DOCSLIB.ORG

Dijagnoze.Pdf

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Str.: 1 18.09.2020 Dijagnoze Oznaka Latinski Naziv Dijagnoze Srpski Naziv Dijagnoze 0 Nepoznata Nepoznata A00 Cholera Kolera A000 Cholera classica Kolera, uzrocnik Vibrio cholerae 01,biotip cholerae A001 Cholera El Tor Kolera, uzrocnik Vibrio cholerae 01,biotip El Tor A009 Cholera, non specificata Kolera, neoznacena A01 Febris typhica et febris paratyphica Tifusna groznica i paratifusna groznica A010 Typhus abdominalis Trbusni tifus A011 Paratyphus A Paratifus A A012 Paratyphus B Paratifus B A013 Paratyphus C Paratifus C A014 Paratyphus, non specificatus Paratifus, neoznacen A02 Salmonelloses aliae Druge infekcije uzrokovane salmonelama A020 Enteritis salmonellosa Zapaljenje tankog creva uzrokovano salmonelama A021 Salmonellosis septica Sepsa uzrokovana salmonelama A022 Infectio per salmonellam localisata Lokalizovana infekcija salmonelama A028 Infectio per salmonellam alia, specificata Druga oznacena infekcija salmonelama A029 Infectio per salmonellam, non specificata Salmonelozna infekcija, neoznacena A03 Shigellosis Dizenterija, uzrocnik Shigellae A030 Dysenteria bacillaris per Shigellam dysenteriae Dizenterija, uzrocnik Shigella dysenteriae A031 Dysenteria bacillaris per Shigellam flexneri Dizenterija, uzrocnik Shigell flexneri A032 Dysenteria bacillaris per Shigellam boydi Dizenterija, uzrocnik Shigella boydi A033 Dysenteria bacillaris per Shigellam sonnei Dizenterija,uzrocnik Shigella sonnei Shigellosis D A038 Shigellosis alia Druga dizenterija A039 Shigellosis, non specifiata Dizenterija, neoznacena A04 Infectiones intestinales bacteriales aliae Druge infekcije creva uzrokovane bakterijama A040 Infectio intestinalis per Escherichiam coli enteropathogenem Balantidijaza, uzrocnik Balantidium coli A041 Infectio intestinalis per Escherichiam coli enterotoxigenem Infekcija creva,uzrocnik enterotoksigena Escherichia coli A043 Infectio intestinalis per Escherichiam coli enterohaemorrhagicam Infekcija creva,uzrocnik enterohemoragijska Escherichia coli A044 Infectio intestinalis per Escherichiam coli alia Druga infekcija creva,uzrocnik Escherichia coli A045 Enteritis campylobacterialis Zapaljenje creva, uzrocnik Campylobacter A046 Enteritis yersiniosa enterocolitica Zapaljenje tankog creva,uzrocnik Yersinia enterocolitica A047 Enterocolitis per Clostridium difficile Zapaljenje creva, uzrocnik Clostridium difficile A048 Infectio intestinalis bacterialis alia,specificata Druga oznacena infekcija creva uzrokovana bakterijama A049 Infectio intestinalis bacterialis, non specificata Infekcija creva, uzrokovana bakterijama ,neoznacena A05 Intoxicationes alimentariae bacteriales aliae Druga trovanja hranom uzrokovana bakterijama A050 Intoxicatio allmentaria staphylococcica Trovanje hranom uzrokovano stafilokokom A051 Botulismus Trovanje konzervisanom hranom od mesa A052 Intoxicato ailmentaria per Clostridium perfringentem (Clostridium welchii) Trovanje hranom,uzrocnik Clostridium perfringens (Clostridium welchii) Str.: 2 18.09.2020 Dijagnoze Oznaka Latinski Naziv Dijagnoze Srpski Naziv Dijagnoze A053 Intoxicatio alimentaria per Vibrionem parahaemolyticam Trovanje hranom,uzrocnik Vibrio parahaemolytica A054 Intoxicatio alimentaria per Bacillum cereum Trovanje hranom, uzrocnik Bacillus cereus A058 Intoxicationes alimentariae bacteriales aliae ,specificatae Druga oznacena trovanja hranom uzrokovana bakterijama A059 Intoxicatio alimentaria bacterialis,non specificata Trovanje hranom uzrokovano bakterijama ,neoznaceno A06 Amoebiasis Amebijaza,uzrocnik patogena ameba A060 Dysenteria amoebica acuta Akutna dizenterija uzrokovana amebama A061 Amoebiasis intestinalis chronica Hronicna amebijaza creva A062 Colitis amoebica non dysenterica Nedizentericko zapaljenje debelog creva uzrokovano amebama A063 Amoeboma intestinale Amebom,tumor creva uzrokovan amebama A064 Abscessus hepatis amoebicus Zagnoj jetre uzrokovan amebama A065 Abscessus pulmonis amoebicus (J99.8*) Zagnoj pluca uzrokovan amebama A066 Abscessus cerebri amoebicus (G07*) Zagnoj mozga uzrokovan amebama A067 Amoebiasis cutanea Amebijaza koze A068 Infectio amoebica loci alterius Infekcija druge lokalizacije uzrokovana amebama A069 Amoebiasis, non specificata Amebijaza, neoznacena A07 Infectiones intestinales protozoicae aliae Druge infecije creva uzrokovane protozoama A070 Balantidiasis Balantidijaza, uzrocnik Balantidium coli A071 Giardiasis (lambliasis) Gjardijaza, uzrocnik Lamblia intestinalis A072 Cryptosporidiasis Kriptosporidijaza, uzrocnik Cryptosporidium A073 Isosporiasis Izosporijaza ,uzrocnik Isospora belli et Isospora hominis A078 Infectiones intestinales protozoicae aliae,specificatae Druge oznacene infekcije creva uzrokovane protozoama A079 Infectio intestinalis protozoica,non specificata Infekcije creva uzrokovane protozoama,neoznacene A08 Infectiones intestinales virales Infekcije creva uzrokovane virusima A080 Enteritis rotaviralis Zapaljenje tankog creva uzrokovano rotavirusima A081 Gastroenteritis acuta Norwalk Akutno Norwalkovo zapaljenje zeluca i tankog creva A082 Enteritis adenoviralis Zapaljenje tankog creva uzrokovano adenovirusima A083 Enteritis viralis alia Druga zapaljenja tankog creva uzrokovana virusima A084 Infectio intestinalis viralis, non specificata Infekcija creva uzrokovana virusima,neoznacena A085 Infectiones intestinales aliae,specificatae Druge oznacene infekcije creva A09 Diarrhoea et gastroenteritis, causa infectionis suspecta Proliv i zeludacno -crevno zapaljenje,verovatno zaraznog porekla A15 Tuberculosis organorum respiratoriorum,per bacteriologiam et histologiam confirm Tuberkuloza organa za disanje potvrdena bakterioloski i histoloski A150 Tuberculosis pulmonis, per microscopiam sputi confirmata Tuberkuloza pluca,potvrdena mikroskopijom ispljuvka A151 Tuberculosis pulmonis, solum culture confirmata Tuberkuloza pluca, potvrdena samo kulturom A152 Tuberculosis pulmonis, per histologiam confirmata Tuberkuloza pluca, potvrdena histoloski A153 Tuberculosis pulmonis, methodis non specificatis confirmata Tuberkuloza pluca, potvrdena neoznacenim metodama A154 Tuberculosis lymphonodorum intrathoracalium,per bacteriologiam et histologiam co Tuberkuloza limfnih cvorova u grudnom kosu,potvrdena bakterioloski i histoloski A155 Tuberculosis laryngis, tracheae et bronchi,per bacteriologiam et histologiam con Tuberkuloza grkljana,dusnika i dusnice,potvrdena bakterioloski i histoloski A156 Pleuritis tuberculosa,per bacteriologiam et histologiam confirmata Tuberkulozno zapaljenje porebrice,potvrdeno bakterioloski i histoloski. Str.: 3 18.09.2020 Dijagnoze Oznaka Latinski Naziv Dijagnoze Srpski Naziv Dijagnoze A157 Tuberculosis pulmonis primaria, per bacteriologiam et histologiam confirmata Primarna tuberkuloza pluca,potvrdena bakterioloski i histoloski A158 Tuberculosis pulmonis,per bacteriologiam et histologiam confirmata alia Druga tuberkuloza pluca,potvrdena bakterioloski i histoloski A159 Tuberculosis organorum respiratoriorum,per bacteriologiam et histologiam confirm Tuberkuloza organa za disanje,potvrdena bakterioloski i histoloski ,neoznacena A16 Tuberculosis organorum respiratoriorum,per bacteriologiam et histologiam non con Tuberkuloza organa za disanje,nepotvrdena bakterioloski i histoloski A160 Tuberculosis pulmonis, bacteriologice et histologice negativa Tuberkuloza pluca, bakterioloski i histoloski negativna A161 Tuberculosis pulmonis, sine exploratione bacteriologica et histologica Tuberkuloza pluca,bez bakterioloskog i histoloskog ispitivanja A162 Tuberculosis pulmonis,sine confirmatione bacteriologica sive histologica Tuberkuloza pluca, bez bakterioloske ili histoloske potvrde A163 Tuberculosis lymphonodorum intrathoracalium Tuberkuloza limfnih cvorova u grudnom kosu A164 Tuberculosis laryngis, tracheae et bronchi Tuberkuloza grkljana,dusnika i dusnice A165 Pleuritis tuberculosa Tuberkulozno zapaljenje porebrice A167 Tuberculosis pulmonis primaria Primarna tuberkuloza pluca A168 Tuberculosis organorum respiratoriorum alia Druga tuberkuloza organa za disanje A169 Tuberculosis organorum respiratoriorum,non specificata Tuberkuloza organa za disanje, neoznacena A17 Tuberculosis systematis nervosi Tuberkuloza nervnog sistema A170 Meningitis tuberculosa (G01*) Tuberkulozno zapaljenje mozdanica A171 Tuberculoma meningium (G07*) Tuberkulozni cvoric mozdanica A178 Tuberculosis systematis nervosi alia Druga tuberkuloza nervnog sistema A179 Tuberculosis systematis nervosi, nonspecificata Tuberkuloza nervnog sistema, neoznacena A18 Tuberculosis organorum aliorum Tuberkuloza drugih organa A180 Tuberculosis ossium et articulorum Tuberkuloza kostiju i zglobova A181 Tuberculosis systematis genitourinarii Tuberkuloza polno-mokracnog sistema A182 Tuberculosis lymphoglandularum peripherica Tuberkuloza perifernih limfnih cvorova A183 Tuberculosis glandularum intestinalium,peritonaealium et mesentericarum Tuberkuloza zlezda creva,trbusne maramice i opornjaka A184 Tuberculosis cutis et subcutis Tuberkuloza koze i potkoznog tkiva A185 Tuberculosis oculi Tuberkuloza oka A186 Tuberculosis auris Tuberkuloza uva A187 Tubercuiosis glandularum suprarenalium Tuberkuloza nadbubreznih zlezda A188 Tuberculosis organorum ailorum,specificatorum Tuberkuloza drugih oznacenih organa A19 Tuberculosis miliaris Rasejana tuberkuloza A190 Tuberculosis miliaris acuta, loci specificati Akutna rasejana tuberkuloza, oznacene lokalizacije A191 Tuberculosis miliaris acuta, locorum multiplicum Akutna rasejana tuberkuloza ,visestrukih lokalizacija A192 Tuberculosis miliaris acuta, non specificata Akutna rasejana tuberkuloza, neoznacena A198 Tuberculosis miliaris alia Druga rasejana tuberkuloza
Recommended publications
  • General Pathomorpholog.Pdf

    General Pathomorpholog.Pdf

    Ukrаiniаn Medicаl Stomаtologicаl Аcаdemy THE DEPАRTАMENT OF PАTHOLOGICАL АNАTOMY WITH SECTIONSL COURSE MАNUАL for the foreign students GENERАL PАTHOMORPHOLOGY Poltаvа-2020 УДК:616-091(075.8) ББК:52.5я73 COMPILERS: PROFESSOR I. STАRCHENKO ASSOCIATIVE PROFESSOR O. PRYLUTSKYI АSSISTАNT A. ZADVORNOVA ASSISTANT D. NIKOLENKO Рекомендовано Вченою радою Української медичної стоматологічної академії як навчальний посібник для іноземних студентів – здобувачів вищої освіти ступеня магістра, які навчаються за спеціальністю 221 «Стоматологія» у закладах вищої освіти МОЗ України (протокол №8 від 11.03.2020р) Reviewers Romanuk A. - MD, Professor, Head of the Department of Pathological Anatomy, Sumy State University. Sitnikova V. - MD, Professor of Department of Normal and Pathological Clinical Anatomy Odessa National Medical University. Yeroshenko G. - MD, Professor, Department of Histology, Cytology and Embryology Ukrainian Medical Dental Academy. A teaching manual in English, developed at the Department of Pathological Anatomy with a section course UMSA by Professor Starchenko II, Associative Professor Prylutsky OK, Assistant Zadvornova AP, Assistant Nikolenko DE. The manual presents the content and basic questions of the topic, practical skills in sufficient volume for each class to be mastered by students, algorithms for describing macro- and micropreparations, situational tasks. The formulation of tests, their number and variable level of difficulty, sufficient volume for each topic allows to recommend them as preparation for students to take the licensed integrated exam "STEP-1". 2 Contents p. 1 Introduction to pathomorphology. Subject matter and tasks of 5 pathomorphology. Main stages of development of pathomorphology. Methods of pathanatomical diagnostics. Methods of pathomorphological research. 2 Morphological changes of cells as response to stressor and toxic damage 8 (parenchimatouse / intracellular dystrophies).
  • Diagnostiek En Therapie in De Dermatologie

    Diagnostiek En Therapie in De Dermatologie

    Diagnostiek en therapie in de dermatologie Leidraad voor co-assistenten Maatschap Dermatologie St. Antonius Ziekenhuis, locatie Nieuwegein St. Antonius Ziekenhuis, locatie Utrecht Polikliniek Houten Polikliniek Vleuterweide Diagnostiek Het stellen van een dermatologische diagnose De dermatologie onderscheidt zich van de andere specialismen vanwege het feit dat het lichamelijk onderzoek voorafgaat aan de anamnese. De anamnese is vervolgens toegespitst op de bevindingen bij het lichamelijk onderzoek, en kan bestaan uit een speciële, dermatologische anamnese en/of een gerichte, interne anamnese. Het is voor het stellen van een dermatologische diagnose van het grootste belang om systematisch te werk te gaan. Dit geldt vooral voor personen met minder ervaring. Met name het systematisch beschrijven van wat je ziet, en vervolgens dit “plaatje” te verwoorden in een zogenaamde “efflorescentie” zijn bij het stellen van een diagnose onontbeerlijk. Een efflorescentie is een zichtbaar bestanddeel van een huidafwijking. Voor een overzicht van de efflorescenties zij verwezen naar pagina 3. De huidafwijking kan monomorf zijn, dat wil zeggen dat het bestaat uit slechts één efflorescentie,maar het kan ook uit enkele of vele efflorescenties zijn opgebouwd. Het is belangrijk bij iedere huidafwijking de meest kenmerkende efflorescentie of combinatie van efflorescenties te kiezen. Zij bepalen de morfologische diagnose, wat op zijn beurt weer een opstapje vormt voor de differentiële diagnose. Op pagina 4 is hiervan een overzicht weergegeven. Een goede richtlijn bij het beschrijven van een afwijking is het zogenaamde “PROVOKE”-systeem. PROVOKE is een acroniem voor: Plaats, Rangschikking, Omvang (aantal, grootte), Vorm, Omtrek (begrenzing), Kleur en Efflorescentie(s). Valkuilen bij het beschrijven kunnen zijn veranderingen die zich in de loop van de tijd met de huidafwijking hebben voorgedaan.
  • Role of Brain Stimulation and the Blood–Brain Interface

    Role of Brain Stimulation and the Blood–Brain Interface

    biomolecules Review Monitoring and Modulating Inflammation-Associated Alterations in Synaptic Plasticity: Role of Brain Stimulation and the Blood–Brain Interface Maximilian Lenz 1,*, Amelie Eichler 1 and Andreas Vlachos 1,2,3,* 1 Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, 79104 Freiburg, Germany 2 Center Brain Links Brain Tools, University of Freiburg, 79110 Freiburg, Germany 3 Center for Basics in NeuroModulation (NeuroModulBasics), Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany * Correspondence: [email protected] (M.L.); [email protected] (A.V.) Abstract: Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood–brain interface, i.e., the blood–brain barrier, Citation: Lenz, M.; Eichler, A.; in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes Vlachos, A. Monitoring and plasticity and modulates vascular function, we argue that clinically employed non-invasive brain Modulating Inflammation-Associated stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and Alterations in Synaptic Plasticity: modulating inflammation-induced alterations in synaptic plasticity.
  • Urticaria from Wikipedia, the Free Encyclopedia Jump To: Navigation, Search "Hives" Redirects Here

    Urticaria from Wikipedia, the Free Encyclopedia Jump To: Navigation, Search "Hives" Redirects Here

    Urticaria From Wikipedia, the free encyclopedia Jump to: navigation, search "Hives" redirects here. For other uses, see Hive. Urticaria Classification and external resourcesICD-10L50.ICD- 9708DiseasesDB13606MedlinePlus000845eMedicineemerg/628 MeSHD014581Urtic aria (or hives) is a skin condition, commonly caused by an allergic reaction, that is characterized by raised red skin wheals (welts). It is also known as nettle rash or uredo. Wheals from urticaria can appear anywhere on the body, including the face, lips, tongue, throat, and ears. The wheals may vary in size from about 5 mm (0.2 inches) in diameter to the size of a dinner plate; they typically itch severely, sting, or burn, and often have a pale border. Urticaria is generally caused by direct contact with an allergenic substance, or an immune response to food or some other allergen, but can also appear for other reasons, notably emotional stress. The rash can be triggered by quite innocent events, such as mere rubbing or exposure to cold. Contents [hide] * 1 Pathophysiology * 2 Differential diagnosis * 3 Types * 4 Related conditions * 5 Treatment and management o 5.1 Histamine antagonists o 5.2 Other o 5.3 Dietary * 6 See also * 7 References * 8 External links [edit] Pathophysiology Allergic urticaria on the shin induced by an antibiotic The skin lesions of urticarial disease are caused by an inflammatory reaction in the skin, causing leakage of capillaries in the dermis, and resulting in an edema which persists until the interstitial fluid is absorbed into the surrounding cells. Urticarial disease is thought to be caused by the release of histamine and other mediators of inflammation (cytokines) from cells in the skin.
  • Histologische Versagensanalyse Von 114 Metall/Metall-Großkopfhüftendoprothesen

    Histologische Versagensanalyse Von 114 Metall/Metall-Großkopfhüftendoprothesen

    Aus der Orthopädischen Universitätsklinik der medizinischen Fakultät der Otto-von-Guericke-Universität Magdeburg Direktor: Prof. Dr. med. C. H. Lohmann Histologische Versagensanalyse von 114 Metall/Metall-Großkopfhüftendoprothesen D i s s e r t a t i o n zur Erlangung des Doktorgrades Dr. med. (doctor medicinae) an der Medizinischen Fakultät der Otto-von-Guericke-Universität Magdeburg vorgelegt von Tina Müller aus Magdeburg Magdeburg Oktober 2016 Dokumentationsblatt Müller, Tina: Histologische Versagensanalyse von 114 Metall/Metall-Großkopfhüftendoprothesen – 2016. – 76 Bl.: 24 Abb., 6 Tab. Die Studie analysierte klinisch, radiologisch, histologisch und anhand intraoperativer Befunde 114 Versagensfälle einer modularen Metall/Metall-Großkopfhüftendoprothese. Alle unter- suchten Patienten zeigten bereits frühzeitig nach Implantation der Primärprothese klinische Symptome, welche auf eine Prothesenlockerung hindeuteten. Schon während der Revisi- onsoperation waren charakteristische Veränderungen im periprothetischen Gewebe makro- skopisch sichtbar. Die gewonnenen Gewebeproben wurden in 5%igem Formalin fixiert. Die histologischen Proben wurden mit Hämatoxylin-Eosin gefärbt, mit monoklonalen anti-CD3- sowie anti-CD68-Antikörpern markiert und auf spezifische Gewebsveränderungen untersucht. Die histomorphologischen Untersuchungen wiesen in der Mehrheit der Fälle eine Fremdkör- perreaktion auf. Mikroskopisch wurden in der Monozyten-/Makrophagenzytologie schwarze Metallpartikel gefunden. Es lässt sich vermuten, dass es bei Verwendung verschiedener
  • Inflammation

    Inflammation

    Inflammation II. 1 Definitions Inflammation is defined as local reaction of vascularized living tissue to local injury, characterized by movement of fluid and leukocytes from the blood into the extravascular space. According the time frame is divided into two categories: acute and chronic. Function: • destroys, dilutes or walls off injurious agents • one of body’s non-specific defense mechanisms • begins the process of healing and repair 1.1 Acute Inflammation Rapid onset, usually short duration Microscopy • neutrophils dominate • other cellular elements are also involved (monocytes/macrophages, platelets, mast cells) • protein rich exudate, especially fibrin Associations • necrosis • pyogenic bacteria 1.2 Chronic Inflammation Usually long duration, but in some cases may be short. May follow acute inflammation or may have an insiduous onset (without an apparent prelude of acute inflammation). Microscopy • mononuclear cells dominate – lymphocytes – plasma cells (plasmocytes) – monocytes/macrophages • other cellular elements are also involved (eosinophils, neutrophils in active“ inflammation)1 ” • In granulomas are typical Langhans cells, large, multinuclear elements on the periphery of tuberculous granulomas. Nuclei are sometimes arranged in a horseshoe shape formation. Foreign body cells are similar, usually smaller, the horseshape formation of nuclei is not present. Both these elements are modified macrophages. • evidence of healing — fibroblasts, capillaries, fibrosis Associations • long term stimulation of immune system, autoimmunity • viral infections
  • Protective Effects of Zinc-L-Carnosine /Vitamin E on Aspirin- Induced Gastroduodenal Injury in Dogs

    Protective Effects of Zinc-L-Carnosine /Vitamin E on Aspirin- Induced Gastroduodenal Injury in Dogs

    PROTECTIVE EFFECTS OF ZINC-L-CARNOSINE /VITAMIN E ON ASPIRIN- INDUCED GASTRODUODENAL INJURY IN DOGS MASTER’S THESIS Presented in Partial Fulfillment of the Requirements for the Master of Science Degree in the Graduate School of the Ohio State University By Mieke Baan, DVM, MVR ***** The Ohio State University 2009 Master’s Examination Committee: Professor Robert G. Sherding, Adviser Professor Stephen P. DiBartola Associate Professore Susan E. Johnson Approved by Adviser Veterinary Clinical Sciences Graduate Program ! Copyright by Mieke Baan 2009 ABSTRACT Zinc plays a role in many biochemical functions, including DNA, RNA, and protein synthesis. The dipeptide carnosine forms a stable complex with zinc, which has a protective effect against gastric epithelial injury in-vitro and in-vivo. This randomized double-blinded placebo-controlled study investigated the protective effects of zinc-L-carnosine in combination with alpha-tocopheryl acetate (vitamin E) on the development of aspirin-induced gastrointestinal (GI) lesions in dogs. Eighteen mixed-breed dogs (mean 20.6 kg) were negative for parasites, and had normal blood work evaluations, and gastroduodenoscopic exams. On days 0 – 35, dogs were treated with 1 tablet (n=6) or 2 tablets (n=6) of 30 mg zinc-L-carnosine/ 30 IU vitamin E q12h PO, or a placebo (n=6). On days 7 – 35, all dogs were given 25 mg/kg buffered aspirin q8h PO. Endoscopy was performed on Days -1, 14, 21, and 35, and GI lesions (hemorrhages, erosions, or ulcers) were scored using a 12-point grading scale. Repeated measures ANOVA was used for statistical evaluation. The significance level was set at p ! 0.05.
  • Mcqs and Emqs in Surgery

    Mcqs and Emqs in Surgery

    1 The metabolic response to injury Multiple choice questions ➜ Homeostasis B Every endocrine gland plays an equal 1. Which of the following statements part. about homeostasis are false? C They produce a model of several phases. A It is defined as a stable state of the D The phases occur over several days. normal body. E They help in the process of repair. B The central nervous system, heart, lungs, ➜ kidneys and spleen are the essential The recovery process organs that maintain homeostasis at a 4. With regard to the recovery process, normal level. identify the statements that are true. C Elective surgery should cause little A All tissues are catabolic, resulting in repair disturbance to homeostasis. at an equal pace. D Emergency surgery should cause little B Catabolism results in muscle wasting. disturbance to homeostasis. C There is alteration in muscle protein E Return to normal homeostasis after breakdown. an operation would depend upon the D Hyperalimentation helps in recovery. presence of co-morbid conditions. E There is insulin resistance. ➜ Stress response ➜ Optimal perioperative care 2. In stress response, which of the 5. Which of the following statements are following statements are false? true for optimal perioperative care? A It is graded. A Volume loss should be promptly treated B Metabolism and nitrogen excretion are by large intravenous (IV) infusions of related to the degree of stress. fluid. C In such a situation there are B Hypothermia and pain are to be avoided. physiological, metabolic and C Starvation needs to be combated. immunological changes. D Avoid immobility. D The changes cannot be modified.
  • Inflammation Hedwig S

    Inflammation Hedwig S

    91731_ch02 12/8/06 7:31 PM Page 37 2 Inflammation Hedwig S. Murphy Overview Of Inflammation Leukocytes Traverse the Endothelial Cell Barrier to Gain Acute Inflammation Access to the Tissue Vascular Events Leukocyte Functions in Acute Inflammation Regulation of Vascular and Tissue Fluids Phagocytosis Plasma-Derived Mediators of Inflammation Neutrophil Enzymes Hageman Factor Oxidative and Nonoxidative Bactericidal Activity Kinins Regulation of Inflammation Complement system and the membrane attack complex Common Intracellular Pathways Complement system and proinflammatory molecules Outcomes of Acute Inflammation Cell-Derived Mediators of Inflammation Chronic Inflammation Arachidonic Acid and Platelet-Activating Factor Cells Involved in Chronic Inflammation Prostanoids, Leukotrienes, and Lipoxins Injury and Repair in Chronic Inflammation Cytokines Extended Inflammatory Response Reactive Oxygen Species Altered Repair Mechanisms Stress Proteins Granulomatous Inflammation Neurokinins Chronic Inflammation and Malignancy Extracellular Matrix Mediators Systemic Manifestations of Inflammation Cells of Inflammation Leukocyte Recruitment in Acute Inflammation Leukocyte Adhesion Chemotactic Molecules nflammation is the reaction of a tissue and its microcircu- blood. Rudolf Virchow first described inflammation as a reaction lation to a pathogenic insult. It is characterized by elabora- to prior tissue injury. To the four cardinal signs he added a fifth: Ition of inflammatory mediators and movement of fluid and functio laesa (loss of function). Virchow’s pupil Julius Cohn- leukocytes from the blood into extravascular tissues. This re- heim was the first to associate inflammation with emigration of sponse localizes and eliminates altered cells, foreign particles, leukocytes through the walls of the microvasculature. At the end microorganisms, and antigens and paves the way for the return of the 19th century, the role of phagocytosis in inflammation to normal structure and function.
  • 5: 1237-1249, 1979 the Naeglerial Causation Of

    5: 1237-1249, 1979 the Naeglerial Causation Of

    Medical Hypotheses 5: 1237-1249, 1979 THE NAEGLERIAL CAUSATION OF RHEUMATOID DISEASE AND MANY HUMAN CANCERS. A NEW CONCEPT IN MEDICINE. R. Wyburn-Mason, 2 Hillbrow, Richmond Hill, Richmond, Surrey, England. ABSTRACT Man and terrestrial animals live in an environment containing free- living amoebae on the surface soil, in pools, fresh water lakes, rivers and streams. They form cysts, which float in the air and which are continually inhaled and found in the nasopharynx and their trophozoites are present in human and animal faeces. Amoebae of the genus, Naegleria, have been demon- strated in all human tissues, both healthy and in larger numbers in those taken from cases of rheumatoid disease, in all human cancers and in the unaffected tissues of cancer patients. They can be killed in vitro by a series of different anti-amoebic substances and treatment of active cases of rheumatoid disease by any of these, either causes cessation of disease activity or a temporary exaggeration of symptoms followed by their lessening or disappearance (Herxheimer reaction), indicating the presence of an amoeba in the affected tissues as the causative organism of the inflammation in this disease in subjects genetically sensitive to the organism. Every internal organ may be involved in the inflammatory response in cases of rheumatoid disease and this also ceases with the above treatments. Many of these internal lesions are premalignant, so that infection with the organism either in sensitive subjects or with pathogenic species, appearsto be the primary cause of cancer in many cases. The presence in the body of Naegleria represents the source of the constant antigenic stimulation thought to be responsible both for rheumatoid disease and for the development of lymphomata and myelomatosis.
  • Dissertation Johann Federhofer.Pdf

    Dissertation Johann Federhofer.Pdf

    Aus dem Lehrstuhl für Innere Medizin I Prof. Dr. med. Jürgen Schölmerich Der Medizinischen Fakultät Der Universität Regensburg Untersuchung der Expression und Regulation von Komponenten des Inflammasoms in primären intestinalen Epithelzellen, Zelllinien, sowie bei Patienten mit Morbus Crohn und Colitis ulcerosa Inaugural – Dissertation zur Erlangung des Doktorgrades der Medizin der Medizinischen Fakultät der Universität Regensburg vorgelegt von Johann Federhofer 2009 Aus dem Lehrstuhl für Innere Medizin I Prof. Dr. med. Jürgen Schölmerich Der Medizinischen Fakultät Der Universität Regensburg Untersuchung der Expression und Regulation von Komponenten des Inflammasoms in primären intestinalen Epithelzellen, Zelllinien, sowie bei Patienten mit Morbus Crohn und Colitis ulcerosa Inaugural – Dissertation zur Erlangung des Doktorgrades der Medizin der Medizinischen Fakultät der Universität Regensburg vorgelegt von Johann Federhofer 2009 Dekan: Prof. Dr. rer. nat. Bernhard Weber 1. Berichterstatter: Prof. Dr. med. Dr. phil. Gerhard Rogler 2. Berichterstatter: PD Dr. med. Stefan Farkas Tag der mündlichen Prüfung: 29.09.2010 The mere formulation of a problem is often far more essential than its solution, which may be merely a matter of mathematical or experimental skill. To raise new questions, new possibilities, to regard old problems from a new angle requires creative imagination and marks real advances in science. (Albert Einstein) Für meine Eltern und Elisabeth Inhaltsverzeichnis VII Inhaltsverzeichnis Inhaltsverzeichnis ...............................................................................................
  • Dr. S. Srinivasa Ravi Dr. Anusha Pilla ABSTRACT KEYWORDS

    Dr. S. Srinivasa Ravi Dr. Anusha Pilla ABSTRACT KEYWORDS

    ORIGINAL RESEARCH PAPER Volume-6 | Issue-12 | December-2017 | ISSN No 2277 - 8179 | IF : 4.176 | IC Value : 93.98 INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH CUTANEOUS MANIFESTATIONS OF INTERNAL MALIGNANCIES – A STUDY OF 217 CASES Oncology Dr. S. Srinivasa D.DLO, MD (DVL), Assistant Professor in DVL, Department of DVL, Rangaraya Ravi Medical College, Kakinada. Dr. Anusha Pilla DDVL, Senior Resident in DVL, Andhra Medical College ,Visakhapatnam. ABSTRACT BACKGROUND : Skin manifestations act as markers for internal malignancy. There may be direct and indirect involvement of skin in various malignancies. Cutaneous manifestations may act as early markers for internal malignancy and various skin manifestations both specific and non specific were seen during the course of malignancy. AIM : The main purpose of this study is to know the incidence and clinical pattern of skin changes both specific and non specific seen in various internal malignancies. MATERIALS AND METHODS : It is an open prospective and observational study. All confirmed malignancy cases attending to the Out patient departments of Radiotherapy and DVL at Government General Hospital, Kakinada were recorded over a period of one year from MAY 2005 to MAY 2006. Total 217 cases of various malignancies were seen during the above period. These cases were clinically evaluated for skin manifestations and the demographic data was noted. These cases were thoroughly clinically examined for various skin manifestations. Relevant haematological, biochemical investigations and skin biopsies were