COLOR ATLAS OF PATHOLOGY PDF

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Color Atlas of Pathology (Thieme ) - dokument [*.pdf] At a Glance 1 Fundamentals of Pathology 2 2 Cellular Pathology 6 3 Connective Tissue . who helped to make the Color Atlas of Anatomy a success. We are particularly of tissues Color Atlas of A Color Atlas of Forensic Pathology. This is a very practical atlas and guide that provides color photo- graphs of appropriate gross and his- tological patterns of various tumors of the central nervous.


Color Atlas Of Pathology Pdf

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حصريا تحميل كتاب color atlas of pathology مجاناً PDF اونلاين r nursus nikolaus riede:(Author n nThe pocket is an excellent reference work that presents . Book Reviews. Pathology: A Color Atlas, by Ivan Damjanov and James Linder,. pp, with illus, $, St Louis, Mo, Mosby (telephone: ), Pathology A Color raudone.info - Ebook download as PDF File .pdf), Text File .txt) or read book online.

Christ, Anat. Institut, Freiburg A-B Prof. Denk, Patholog. Freudenberg, Patholog. Hansen, Univ. Augenklinik, Freiburg 75D, 81F Dr. Hellerich, Patholog. Institut, Freiburg E Prof. Herbst, Patholog. Institut, Freiburg C Dr.

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Ihling, Patholog. Institut, Freiburg E,E, Prof. Koch, Patholog. Mall, Patholog. Institut, Darmstadt G Prof. Meister, Patholog. Mihatsch, Patholog.

AN ATLAS OF GENERAL PATHOLOGY

Mittermayer, Abt. Olah, Anatom. Peter, Abt. Rheumatologie, Univ. Rintelen, Univ. Rohrbach, Patholog. Institut, Freiburg 81A-B Prof. Saeger, Abt. Pathologie, Marienkrankenhaus Hamburg A Prof. Schaefer, Patholog.

Schlote, Neurolog. Schuppli, Univ. Spycher, Patholog. Staubesand, Anatom. Steinmann, Univ. Sterry, Univ. Stolte, Patholog. Institut, Bayreuth C Dr. Technau, Patholog. Torhorst, Patholog. Institut, Basel G, A W. Wiestler, Neuropatholog. Wittekind, Patholog. Institut, Leipzig A-D Prof. Wehner, Patholog. Wetterauer, Abt. Urologie, Univ. Yoshi, Mikrobiol.

Institut, Univ. Carruthers GB. The different types of malignant lymphoma and leukemia are the most frequent hematopoietic tumors. Characterization of tumor cell populations in companion animals is increasingly facilitated by immunohistochemical methods.

In several species e. Bone marrow, diaand metaphysis of femur. Red blood forming and yellow fatty bone marrow displaced bygelatinous andtranslucent material traversed bysmall blood vessels.

Atrophy of hematopoietic tissue dueto cachexia. Bone marrow, mid-diaphyseal area of femur. Increased number of immature myeloid cells myeloblasts and megakaryocytoblasts , few normoblasts. Leukocytosis dueto infection. Adult cat. Nitrate nitrite poisoning. Random, loosely arranged meshwork of delicate fibrin fibrils, after settling out and coagulation of stagnant blood.

In a neighboring vessel accumulation of leukocytes as a buffy coat between plasma and red clot. Concentrically arranged, densely packed aggregations of fibrin fibrils, deposited in flowing blood. The thrombus is attached to the damaged arterial wall,and is covered by a red clot. Pseudomembranous rhinitis. Surface of thrombus covered by endothelium. Formation of newcanals lined byendothelium allowing some blood flow. Many small hemorrhages. Defective hemostasis following immune-mediated destruction of thrombocytes by maternal antibodies in colostrum.

Although primary plug formation by platelets is impaired, coagulation isstill possible, preventing larger hemorrhages. Porcine thrombocytopenia purpura. Newborn piglet. Adrenal gland, sagittalsection. Extensive cortical hemorrhages dueto consumption of clotting factors and loss of platelets by disseminated intravascular coagulation DIC. Hemorrhages of similarsize may also be due to primary vascular damage e. Escherichia coli endotoxic shock.

Glomerular capillaries obstructed by hyaline microthrombi platelets and fibrin , causing oliguria or anuria. Protein casts in Bowman'sspace and mosttubules. Hyaline droplets, due to protein pinocytosis cf. Acute tubular necrosis often occurs during DIC see Fig.

Shock following experimental Trypanosoma bruce; infection. Mediastinal tumorcomposed of epithelial cells with non-tumorous lymphocytes. Network of large, pale staining, epithelial cells sometimes resembling stromal cells; mature lymphocytes in meshes.

Peripheral lymph node. Relative cell-poorcortical andparacortical areas containing increased numbers of hypertrophic macrophages several of which formed syncytial giant cells arrows. Circo-virus infection: Pig, 3 months. Lymph nodes, cut surface. Accumulation of erythrocytes in large peripherally located sinuses and paratrabecular sinuses, resulting in 'marbling',and indicating hemorrhage in the drainage area.

Classical swine fever. Color Atlas of Veterinary Pathology.

All rights reserved. Gruys J. We are much indebted to E. Pulmonary stenosis. Critical stenosis of a unicommissural valve in an infant. Dome-shaped acommissural valve. Rheumatic carditis is less common today than it was in the preantibiotic era. I-I I. Rheumatic Heart Disease Rheumatic fever is an immune-mediated systemic inflammatory disease related to sensitization of the body to beta hemolytic group A streptococci.

At higher magnification one can see that the Aschoff body is composed of macrophages. Rheumatic carditis in an active phase. Coarctation of the aorta is the most common form of congenital vascular obstruction Fig. Aschoff body composed of macrophages and lymphocytes is found in the interstitial plane of the myocardium. An active rheumatic fever causes typical lesions. It is associated with a V-shaped invagination of the aorta. They most often are found in the myocardium and the subendocardial connective tissue.

Even though rheumatic heart disease may involve all parts of the heart and is thus a pancarditis. Coarctation of the aorta. It often is associated with other cardiac anomalies. Aschoff bodies heal by scarring. In the granulomatous stage. Mitral valves Fig. Acute endocarditis presents with small translucent vegetations.

Deposits of fibrin and underlying inflammation may extend onto the left atrial parietal endocardium and less often onto the chordae tendineae or papillary muscles. Clinically chronic valvular changes present as stenosis or insufficiency. The deformed valves tend to calcify and become infected. Rheumatic valvulitis presents in the form of verrucous endocarditis characterized by the formation of tiny translucent nodules on the atrial side of atrioventricular valves and on the ventricular surfaces of semilunar valves Fig.

The valves. Higher magnification of the vegetation and the inflamed value. Acute rheumatic endocarditis. Histologically the vegetations are composed of fibrin covering the valve.

Within 6 to 8 weeks the valves contain relatively thick-walled blood vessels. Resolution of this inflammation results in scarring. The chordae tendineae become shortened. Histologically the lesion is composed of fibrin covering a valve that is infiltrated with mononuclear inflammatory cells.

Valvular infection is more common and clinically more important. The infected valves are covered with luscious. The vegetation consists of fibrin and bacteria.

II A B Fig. The valve is covered with large. Acute bacterial endocarditis. The valves are deformed fused and the orifice is stenosed. Infective Endocarditis Inflammation may involve the valves or mural endocardium. Chronic rheumatic endocarditis of mitral valve. It most often is caused by gram-positive bacteria such as Streptococcus pneumoniae and Staphylococcus aureus. Chronic rheumatic endocarditis of aortic valve.

View from the opened left heart. Stenotic orifice seen from the left atrium. Acute bacterial endocarditis superimposed on chronic healing endocarditis. Potential Complications of Infective Endocarditis Fig.

Infective endocarditis of immunosuppressed persons may be caused by uncommon bacteria and even fungi Fig. Valvular deformities and thickened chordae tendineae are evidence of the chronic process. Infective endocarditis affects valves of the left heart more often than those of the right heart. Fungal hyphae can be demonstrated in the vegetation by Gomori methenamine-silver stain.

Infective endocarditis with extensive destruction of the valve. Acute bacterial endocarditis superimposed on chronic rheumatic endocarditis. The arrow points to a microabscess formed in the central part of the vegetation. Factors that predispose to infection include congenitally deformed valves and preexisting valvular lesions such as those caused by rheumatic fever Figs.

Fungal endocarditis. Other complications of infective endocarditis are listed in Table The valve appears irregularly thickened and deformed.

Greatly thickened tricuspid valve and chordae show a whitish "onlay. Floppy mitral valve.

Chordae tendineae are variably thickened and focally fused. Small vegetations typically are found along the line of closure on otherwise normal valves Fig.

The greatest redundancy and gelatinous change are noted in the posterior leaflet to the right. Aortic insufficiency may result from the dilatation of the aortic valve annulus caused by a variety of diseases such as rheumatic fever. Nonbacterial thrombotic endocarditis. Floppy mitral valves are common but they rarely cause clinically significant changes unless they are associated with myxomatous transformation.

The valves are deformed by nodular calcifications within the cusps Fig. The line of closure is covered with fine uniform vegetations. In floppy valve syndrome the valve cusps expand.

Degenerative calcific aortic stenosis represents an agerelated lesion that typically is found in the elderly. Histologically the vegetations are composed of fibrin attached to a normal valve. Carcinoid heart syndrome.

It is characterized by fibrotic changes in the endocardium of the right ventricle. Histologically such vegetations resemble bland fibrin thrombi Fig. The tricuspid and pulmonary valves have focal or diffuse plaques of glycosaminoglycan-rich. Carcinoid heart disease is a complication of intestinal carcinoids metastatic to the liver.

The left ventricle also is involved in one third of patients examined at autopsy. Histologically it is classified descriptively according to the predominant cell type infiltrating the myocardium or the pattern of reaction.

Color Atlas of Veterinary Pathology

The calcific nodules are most prominent inside the cusps arrow. Pathogens rarely. Close-up view. I Focal endocardial thickening below the aortic valve is indicative of regurgitation. Degenerative calcific aortic stenosis. Myocarditis Inflammations of the myocardium are classified as 1 infectious.

Superior view of tricuspid. Similar case with more prominent calcification. The commissures are focally fused. Aortic insufficiency due to dilatation of the aortic root. The aorta has a thickened wall and its luminal surface is covered with fibrous plaques and focal ulcerative calcific changes.

Pathologically myocarditis is classified as acute or chronic. Giant cell myocarditis with multinucleated giant cell and neighboring macrophages stained brown with an antibody CD Giant cell myocarditis with multinucleated giant cells positive for muscle-specific a-actin monoclonal antibody staining.

Some of the giant cells in the same heart were derived from muscle cells. Active myocarditis of the predominantly lymphocytic type. Ventricular myocardium with myocarditis and clusters of cells immunoreactively identified as macrophages.

Ventricular myocardium with active myocarditis and myocytolysis arrows. The cytolysis is associated with an infiltrate of activated immune cells in a child with suspected viral myocarditis. Isolated myocytes are surrounded by the infiltrate in a background of what appears to be edema. Although this multinucleated cell is immunonegative.

The "punched-out" lesions of myocyte necrosis are best defined by lack of positive staining arrows with monoclonal antibody to muscle-specific a-actin. Microscopic appearances of myocarditis. Ventricular myocardium with influenza A-related myocarditis in a young child. It may present histologically as lymphocytic. Cardiac transplant rejection. Myocardium contains aggregates of neutrophils. Transplant rejection is accompanied by an immunemediated myocarditis Fig.

Chagas disease. Myocardial abscess caused by sepsis rarely contains identifiable bacteria Fig. Necrosis of cardiac myocytes is more prominent than the inflammatory infiltrate. Diphtherial myocarditis.

Myocardial cell necrosis with myophagocytosis in a patient with diphtherial pharyngitis is by inference classified as diphtherial. Myocytes contain Trypanosoma cruzi. Idiopathic myocarditis is the most common type of myocardial inflammation identified at autopsy. Myocardial abscess. The type of rejection may be classified by endocardial biopsy as: The dilated heart shows foci of scarring "replacement fibrosis" Fig. Eosinophilic myocarditis.

There is replacement fibrosis in the myocardium. I7 Fig. There is a mural thrombus in the left ventricle. Dilated cardiomyopathy systolic disorder is found in patients with hemochromatosis. Thrombi tend to form in the dilated ventricle and there typically is functional mitral insufficiency.

Cardiomyopathy Cardiomyopathies are diseases characterized by cardiac dysfunction in which the main abnormality lies in the working myocardium. Dilated cardiomyopathy. Ventricles and atria are dilated. Both the primary and the secondary categories have three possible functional states: Typically it is found in the end stages of ischemic heart disease and in hypertensive heart disease.

Cardiomyopathies are divided into two groups: The interstitium contains infiltrates of lymphocyte and eosinophils. Specific and less specific causes of dilated. These diseases typically impede the diastolic filling of the cardiac chambers and reduce systolic ejection of blood. Hypertrophic cardiomyopathy diastolic disorder is found in patients with Friedreich ataxia. Restrictive cardiomyopathy diastolic and systolic disorder may be caused by pathologic processes involving the endocardium e.

The pathologic changes depend on the process that has caused the disturbance. Congenital hypertrophic cardiomyopathy with asymmetric septa hypertrophy. Cor pulmonale causes right ventricular hypertrophy. The most common cause of left ventricular hypertrophy is arterial hypertension. In all these diseases there is marked hypertrophy of the cardiac myocytes. Amyloidosis of the heart. Histologically the cardiac myocytes are hypertrophied and show branching and disarray.

The ventricular myocardium appears thickened but pale. There also is considerable interstitial fibrosis. Electron microscopy shows pericellular amyloid fibers. The cardiac myocytes are surrounded by hyalinized material. I9 Fig. Congenital hypertrophic cardiomyopathy. Consequences and potential outcomes of coronary atherosclerotic plaque rupture are outlined in Diagram Narrowing or occlusion of coronary arteries typically causes myocardial ischemia.

Soft lipid-rich atherosclerotic plaques tend to rupture and provoke thrombus formation in the lumen of the coronary Fig.

Coronary Atherosclerosis Atherosclerotic plaques of coronary arteries have the same morphologic features as plaques in other sites. Concentric plaque causing narrowing of the coronary artery. In cross section the plaque. The plaque projects outward rather than inward. Coronary artery with a fibrolipid plaque.

Some lesions are composed only of fibrous tissue and are calcified. The presence of multiple vascular channels inside a coronary artery indicates recanalization Fig. Plaques may be eccentric Fig. Coronary thrombi may be lysed through the action of fibrinolytic enzymes. Eccentric plaque causing narrowing of the coronary artery. Rupture of atheroma also may cause microemboli and fibrin thrombi in the distal small branches of the coronary artery system Fig.

There is a small tissue in the plaque. In this picro-Mallory trichome—stained slide. The lumen of the coronary artery has been subdivided into several channels by fibrous strands.

This small artery is occluded by a mass composed of platelets blue. Potential outcomes of coronary plaque rupture. Microemboli in small intramyocardial vessels. Coronary artery recanalization.

Coronary thrombus. By clinical history this infarct was six days old. Contraction band necrosis in which the cytoplasm of myocardial cells contains densely eosinophilic bands also may be seen but it is more typical of reperfusion injury Fig. The infarcted area is invaded by neutrophils two to three days after the coronary occlusion Fig. Transmural myocardial infarct. The pattern of infarction is best appreciated at autopsy by staining slices of cross-sectioned heart enzyme histochemically to demonstrate dehydrogenase activity.

Myocardial Infarction Myocardial infarction represents the major consequence of coronary artery occlusion. Granulation tissue gives rise to fibrotic scars. Normal myocardium is blue. The pale areas involving the anterior and septal wall of the left ventricle represent the infarct caused by occlusion of the anterior branch of the left coronary artery.

Myocardial infarct. External cardiac rupture. The tissue was stained to demonstrate succinic dehydrogenase activity. Rupture of the septum can cause an acute left-to-right shunt and the rupture of papillary muscle Fig. Histologic changes indicative of myocardial infarction appear approximately 6 to 12 hours after occlusion but the definite signs of necrosis can be identified only after 24 hours. Complications of Myocardial Infarction The outcome of myocardial infarction depends on many variables and includes a spectrum of clinical pictures from sudden death to complete recovery.

The yellow necrotic area is surrounded by a hemorrhagic red rim. Myocardial infarcts can be localized or diffuse. Subendocardial infarct. The transverse section of ventricles was stained to demonstrate succinic dehydrogenase activity. Macrophages appear three to five days after the onset of ischemia and a fully established granulation tissue develops over a few days. Infarcted areas appear pale 12 hours after the onset of necrosis due to loss of enzyme activity in necrotic cells Figs.

On gross examination the infarcted myocardium initially is redder than the surviving adjacent tissue at 12 hours after occlusion of the coronary and then becomes paler.

The subendocardial pale areas correspond to the infarct. The myocardial cells become hypereosinophilic. The cytoplasm of myocytes contains deeply eosinophilic bands.

Myocardial infarct 24 hours after occlusion of the coronary artery. Rupture of a transmural infarct. The necrotic myocytes have deeply eosinophilic amorphous cytoplasm. Pericardium is filled with blood as a complication of cardiac rupture. In this three-day-old infarct the necrotic myocardial cells are surrounded by neutrophils.

Contraction band necrosis. Adjacent surviving cells appear pale and vacuolated. Ventricular aneurysm. Ventricular aneurysms form at the site of large scars replacing infarcted myocardium of the left ventricle Fig. Mural thrombus overlying a massive myocardial infarct. Rupture of the interventricular septum. The bulging aneurysm has a thin fibrotic wall. Papillary muscle rupture. Courtesy of Dr. Mural thrombi form over the infarcted areas Fig.

Fred Bosman. Hematopericardium is a complication of heart rupture. Hydropericardium is a common complication of congestive heart failure and generalized edema. The surface of the heart is covered with a layer of fibrin. Fibrinous pericarditis. Pericardial diseases present in several pathologic forms: The surface of the epicardium is covered with fibrin. There is granulation tissue under the layer of fibrin.

The pericardium often is involved. Pericarditis also is a common complication of myocardial infarction. The layer on the surface of the epicardium consists of fibrin and granulation tissue. Constrictive pericarditis. The inflammatory infiltrate is composed of macrophages.

Tuberculous pericarditis. The heart is encased in a thick layer of white fibrous tissue. Fibrinohemorrhagic pericarditis.

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The heart is covered with blood-tinged fibrin. High-power view of stellate and elongated lepidic cells and hemosiderin laden macrophages.

Rhabdomyomas are cardiac tumors of infancy and childhood Fig. The external surface is smooth and the tumor appears lobulated and myxomatous. Typically myxomas are benign tumors. The tumor may occlude the mitral orifice as a "ball valve. Cardiac myxoma in the left atrium. The most common tumor is myxoma Fig. Metastases to the heart are more common than primary tumors.

They may be found on the epicardial surface. Primary tumors of the pericardium are histologically classified as benign or malignant mesotheliomas or hemangiosarcomas Fig. Less often they occur in the right atrium or attached to the valves. There also are thin-walled blood vessels. The tumor is composed of elongated cells surround by myxomatous matrix that stains pink.

This hemorrhagic tumor was found encasing the heart. The tumor presents as a myocardial mass. The tumor is composed of glycogen-rich cells that have clear cytoplasm. Hemangiosarcoma of the pericardium. Metastatic melanoma of the epicardium. Histopathology Contreras-Mejuto F. Aretz HT: Lancet Virmani R: Cardiac rhabdomyoma. Chest Bulkley BH. Davies MJ: Pardo-Mindan FJ. Edwards JE: Clinical and pathologic features of metastatic neoplasms of the pericardium.

Maron BJ: Hypertrophic cardiomyopathies. Cowan D. Burke AP. Semin Diagn Pathol 9: The pathology of cardiovascular prostheses.

Winters GL: The challenge of endomyocardial biopsy interpretation in assessing allograft rejection. Cardiac myxoma. Klacsmann PG. A clinicopathologic study.

Dickens P. Olson LJ.

Curr Opin Cardiol Chan AC: Tumors of the heart. Cancer Hutchins GM: The changed spectrum of purulent pericarditis. Am J Med An 86 year autopsy experience in patients. A study of cases spanning 15 years. Altrichter PM. Mod Pathol 4: Edwards WD et al: Surgical pathology of the pulmonary valve. Am J Clin Pathol Hum Pathol Primary sarcomas of the heart.

A year experience with a review of A look at the last five years. Coronary artery remodeling and the assessment of stenosis by pathologists. Lam KY. Pathology of heart transplant through endomyocardial biopsy. Arch Pathol Lab Med Lazano MD. Silver MD: Cardiac pathology. Mayo Clin Prot Hum Pathol 5: The Dallas criteria. Thickened arterioles in kidney of a diabetic man appear homogeneously pink. It has little or no clinical significance.

In the large elastic arteries it causes changes indistinguishable from those of atherosclerosis. Hyperplastic arteriolosclerosis.

It may accompany hypertension or diabetes and is a common feature of involutional atrophy e. Chronic benign hypertension affects all arteries and arterioles. Included under this term are four pathologic entities: Hypertensive arteriosclerosis may be divided clinically and to some extent pathologically into chronic benign and accelerated malignant types. Hyperplastic arteriolosclerosis is characterized by narrowing of the lumen of arterioles due to the concentric proliferation of smooth muscle cells in the vessel wall Fig.

Arterioles have narrow lumen due to layers of fibrous tissue. Malignant hypertension is characterized by hyperplastic arteriolar changes that often are accompanied by fibrinoid necrosis of the vessel wall Fig. It typically is found in malignant hypertension. In hyaline arteriolosclerosis the wall of arterioles appears thickened by homogeneously glassy pink material " hyaline" Fig.

Splenic arterioles in an elderly nondiabetic man. Monckeberg medial calcific sclerosis is an age-related degenerative process in which the media of large and mediumsized muscular arteries undergoes calcification Fig. It often is prominent in the spleen.. Hyaline arteriolosclerosis. The lumen of the arteriole is narrowed due to concentric proliferation of smooth muscle cells in the vessel wall "onionskin lesion".

Monckeberg medial calcific sclerosis. Immunofluorescence microscopy shows deposits of fibrin in the vessel wall. The vessels show hyperplastic changes and narrowing of the lumen. The wall of the arteriole is infiltrated with fibrin and appears magenta red. Fibrinoid necrosis. Systemic sclerosis. Media of this elastic artery shows a discrete area of calcification. The arterial wall is thickened and contains increased amounts of collagen and elastic tissue.

Hypertensive change in muscular arteries. It contains yellow. Ulcerated atheromas are seen in the aorta above the renal arteries. Atherosclerotic aneurysm. Fatty streak. Severe atherosclerosis of aorta. Atheroma consists of amorphous cellular debris and cholesterol crystals walled off by fibrous tissue.

The intima contains fat-laden foam cells that stain with oil red O. Fatty streaks in the aorta of an adolescent boy. These changes lead to diffuse intimal thickening followed by eccentric intimal thickening and ultimately to formation of fibrous plaques.The thrombus is attached to the damaged arterial wall,and is covered by a red clot.

We are still conscious of the need to preserve the original aim of understanding disease and disease processes. Invasive carcinomas show variable degrees of keratinization Figs. Peripheral adenocarcinoma. In this picro-Mallory trichomestained slide, collagen is blue and the thrombus is red. Coronary Atherosclerosis Atherosclerotic plaques of coronary arteries have the same morphologic features as plaques in other sites.

The information is relevant to a wide range of medical specialists and health-care workers involved in the diagnosis and management of patients with AIDS.

Pathologically myocarditis is classified as acute or chronic. The authors deserve congratulations for the well-chosen pictures, some of which cannot be described otherwise than stunning and memorable. Occasionally the stroma of nasal polyps may contain atypical stromal cells with dysplastic or bizarre nuclei.

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