Cardiovascular System Pathology PDF

PATHOLOGY OF CARDIOVASCULAR SYSTEM Developmental anomalies: Persistent right aortic arch (Vascular ring anomaly) Right aortic arch persists, resulting in displacement of esophagus & trachea to the left. Both trachea and esophagus become locked up in a vascular ring formed by...

PATHOLOGY OF CARDIOVASCULAR SYSTEM Developmental anomalies: Persistent right aortic arch (Vascular ring anomaly) Right aortic arch persists, resulting in displacement of esophagus & trachea to the left. Both trachea and esophagus become locked up in a vascular ring formed by arch of aorta, pulmonary artery, base of heart, and ligamentum arteriosum (or ductus arteriosus). This ring causes partial obstruction of trachea and/or esophagus. It has been reported in dogs, cats, cattle, and horses. Significant clinical signs include – dysphagia and regurgitation since the vascular ring encircles and compress the esophagus and trachea. At necropsy, portion of esophagus anterior to obstruction is usually dilated. Persistent right aortic arch Relations of the aorta, trachea, esophagus and other heart structures Patent ductus arteriosus: Ductus arteriosus is a short blood vessel which connects pulmonary artery to aorta in foetal life. Normally after birth this duct is sealed and remains in the form of a ligamentum arteriosum. Ductus arteriosus remains open and blood is shunted between aorta and pulmonary artery. It may lead to  Congestive heart failure  Pulmonary hypertension  Cyanosis due to mixing of venous and arterial blood.  Inter-ventricular septal defects: In foetal life, no partition in ventri- cles and there is only one chamber divided into two right and left by inter-ventricular septum. Inter-ventricular septum does not develop completely – mixing of blood from both chambers. It is responsible for thickening of myocardium, roughening of endo- cardium and cyanosis. Large patent interventricular septal defect in a two-month-old calf.  Inter-atrial septal defect: Incomplete partition of atrium. Continuous overload on right side of heart leading to pulmonary hyper- tension and hypertrophy of right side myocardium. A small defect in septum may persist throughout the life of animal without causing any clinical illness. TRANSPOSITION OF THE GREAT VESSELS (Transposition of aorta) The aorta and pulmonary artery may be transposed. Aorta arising from right ventricle and pulmonary artery from the left ventricle (Abnornal). Arterial side of heart on the right and venous side on the left - No significant clinical signs are encountered. However, if aorta originates from the venous side and pulmonary artery from the arterial side, death occurs. (Create problems when aorta arises from venous ventricle and pulmonary artery from arterial side). Transposition of Great Arteries Tetralogy of Fallot (TOF or “Tet") is a complex condition of several congenital defects that occur due to abnormal deve- lopment of fetal heart during the first 8 weeks of pregnancy. These problems include the following: Pulmonary stenosis. Ventricular septal defect. An overriding, dextraposed aorta (that receives blood from both the left and right ventricles). Right ventricular hypertrophy (which is secondary to the other defects). Tetralogy of Fallot has been reported in dogs, cats, horses, and cattle. Affected animals are stunted and mucous membranes are cyanotic – increased pulse & respiratory rates and a murmur is heard. “Blue babies” in case of humans.  Above the large membranous ventricular septal defect is an overlying, straddling aorta (Ao). There is also severe pulmonic stenosis (arrow) with massive right ventricular hypertrophy. Ectopia cardis: Literally, "heart in the wrong place”. Heart lies outside the thoracic cavity – usually under the subcutaneous tissue of lower cervical region or in the abdominal cavity. Most frequently seen in cattle. Usually secondary to sterna cleft or failure of thoracic cavity to close normally. Some animals can survive for several days to months. Dextrocardia - Heart is on the right side rather than the left. Acardia – complete absence of heart. Diplocardia – presence of two hearts. HYDROPERICARDIUM Accumulation of excess serous fluid in the pericardium. It is caused by those factors responsible for generalized and/or local edema. The volume of fluid varies greatly. The rate at which fluid accumulates is important. If fluid accumulates rapidly, pericardium is placed under considerable tension (generalized venous congestion). However, when fluid accumulates slowly, there is time for the pericardium to stretch and adapt. Most diseases of pericardium are secondary to diseases – in the heart, lungs, pleura, and other sites in the body. HEMOPERICARDIUM Accumulation of pure blood in the pericardial sac. The condition is uncommon in animals except in the following instances: Following cardiac punctures. Spontaneous rupture of the intrapericar- dial aorta in horses. In uremic dogs with ulcerative atrial endocarditis. Following rupture of the coronary artery. CARDIAC TAMPONADE refers to compression of the heart subsequent to accumulation of any fluid within pericardial sac.  INFLAMMATION OF THE HEART PERICARDITIS: Inflammation of both parietal and visceral surfaces of pericardium characterized by accumulation of exudates (serous, fibrinous or suppurative) within the sac. Causes- Almost always infectious  Infectious agents- by blood stream (haematogenous) or lymphogenous usually reach by extension from surrounding structures and/or  Trauma- traumatic pericarditis, bullet wounds etc.  Depending upon the exudates- 1. Fibrinous Pericarditis Characterized by an accumulation of fibrin within the pericardial sac. Exudation of fluid is not a prominent feature. Grossly,  Pale yellow fibrinous or sero-fibrinous exudates deposition on pericardial surfaces and pericardial sac (adhesion leads to shaggy heart/bread-butter appearance /cor rugosum) Microscopically,  infiltration of inflammatory cells and RBCs in the fibrinous meshwork. Congested pericardium Etiology- Blackleg, pasteurellosis, contagious bovine pleuropneumonia, sporadic bovine encephalomyelitis, and some forms of neonatal coliform infections.  2. Purulent Pericarditis Characterized by accumulation of pus in pericardial sac. It occurs most commonly as a result of traumatic perforation by a foreign body originating from the reticulum (TRP). Also, in traumatic pericarditis the exudate may be fibrinous or fibrino-purulent in nature. Pus within the pericardial sac may appear as a thin cloudy exudate, as creamy exudate, or as a purulent exudate. The accumulation of pus – tension on the pericardium (congestive heart failure). In both fibrinous and purulent pericarditis, healing is usually by organization. Ultimately, adhesive pericarditis. Thus, considerable pressure is exerted, and heart muscles become more or less rigid (constrictive pericarditis). Purulent Pericarditis 3. Traumatic Pericarditis Occurs in cattle as a result of traumatic perforation of pericardium by a foreign body originating in the reticulum (traumatic reticulitis). Ingested foreign bodies enter reticulum; pierce wall of the reticulum, overlying peritoneum and diaphragm – enter the thoracic cavity. Subsequently the foreign body may enter the pericardial sac (as well as the myocar- dium and endocardium) resulting in an exudative pericarditis).  ENDOCARDITIS Inflammation of the endocardium. Etiology/ Occurrence: Chronic septicemic diseases caused by Actino -myces pyogenes, Erysipelothrix rhusiopathae, Staphylococci, Streptococci, Pseudomonas aeruginosa and Clostridial infections. Gross changes: Lesions in heart valves or wall of atrium/ventricles. Presence of thrombi on endocardium. Vegetative/cauliflower like growth on endocardium either in valves (Valvular vegetative endocarditis e.g. Swine erysepalas) or in wall (Mural vegetative endocarditis). Dilation of heart chambers. Microscopic changes: Infiltration of thrombocytes, neutrophils, macrophages and lymphocytes. Masses of bacterial organisms can be seen. Underlying endocardium and myocardium shows the presence of fibrin network and infiltration of RBC, neutrophils & macrophages.  Exuberant valvular endocarditis in a cow’s tricuspid valve (large thrombi that appear adhered to the cusps block the blood flow between the right atrium and the right ventricle. On the right, note that the left heart chambers exhibit milder lesions of mitral valve endocarditis). Vegetative endocarditis in a cow.  MYOCARDITIS Inflammation of myocardium, the middle layer of heart. It may be suppurative, eosinophilic or lymphocytic depending on the type of exudate. Etiology: Toxins/Poisons; Bacteria/Virus; Parasites; Drugs/Chemicals Gross changes: Dark red or cyanotic due to accumulation of blood. Abscesses in myocardium – yellow / green pus oozes out. Yellowish white streaks of necrosis in myocardium. Presence of cyst encapsulated by fibroplasia (cysticercosis). Microscopic changes: Hyperemia and hemorrhages in myocardium. Infiltration of neutrophils, eosinophils or lymphocytes. Coagulative necrosis of muscle fibers. In chronic cases, proliferation of fibrous connective tissue.  Myocarditis  MYOCARDITIS Inflammation of the myocardium, usually secondary to a wide variety of systemic diseases (Hematogenous). The lesions are usually focal and may be overlooked on causal gross inspection. Suppurative myocarditis: Associated with presence of pyogenic organisms, abscess formation is common. Eosinophilic myocarditis: Characterized by an infiltration of eosinophils in the myocardium. Condition is occasionally observed in cattle, and cause is unknown. In addition, an eosinophilic myocarditis is observed in animals given excessive amounts of sulfonamides and occasionally in penicillin hypersensitivity. Parasitic myocarditis: - May be caused by a variety of parasites.  HEART FAILURE Inability of heart to maintain adequate blood supply – death. Myocardium is no longer able to compensate for increase in workload. “Congestive Heart Failure” is the clinical syndrome – charac- terized by pulmonary and/or generalized venous congestion and low cardiac output. Subsequently, retention of sodium and water (decreased renal flow and adrenal cortical mechanisms). This further distends the venous bed – heart delivery? Clinical signs – secondary effects of a failing circulation. Lesions - most prominent and extensive in the lungs and liver. Ability of heart to respond to circulatory demands over and above those of animal at rest is referred to as cardiac reserve. Any cardiac lesion which impairs the efficiency of the heart reduces the cardiac reserve. When cardiac reserve is exhausted and circulatory require- ments at rest can no longer be met - "congestive heart failure"  Acute cardiac failure Sudden failure of contraction of the heart leading to death within minutes. Etiology: Anoxia; Drugs/poisons; Shock Cardiac temponade; Myocardial necrosis Sudden occlusion of aorta and/or pulmonary artery Gross changes: Cardiac temponade. Occlusive thrombus. Pulmonary congestion. Dilatation of heart particularly of right ventricle. Microscopic changes: Myocardial necrosis. Centrilobular necrosis in liver “nut meg liver”. In prolonged cases, congestion & oedema in visceral organs.  Chronic cardiac failure Inability of heart to maintain balance between its output and venous return of blood. It can be further divided into two: Left sided heart failure Right sided heart failure Left sided heart failure is caused by myocardial damage and characterized by congestion & edema in lungs with hypertrophy of alveolar lining cells. Right sided heart failure is caused by a disease of lungs or pulmonary vasculature and mostly occurs after a left sided heart failure.  LEFT SIDED HEART FAILURE Characterized by congestion and oedema in lungs with hypertrophy of alveolar lining cells. Etiology: Myocardial degeneration/ necrosis Aortic and mitral valve disease Hypertension Gross changes: Congestion and oedema in lungs Chronic dilatation of heart Microscopic changes: Congestion of alveolar vessels Oedema in lungs Hypertrophy of alveolar lining cells Alveolar macrophages contain hemosiderin pigment also called “heart failure cells”.  LEFT SIDED HEART FAILURE Clinical signs – primarily pulmonary (lungs), dyspnoea on exertion, cough, and orthopnea. Common causes: Myocarditis, Degeneration of the myocardium, Stenosis and insufficiency of the mitral and semilunar valves, and Congenital heart diseases. Progressive dilatation of the left ventricle and atrium which may be followed by left ventricular and atrial hypertrophy. Pulmonary (lung) congestion, edema, and induration ensue. Reduction in pulmonary vital capacity and impaired gaseous exchange result in hypoxic stimulation of the carotid sinus. Eventually, the right heart failure develops subsequent to increased pulmonary resistance and increased pressure in the pulmonary artery. Coughing in dog – most distinctive and alarming feature.  Left sided heart failure – Pulmonary congestion, edema and hemosiderin laden alveolar macrophages (heart failure cells) Right sided heart failure – Hepatic congestion, nutmeg liver and hepatic congestion (histology)  RIGHT SIDED HEART FAILURE Caused by a disease of lungs or pulmonary vasculature and mostly occurs after a left sided heart failure. Etiology: Left sided heart failure Pulmonary lesions, congestion Gross changes: Congestion of visceral organs Subcutis oedema and ascites Pulse in jugular vein Microscopic changes: “Nutmeg appearance” in liver due to centrilobular necrosis. Atrophy, necrosis and fibrosis in liver. Congestion in visceral organs.  RIGHT SIDED HEART FAILURE - Ascites (Hydroperitoneum) and Hydrothorax Generalized edema (Anasarca)  RIGHT SIDED HEART FAILURE Clinical signs of generalized venous congestion, include distension of jugular & other superficial veins, liver & spleen enlargement, accumula- tion of fluid in serous cavities and in tissues (generalized edema). Common causes: Left-sided heart failure, myocardial degeneration, myocarditis, factors that cause increased pulmonary resistance, hydropericar- dium, exudative pericarditis, endocarditis & defective tricuspid & semilunar valves. Progressive dilatation of right ventricle and atrium which may be followed by right ventricular and atrial hypertrophy. Blood accumulates in the vena cava – generalized venous congestion. Centrilobular congestion, degeneration, necrosis, and fibrosis of liver. Splenic red pulp becomes engorged, generalized edema (ascites, etc.). Eventually, right heart failure Generalized edema is a prominent feature In horse and cow, a dependent subcutaneous edema is expected Subcutaneous edema is scant or absent in other species. In dog, in peritoneal cavity (ascites), whereas in cat - in thorax (hydrothorax) Corpulmonale – heart failure due to lung disease.  BRISKET DISEASE (OR HIGH ALTITUDE DISEASE) A condition of slow cardiac failure, which occurs at 2500 meters sea level or above where pressure of air is low. Etiology: Low oxygen in environment. Decreased atmospheric pressure of air. In native cattle morbidity rate is only 2% and in imported cattle at hills it is up to 40%. Gross changes: Dilatation of heart Hypertrophy of ventricular wall Chronic passive congestion in visceral organs Oedema in sternal region in between forelegs Microscopic changes: Nut meg liver due to chronic passive congestion Polycythemia Hypertrophy of muscle fibers in myocardium Brisket disease (High altitude disease)  BRISKET DISEASE (OR HIGH ALTITUDE DISEASE) (High mountain disease/Pulmonary Hypertensive Heart Disease) Develops subsequent to chronic hypoxia that causes increased pulmonary vascular resistance and increased pulmonary arterial pressure. It is characterized by dilatation and hypertrophy of the right ventricle and atrium with the ultimate development of cardiac decompensation & signs related to "congestive heart failure". Affected cattle reside at usually above 7,000 feet. There is a failure of the cardio-respiratory system to adjust to the chronic anoxia. The disease usually develops slowly and generalized edema is a prominent feature. Edematous swelling in the ventral pectoral region is responsi- ble for the term "brisket disease".  BRISKET DISEASE (OR HIGH ALTITUDE DISEASE) Due to chronic venous congestion, liver lesions may vary from early "nutmeg" appearance to severe centrilobular fibrosis. Lungs exhibit varying degrees of atelectasis & emphysema. Microscopically, hypertrophy of media of small pulmonary arteries may be observed. Young cattle are more susceptible than adults. Morbidity rate is highest in animals exposed to high altitudes for the first time. In animals transported from low altitudes to about 10,000 feet, the incidence of severe pulmonary hypertension may not affect more than 2%.  Brisket disease (High altitude disease) Right side of heart (RVFW = right ventricular free wall) is markedly enlarged relative to left side (LVFW). In healthy animals, left side of heart wall is heavier than right, as it has to pump blood to entire body, with exception of lungs. Right side is lighter, since it only has to pump blood to lungs. In brisket disease, the extra workload on the right side of the heart causes that side to initially undergo get bigger. Eventually, this side of the heart fails. As a result of the right sided heart failure, blood backs up in the liver, causing the liver to enlarge. Fluid accumulates in the abdominal cavity (ascites). The liver has a characteristic reticulated pattern that resembles a cross-section of a nutmeg, hence the term "nutmeg liver", one of the hallmarks of brisket disease.  Mulberry heart disease It is characterized by firm contraction of heart and petechial hemorrhages on pericardium giving the appearance of mulberry. Etiology: Not known May be enterotoxemia / poisoning Gross changes: Contraction of heart with petechial hemorrhages on pericardium looking like mulberry “Mulberry heart disease”. Hydropericardium, hydroperitoneum and pulmonary oedema. Oedematous fluid has high protein content resulting in clot formation. Congestion of fundic portion of stomach. Microscopic changes: Congestion on serosa of visceral organs.  ARTERITIS Inflammation of arteries characterized by infiltration of neutrophils, lymphocytes and macrophages in the media and intima of arterial wall. Etiology: Chemicals; Thermal Virus e.g. Equine viral arteritis Pyogenic bacteria Parasite e.g. Strongylus vulgaris Gross changes: Hyperemia Conjunctivitis, oedema of eye Presence of thrombi in artery Microscopic changes: Thrombi in artery involving intimal layer. Equine viral arteritis virus causes infiltration of lymphocytes and macrophages in media. Occlusion of lumen of arteries due to thickening of wall. In parasitic arteritis, parasitic thrombi may be present along with inflammatory reaction in intimal layer.  ANEURYSM OF ARTERIES Aneurysm is dilation of an artery or cardiac chamber leading to formation of sac. An aneurysm is a pathological, more or less circumscribed, dilatation of an artery (or chamber of the heart). Arterial wall is composed of stretched intima and adventitia with only remnants of media. There is a tendency for aneurysms to enlarge progressively and to ultimately rupture. A false aneurysm is a blood-containing cavity that communi- cates with the arterial lumen – wall is formed from surroun- ding tissues. A dissecting aneurysm is characterized by the presence of blood between the layers of arterial wall (usually in media). Blood current gains access to a defect in media & resulting blood pressure forces blood for some distance between layers.  ANEURYSM OF ARTERIES Etiology: Aflatoxin; Infectious emboli Weak vessel wall due to rupture Fracture or necrosis of medial layer of large blood vessel. Arteriolosclerosis Gross changes: Fracture or necrosis of medial layer of large blood vessels permitting parallel blood circula- tion till next division of blood vessel is called as Dissecting aneurysm or False aneurysm. Formation of sac in the artery due to dilation “True aneurysm”. Microscopic changes: Rough intimal layer Wall of blood vessel damaged with inflammatory exudates. ARTERIOSCLEROSIS – hardening of the arteries. 3 types depending on their size and etiological factors: Atherosclerosis Medial sclerosis Arteriolosclerosis Atherosclerosis - hardening and thickening of intimal layer of large arteries and aorta due to proliferation of connective tissue, hyaline degeneration, infiltration of fat/lipids and calcification. These changes may lead to loss of elasticity of artery (Athere means mushy substance). Medial sclerosis involve medium sized muscular arteries and characterized by fatty degeneration and hyalinization of muscular tissue of medial arteries leading to necrosis. This is also known as Monckeberg’s medial sclerosis. Arteriolosclerosis affects arterioles in kidneys, spleen & pancreas and is characterized by hyperplasia of intimal cells of arterioles producing concentric lamellations occluding their lumen.  ATHEROSCLEROSIS Etiology: Exact cause is not clear Hypercholesterolemia and hyperlipidemia Hypertension Gross changes: Fatty streaks running parallel in the direction of the artery. Intimal layer of aorta/ coronary arteries is elevated due to plaques which are white/ yellow, fibrous and occluding the lumen of vessel. Occlusion of artery may lead to ischemia and infarction. Microscopic changes: Macrophages are filled with lipid droplets including cholesterol, fatty acids, triglycerides and phospholipids. Fragmented internal elastic lamina in the intimal layer of artery. Proliferation of altered smooth muscles may become metaplastic to macrophages. Deposition of mucoid ground substance and collagen fibres. Hyalinization of CT “ Fibrous plaques” Presence of fat droplets in between the lesion. Arteriosclerosis of Coronary Arteries and Small arteries  MEDIAL SCLEROSIS Etiology: Old age Excessive administration of epinephrine (adrenaline) Nicotine Vitamin D toxicity Hyperparathyroidism Gross changes: Hardening of medium sized arteries Hyaline, fatty changes and calcification of arterial wall Microscopic changes: Fatty changes, hyalinization of muscular layer of medium sized arteries. Necrosis of myofibrils Calcification  ARTERIOLOSCLEROSIS It affects arterioles in kidneys, spleen and pancreas and is characterized by hyperplasia of intimal cells of arterioles producing concentric lamellations occluding their lumen. Etiology: Hypertension Gross changes: No characteristic macroscopic lesion Atrophy of organ, hardening Microscopic changes: Proliferation of cells present in intima of blood vessels Swelling and necrosis of cells in medial layer leading to occlusion of lumen Calcification in chronic cases Phlebitis – inflammation of veins characterized by presence of inflammatory exudate, thickening of wall & dilatation of lumen The condition is less common than arteritis. Acute phlebitis occurs in "naval infection"(omphalophlebitis) of calves, lambs and foals. The resulting bacteremia may lead to acute death or give rise to widespread suppurative lesions (abscesses). Etiology / Occurrence: Naval infection in calves Uterine infections In jugular vein due to improper intravenous infection. Varicose veins are dilated and elongated veins following irregular and tortuous course. Telangiectasis is marked dilation of veins particularly of sinusoidal capillaries in one or more lobules in liver. Varicose veins  PHLEBITIS Gross changes: Wall of vein is thickened Vein contain large thick necrotic material Lumen dilated Inner surface of vein is rough and hyperemic. Microscopic changes: Infiltration of neutrophils in wall of veins. Sometimes calcification may also present. Wall of vein becomes thick due to inflammatory cells and/or proliferation of fibrous tissue. Varicose Veins: Dilated and elongated veins are referred to as varicose veins. Such veins follow an irregular and tortuous course and hold an abnormally large amount of blood. Varicose veins are less common in animals than in man.  Lymphangitis Inflammation of lymph vessels characterized by aggregation of lymphocytes around lymphatics, edema of dependent parts and distension of lymphatics. In most instances, the involved vessels are so small as to have no significance. Lymphangitis is associated with several specific diseases. Anthrax in dogs, pigs & horses (acute thrombolic lymphan- gitis). Mycobacterium infections (granulomatous lymphadenitis) and cutaneous glanders of horses (ulcerative lymphangitis). Etiology/Occurrence: Corynebacterium ovis causes caseous lymphangitis and lymphadenitis; Equine epizootic lymphangitis.  Lymphangitis Gross lesions: Lymphatics are seen thickened, reddish streaks and painful to touch. Distension of subcutaneous lymph vessels, nodules of lymphoid aggre- gates. Oedema due to failure of lymphatic drainage. Nearest lymph glands that drain the area are inflammed, swollen and painful. Microscopic changes: Lymphoid aggregation around lymphatics. Lymphatics distended. Oedema of dependent tissue.