change into mere collections of bacteria break loose from the deposits REGENERATIVE CHANGES 197 on the valves, or, at all events, particles so minute that they do notstick until they reach the capillaries, in which case quite small andmore rounded metastatic foci form as a result. (See also Thrombosisand Emholism, p. 208 et seq.) If the endocarditis does not cause death before the heisfht of theprocess is reached, regenerative changes set in (Fig. 97). There are. Fio. 97.—Endocarditis Verrucosa in Process of Healino. x 330. (Alum cochineal.)o, Valve thronabus ; h, Small round cells; c, Larger epithelioid cells (fibroblasts). then found in the deeper parts of the valve, besides small mononuclearcells, larger epithelioid or spindle-shaped elements, which togetherwith the newly-formed blood-vessels (derived from those already exist-ing in the valves or neighbouring myocardium) form an embryonictissue which invades the necrotic parts of the valves and thethrombotic deposits, and finally replaces them. As it eventuallychanges into a connective tissue which becomes progressively poorerin cells and firmer, it produces the well-known thickenings, adhesionsand shrinkages of the valve-curtains and chordae tendineae, whichmay lead to insufficiency of the valvylar apparatus. The phase ofthe process last described is termed by many chronic endocarditis,under which desi
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Keywords: ., bookcentury1800, bookdecade1890, booksubjectpatholo, bookyear1895
