Pathological Anatomy - 1 Lecture # 7

Haemodinamic disorders. Notion about general and local haemodinamic disorder, their interrelation, classification. Morphology of acute and chronic insufficiency. Lecture # 7 PLAN: 1. 2. 3. 4. 5. 6. 7. Kinds of haemodinamic disorders. Hyperemia (active congestion). Congestion (passive venous congestion). Ischemia & infarction. Oedema. Morphology of acute and chronic insufficiency. Hemorrhage.

HYPEREMIA (Active Congestion) Increased blood volume caused by dilatation of arterioles is called hyperemia. The affected part becomes redder due to engorgement with oxygenated blood. Causes of local hyperemia Physiological (I) Sympathetic neurogenic mechanism as in blushing. (2) Increased muscular activity during exercise. Pathological (I) Inflammation. (2) Poisons & toxins. (3) Angioneurotic disorder. (4) Collateral blood supplying. (5) Post anemic. (6) Due to increasing of barometric pressure. (7) Due to formation of arterial-venous fistula. CONGESTION (passive venous congestion) It is an increased volume of blood resulting from impaired venous drainage. The affected tissue becomes bluish (cyanosed) due to accumulation of deoxygenated hemoglobin. Local acute venous congestion: It occurs due to sudden obstruction of the venous return e.g. venous thrombosis and strangulation of hernia.

Pathological Anatomy - 1 Lecture # 7

Local chronic venous congestion: It is caused by prolonged gradual obstruction of veins caused by enlarged lymph nodes or tumor compressing the veins, it may occur in case of portal hypertension. General acute venous congestion: It occurs in acute heart failure in which there is raised venous pressure and overdistension of the viscera e.g. acute hepatic and pulmonary congestion in acute heart failure. General chronic venous congestion: It occurs in chronic heart failure resulting in chronic congestion of viscera such as liver and lungs. Chronic venous congestion of lung Causes Chronic left ventricular failure (left sided heart failure). Mitral stenosis. Macroscopic features Lungs are tougher in consistency than normal and color of the lungs becomes brownish. This condition is called brown induration of the lungs. Microscopic features (a) The alveolar septa are thickened and fibrotic. (b) Small hemorrhages are present within the alveoli. (c) The lungs show abundant evidence of previous hemorrhages because alveoli are filled with macrophages containing hemosiderin. These hemosiderin containing macrophages are called "heart failure cells, which give the lung its brown colour. Chronic venous congestion of liver Causes: (a) Chronic right ventricular failure. (b) Hepatic vein obstruction. Macroscopic features Enlargement of liver. Microscopic features (a) Central region of hepatocyte becomes congested while peripheral region is uncongested appearing yellow. This red and yellow mottling gives the liver a characteristics appearance called "nutmeg liver". (b) There is centrilobular necrosis of hepatocytes. (c) In severe and long standing heart failure hepatocytes becomes fibrotic, this condition is called "cardiac cirrhosis".

Pathological Anatomy - 1 Lecture # 7

Chronic venous congestion of spleen Causes: (a) right heart failure (b) Portal hypertension in cirrhosis of liver. Macroscopic features Enlargement of spleen, it deeply congested, tense, cyanotic. Sectioned surface is gray tan. Microscopic features (a) Red pulp shows congestion & marked sinusoidal dilatation with areas of recent & old haemorrhages. (b) Deposits of haemosiderin pigment & calcium salts on fibrous connective tissue & elastic fibres. Chronic venous congestion of kidney Macroscopic features Kidneys are slightly enlarged and the medulla is congested. Microscopic features (a) Tubules may show degenerative changes like cloudy swelling & fatty change. (b) The glomeruli may show mesangial proliferation. Heart failure Occurs when the ventricular muscle is incapable of maintaining a circulation adequate for the needs of the body producing symptoms on exercise & at rest. Right Ventricular Failure It results from increased hydrostatic pressure in the venular ends of systemic capillaries. This increased hydrostatic pressure pulls the fluid out of the vessels into the interstitial space resulting in edema of dependent parts of the body. Left ventricular failure When there is left ventricular failure alone, the retained water tends to accumulate in the lungs because of increased pulmonary venous pressure (called pulmonary edema). The pulmonary edema also develops in renal failure, adult respiratory distress syndrome (ARDS), pulmonary infections and hypersensitivity reactions. EDEMA Accumulation of excess fluid in the interstitial tissue spaces or body cavities is called edema.

Pathological Anatomy - 1 Lecture # 7

Depending on the site, collection of fluid in the different parts of the body cavities is designed as: - Hydrothorax. Collection of fluid in pleural cavity. - Hydropericardium: Excessive fluid in pericardial sac - Hydroperitonium (also called ascites): Collection of fluid in peritoneal cavity. - Anasarca the severe and generalized edema producing marked swelling of all tissues and organs in the body particularly in the subcutaneous tissue is called anasarca. Edema mechanism: Leaky vessels inflammation. Increased capillary hydrostatic pressure Venous obstructions Cardiac failure Decreased Osmotic pressure Hypoproteinemia liver disease, anemia. Lymphatic obstruction Elephantiasis TYPES OF EDEMA (1) Localized edema. (2) Generalized edema. Localized edema Causes of localized edema are: a) Increased vascular permeability due to inflammatory or allergic reactions. b) Impaired venous drainage due to thrombosis or compression of veins by external pressure (due to tumor, surgical dressing). c) Obstruction of lymphatics by inflammation or radiation. Generalized edema Causes of generalized edema are: a) Cardiac failure. b) Constrictive pericarditis. c) Renal diseases e.g. nephrotic syndrome and glomerulonephritis. d) Liver cirrhosis. e) Protein malabsorption, starvation. f) Toxemia of pregnancy.

Pathological Anatomy - 1 Lecture # 7

Kinds: Cardiac edema Renal edema Edema of hypoproteinemia ISCHEMIA (isch- is restriction, hema or haema is blood) is a restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue. Acute ischemia leads to dystrophya & necrosis. Chronic ischemia leads to athrophy of parenchyma & sclerosis of stroma. INFARCTION An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage or both in a particular area. CAUSES: Thrombi and emboli in 99% of cases. Local spasm of the artery. Extrinsic compression of a vessel by tumor. Traumatic rupture of the artery. TYPES: According to contamination Septic infarct. Bland or aseptic infarct. WHITE OR PALE INFARCT This type of infarct usually occurs: a) In solid organs e.g. heart, spleen, kidney. b) Due to arterial occlusion. RED OR HEMORRHAGIC INFARCT This type of infarct usually occurs: a) in loose tissue (e.g. lung) that allows blood to collect in the infarcted zone. b) Due to venous occlusion or both arterial and venous occlusion.

Pathological Anatomy - 1 Lecture # 7

c) In tissues with double circulation e.g. lung and small intestine in which blood flow continues to the infarcted area from unobstructed vessel giving the red or hemorrhagic appearance, (but this amount is not sufficient to rescue the ischemic tissue). d) When blood flow is re-established to a site of previous arterial occlusion and necrosis (by drugs or surgical procedure). MORPHOLOGY OF INFARCT 1. There is ischemic coagulative necrosis of the affected area (except brain). 2. All infarcts, red and white tend to be wedge shaped, with the occluded vessel at the apex and the periphery of the organ forming base. 3. In solid organs, the relatively few extravasated red cells are lysed and the released hemoglobin is converted to hemosiderin giving the colour of the infarct pale. In spongy organs, hemorrhage is so extensive that the infarct cannot become pale. Instead it becomes more brown with time. 4. An inflammatory response begins to develop along the margin of infarcts within a few hours and is usually well defined within 1 or 2 days. 5. Ischemic necrosis in CNS results in liquefactive necrosis (not coagulative necrosis). 6. Septic infarctions may arise when embolization occurs by a fragment of a bacterial vegetation from a heart valve or when bacteria seed an area of necrotic tissue. In these cases the infarct is converted into an abscess. HEMORRHAGE Rupture or laceration of a blood vessel with extravasation of blood is called hemorrhage. Etiology of hemorrhage Localized causes: (a) Trauma (b) Abnormality of vessels due to aneurysm, arteriosclerosis and local vascular infection (c) Necrosis and rupture of the heart (d) Neoplastic (cancer) invasion Generalized causes. (a) Defects of coagulation mechanism in diseases such as hemophilia, hyperprothrombinemia, and hypofibrinogenemia. (b) Platelet abnormalities such as purpura and thrombocytopenia (c) Vascular abnormalities which may be allergic (anaphylaloid purpura) or hereditary (telangiectasis). Clinical features

Pathological Anatomy - 1 Lecture # 7

Clinical features depend on amount of blood loss, rate and site of the hemorrhage. 1. Larger or more rapid loss of blood may result in hypovolemic shock. 2. Small amount of hemorrhage is not lethal in soft tissues while could be lethal in brain. 3. Chronic blood loss may result in iron deficiency (essential for new RBC production) resulting in anemia. Important definitions (a) Hematoma: A localized collection of blood within a tissue is called hematoma. (b) Petechiae: Smaller hemorrhage in skin and serous membrane up to 1 mm is called petechiae. (c) Purpura: hemorrhage from 1 mm to l cm is called purpura. (d) Echymosis: Large bruise. (e) Hematemesis: vomiting of blood. (f) Hemoptysis: Expectoration of blood from respiratory tract. (g) Melena: Blood in feces. (h) Hematuria: Blood in urine.