المرحلة الثالثة م. هالة عباس ناجي Ischaemia It means local anemia, it is characterized by a decrease amount of blood in an organ or region. Causes of Ischemia: *1.External pressure upon an artery e.g: by a rapidly growing neoplasm. *2.Narrowing of the lumen of an artery as in case of artery sclerosis or verminous thrombosis and embolism of the branches of the anterior mesenteric artery in the horse. The effect of the decreased amount of blood in a region depend on the following: 1.The degree of occlusion of the affected blood vessel. 2.The rate of closure. 3.The amount of anastomosis. 4.The kind of tissue affected. 5.The size of the occluded vessel. Some of the main arteries of limbs have proportionally small anastomotic connections. The sudden occlusion of one of these vessels result in a sever ischemia in the part, while the gradual occlusion of such vessel by atheroma causes no ill effect because there is time for the development of efficient collateral circulation. The result of sudden embolism or thrombotic occlusion of an end artery or an artery which has poor collateral anastomosis is sudden ischemia of the involved tissue and it's consequent necrosis or infarction.
Infarction It's an area of coagulative necrosis due to a sudden ischemia as a result of the sudden obstruction of the arterial supply to the area. Pathogenesis:- As an embolus or thrombus occludes an end artery the stagnated blood soon becomes deficient in oxygen and loaded with carbon dioxide and other waste products of cell metabolism. This luck of nutrition and accumulation of waste products are injurious both of the part involved. The damage of the capillary wall permits edema and hemorrhage to occur. The paranchymatous cells become swollen, granular and the nuclei gradually lose their characteristic staining reaction. Further degenerative changes then occur in the cell elements. They undergo necrosis and their cytoplasm appears coagulated. In this type of necrosis, the cells and the tissues retain their form and relative position ( coagulative necrosis). The necrosis begins in the center of the area within 24 hrs. after the onset and extends towards the periphery. At the same time, changes occur in the blood. The erythrocytes become haemolysed and the hemoglobin is removed by leucocytes. The area assumes a pale or anemic appearance. The dead tissue give rise to toxic substances which in turn induce an inflammatory reaction in the surrounding tissue. The zone is characterized by dilated capillaries and a collection of leukocytes ( line of demarcation). The blood pigment aggregate together at the margin in the form of haematoidin crystals, giving a yellow colour to the capsule of the infarct. The necrotic cells in the infarct gradually undergo autolysis and disappear. Newly formed connective tissue replaced them.
Varieties of Infarcts: There are 2 types:- 1. Red or hemorrhagic infarct. 2. Pale, anemic or white infarcts. The infarcts are filled with blood while in the white ones the blood carpusles never get beyond a thin peripheral zone, leaving the bulk of the lesion with pale colour. It's said that all infarcts are hemorrhagic before disappearance of blood cells by autolytic processes, usually 2 or 3 days. Infarcts of dense solid organs as the kidney appears always anemic, those in the previous tissue of lung are always hemorrhagic. Macroscopic appearance: 1. Most infarcts, particularly those of the spleen, kidney, lungs and brain are cone shaped, with the apex at the point of embolism or thrombosis and with the base at the surface of the organ. 2. In early stages, the area is swollen and dark red due to distention of the capillaries with blood. After 48 72 hrs. it becomes pale with a red margin. This is the result of the necrosis and inflammatory border. Infarcts of different organs: SPLEEN: an infarct of spleen appears as ale, red in colour at first, then dark red when hemorrhage occurs. On section, the infarct appear triangular in shape. The infarct takes a long time to lose the hemoglobin of red cells and to turn yellowish white in colour. In late stages, fibrosis occurs in the infarct. All structure details of the pulp and lymphoid follicles are lost, and extensive interstitial hemorrhage can be seen. HEART: 1. The cardiac infarct is caused by the occlusion of the coronary artery.
2. The infarct heals by fibrous replacement. 1. The affected muscle fibers appear swollen and granular. 2. The striations are lost. 3. The fibers stain more deeply acidophilic. LUNG: 1. The cause is emboli brought in via the pulmonary artery. 2. The pulmonary infarcts are always hemorrhagic. LIVER: Because of it's double blood supply, infarcts of the liver are rare and always if happened, hemorrhagic. KIDNEY: 1. The infarct appears on the convex border as a pale red cuboidal area which is raised on the surface and is surrounded with zone of congestion. 2. On section, the infarct is seen to be wedge like or triangular in shape. 1. A pink area of structurless degenerating or necrotic tissue is seen. 2. The epithelium of the secreting tubules soon degenerates, the cells swell and the nuclei lose their staining reaction. Termination of Infarction: 1. If exposed to the invasion of saprophytic bacteria which gangrene results. 2. If invaded by pyogenic organisms, abscess will be formed. 3. A small infarct undergoes autolysis and thus it's liquefied material gets absorbed and removed gradually and then replaced by fibrous tissue. 4. A large infarct which fails to be removed becomes encapsulated by fibrous tissue and it's dead material may become the scot of dystrophic calcification.
Oedema or Edema Odema mean the pathological accumulation of fluids in the tissue spaces, serous cavities, pulmonary alveoli or inside cells. Odema may be localized or generalized: *In localized oedema: the total amount of fluids in the body is within the normal limits, but because of a localized pathological process, the distribution of the body fluids goes along and an abnormal quantity of it gets retained in the tissue involved. *In generalized Odema: the total amount of fluids in the body increases and thus the body weight shows a daily increase. - when edema is sever and generalized and causes swelling of the subcutaneous tissues it's called: ( anasarca). - collection of edema fluid in peritoneal cavity known as : (ascites). - in the pleural cavity : (hydrothorax). - in the pericardial sac : ( hydropericardium or pericardial effusion). - accumulation of fluid in tunica vaginalis or testicles called: ( hydrocele). The edema fluid is non inflammatory and is referred to as a transudate which differ from edema as in this table: Exudate ( inflammatory edema) Transudate (non-inflammatory edema 1. Cloudy 1.Clear. 2. Thick, creamy and contain tissue 2. Thin, watery, resembles lymph and not fragments. contain tissue fragments 3. May have an odor. 3. No odor. 4. Acidic. 4.Alkaline 5. Colour: white, yellow or red. 5.color like watery or pale yellow. 6. Specific gravity: 1.020. 6.specific gravity : 1.012
7. High protein content. 7.Low protein content. 8. Coagulate. 8.Dose not coagulate. 9. High cell count (RBC,WBC) 9.Low cell count. 10. High enzyme content. 10.Low enzyme content. 11. Bacteria may be present. 11.No bacteria are present. 12. Associated with inflammation. 12.No association with inflammation. Causes of Oedema: 1. Increase hydrostatic pressure: this may result from an impaired venous return, this occurs in general or local passive hyperemia. 2. Reduced plasma osmotic pressure: results from excessive loss or reduced synthesis of serum albumin. In cattle and sheep: this occurs as a result of heavy infestation with trichostrongyles ( stomach worm) and either intestinal parasites, also in renal injury, liver diseases and starvation. 3. Lymphatic obstruction: result from inflammatory or neoplastic obstruction. It's also observed when tumors or thrombi are found within lymphatics or lymph nodes parasites. 4. Sodium and water retention: failure to excrete sodium in the urine resulting in water retention dose lead to generalized edema. Which occur in congestive heart failure, nephrosis and nephritis. Pathogenesis: Oedema is the result of an increase in the forces that tend to move fluids from the intravascular compartment into the interstitial tissue spaces. The exchange between intravascular and interstitial compartment is governed by Sharling's forces. According to sharlings hypothesis, the normal fluid balance is maintained by two opposing sets of forces, namely, vascular hydrostatic pressure and plasma osmotic pressure. Fluids moves from intravascular to the interstitial
compartment at the arteriolar end of the microcirculation largely under the influence of the hydrostatic pressure. It returns to the intravascular compartment at the venular end mainly because of osmotic pressure. Macroscopically: The edematous part is swollen, increased in weight and if external, cold temperature of extremities is lower than normal because of the suppressed rate of flow of blood in the area. Color is less intense than normal and pain is absent. The swollen tissue has a firm and doughy consistency. It pits on pressure: meaning that if finger is pressed into the edematous tissue, then finger is removed, the pit remains for a moment. The spaces between adjacent cells, fibrils or other structures are enlarged. During life, they were filled with fluid, they may contain a finely granular material that stains pink with eosin. Atrophy of the paranchymatous cells and fibrosis occur in the area.