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Inflammation and Degeneration of Arteries Aneurism

vessel, blood, artery, walls, inner, formed and sac

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Inflammation of the inner coat of arteries is characterized by patches of thickening due to increased cell development. The thickened patches encroach on the channel of the vessel, and may block it. The disease depends in some cases on syphilis or other bad conditions of the system, such as defective diet, intemperance, over-exposure to cold, &e., would produce. Sometimes it is a consemence of other diseases.

The symptoms are mainly due to the ob struction to the flow of blood. Thus the part which is supplied by blood from the vessel will be improperly nourished, and may pass into gangrene (mortification) if the vessel be blocked. Where the blocking and inflammation are clue to a clot filling up the vessel, pain and tender ness are felt in the line of the vessel.

Degeneration is an accompaniment of in flammation. The cell growth of the inflamed patches breaks down into fatty material, and, if this be swept away by the current of blood, an ulcer is left on the inner coating of the vessel. If the degeneration has passed deeply into the substance of the wall of the vessel, that part will be seriously weakened, liable to stretch or burst, and thus aneurism may be produced. Atheroma is the term applied to this degenera tive change in an artery. Another form of de generation is the calcareous. Chalky material becomes deposited in thin plates in the inner coat of the vessel, and sometimes throughout the muscular coat of the wall of the vessel as well. The vessels lose their elasticity in con sequence, and become quite hard. In vessels that lie near to the surface the rigid tubes are easily felt by the finger, and clearly indicate what is going on.

Aneurism (Greek, aneuruno, to widen or dilate) is a pouch-like swelling or bulging formed in connection with an artery. The true aneurism is formed of a part of the wall of the artery which has been unable to resist the pressure of the blood within the vessel and has slowly bulged out. This usually happens in an artery that is the seat of fatty or calcareous degeneration, by which its walls have been weakened. The walls of the sac of the aneu rism are thus formed of the walls of the artery, but do not necessarily exhibit all the three coats possessed by a healthy artery (see p. 305). An

aneurism may be formed in connection with a vessel by rupture of the vessel occurring, through a diseased part of the wall, for ex ample. If the escaped blood is hemmed in by the tissues surrounding the artery, so as to form a sac, while, at the same time, the opening in the vessel remains as a means of communica tion, a false aneurism is formed. A wound from the outside may occasion aneurism in a similar way.

The causes of aneurism are thus disease of the arterial walls, diminishing their power to resist the pressure of blood from within, or injury of the vessel by violence from without. Strains, excessive and sudden muscular effort, &e., may lacerate the coats of an artery and so diminish its resistance as to lead to aneurism. Men are more liable to it than women, and it is chiefly a disease of advanced life, though it does occur in the prime of life.

The usual history of an aneurism is that, being caused by a yielding of the walls of the artery before the pressure of the blood, and that pressure being constant, the yielding is apt to continue, the more because, as the sac enlarges, its walls must become thinner. As it expands it exerts pressure on the tissues and organs which are in the neighbourhood. Some times, owing to the pressure, neighbouring parts become matted to its walls, and do something to prevent its bursting. Within the sac also changes take place. The inner surface is rougher than the usual smooth inner lining of a blood vessel, and the blood in the pouch may be more or less stagnant, depending on the size of open ing from the artery into the pouch. Both of these conditions tend to produce coagulation of the blood. Fibrin is separated from the blood and deposited on the inner surface of the sac. This often goes on till layer after layer of fibrin is formed. In such a way it is possible for the sac to become filled up, in time, by a mass of fibrin clot, and for a cure to be effected natu rally. Various causes, however, frequently co operate to prevent such a desirable result, and as a rule the aneurism enlarges, unless means are successfully adopted to prevent it.

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