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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.

Total anomalous pulmonary venous connection Aortic stenosis 7. The most common cardiac malformations in descending order of frequency are 1. Atrioventricular septal defect Cardiac and vascular shunts.

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.

Of pdf pathology atlas color

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.

AN ATLAS OF GENERAL PATHOLOGY

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. 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.

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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.

Atherosclerotic aneurysms most often are located in the abdominal aorta. Atherosclerosis of the splenic artery leads to formation of cirsoid aneurysms Fig. The calcified blood vessels appear serpentine. An aneurysm is a dilatation of the aorta or any other major artery.

Berry aneurysms are related to a defect in the muscle layer of cerebral arteries Fig. The blood has filled the space formed by the forcible separation of intima and media of the aorta. Layers of the aortic wall are loose and have been separated by blood. Atheromatous plaques.

Pathology pdf color atlas of

Dissecting aneurysm of the aorta. Berry aneurysm of the circle of Willis arrow. They typically occur in the thoracic aorta Fig. Weakening of the arterial wall may lead to aneurysm formation. Dissecting aneurysm of the thoracic aorta. Hypertension combined with cystic medial necrosis may lead to the formation of dissecting aneurysms even in the absence of atherosclerosis Fig.

Syphilitic aneurysms are a consequence of infection with Treponema pallidum. Cirsoid aneurysm of splenic artery. The earliest changes. The aortic arch is dilated. Syphilitic aneurysm. Histoplasma capsulatum has invaded the meningeal arteries. Aortic lesions typical of tertiary syphilis are caused by a tendency of Treponema pallidum to cause inflammation of vasa vasorum of the aorta Fig.

Hematogenous dissemination of viruses. Granulomatous giant cell vasculitis of cerebral arteries. Infection-induced vasculitis is an inflammation caused by invasion of the vessel wall by pathogens.

Fungal vasculitis. Rickettsia have a predilection for the endothelial cells of capillaries. Pathogens can gain entry into the vessel wall from outside i. Fungal vasculitis is a common complication of pneumonia caused by Aspergillus or Rhizopus in which these fungi invade the pulmonary arteries and veins from outside. This patient had a herpes zoster virus infection.

Fungal meningitis can spread to the cerebral vessels Fig. Injury of these small nutrient vessels of the aorta results in scarring of media. Viruses are considered to cause granulomatous vasculitis of the central nervous system Fig Intima has a "tree-bark" appearance. Immunofluorescence Rickettsia ricketsii causes segmental necrosis. Rocky Mountain spotted fever. Infection with Fig.

The media of the aorta shows focal loss of elastic fibers and scarring caused by ischemia. Syphilitic aortitis. A B pallidum infection caused infiltrate around vasa vasorum composed of lymphocytes and plasma cells. Immune-mediated Vasculitis Vasculitis may be caused by antibody-mediated and cellmediated mechanisms elicited by a variety of antigens. For practical reasons it is best to classify vasculitides in three groups according to the type of blood vessel involved: Histologically it presents as a granulomatous inflammation.

Diagram 2-I. The infiltrate typically contains multinucleated giant cells. Right lateral view of the heart of an infant who died of Kawasaki disease.

Destruction of the media of the aorta is a consequence of a granulomatous inflammation. Modified from Jennette JC et al: Arthritis Rheum Vasculitis clinical syndromes.

Takayasu arteritis. Takayasu arteritis involves the aorta and its major branches. Kawasaki disease. The infiltrate contains multinucleated giant cells. The causative antigens cannot be identified in many cases and the exact pathogenesis of many lesions is only partially understood. There is pronounced thickening and immense prominence of all coronary arteries due to a combination of ectasia and intimal thickening. Klima T. Spjut HJ. Lie JT: Histopathologic specificity of systemic vasculitis.

Am J Pathol A defense mechanism gone awry. Further Reading Jennette JC. Chandler AB. Polyarteritis nodosa is a necrotizing inflammation of medium-sized or small arteries Fig. A small subcutaneous artery shows focal fibrinoid necrosis and transmural inflammation extending into the perivascular tissue.

Circulation Destruction of the vessel wall often leads to formation of microaneurysms Fig. Polyarteritis nodosa. Small dermal vessels are infiltrated with IgA as demonstrated by immunofluorescence microscopy in this slide stained with antibodies to IgA.

Ledford DK: Immunologic aspects of vasculitis and cardiovascular disease. Henoch-Schinlein purpura. Rheum Dis Clin NAm In HSP this leukocytoclastic vasculitis typically is associated with a deposition of immunoglobulin A IgA in the wall of small vessels Fig.

American Heart Association. Stary HC. Pretre R. Andrassy K et al: Nomenclature of systemic vasculitides: Dinsmore RE et al: A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis.

Falk RJ. Aortic dissection. Dermal venules show signs of leukocytoclastic vasculitis. JAMA The pancreatic artery forms an aneurysm that is filled with a thrombus. Ross R: Rous-Whipple Award Lecture. Kawasaki disease often involves coronary arteries. Coelho A et al: The morphology of ascending aortic aneurysms. Henoch-Schonlein purpura HSP and drug-induced vasculitis are examples of small vessel vasculitis.

Parums DV: The arteritides. Small vessel vasculitis. Such lesions predispose to thrombosis. These pathologic processes can be caused by infectious agents.

Pathology pdf color atlas of

The pathologic findings in such conditions are banal and nondiagnostic. Uncommon infections such as nasal infection caused byKlebsiella rhinoscleromatis Fig. Nasal biopsy showing numerous foamy histiocytes Mikulicz cells. Chronic inflammation may result in the formation of nasal polyps. Histologically nasal polyps represent edematous mucosa infiltrated with inflammatory cells.

Allergy is a common cause of rhinitis. Slides stained with Warthin-Starry stain show numerous intracellular coccobacilli corresponding to Klebsiella rhinoscleromatis. Right nasal cavity and posterior wall of left maxillary sinus are involved. Myospherulosis is a form of inflammation related to packing of nasal cavities with gauze that contains petroleum jelly Fig. CT scan of paranasal sinus in year-old man with rhinoscleroma. Such changes usually are found in polyps with ulcerated surface epithelium.

For example. Occasionally the stroma of nasal polyps may contain atypical stromal cells with dysplastic or bizarre nuclei. Inflammation may be caused by chronic strain or irritation. Granulation tissue is seen in the nasal cavity. The inflamed nasal mucosa contains round sporangia of RhinoSporangium filled with spores and surrounded by multinucleated giant cells.

The central sac. Nasal polyp. The edematous stroma contains scattered bizarre cells between the dilated blood vessels. Chronic laryngitis. As seen through the laryngoscope. Juvenile nasopharyngeal angiofibroma is a benign mesenchymal tumor restricted to adolescent boys and young men Fig.

Exophytic and endophytic papillomas together account for 95 percent of all nasal lesions Fig. Multiple papillomas are usually found in preschool children.

Color Atlas of Pathology

These lesions represent edema of connective tissue. Nasal papillomas. These lesions typically contain human papilloma virus type 6 and There is no reliable way to histologically predict recurrence. Oak Park. They also may be located inside the wall of each organ or may cause focal thickening. Nonepithelial tumors are less common. Schneiderian papilloma.

Laryngeal papillomas are lined by nonkeratinizing squamous epithelium. These papillomas are lined by basaloid cells that occasionally show squamous differentiation. Proliferation of monotonous. The tumor involves the nasal cavity extending onto the septum and lateral wall. The tumor is exophytic but focally it shows features of an inverted papilloma. Papillomas most often originate from nasal or laryngeal epithelium. Histologically these tumors are composed of gaping. Vocal cord nodules and solitary laryngeal polyps of adults are common nonneoplastic tumefactions related to strain and abuse of voice Fig.

Nasopharyngeal carcinoma accounts for 85 percent of all malignant tumors of this site. Bilateral polypoid nodules of vocal cords. As viewed through the nasal speculum. Juvenile nasopharyngeal angiofibroma. Histologically these tumors show prominent keratinizations and tend to invade the underlying tissues. Three histologic subtypes are Malignant tumors of the upper respiratory tract are mostly of epithelial origin and histologically represent squamous cell carcinomas.

The irregularly shaped. The polypoid mass consists of edematous. Both variants stain with antibodies to neurofila: It may show typical features of neuroblastoma of other sites such as fibrillary stroma.

Nasal tumors. Vocal cord nodule "singer's node". Wherever possible, we have in- cluded the normal structures of the most im- portant organs and tissues for the sake of com- parison. Such a visual comparison makes a more lasting impression and conveys a better understanding of the altered structure than any verbal description. Macrostructure and microstructure: Physicians who perform open or endoscopic surgery are routinely confronted with the macroscopic as- pects of disease processes.

For this reason, we have attached great importance to including both macroscopic and microscopic images of tissue changes.

Pathology A Color Atlas.pdf

To illustrate histologic changes, we have used modern research and diagnostic techniques such as enzyme histochemical stu- dies, immunohistochemical studies, and lectin histochemical studies; and with the aid of elec- tron microscopy and molecular biology, we have expanded our coverage to include ultra- structural and supramolecular changes.

Diagrams and cartoons: Many concepts and dis- ease processes cannot be suitably illustrated with histologic images. To facilitate an under- standing of these concepts and processes, we have employed a concept that concentrates on representing the essential elements in- volved, wherever possible in the form a linear progression. To prevent the book from becom- ing overly tedious as a result of this objective presentation of information, we have taken the liberty of representing certain disease pro- cesses in the form of pathologic cartoons.

In this manner, we use a combination of text and images to examine those abnormal mani- festations of life processes that lead to suffering. In this manner, pathology makes an important contribution to society as a whole.

For a society that is oblivious to indi- vidual suffering is ruthless and inhuman. More- over, the study of suffering can represent a gain for the individual as well. For it may well be that the only reason our soul is encased in a body is to allow it to experience that most important aspect of all creation: Acknowledgements Here, I would like to express my thanks to all who have helped to make this book possible in its present form. I also extend my thanks to those colleagues who have assisted us by providing image material: Adler, Patholog.

Institut, Freiburg B-D Prof. Kliniken, Fulda A Prof. 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. Ihling, Patholog. Institut, Freiburg E,E, Prof. Koch, Patholog. Mall, Patholog. Institut, Darmstadt G Prof. Meister, Patholog. Mihatsch, Patholog. 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. Halsema, 1. Heystek and J. Lek were involved in the preparation of the atlas. The hematopoietic system includes the lymphoreticular e. Peyers' patches, thymus, tonsils and Bursa of Fabricius , and blood and bone marrow. Its cellular components provide oxygen transport erythrocytes and protective responses to infectious and non-infectious agents lymphoid cells, mononuclear phagocytic cells, granulocytes and supportive tissues.

In addition, degenerative changes of erythrocytes, circulatory disturbances and abnormal deposits may occur. In cachexia the hematopoietic tissue in the bone marrow can be displaced by gelatinous, almost translucent material, the serous atrophy of bone marrow. Non- infectious agents can induce atrophic changes, either by 'exhaustion' of the response capacity of the tissue or as a direct or indirect effect on the effector cells. High levels of glucocorticoids may cause lymphodepletion in lymphoid tissues.

Filtering of lymph in the lymph nodes with deposition or processing of filtered material may reveal important information. The same applies to the filtering of blood in the spleen. Reactive Ilyperplasia of hematopoietic tissue can expand into and replace fatty bone marrow. Mostly, the myeloid cell series is involved and the process will result in leukocytosis in the. Because of the close relation between adapiiue reactioitv and inflammatory reaction these two processes are often difficult to distinguish, especially based on gross morphology.

Humoral immune reactivity is evidenced by B-cell hyperplasia with large secondary follicles and many plasma cells in the medullary cords of the lymph nodes, and cellular immunity evidenced by hyperplasia of the paracortical zones lymph nodes or periarterial lymph sheaths PALS, spleen. Most hyperplastic reactions are non-specific in that they do not reveal the identity of the agent responsible. When characteristic inflammatory changes like suppuration, necrosis or caseation are visible in lymph nodes or spleen, lymphadenitis and splenitis are appropriate terms.

Neoplasms of the hematopoietic system are also relatively common in both companion animals and production animals and are classified according to their histogenetic lineage.

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.