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Basic knowledge of general and special pathology (Springer textbook)

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Springer textbook

Ursus-Nikolaus Riede Martin Werner Nikolaus Freudenberg

Basic knowledge of general and special pathology With the collaboration of JP Baak, HE Blum, B. Brand-Saberi, M. Braun-Falco, J. Finke, P. Fisch, U. Gerlach, K. Höpker, G. Kayser, J. Lütschg, D. Mattern, H. Matthys, K. Müller, AJ Olah, M. Orlowska-Volk, J. Seufert, K. Warnatz, U. Wetterauer, N. Weyer, A. zur Hausen With an afterword by S. von Boletzky

With 391 illustrations, 76 tables and 47 authentic cases

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Professor Dr. med. Ursus-Nikolaus Riede Professor Dr. med. Martin Werner Professor Dr. Dr. h.c. Nikolaus Freudenberg Institute for Pathology University Hospital Freiburg Breisacher Str. 115a 79106 Freiburg

ISBN 978-3-540-79213-0 Springer Medizin Verlag Heidelberg Bibliographic information from the German National Library The German National Library lists this publication in the German National Bibliography; detailed bibliographic data are available on the Internet at http://dnb.d-nb.de. This work is protected by copyright. The resulting rights, in particular those of translation, reprinting, presentation, extraction of figures and tables, radio broadcasting, microfilming or duplication in other ways and storage in data processing systems, are reserved, even if only in part. A reproduction of this work or parts of this work is only permitted in individual cases within the limits of the statutory provisions of the copyright law of the Federal Republic of Germany of September 9, 1965 in the currently applicable version. In principle, it is subject to remuneration. Infringements are subject to the penal provisions of the Copyright Act. Springer Medizin Verlag springer.de © Springer Medizin Verlag Heidelberg 2009 Product liability: The publisher cannot accept any liability for information on dosage instructions and application forms. Such information must be checked for correctness by the respective user on a case-by-case basis using other literature sources. The reproduction of common names, trade names, etc. in this work does not justify the assumption that such names are to be regarded as free within the meaning of the trademark and trademark protection legislation and therefore may be used by everyone, even without special identification. Planning: Christine Trotta, Peter Bergmann, Heidelberg Project management: Rose-Marie Doyon, Heidelberg Editing: Dr. Monika Merz, Sandhausen Cover design & design: deblik Berlin Cover picture: "Transformationsmuster 2008" by Eugen Roth, Ludwigshafen Typesetting: Fotosatz-Service Köhler GmbH, Würzburg SPIN: 12046379 Printed on acid-free paper

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The violence doesn't start when someone strangles you. It starts when someone says: "I love you: You are mine!" The violence does not start when the sick are killed. It begins when someone says: "You are sick: you have to do what I say!" From: "Violence" by Erich Fried, Jewish, British-Austrian, political poet 1921–1988

Foreword Every disease develops a tissue "face" which, depending on the level of training, puts the clinician on the right diagnostic trail if he knows about it. The general practitioner can be expected to see or feel the pathological process as such when inspecting a patient. The specialist must recognize it to the extent that it removes the diagnosis-relevant tissue from the right place in the form of a biopsy so that the pathologist can make the therapy-relevant diagnosis. The present book is therefore based on the knowledge requirements of a general practitioner and a biopsy / surgical doctor; it includes the "basics" of pathology. This goal is already reflected in the first chapters, which only deal with the clinically important changes in shape and color as well as tissue destruction and are intended to be understood as diagnostic instruments. In the conception of the present book "Basic Knowledge of Pathology" we started from the knowledge that about 95% of all diseases, as they occur in the patient population of a general practice, belong to the "very frequent" or "frequent" cases that he himself diagnoses. For him, 4.9% of the remaining cases are "less frequent" or even "rare"; he will refer them to a specialist for reliable clarification and correct therapy. The remaining 0.1% cases are "very rare" or even a "rarity", of which only a few are known in world literature. You belong in the hands of an expert. According to this rating scale, the individual diseases were included in this book in collaboration with clinically active doctors and their frequency was already mentioned in the respective definition, although disease rarities were also discussed if they belong to the pathogenetic understanding of a general practitioner. Without slipping to the level of a telephone book, in which many people appear but the plot is missing, the content of the knowledge material in this book has been streamlined so that its content reflects basic knowledge. Every disease is based on its own development process. The causal pathogenesis mostly reflects the reaction structure of the triggering factors, whereas the formal pathogenesis describes the reaction process through which a disease receives its tissue peculiarity, by which it can be recognized and thus diagnosed by the pathologist. In many cases, however, a pathological diagnosis does not conceal a uniform causal pathogenesis, which means that the diagnosis made on the tissue changes is often the morphological resultant of various trigger mechanisms, which therefore also explains why patients with the same diagnosis sometimes respond differently to the same therapy . This fact is taken into account in this textbook by defining certain illness terms as group names, collective terms or reaction patterns. If one compares the formal pathogenetic reaction processes of the individual diseases, it is noticeable that certain processes occur in the same or similar form in other diseases and that the same cellular-molecular mechanisms are controlled. We call them "reaction patterns". They are worked out in the first sections of "General Pathology" and are only mentioned as "Patterns" with a corresponding chapter reference in the treatment of "Special Pathology". The same applies to the images. They have been chosen to illustrate, wherever possible, both general and specific aspects of the pathology or even response patterns. Correspondingly, the same figure is often referred to in several places in the text. If organ- or tissue-specific reaction patterns appear in a chapter, these are placed in front of the individual diseases. The pathology serves on the one hand as the basis of an evidence-based therapy, but also, as in the case of an autopsy, of quality assurance, in which the diagnoses made in the clinic are compared with the diagnoses made on the tissue. Because around the world around a third of all diagnoses made in clinics are incorrect or at least in need of correction. Unfortunately, this is not known to all clinicians. In this context I cannot get rid of the remark of the clinic boss who, before I carried out the autopsy of a deceased at the request of the relatives,

VII Foreword

greeted with the words: “We can save this section. The patient died of a pulmonary embolism. What else do you want now? ”When the autopsy revealed that he had overlooked a“ heparin-induced thrombocytopenic syndrome ”(7 chap. 26.2.3.1), which was decisive for the patient's death, he was meek. Not least because of this, I have included a number of "clinical cases" in the book. Without exception, they are authentic and, on the one hand, give an insight into the everyday life of a pathologist and, on the other hand, teach how to apply the knowledge conveyed in this textbook. When processing the cases, it was sometimes difficult for me to leave out the emotions completely. That's why I leave it to the reader to decide how much they read between the lines. If you get respect for the patient in the process, you will have understood the basis of this textbook. Freiburg in autumn 2008 Ursus-Nikolaus Riede on behalf of everyone involved in the creation of this book

Dedication We dedicate this book to the two Chinese doctors and friends

Wu Zhongbi (3/19/1919 - 11/14/2007) After a poor youth in Shanghai and Nanjing, he was drawn into the maelstrom of the anti-Japanese war. For years he was on the run, so that his feet kept bleeding through the straw shoes. Regardless of this, he passed his Abitur in 1939 and studied medicine and learned German at Tongji University - then still in Shanghai. In 1946 he became an assistant doctor in pathology, where he was appointed lecturer in 1950. Mao Tsedong immediately ordered Tongji University to be relocated to Wuhan. Wu Zhongbi had to go with - on foot! - and became an associate professor there in 1956. During the Cultural Revolution (1966-1976) the Red Guards humiliated and harassed him in the worst possible way. But in 1976 he was appointed full professor. Thanks to his razor-sharp mind and his excellent knowledge of German, his scientific work was extremely successful. She was crowned by his research into schistosomes as the causative agent of schistosomiasis, which eventually led to the development of a vaccine. As a founding member of the German-Chinese Society for Medicine, he contributed significantly to the understanding of both peoples; even more, he became the Chinese patron saint of medical-scientific exchange, with whom he brought many young doctors to Germany for further training. Prof. Wu died in 2007 of complications from colon cancer.

Qiu Fazu (December 6, 1914 - June 14, 2008) The son of a noble family, he passed his Abitur in Shanghai, where he studied medicine from 1933–1936, learned German and completed his studies in Munich in 1939 as a Humboldt fellow. In 1944 he was assigned to the Bad-Tölz military hospital as a surgeon, where he succeeded in stopping a transport of Jews and saving them from certain death in the Dachau concentration camp by branding everyone with typhoid fever and hospitalizing them off the street. In 1946 he returned to Shanghai with his real Bad Tölzer wife, where he took over the management of surgery. In 1951 he was posted to the Korean War as a surgeon. But in 1952 he was appointed professor of surgery at Tongji University in Shanghai. However, this did not prevent the Red Guards from relegating him to gardening during the Cultural Revolution. Meanwhile, he had to hide his wife in the attic as a foreigner. He then became a pioneer of Chinese abdominal surgery and immediately carried out the first liver transplants, while his wife excelled as a German lecturer. He too became a founding member of the German-Chinese Society for Medicine. When Prof. Wu Zhongbi fell ill with colon cancer in 2007, the aged Prof. Qui insisted on operating his friend himself. The operation was successful, but the tumor has already metastasized.

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the authors

[email protected]

[email protected]

[email protected]

Ursus-Nikolaus Riede was born in 1941. Study of medicine in Basel. General practice doctor. Resident at the AO Institute Davos with Prof. H. Willenegger, at the Anatomical Institute with Prof. R.K. Schenk and at the Pathological Institute of the University of Basel with Prof. Dr. H.-U. Zollinger, as well as at the Pathological Institute of the University of Freiburg with Prof. Dr. W. Sandritter. 1973 habilitation. 1978 specialist, adjunct professor. 1980 Rudolf Virchow Prize of the German Society for Pathology. 1980 E. K Frey Prize of the German Society for Internal Intensive Care Medicine. Editor and author of standard textbooks for "General and Special Pathology". Martin Werner born in 1961. Studied medicine in Mainz, Cologne and Homburg / Saar. Assistant doctor at the Institute for Human Genetics with Prof. Dr. K.D. Zang, at the Women's Clinic of Saarland University with Prof. Dr. G. Bastert and at the Pathological Institute of the University of Hanover with Prof. Dr. A. Georgii. 1993 habilitation. 1995 specialist. 1996 specialist in molecular pathology. 1996 Prize of the International Society for Histochemistry and Cytochemistry. 1997 C3 professorship at the Technical University of Munich. 2001 C4 professorship, director of the Institute for Pathology at the University of Freiburg. Nikolaus Freudenberg born in 1944. Study of medicine in Erlangen and Frankfurt / M. Assistant doctor at the Anatomical Institute with Prof. Dr. J. Dust sand and Pathological Institute of the University of Freiburg with Prof. Dr. W. Sandritter. 1976 medical specialist. 1977 habilitation. 1984 adjunct professorship. Medical director of the cytopathology section at the Institute for Pathology at the University of Freiburg. 1992-1998: Dean of Studies. 1999 Awarded an honorary doctorate by the Semmelweis University in Budapest. 1989-2007 secretary, since 2008 president of the German Society for Cytology.

Basic knowledge of general and special pathology

Clinic: Tips for everyday life: What do I do with the patient?

Introduction: At a gallop through the topic: What is it, what does one die of?

Control system: Quick overview for a clear view: where can I find what?

Glossary: ​​Understand what the term means: what are we actually talking about?

Take-homemessage: A profile that you should remember: A "must-have"!

Content structure: A guidance system for text strangers: How do I get where?

Over 390 images: Sustainable insights into the essentials: How should I imagine that?

Linear text structure of lists for short-term memory

Navigation: Locating order: where am I here?

Keyword: Highlighted in Bold: What Is Really Important?

References to figures, tables and chapters: The chance for career changers: Was there anything before?

Deepening knowledge: Well drilling for knowledge: A "nice-to-have".

Selected exemplary images mostly with reference to general and special pathology (colliquation necrosis, liver abscess)

Diagnostics: a look that matters: where, how what?

Give us your opinion! Ÿ www.lehrbuch-medizin.de

List of Abbreviations DEF FPG KPG MAK

Definition formal pathogenesis causal pathogenesis macroscopy

MIK KLN KPL

Microscopy (histology) clinic, clinical aspects complications

Explanation of important abbreviations Oncogenes / proliferation factors BCR (breakpoint cluster region) → forms a permanently proliferative fusion transcript with c-abl c-abl (Abelson murine leukemia virus = abl-tyrosine protein kinase) → signal transduction, growth control. Inhibitor: Imatinib c-ets family (avian erythroblastosis virus) → transcription factors cooperating with nuclear factors → mitogenic, transforming and development-controlling effect (Down syndrome) c-myc (myelocytomatosis virus) → transcription factor → stimulation of proliferation with consecutive virus differentiation block c-kitv (catarcoma ; kit = kitten) → receptor tyrosine kinase for stem cell factor CD34 → development of haematopoietic stem cells. Inhibitor: Imatinib c-ras (Kirsten rat sarcoma virus) → generator of c-AMP as a second messenger substance → mitogenic and transforming effect K-ras (mutated form in colorectal cancer) does not react to anti-EGFR therapy with cetuximab c-ret (rearranged during transfection → Proto-oncogene) → Receptor tyrosine kinase for neurotropic factors → Control of epithelial morphogenesis FAK (focal adhesion kinase) → Protein kinase activation through cell anchoring → Cell survival Her2 / neu (human epidermal growth factor receptor-2) → Proliferation stimulator and apoptosis blocker. Inhibitor: Herceptin (trastuzumab) HIF-1 (hypoxia inducible factor) → transcription factor for oxygen-dependent expression, among others. of VEGF and TGF; Key factor for cell adaptation to hypoxia JAK (Janus kinase) → simultaneous cytokine and growth factor activation → cell development, growth control, homeostasis MAP kinase → (mitogen-activated protein kinase) → cell regulation in development, neoplasia, inflammation NFκB (nuclear factor kappa light chain -enhancer of activated B cells) → central transcription factor in immune and inflammatory reactions Development genes FLI (flightless drosophila homolog gene) → migration-controlling transcription factor v. a. in embryonic mesoderma development HOX genes (Homeobox) → development control genes → embryonic patterning (patterning) SHH gene (sonic hedgehog) → development genes in embryonic polarization

Inhibitor: Rapamycin VHL (von-Hippel-Lindau) → gatekeeper gene → controls the degradation of HIF-1 and its VEGF formation. Inhibitors: Sorefinib, Sunitinib WT-1/2 (Wilm's tumor) → suppressor / differentiation genes → urogenital development

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Table of contents 5

Pattern of necrosis. . . . . . . . . . . . . . . . . .

33

5.1 5.2 5.3 5.4 5.5

U.N. Riede, H.E. Blum, N. Freudenberg, M.Werner Focal cytoplasmic necrosis. . . . . . . Shrink necrosis. . . . . . . . . . . . . Coagulation necrosis. . . . . . . . . . . Colliquational necrosis. . . . . . . . . . . Necrosis elimination pattern. . . . . .

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33 33 34 35 35

6

Adaptation pattern. . . . . . . . . . . . . . . .

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6.1 6.2 6.3

U.N. Riede, H.E. Blum, N. Freudenberg Catabolic Pattern. . . . . . . . . . . . . . . . . . Anabolic pattern. . . . . . . . . . . . . . . . . . . Reparative pattern. . . . . . . . . . . . . . . . .

41 42 44

I Basics 1

Introduction and methodology. . . . . . . . . . .

U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner 1.1 Histopathology. . . . . . . . . . . . . . 1.2 Quick cut. . . . . . . . . . . . . . . 1.3 Crush preparation. . . . . . . . . . . 1.4 cytology. . . . . . . . . . . . . . . . . . 1.5 electron microscopy. . . . . . . . . 1.6 Immunohistochemistry. . . . . . . . . . . . 1.7 Molecular Pathology. . . . . . . . . . . 1.8 autopsy. . . . . . . . . . . . . . . . . . . 1.9 (individual) death. . . . . . . . . . . . . . 1.10 autolysis. . . . . . . . . . . . . . . . . . . 1.11 Disease Terminology. . . . . . . . .

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2

Diagnostic strategies - shape patterns. . . . .

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2.1 2.2 2.3 2.4

U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner 2D elements. . . . . . . . . . . . . . . . 3D elements. . . . . . . . . . . . . . . . Hollow organ pattern. . . . . . . . . . . . . Parenchymal pattern. . . . . . . . . . . . .

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9 11 14 17

3

Diagnostic strategies - color swatches. . . . .

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3.1 3.2 3.3 3.4 3.5 3.6 3.7

U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner Weiss. . . . . . . . . . . . . . . . . . . . . Blue. . . . . . . . . . . . . . . . . . . . . . Green. . . . . . . . . . . . . . . . . . . . . Yellow. . . . . . . . . . . . . . . . . . . . . . Red. . . . . . . . . . . . . . . . . . . . . . Brown. . . . . . . . . . . . . . . . . . . . . Black . . . . . . . . . . . . . . . . . . .

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II Cellular Response 4

Cellular death pattern. . . . . . . . . . . .

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4.1 4.2

U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner Programmed cell death. . . . . . . . . . . . . . Alternative cell death. . . . . . . . . . . . . . . . . .

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III Metabolism 7

Inorganic metabolism. . . . . . . . .

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7.1 7.2 7.3 7.4

U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner Hypoxia. . . . . . . . . . . . . . . . . . . Calcium. . . . . . . . . . . . . . . . . . . Iron. . . . . . . . . . . . . . . . . . . . . Copper. . . . . . . . . . . . . . . . . . . .

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55 57 58 59

8

Intermediate metabolism. . . . . . . . . . . .

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8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 8.9

U.N. Riede, H.E. Blum, N. Freudenberg Carbohydrates. . . . . . . . . . . . . . Lipids. . . . . . . . . . . . . . . . . . . . Lipoproteins. . . . . . . . . . . . . . . Sphingolipids. . . . . . . . . . . . . . Nucleotides. . . . . . . . . . . . . . . . Amino acids . . . . . . . . . . . . . . . Urea cycle. . . . . . . . . . . . . Serum proteins. . . . . . . . . . . . . . Heme synthesis. . . . . . . . . . . . . . .

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62 64 66 68 70 71 73 73 74

9

Structural metabolism. . . . . . . . . . . . . .

76

9.1 9.2 9.3 9.4

U.N. Riede, H.E. Blum, N. Freudenberg collagen. . . . . . . . . . . . . . . . . . Proteoglycans. . . . . . . . . . . . . . Microfibrils. . . . . . . . . . . . . . . Elastin. . . . . . . . . . . . . . . . . . .

76 79 80 83

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Table of Contents

IV Incorrect circulation 10

Generalized cycle. . . . . . U.N. Riede, H.E. Blum, N. Freudenberg Arterial Hypertension. . . . . . . . . . Pulmonary hypertension. . . . . . . . . . Portal hypertension. . . . . . . . . . . . Circulatory shock. . . . . . . . . . . . . Bleeding. . . . . . . . . . . . . . . . . .

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11.1 11.2 11.3 11.4 11.5

Localized circulation. . . . . . . . U.N. Riede, H.E. Blum, N. Freudenberg Thrombosis. . . . . . . . . . . . . . . . Embolism. . . . . . . . . . . . . . . . . . Microcirculatory inflammation. . . . Arterial circulation. . . . . . . . . . Venous circulation. . . . . . . . . . .

12

Edema. . . . . . . . . . . . . . . . . . . . . . . . . 104

12.1 12.2 12.3 12.4

U.N. Riede, N. Freudenberg Hydrostatic Edema. . Oncotic edema. . . . Vascular edema. . . . . Lymphedema. . . . . . .

10.1 10.2 10.3 10.4 10.5

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V Individuality assurance 13

Inflammation. . . . . . . . . . . . . . . . . . . . . 109

U.N. Riede, H.E. Blum, N. Freudenberg 13.1 Acute exudative inflammation. . . . . . . . . . 115 13.2 Chronic inflammation. . . . . . . . . . . . . . 122 13.3 Causal forms of inflammation. . . . . . . . . . . 129

14

Immunopathology. . . . . . . . . . . . . . . . 133

K. Warnatz, U.N. Riede 14.1 Hypersensitivity reaction. . . . . . . . . . 133 14.2 Autoimmune Disease. . . . . . . . . . . . . . . 140 14.3 Immunodeficiencies. . . . . . . . . . . . . . . . . . . . 145

VI Incorrect growth 15

Malformations. . . . . . . . . . . . . . . . . . . 151

U.N. Riede, B. Brand-Saberi 15.1 Etiology. . . . . . . . . . . . . . . . . . . . . . . . 151 15.2 Causal Pathogenesis. . . . . . . . . . . . . . . . . 152

15.3 15.4 15.5 15.6

Formal pathogenesis blastopathy. . . . . Embryopathy (EP). Fetopathy (FP). . . .

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Neoplasms / neoplasia. . . . . . . . . . . 163

U.N. Riede, N. Freudenberg, P. Fisch, M. Werner 16.1 Etiology. . . . . . . . . . . . . . . . . . . . . . . . 16.2 causal pathogenesis. . . . . . . . . . . . . . . . . 16.3 Formal Pathogenesis. . . . . . . . . . . . . . . . 16.4 Tumor classification. . . . . . . . . . . . . . . 16.5 Dysontogenic tumor. . . . . . . . . . . . 16.6 Non-epithelial tumor. . . . . . . . . . . . . . 16.7 Semimalignant tumor. . . . . . . . . . . . . . . . 16.8 Benign epithelial tumor. . . . . . . . . . . . . . . 16.9 Malignant epithelial tumor. . . . . . . . . . . . . . . 16:10 Cancer of Unknown Primary (CUP). . . . . . .

154 157 159 160

164 174 181 188 188 189 192 192 194 200

VII circuit: piping system 17

Arteries. . . . . . . . . . . . . . . . . . . . . . . . 203

17.1 17.2 17.3 17.4

U.N. Riede, N. Freudenberg Fibrodestructive Patterns. . Mucodegenerative Patterns Dilatation Patterns. . . . . . Inflammation patterns. . . .

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Veins. . . . . . . . . . . . . . . . . . . . . . . . . 213

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U.N. Vineyard 18.1 Fibrodestructive Pattern. . . . . . . . . . . . . . 213 18.2 Inflammation Pattern. . . . . . . . . . . . . . . . 213

19

Lymph vessels. . . . . . . . . . . . . . . . . . . . 215

U.N. Vineyard 19.1 Malformation pattern. . . . . . . . . . . . . . . . 215 19.2 Inflammation Patterns. . . . . . . . . . . . . . . . 215

20

Vascular neoplasm pattern. . . . . . . . . . . . . 216

20.1 20.2 20.3 20.4 20.5 20.6

U.N. Riede hemangiomas. . . . . Lymphangioma. . . . Glomus tumor. . . . Hemangiopericytoma Kaposi's sarcoma. . . . Angiosarcoma. . . . .

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XV Table of Contents

VIII Circulatory system: pumping system (heart) 21

Cardiac malformation pattern. . . . . . . . . . . . 221

21.1 21.2 21.3 21.4 21.5 21.6 21.7

U.N. Riede atrial septal defects. . . . . . . . . Ventricular septal defects. . . . . . . . Open ductus arteriosus. . . . . . Transposition of the great vessels. . Coarctation of the aorta. . . . . . . . . Proximal aortic / pulmonary stenosis, Fallot tetralogy. . . . . . . . . . . . .

22

Cardiac adaptation pattern. . . . . . . . 225

22.1 22.2 22.3 22.4

U.N. Riede congestion hypertrophy. . Heart failure. . . . . . . . . Coronary artery disease (CHD) heart attack. . . . . . . . . . . .

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Endocardium. . . . . . . . . . . . . . . . . . . . . . . 232

23.1 23.2 23.3 23.4 23.5

U.N. Vineyard elastosis pattern. . . . . . . . Calcification pattern. . . . . Mucodegenerative Patterns Inflammatory Patterns. . . . Neoplasm pattern. . . . . .

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Myocardium. . . . . . . . . . . . . . . . . . . . . . . 236

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232 232 232 232 234

U.N. Vineyard 24.1 Fibrodestructive patterns. . . . . . . . . . . . . . 236 24.2 Patterns of inflammation. . . . . . . . . . . . . . . . 237 24.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 239

25

Pericardium. . . . . . . . . . . . . . . . . . . . . . . . 240

U.N. Vineyard 25.1 Incorrect circulation pattern. . . . . . . . . . . . . . . 240 25.2 Inflammation Patterns. . . . . . . . . . . . . . . . 240 25.3 Neoplasmic Pattern. . . . . . . . . . . . . . . . . . 241

IX Circulation: Haematopoiesis / Lymphopoiesis 26

Bone marrow. . . . . . . . . . . . . . . . . . . 245

26.1 26.2 26.3 26.4

U.N. Riede, J. Finke, M. Werner Hereditary cytopenia. . . . . . Acquired cytopenia. . . . . Hereditary malfunction. . . . Neoplasm pattern. . . . . . . .

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245 245 251 254

27

Lymph nodes. . . . . . . . . . . . . . . . . . . 262

U.N. Riede, J. Finke, M. Werner 27.1 Inflammation Patterns. . . . . . . . . . . . . . . . 262 27.2 Tumor-like patterns. . . . . . . . . . . . . . . . 264 27.3 Neoplasmic Pattern. . . . . . . . . . . . . . . . . . 265

28

Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . 273

28.1 28.2 28.3 28.4 28.5 28.6 28.7

U.N. Riede malformation pattern. . . . . Miscirculation pattern. . . . Inflammation patterns. . . . . Metabolic disorder pattern dysfunction pattern. . . . . Tumor-like patterns. . . . . Neoplasm pattern. . . . . . .

29

Thymus. . . . . . . . . . . . . . . . . . . . . . . . 277

29.1 29.2 29.3 29.4

U.N. Riede, J. Finke Malformation Pattern Inflammation Pattern Tumor-like Pattern Neoplasmic Pattern. .

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273 273 274 275 275 275 276

277 277 277 277

X respiratory system 30

Nose, sinuses. . . . . . . . . . . 283

U.N. Riede 30.1 Inflammation Pattern. . . . . . . . . . . . . . . . 283 30.2 Neoplasmic Pattern. . . . . . . . . . . . . . . . . . 284

31

Throat. . . . . . . . . . . . . . . . . . . . . . . . 286

U.N. Vineyard 31.1 Malformation pattern. . . . . . . . . . . . . . . . 286 31.2 Inflammation Pattern. . . . . . . . . . . . . . . . 287 31.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 288

32

Larynx. . . . . . . . . . . . . . . . . . . . . . . 290

U.N. Riede 32.1 Inflammation Pattern. . . . . . . . . . . . . . . . 290 32.2 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 291

33

Tracheobronchial system. . . . . . . . . . . . 293

33.1 33.2 33.3 33.4

U.N. Riede, H. Matthys Stenosis pattern. . . . . Dilation pattern. . . Inflammation patterns. Neoplasm pattern. . .

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293 294 294 297

XVI

Table of Contents

34

Lungs. . . . . . . . . . . . . . . . . . . . . . . . . 298

34.1 34.2 34.3 34.4 34.5

U.N. Riede, G. Kayser, N. Freudenberg, H. Matthys false circulation pattern. . . . . . . . . Malfunction pattern. . . . . . . . . . Inflammation patterns. . . . . . . . . . Fibrodestructive Patterns. . . . . . . . Neoplasm pattern. . . . . . . . . . . .

35

Pleura. . . . . . . . . . . . . . . . . . . . . . . . . 317

35.1 35.2 35.3 35.4

U.N. Riede, N. Freudenberg, H. Matthys Malfunction Patterns. . . . . . . . . . . Inflammation patterns. . . . . . . . . . . Fibrodestructive Patterns. . . . . . . . . Neoplasm pattern. . . . . . . . . . . . .

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298 300 302 311 312

317 317 318 318

XI digestive organs: head intestine oral cavity. . . . . . . . . . . . . . . . . . . . . 323

36.1 36.2 36.3 36.4 36.5

U.N. Riede, N. Weyer Malformation Pattern Inflammation Pattern Hyperplasia Pattern. Pre-neoplasia pattern neoplasia pattern. .

37

Chewing apparatus. . . . . . . . . . . . . . . . . . . . . 328

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40 40.1 40.2 40.3 40.4 40.5 40.6

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323 323 325 325 326

41.1 41.2 41.3 41.4 41.5 41.6 41.7

Salivary glands. . . . . . . . . . . . . . . . . . 332

38.1 38.2 38.3 38.4

U.N. Riede, N. Weyer Malfunction Patterns Inflammation Patterns Tumor-like Patterns Neoplasmic Patterns. .

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332 332 333 333

XII digestive organs: foregut 39

Esophagus. . . . . . . . . . . . . . . . . . . . . 339

U.N. Riede, H.E. Blum, M. Werner 39.1 Malformation Patterns. . . . . . . . . . . . . . . . 339 39.2 Dilation Pattern. . . . . . . . . . . . . . . . . . 339

. . . . . . . . . . . . . . 344 . . . . . .

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344 344 345 346 346 347

Small intestine. . . . . . . . U.N. Riede, H.E. Blum malformation pattern. . Malfunction pattern. . Dilation pattern. . . . Miscirculation pattern. Inflammation patterns. . Tumor-like patterns. . Neoplasm pattern. . . .

. . . . . . . . . . . . . . 353 . . . . . . .

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353 353 353 354 355 358 358

XIV digestive organs: rectum

U.N. Riede, N. Weyer 37.1 Patterns of Inflammation. . . . . . . . . . . . . . . . 328 37.2 Tumor-like patterns. . . . . . . . . . . . . . . . 329 37.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 330

38

Stomach. . . . . . . . . . . U.N. Riede, H.E. Blum malformation pattern. . Miscirculation pattern. Inflammation patterns. . Peptic ulcer disease. . . . . . Tumor-like patterns. . Neoplasm pattern. . . .

XIII Digestive organs: midgut 41

36

. . . . .

39.3 Incorrect circulation patterns. . . . . . . . . . . . . . . 340 39.4 Inflammation Patterns. . . . . . . . . . . . . . . . 340 39.5 Neoplasmic Pattern. . . . . . . . . . . . . . . . . . 341

42

Colon. . . . . . . . . . . . . . . . . . . . . . . 363

42.1 42.2 42.3 42.4 42.5 42.6

U.N. Riede, H.E. Blum, M. Werner, J.P. Baak malformation pattern. . . . . . . . . . . . . . Dilation pattern. . . . . . . . . . . . . . . . Miscirculation pattern. . . . . . . . . . . . . Inflammation patterns. . . . . . . . . . . . . . Tumor-like patterns. . . . . . . . . . . . . . Neoplasm pattern. . . . . . . . . . . . . . . .

43

Anal canal. . . . . . . . . . . . . . . . . . . . . . 373

43.1 43.2 43.3 43.4 43.5

U.N. Riede, H.E. Blum malformation pattern. . Miscirculation pattern. Inflammation patterns. . Tumor-like patterns. . Neoplasm pattern. . . .

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363 363 364 364 368 369

373 373 373 374 374

XVII Table of Contents

XV peritoneum

XVII urinary organs

44

Peritoneum. . . . . . . . . . . . . . . . . . . . . . . 379

44.1 44.2 44.3 44.4

U.N. Riede, H.E. Blum malfunction pattern dilation pattern. . Pattern of inflammation, neoplasmic pattern. .

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379 379 379 380

XVI digestive organs: hepatopancreas 45

Liver. . . . . . . . . . . . . . . . . . . . . . . . . 385

45.1 45.2 45.3 45.4 45.5 45.6 45.7

U.N. Riede, A. zur Hausen, H.E. Blum malformation pattern. . . . . . . . . . Metabolic disorder pattern. . . . . Miscirculation pattern. . . . . . . . . Inflammation patterns. . . . . . . . . . Toxic patterns. . . . . . . . . . . . . Tumor-like patterns. . . . . . . . . . Neoplasm pattern. . . . . . . . . . . .

46

Intrahepatic biliary tract. . . . . . . . . 406

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389 389 392 394 400 402 402

U.N. Riede, H.E. Blum 46.1 Malformation Pattern. . . . . . . . . . . . . . . . 406 46.2 Patterns of inflammation. . . . . . . . . . . . . . . . 406 46.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 408

47

Extrahepatic biliary tract. . . . . . . . . 409

47.1 47.2 47.3 47.4

U.N. Riede, H.E. Blum malformation pattern. . . . . Metabolic disorder pattern Inflammatory pattern. . . . . Neoplasm pattern. . . . . . .

48

Pancreas. . . . . . . . . . . . . . . . . . . . . . . 413

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409 409 411 411

U.N. Riede, H.E. Blum 48.1 Malformation Pattern. . . . . . . . . . . . . . . . 413 48.2 Patterns of inflammation. . . . . . . . . . . . . . . . 413 48.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 416

49

Kidneys. . . . . . . . . . . . . . . . . . . . . . . . . 421

49.1 49.2 49.3 49.4 49.5 49.6 49.7

U.N. Riede, K. Höpker Malformation Pattern. . . . . Miscirculation pattern. . . . Malfunction pattern. . . . . Metabolic disorder pattern Inflammatory pattern. . . . . Malfunction pattern. . . . . Neoplasm pattern. . . . . . .

50

Urinary tract. . . . . . . . . . . . . . 445

50.1 50.2 50.3 50.4 50.5

U.N. Riede, U. Wetterauer Malformation Pattern. . Dilation pattern. . . . Stenosis pattern. . . . . . Inflammation patterns. . Neoplasm pattern. . . .

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421 423 425 426 428 439 439

445 446 446 448 449

XVIII Reproduction: Male Organs 51

External genitals. . . . . . . . . . . . . . . . . 455

51.1 51.2 51.3 51.4 51.5

U.N. Riede, U. Wetterauer Malformation Pattern. . Malfunction pattern. . Inflammation patterns. . Pre-neoplasm pattern. . Neoplasm pattern. . . .

52

Prostate. . . . . . . . . . . . . . . . . . . . . . . . 458

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455 455 456 457 457

U.N. Riede, U. Wetterauer 52.1 Inflammation Patterns. . . . . . . . . . . . . . . . 458 52.2 Stenosis Pattern. . . . . . . . . . . . . . . . . . . . 459 52.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 459

53

Epididymis. . . . . . . . . . . . . . . . . . . . 463

U.N. Riede, U. Wetterauer 53.1 Inflammation Patterns. . . . . . . . . . . . . . . . 463 53.2 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 463

54

Testicles. . . . . . . . . . . . . . . . . . . . . . . . . 464

54.1 54.2 54.3 54.4

U.N. Riede, U. Wetterauer Malformation Pattern. . Malfunction pattern. . Miscirculation pattern. Inflammation patterns. .

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464 465 466 467

XVIII

Table of Contents

54.5 Tumor-like patterns. . . . . . . . . . . . . . . . 468 54.6 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 468

XIX reproduction: female organs 55

Vulva. . . . . . . . . . . . . . . . . . . . . . . . . . 475

55.1 55.2 55.3 55.4

U.N. Riede inflammation pattern Tumor-like pattern Preneoplasia pattern Neoplasia pattern. .

56

Vagina. . . . . . . . . . . . . . . . . . . . . . . . . 479

56.1 56.2 56.3 56.4

U.N. Riede, N. Freudenberg Malformation Patterns. . . Inflammation patterns. . . Tumor-like patterns. . . Neoplasm pattern. . . . .

57

Uterus. . . . . . . . . . . . . . . . . . . . . . . . . 481

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475 476 476 477

62

Ovaries. . . . . . . . . . . . . . . . . . . . . . 495

62.1 62.2 62.3 62.4

U.N. Riede, M. Orlowska-Volk Malformation Patterns. . . . . Inflammation patterns. . . . . Tumor-like patterns. . . . . Neoplasm pattern. . . . . . .

63

Placenta. . . . . . . . . . . . . . . . . . . . . . . 502

63.1 63.2 63.3 63.4 63.5

U.N. Riede, M. Orlowska-Volk Malformation Patterns. . . . . Malfunction pattern. . . . . Miscirculation pattern. . . . Inflammation patterns. . . . . Neoplasm pattern. . . . . . .

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495 495 495 496

502 503 504 504 505

XX skin organ. . . .

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479 479 480 480

U.N. Riede, N. Freudenberg 57.1 Malformation Patterns. . . . . . . . . . . . . . . . 481

58

Cervix uteri. . . . . . . . . . . . . . . . . . . . . 482

58.1 58.2 58.3 58.4

U.N. Riede, N. Freudenberg Inflammation Patterns. . . Tumor-like patterns. . . Pre-neoplasm pattern. . . Neoplasm pattern. . . . .

59

Endometrium. . . . . . . . . . . . . . . . . . . . 486

59.1 59.2 59.3 59.4 59.5

U.N. Riede, M. Orlowska-Volk, J.P. Baak malfunction pattern. . . . . . . . . . . Inflammation patterns. . . . . . . . . . . Tumor-like patterns. . . . . . . . . . . Pre-neoplasm pattern. . . . . . . . . . . Neoplasm pattern. . . . . . . . . . . . .

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482 482 482 483

64

Skin . . . . . . . . . . . . . . . . . . . . . . . . . . 509

U.N. Riede, M. Braun-Falco 64.1 Inflammation Pattern. . . . . . . . . . . . . . . . 510 64.2 Tumor-like patterns. . . . . . . . . . . . . . . . 513 64.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 513

65

Mammary gland. . . . . . . . . . . . . . . . . . . . . . 522

65.1 65.2 65.3 65.4

U.N. Riede, J.P. Baak, D. Mattern Malformation Pattern. . . . . . . Inflammation patterns. . . . . . . Tumor-like patterns. . . . . . . Neoplasm pattern. . . . . . . . .

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522 522 523 524

XXI endocrine organs. . . . .

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486 487 487 487 488

Myometrium. . . . . . . . . . . . . . . . . . . . 491 U.N. Vineyard 60.1 neoplasia pattern. . . . . . . . . . . . . . . . . . 491

66

Neurohypophysis. . . . . . . . . . . . . . . . . 535

U.N. Riede, J. Seufer 66.1 Malfunction Pattern. . . . . . . . . . . . . . . . 535

60

67

61

U.N. Riede, J. Seufer 67.1 Hyperplastic Patterns. . . . . . . . . . . . . . 536 67.2 Neoplastic patterns. . . . . . . . . . . . . . . 536 67.3 Malfunction patterns. . . . . . . . . . . . . . . . 538

Tuba uterina. . . . . . . . . . . . . . . . . . . . 493

U.N. Vineyard 61.1 Malformation pattern. . . . . . . . . . . . . . . . 493 61.2 Inflammation Pattern. . . . . . . . . . . . . . . . 493 61.3 Tumor-like patterns. . . . . . . . . . . . . . . . 494

68

Adenohypophysis. . . . . . . . . . . . . . . . . 536

Adrenal cortex. . . . . . . . . . . . . . . . 541

U.N. Riede, J. Seufer 68.1 Circulatory patterns. . . . . . . . . . . . . . . 541 68.2 Patterns of inflammation. . . . . . . . . . . . . . . . 541 68.3 Hyperplasia Pattern. . . . . . . . . . . . . . . . . 541

XIX Table of Contents

68.4 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 542 68.5 Malfunction patterns. . . . . . . . . . . . . . . . 543

69

Adrenal medulla. . . . . . . . . . . . . . . . 547

U.N. Riede, J. Seufer 69.1 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 547

70

Thyroid. . . . . . . . . . . . . . . . . . . . . 549

70.1 70.2 70.3 70.4

U.N. Riede, N. Freudenberg, J. Seufer Inflammation Pattern. . . . . . . . . Hyperplasia pattern. . . . . . . . . . Malfunction pattern. . . . . . . . . Neoplasm pattern. . . . . . . . . . .

71

Parathyroid gland. . . . . . . . . . . . . . . . 557

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549 551 553 554

U.N. Riede, J. Seufer 71.1 Hyperplasia pattern. . . . . . . . . . . . . . . . . 557 71.2 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 557 71.3 Malfunction patterns. . . . . . . . . . . . . . . . 558

72

Island organ. . . . . . . . . . . . . . . . . . . . . . 562

U.N. Riede, J. Seufer 73.1 Malfunction patterns. . . . . . . . . . . . . . . . 562 73.2 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 563

XXII Nervous System 74

76

Skeletal muscles. . . . . . . . . . . . . . . . 605

76.1 76.2 76.3 76.4 76.5

U.N. Riede, K. Müller, J. Lütschg Myopathic Patterns. . . . . . . . . . . . . . . Neurogenic atrophic pattern. . . . . . . . . . Endplate Damage Pattern. . . . . . . . . Inflammation patterns. . . . . . . . . . . . . . . . Neoplasm pattern. . . . . . . . . . . . . . . . . .

77

Bone tissue. . . . . . . . . . . . . . . . . 612

77.1 77.2 77.3 77.4 77.5 77.6

U.N. Riede, U. Gerlach Malformation Pattern. . . . . Metabolic disorder pattern, necrosis pattern. . . . . . . . . Inflammation patterns. . . . . Tumor-like patterns. . . . . Neoplasm pattern. . . . . . .

78

Joints. . . . . . . . . . . . . . . . . . . . . . . . 627

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605 607 608 609 610

612 614 619 620 621 622

Diffuse neuroendocrine system. . . . . 560

U.N. Riede, J. Seufer 72.1 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 560

73

XXIII Movement System

U.N. Vineyard 78.1 Fibrodestructive patterns. . . . . . . . . . . . . . 627 78.2 Patterns of inflammation. . . . . . . . . . . . . . . . 628

79

Tendofascial tissue. . . . . . . . . . . . . . . 633

79.1 79.2 79.3 79.4

U.N. Riede Fibrodestructive Patterns Inflammatory Patterns. . Tumor-like patterns. . Neoplasm pattern. . . .

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633 633 633 634

Central nervous system. . . . . . . . . . . . . . 567

U.N. Riede, K. Müller 74.1 Malformation Patterns. . . . . 74.2 Incorrect circulation patterns. . . . 74.3 Injury Pattern. . . . . . 74.4 Infantile cerebral palsy. . . 74.5 Malfunction Patterns. . . . . 74.6 Patterns of Metabolic Disorders 74.7 Toxic Patterns. . . . . . . . 74.8 Neurodegenerative Patterns. 74.9 Inflammation Pattern. . . . . 74.10 neoplasm pattern. . . . . . .

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567 571 574 575 576 577 579 580 583 590

Epilogue. . . . . . . . . . . . . . . . . . . . . . . . . . 639 Acknowledgments. . . . . . . . . . . . . . . . . . . . . . . . 641 Disclosure about a biopsy. . . . . 642 Disclosure about an autopsy. . . 642 Subject index. . . . . . . . . . . . . . . . . . . . . . 645

75

Peripheral nervous system. . . . . . . . . . . 598

U.N. Riede, K. Müller 75.1 Peripheral neuropathic patterns. . . . . . . . . 598 75.2 Patterns of inflammation. . . . . . . . . . . . . . . . 599 75.3 Neoplasmic pattern. . . . . . . . . . . . . . . . . . 600

I.

Basics 1

Introduction and methodology

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U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner

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Diagnostic strategies - shape patterns

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U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner

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Diagnostic strategies - color swatches

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U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner

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1 Introduction and methodology U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner>> Introduction Pathology is the medical subject that uses scientific methods to analyze the development mechanisms as well as the molecular genetic and morphological manifestations of a disease. Almost every disease is accompanied by a disorder that affects the structure of organs, tissues, cells or organelles. Therefore, the pathologist can assign tissue changes to a specific disease on the basis of removed tissue or cells, be it 4 through a hollow needle (needle biopsy), 4 through the endoscope (brush, forceps biopsy) or 4 through open excision derive their sequence.

Glossary Diagnostic forms of tissue collection Biopsy: small tissue sample, 1 cm resected material: removed diseased organ part, tumor extirpate: distant diseased organ, tumor amputate: distant extremity abladate: removed outer tissue Exkochleation: scraping a diseased focus from a tissue Enucleation: removal of a diseased organ tissue / Tumors Abradate: Scraping off a diseased tissue from a surface. Morcellement: Removal of a tissue / organ by dismembering it. Lumpectomy: Removal of a tumor and a safety margin

Ë Take-home-message Prerequisite for a biopsy assessment 4 Sufficient amount of biopsy material 4 Clinical information on disease, organ, location of removal 4 Adequate fixation (mostly 4% formaldehyde) 4 Paraffin embedding 4 Production of 4 μm thick tissue sections 4 Adequate tissue staining (mostly hematoxylin-eosin)

There is no legal obligation to provide biopsy protection for therapeutic action, but there is a clear justification and documentation. In addition, the histological diagnosis (until now!) Is the safest and cheapest. 1.1

Histopathology

Process flow

Tissue extraction 7 adequate fixation (mostly 4% formaldehyde) 7 possibly tissue decalcification 7 tissue drainage with alcohol in increasing concentration 7 embedding in paraffin 7 production of 4 μm thick tissue sections 7 deparaffinization of the tissue sections 7 tissue section application on microscope slide 7 tissue staining (mostly hematoxilin) ​​7 Diagnosis, . Fig.13.12 Processing time

4 single rush procedures: 6 hours 4 routine procedures: 12 hours accuracy (almost) 100%. Use of standard procedures. 1.2

Quick cut

Process flow

Tissue removal 7 Biopsy sent to pathologist in unfixed state 7 Production of frozen sections 7 Tissue staining (hematoxilin-eosin). Processing time Specialist microscopic assessment within 5–10 minutes Accuracy Due to the fast fixation process and the greater incision thickness less than with conventional fixation, 98%. Use During a surgical procedure to secure the further operative procedure, e.g. B. Tumor Exclusion.

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Chapter 1 · Introduction and methodology

clinic

1

It is important to talk to patients about the procedure and the benefits of a biopsy. You will find a suggestion for an appropriate »informative discussion« with the patient in the appendix on page 642.

1.3

Crush preparation

Process flow

Stereotactic control 4 needle biopsy 4 tissue squeezing between two microscope slides,. Fig.74.11

4 staining 4 specialist assessment of the cells contained therein. Processing time 5–10 minutes, accuracy 95%. Application Unclear mass in the brain. 1.4

cytology

Puncture cytology process flow

Piercing a diseased organ with a thin needle (fine needle biopsy) 4 Sucking in the cells with a syringe 4 Pressure equalization before pulling the needle out of the tissue 4 Streaking the cells on a slide,. Fig.13.3. Processing time 30 minutes.High accuracy. Application of tumor exclusion diagnostics. Exfoliative cytology process flow

Cell smear from tissue surface or centrifuged cells from body fluids → staining,. Fig. 58.1a – d. Processing time 30 min. Application of tumor exclusion diagnostics.

1.5

Electron microscopy

Process flow

Pre-fixation of a max. 1 mm biopsy sample with a buffered glutaraldehyde / paraformaldehyde mixture 4 Post-fixation with lipophilic osmic acid (cell membrane display!) 4 Embedding in synthetic resin (araldite) 4 Production of ultra-thin sections (70 nm) 4 Contrasting with heavy metal salts such as lead microscope and analysis of the uranyl calcium. Processing time 3 days. Accuracy Depending on the question. application

4 Virus detection 4 Assessment of membrane changes 4 Detection of metabolic products 1.6

Immunohistochemistry

Process flow

Binding of an antibody (primary antibody) to a specific cell / tissue antigen (primary reaction) 4 Binding of a second antibody against the antigen-antibody complex of the primary reaction (secondary reaction), 4 Visualization by coupling with a marker molecule (fluorescent dye, enzyme, colloidal gold). Primary antibodies can be: 4 Polyclonal antibodies: Antibody mixture against different epitopes of the applied antigen by immunizing an animal species with purified antigen. Occasionally cross reactions with other antigens. 4 Monoclonal antibodies: Antibodies produced by 1 appropriately immunized cell after immortalization and multiplication, i. H. Formation of only 1 type of antibody with high specificity against 1 epitope of the applied antigen,. Fig. 14.4,. Fig. 27.2. Processing time 5 hours. Accuracy Rarely false positive results. Application of tumor diagnostics.

5 1.8 · Autopsy

1.7

Molecular pathology

A distinction is made: 4 DNA analysis: direct assessment of the functional state of a gene 4 RNA analysis: indirect assessment of the functional state of a gene Methodology

4 Hybridization (hybrida, Latin = bastard): Principle: Binding (hybridization) of a synthesized or cloned copy sample (DNA or cDNA) known in its sequence to the corresponding complementary nucleotide sequence that is suspected in the sample to be examined. 4 Polymerase chain reaction (polymerase chain reaction, PCR): This allows DNA resp. Propagate cDNA fragments. PCR sequence: heat denaturation of the DNA extract → cooling. Hybridization of the 2 primers in the form of short DNA sequences flanking the gene segment in question to their specific complementary sequence. Heat-stable DNA polymerase (starting from the primers) reads the respective template strands and synthesizes the corresponding complementary strand → duplication of the specific template DNA after each cell cycle → amplification of the gene segment sought. 4 DNA sequence analysis: Base-specific breakdown of the synthesis of the 5‘-3‘ strand of the DNA segment to be sequenced → Formation of DNA fragments of different sizes, the size of which reflects the position of the respective nucleotide base → Determination of the base sequence of the analyzed DNA segment. 4 Cytogenetics: Chromosome examination of vital cultured cells → metaphase preparation → karyotyping using different banding techniques. Processing time 3 days. Accuracy Depending on the question. application

4 Infection: Detection of pathogen DNA 4 Hereditary disease: Detection of DNA changes 4 Diagnostics: Detection of tumor-specific mutations

1

4 Prognostics / Prediction: Evidence of oncogene amplification / tumor suppressor gene defects with prognostic and therapeutic relevance. 1.8

autopsy

DEF Internal examination according to pathological-anatomical criteria. If the organs are presented to the clinician by the pathologist, it is an autopsy (obducere, Latin = to present). The autopsy means a major intervention for the deceased and the relatives, on the basis of which 4 the suffering and the history of the suffering are traced or determined, 4 the clinical diagnoses are checked, 4 the ailment leading to death is determined, 4 the pathogenetic reaction sequence of all pathogenic processes is ensured and 4 the genetic causes of an illness are often also clarified. Administrative autopsy

In legally prescribed cases with sudden death from an unclear or unnatural cause or death due to third-party / self-fault. Order: Public Prosecutor. Implementation: (mostly) forensic doctors. Epidemic autopsy

In cases where there is no clinical suspicion of a contagious infectious disease. Order: Health Department. Execution: pathologist. Clinical autopsy

For those who have died in hospital (quality assurance!). Implementation: Pathologist, but only with the consent of relatives or the patient himself (living will). Insurance autopsy

Required by the insurance company in the event of 4 sudden death from an unclear and / or unnatural cause, 4 occupational exposure to noxious substances. Execution: pathologist. Clinic It is important to speak objectively with relatives of a deceased person about the benefits of an autopsy. You will find a suggestion for an appropriate »informative discussion« with relatives in the appendix on page 642.

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Chapter 1 · Introduction and methodology

Ë Take-home-message Autopsy 4 The autopsy is the only method for uncovering external influences or treatment errors (quality assurance!). 4 Rejection of an autopsy by relatives, never if there is an insurance claim!

Ì Deepening of knowledge Probability of error in clinical (main) diagnoses 4 Probability of error in all diagnoses made for a patient in the clinic: 30% 4 Incorrect diagnosis of pulmonary embolism, myocardial infarction: 50% 4 Incorrect diagnosis of liver cirrhosis: 30% 4 Incorrect diagnosis of liver, biliary tract and kidney carcinoma : 50%

1.9

(Individual) death

DEF Irreversible extinction of the vital functional processes of an individual, recognizable by signs of death. 1.9.1 Dying DEF Process leading to biological death of a patient with a phased course. KPG trigger mechanisms Death occurs in a patient when certain major organs fail to function properly. In most cases, intensive medical measures can delay the failure of a main organ (Vita reducta!) Until a multiple organ failure occurs. With regard to dying, these main organs are also referred to as "death entry gates" (atria mortis). 4 Heart: The pump function goes out, resulting in cardiac insufficiency and cardiac arrest. 4 Brain (trunk, midbrain): failure of the vegetative centers, such as the respiratory center under the image of brain death. 4 lungs: loss of gas exchange function, resulting in respiratory insufficiency with suffocation. 4 Liver: loss of detoxification function, resulting in liver insufficiency with general metabolic poisoning and resulting hepatic coma (unconscious disturbance of consciousness).

4 Kidneys: loss of the toxin excretion function, resulting in renal insufficiency with acute kidney failure. The process of dying takes place in 3 phases: 4 Agony (Gr. = Agony): State of reduced life (Vita reducta) with liver and / or kidney failure (7 Ch. 45, 7 Ch. 49) 4 Clinical death (relative death): Condition with circulatory and / or respiratory arrest or multiple organ failure 4 Intermediate life (premortal phase): phase until brain function ceases Clinical phases of death The patient experiences the awareness of having to die in the foreseeable future in the following phases: 1st phase of not wanting to be aware of the Diagnosis and the resulting isolation from society 2nd phase of anger (heteroaggression, "Why me?") 3rd phase of negotiating with good administration before God and hospital staff, so to speak, to obtain a deadline extension 4th phase of depression (autoaggression) with grief the loss of a part of the body and / or a share in society due to illness (awareness of replaceability) 5th phase of consent with need n oh rest, sleep, redemption

1.9.2 Signs of death Uncertain signs of death (clinical death) Cardiac arrest, pulselessness, respiratory arrest, lack of reflexes, drop in temperature Clinical brain death criteria 4 EEG zero line over 24 h 4 Two angiographic evidence at intervals of 30 min of the cerebral circulation 4 irreversible absence of spontaneous breathing 4 irreversible areflexia (Corneal, pupillary reflex!).

7 1.11 · Disease terminology

Sure signs of death 4 death spots (Livores): red-violet, pushable spots (. Fig. 3.11b) in the deepest parts of the body, because the severity of the blood accumulates in the venous system there after the cardiac arrest. 4 Rigor mortis: It begins cranially 3–6 hours after death due to an ATP deficiency and consecutive actin and myosin filament cross-linking. It progresses caudally. Solution of rigor mortis from caudal to cranial (Nysten rule). 4 Autolysis (corpse putrefaction): 7 chap. 1.10. 1.10

Autolysis

DEF Morphological correlate for the death of whole body tissue or a separated organ / tissue, e.g. B. Amputate. KPG trigger mechanism The organism no longer develops any resistance to massive damage, so that the tissue dissolves due to the following mechanisms: 4 by its own lysosomal enzymes (autolysis), 4 by anaerobes that are post-mortem or already intravitally from the inner (intestinal lumen) or outer surface of the body (Skin) have penetrated the organism, putrefaction develops, 4 due to the action of gastric acid, a softening of the stomach wall develops (gastromalacia acida). Ì Deepening knowledge of factors influencing autolysis 4 high core temperature of the deceased (fever, sepsis) 4 "thermal insulation" of the deceased by a layer of skin fat 4 high ambient temperature 4 hardly any heat-conducting ambient medium Casper's rule Comparable putrefaction at comparable temperatures: 1 week air, 2 weeks water, 8 weeks Earth.

Ë Take-home-message Necrosis: the death of tissue in the living organism. Autolysis: death of tissue in the dead (partial) organism.

1.11

1

Disease terminology

Glossary Statistical measures Average life expectancy: time span after 50% death of a certain population group, e. B. Women. Incidence: Number of new cases of a specific disease per year and per 100,000 population. Prevalence: the number of people suffering from a specific disease on a given day per 100,000 population. Morbidity: Number of people suffering from a specific disease per year and per 100,000 population.Mortality: Number of people who die from a particular disease per year and per 100,000 population. Lethality: the ratio of the number of people who have died from a certain disease to the number of people who are sick.

health

State of perfect physical, mental, social well-being (WHO definition). illness

Disturbance of those life processes that change the organism of a person or parts of it in such a way that it becomes clinically or socially in need of help. etiology

Is concerned with the trigger mechanism of a certain disease / malformation and thus with the question of which damaging processes can be considered as the cause. All diseases are triggered by tissue / cell damaging influences that act individually or together on the organism and have the following properties: 4 animated-exogenous, such as viruses, bacteria, fungi, parasites 4 animated-endogenous, such as inflammatory, immune, tumor -Cells 4 inanimate-exogenous, such as physico-chemical noxae 4 inanimate-endogenous, such as genetic, metabolic, circulatory disorders

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Chapter 1 · Introduction and methodology

Causal pathogenesis

Is concerned with the interplay between the causes of disease and the willingness of the organism that leads to the manifestation of a disease and explains its trigger mechanism. Formal pathogenesis

Is concerned with those reaction processes that are responsible for the structural change of a tissue in the course of a disease and that give a disease a tissue-like face.

All damaging influences are either 4 so intense that they cause cells / tissue to die or 4 can be overcome by the affected tissue by means of an adaptation reaction or 4 decouple the affected cells from the physiological regulatory mechanisms. This results in the tissue changes that are typical of the disease.

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2 diagnostic strategies - shape pattern U.N. Riede, H.E. Blum, N. Freudenberg, M. Werner>> Introduction

Ì Deepening knowledge of the sectional structure transformation principle

The term form pattern encompasses a series of formal pathogenetic principles which shape the macroscopically detectable tissue changes of the various diseases and which represent the tools for making a diagnosis through clinical inspection.

A 3-dimensional structure (3-D structure) loses 1 dimension through a tissue cut. Morphological consequences of this are: 4 sphere becomes disc, tube becomes circle, 4 surface becomes line, membrane becomes line, 4 line becomes point, fiber becomes point.

Glossary Necrosis: Dead tissue area that has become visible in the living organism. Detritus: "cell debris" from the corpse of cells. Infarct: necrosis as a result of a blood flow stop. Cytology: neutrophils and cell debris. Inflammation: vascular and cellular defense reaction of the living organism to harmful noxa (suffix "-itis"). Tumor: circumscribed new cell / tissue formation through autonomous and deregulated cell growth. Neoplasia: generic term for tumor-like tissue / cell new formations (suffix "-om"). Infiltration, in the medical sense: passive penetration of solid / liquid substances into a tissue. Infiltration, in the histological sense: active, (mostly) localized penetration of non-localized cells in the form of inflammatory cells or tumor cells into a tissue. Attention: The term infiltration does not apply to the passive erythrocyte leakage into the tissue or to the multiplication of local cells! Proliferation, (proles ferre, Latin = to produce offspring): mitotic cell proliferation. Degeneration: Replacement of a fully-fledged tissue with a functionally inferior tissue. Synchronous: simultaneous manifestation of a lesion. Metachron: staggered manifestation of a lesion.

Ë Take home message Every doctor must master these minimum diagnostic requirements in order to be able to take meaningful biopsy material from the correct tissue sites for pathohistological / cytological examination.

2.1

2D elements

DEF umbrella term for two-dimensional damage

patterns that manifest themselves on the surface or on the cut surface of an organ / tissue. 2.1.1

Surface elements

DEF characterization of 2D lesions with regard to their area distribution (. Fig. 2.1).

. Fig.2.1. Pathomorphological basic elements: surface elements

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Chapter 2 · Diagnostic Strategies - Shape Patterns

2.1.1.1 Diffuse lesion DEF (syn .: indistinctly delimited lesion) Lesion without sharp delimitation to the surrounding tissue due to the following processes: 4 Storage of inflammatory, congestion-related fluids (. Fig. 12.1) or metabolic products. 4 Infiltration by mobile or sedentary cells in the case of inflammation or tumor. Clinical features In the case of a diffuse lesion, a biopsy is indicated if a tumor is suspected.

2.1.1.2 Large lesion DEF macrofocals, d. H. palpable, well-circumscribed lesion several centimeters in size (. Fig. 5.7,. Fig. 13.7). Clinical features In the case of a large lesion, a biopsy is indicated.

2.1.1.3 Small lesion DEF microfocal, d. H. Well-circumscribed, barely palpable lesion at the limit of visibility (. Fig. 9.7). Clinical features In the case of a small lesion, there is no indication for a biopsy due to the risk of the »wrong target«. If a tumor is suspected, however, an excision is advisable.

. Fig 2.2. Basic pathomorphological elements: contour patterns

2.1.1.4 Multiple lesions DEF (Syn .: multifocal lesions) Syn- / metachronic occurrence of several foci within a tissue / organ (. Fig. 34.6). 2.1.1.5 Systemic lesions DEF syn- / metachronous occurrence of numerous lesion foci within the whole organism or within an organ system due to the following processes: 4 metabolic with storage in or damage to a cell / tissue system, 4 inflammatory with spreading of pathogens, 4 neoplastic with cell seeding or neoplasia of a system 2.1.2

Contour elements

DEF outline characterization of 2D elements

(. Fig. 2.2). 2.1.2.1 Blurred contour It is the result of the following tissue changes: 4 Infiltration: Diffuse tissue penetration with 5 fluids such as water / blood serum (. Fig. 12.1), 5 metabolic products such as fat, pigment (. Fig. 8.4), 5 environmental gases such as Air, bacterial gases, 5 circulating cells such as inflammatory cells, v. a. in acute inflammation (. Fig. 64.1), 5 proliferating local cells, such as tumor cells (. Fig. 16.2,. Fig. 45.8,. Fig. 65.4,. Fig. 74.8), 5 proliferating fibroblasts with scarring (. Fig. 11.6, . Fig. 34.8a).

11 2.2 3D elements

2

Clinic palpable findings Fluid retention: painless, resilient tissue swelling, e.g. B. Edema. Metabolic product storage: painless, doughy tissue thickening, e.g. B. Obesity. Gas retention: painless, crackling tissue thickening, e.g. skin emphysema. Circulating inflammatory cells: painful red swelling. Circulating and / or local tumor cells: non-painful, coarse elastic swelling. Scarring: not painful, hard and tough tissue compression.

. Fig. 2.3. Basic pathomorphological elements: structural patterns

2.1.3

Structural elements

DEF with regard to characterization of 2D lesions

their tissue distribution (. Fig. 2.3). 4 Cell / tissue shrinkage due to the following trigger mechanisms: 5 Diffuse-progressive reduction of local cells in a tissue in degenerative or autoaggression diseases (. Fig. 6.9,. Fig. 48.1,. Fig. 74.4). 5 Diffuse-progressive decrease in circulating cells (erythrocytes) in a tissue. 5 Subtotally simultaneous destruction of parenchyma cells in an organ with subsequent wrinkling of the capsule (. Fig. 10.1). 2.1.2.2 Sharp contour This is the result of the following focal lesions mentioned in the "surface defect patterns": 4 cell death with / without inflammatory demarcation due to the following processes: 5 blood flow stop → infarction (. Fig. 5.1), 5 degenerative cell / tissue loss → apoptosis (. Fig. 15.4), 5 necrotic-enzymatic cell / tissue fusion → tissue liquefaction → abscess formation (. Fig. 5.4). 4 Cell proliferation: 5 passive with erythrocyte proliferation due to blood congestion (. Fig. 45.2), 5 active with (primarily chronic) inflammatory cell infiltration (. Fig. 34.6), 5 active with encapsulated tumor cell growth (. Fig. 16.1).

2.1.3.1 Diffuse structure DEF (Syn .: blurred structure) opposite

Surrounding area, indistinctly demarcated lesion on the tissue surface or on the organ / tissue cut surface (7 Section 2.1.1.1): 4 Tissue compression due to cellular infiltration or tissue compression (. Fig. 13.7) 4 Tissue loosening due to infiltration with air or with fluid (. Fig. 12.1 ). 2.1.3.2 Striated, stringy structure DEF Striated structure densities in the tissue with preference for direction (. Fig. 34.8a). 2.1.3.3 Reticular structure DEF Reticular structure compression in the tissue without directional preference (reticulum, Latin = net,. Fig. 16.6,. Fig. 34.7). 2.1.3.4 Cystic / cancellous structure On the cystic or cancellous structure, 7 Chap. 2.2.3. 2.2

3D elements

DEF umbrella term for three-dimensional damage

patterns as they appear after the 3D reconstruction of the tissue sections and / or in the imaging. 2.2.1

Surface defect pattern

Clinical features A lesion with a sharp contour is indicated for a biopsy.

DEF Inspectorally detectable damage patterns as a result of local tissue destruction from an external body surface (skin, 7 Chap. 64) or from internal

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Chapter 2 · Diagnostic Strategies - Shape Patterns

2.2.1.5 Fistulous lesion Fistula, (fistula, Latin = pipe): Pathological, narrow tubular connection between 4 1 hollow organ with 1 other hollow organ, 4 1 hollow organ and the skin surface, 4 2 duct systems.

2

Healing: scarring defect healing. 2.2.2. Fig 2.4. Basic pathomorphological elements: surface lesions

Surfaces (mucous membrane, serosa) extend deep into the underlying tissue (. Fig. 2.4). 2.2.1.1 Erosive lesion Erosion: Flat, pit-like tissue defect as a result of trauma, inflammation or necrosis in the area of ​​an epithelial-covered surface of the skin, the duct systems (. Fig. 64.1) or the mucous membranes of hollow organs, v. a. Aerodigestive tract (. Fig. 3.17). The lesion basically only affects the epithelial layer and not the underlying vascular layer of connective tissue. Healing: complete, with no remaining defect. 2.2.1.2 Pseudomembranous lesion Pseudomembrane: membrane-like, flat deposits of fibrin and cell debris (detritus) on the erosively damaged surface of hollow organs, such as the aerodigestive tract (. Fig. 13.5). 2.2.1.3 Ulcerative lesion Ulcer: Hemispherical tissue defect on an epithelial-covered surface such as the skin, the ducts or the mucous membrane of hollow organs (. Fig. 5.13,. Fig. 16.2). The lesion crosses the epithelial layer and injures the underlying vascular layer of connective tissue, resulting in profuse bleeding in a fresh lesion. Healing: scarring defect healing. 2.2.1.4 Fissural lesion Fissure, (fissus, Latin = split): Ax-like, deeply penetrating lesion 4 due to overstretching (mostly single) or 4 due to inflammation, (mostly multiple, e.g. in Crohn's disease, 7 chap. 41.5.5). Healing: possibly defect healing.

Surface growth pattern