QUESTIONS AND ANSWERS 149 



eases, valvular diseases, etc., tumors or adherent pericardium creat- 

 ing pressure from without, disease of the heart muscle itself. 



Lesions : increased volume and weight of the heart ; walls thick- 

 ened, hard and firm. 



What pathological changes may follow mitral stenosis? 



Hypertrophy of the left auricle, pulmonary congestion, hyper- 

 trophy of the right ventricle and right auricle ; pulmonary oedema, 

 bronchial catarrh and hepatic congestion. 



Describe the lesions of pericarditis. 



Acute form: fibrinous membranes on the pericardium; fluid 

 exudate, clear (or cloudy from pus), in varying amounts distends 

 the pericardial sac. Passive hyperemia of the lungs and liver and 

 cedematous infiltrations may occur. 



Chronic form: connective-tissue proliferation, thickening and 

 adhesions of the pericardial sac. 



What is the difference between active and passive congestion? 



Active congestion arises from an increase in the arterial supply 

 on account of the dilatation of the lumen of the blood-vessels to the 

 part. Passive congestion arises through a retardation or obstruc- 

 tion of the flow of blood from the veins and a passive yielding of 

 the vessel-walls to intravascular pressure. 



Define (a) embolism, (b) aneurism, (c) lymphangioma, (d) myocar- 

 ditis. 



(a) The plugging of a blood-vessel by a clot or obstruction 

 which has been brought to its place by the blood-current. 



(b) A sac formed by the dilatation of the walls of an artery and 

 filled with blood. It may be a true aneurism which contains one 

 or more of the coats of the artery, or a false aneurism in which all 

 of the coats are absent, the blood being retained by the surrounding 

 tissues. 



(c) A tumor composed of dilated Ijonphatic vessels. 



(d) Inflammation of the heart muscle. 



Discuss verminous aneurisms of the coeliac or mesenteric arteries of 

 the horse. 



They are due to the larvse of the sclerostoma equinum which 

 enter the blood-stream from the intestines, are carried to the coeliac 

 artery and enter the vasa vasorum of the same and cause infarction 

 in the media of the vessel, and then meso-arteritis, or peri- and 

 endarteritis. This leads to formation of a thrombus and narrowing 

 of the Itimen of the vessel, providing dilatation is not commensurate 

 with the diminution in calibre. The inflamed vessel-wall, losing its 

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