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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). -
15. Dermatology Eponyms
Dermatology Eponyms DERMATOLOGY EPONYMS – PHENOMEN / SIGN – LEXICON (D) Brzeziński Piotr1, Wollina Uwe2, Poklękowska Katarzyna3, Khamesipour Ali4, Herrero Gonzalez Jose Eugenio5, Bimbi Cesar6, Di Lernia Vito7, Karwan Krzysztof 8 16th Military Support Unit, Ustka, Poland. [email protected] 2Department of Dermatology & Allergology, Hospital Dresden-Friedrichstadt, Academic Teaching Hospital of the Technical University of Dresden, Dresden, Germany [email protected] 3Mazowiecki Branch of the National Health Fund, Warsaw, Poland [email protected] 4Center for Research and Training in Skin Diseases and Leprosy, Tehran University of Medical Sciences, Tehran, Iran [email protected] 5Malalties Ampul.lars i Porfíries, Departament de Dermatologia, Hospital del Mar, Barcelona, Spain [email protected] 6Brazilian Society of Dermatology [email protected] 7Department of Dermatology, Arcispedale Santa Maria Nuova, Reggio Emilia, Italy [email protected] 8The Emergency Department, Military Institute of Medicine, Warsaw, Poland [email protected] N Dermatol Online. 2011; 2(3): 158-170 Date of submission: 08.04.2011 / acceptance: 29.05.2011 Conflicts of interest: None DANIELSSEN’S SIGN Anesthetic leprosy. A form of leprosy chiefly affecting the nerves, marked by hyperesthesia succeeded by anesthesia, and by paralysis, ulceration, and various trophic disturbances, terminating in gangrene and mutilation. In 1895 I presented to the Ohio State Medical Society two sisters, natives of Ohio, who manifested appearances of anesthetic leprosy. Synonyms: Danielssen disease, Danielssen-Boeck disease, dry leprosy, trophoneurotic leprosy. OBJAW DANIELSSENA Anesthetic leprosy. Postać trądu głównie wpływająca na nerwy, początkowo charakteryzuje się oznaczone przeczulicą, następcą znieczulicą i paraliŜem, owrzodzeniem i róŜnymi zaburzeniami troficznymi, kończąca się w gangreną i okaleczeniem. W 1895 roku przedstawiono w Ohio State Medical Society dwie siostry z Ohio, u których występowały objawy anesthetic Figure 1. -
Classification of Thyroid Tumors Benign Tumors - Adenoma 1
DERMATOPATHOLOGY PATHOLOGY OF ENDOCRINE SYSTEM Thyroid carcinoma, Hashimoto thyroiditis, Graves‘ disease, neuroendocrine tumor, Institute of Pathological Anatomy melanoma, pigmented naevus, psoriasis, eczema FM CU BA DERMATOPATHOLOGY • 10-year-old boy with a pigmented lesion on his shoulder, sharply demarcated from the surrounding skin, with a diameter of 2.3 cm, dark brown in color, without noticeable changes. CASE NO. 1 ➢Suggested examinations? ➢Your diagnosis? ➢Describe the microscopic finding. Pigmented nevus of the skin Congenital pigmented nevus of the skin PIGMENTED NEVUS • benign skin formation arising as a result of melanocyte accumulation • the most common skin lesion of the white race • most nevi form in childhood and adolescence Classification of nevi according to the position of growth in the skin • Junctional nevus - nests of melanocytes are found at the dermo-epidermal junction • Mixed nevus - nests of melanocytes are found at the junction but also in the dermis • Intradermal nevus - clusters of melanocytes are found in the upper part of the dermis WITHOUT connection with the epidermis Histological variants of pigmented nevus • Congenital nevus • Blue nevus • Halo nevus • Familial dysplastic nevus Mixed pigmented nevus Junctional pigmented nevus Intradermal pigmented nevus • 73-year-old patient was admitted to hospital for progressive weakness, shortness of breath. You notice that both the skin and the sclera are icteric. • laboratory hyperbilirubinemia, hypoalbuminemia and mineral imbalance, positive oncomarkers (S100) • abdominal ultrasound with spherical structures found in the liver parenchyma • personal medical history - malignant melanoma of the eye CASE NO. 2 30 years ago, CLL 3 years ago, now in remission ➢Suggested examinations? ➢Your diagnosis? ➢Complications? ➢Describe the microscopic finding. -
Spontaneous Regression of Divided Nevus of the Eyelid Evaluated by Dermoscopy Leaving a Hypopigmented Lesion
Case Report Spontaneous regression of divided nevus of the eyelid evaluated by dermoscopy leaving a hypopigmented lesion Danang Tri Wahyudi1, Izzah Aulia2, Aida S.D. Hoemardani1, Agassi Suseno Sutarjo1 1. Department of Dermatology and Venereology, Dharmais National Cancer Hospital, Jakarta, Indonesia 2. Department of Dermatology and Venereology Faculty of Medicine Universitas Indonesia/ Dr. Cipto Mangunkusumo National Central General Hospital Jakarta, Indonesia Email: [email protected] Abstract Background: Divided nevus, also known as “kissing nevus,” is a rare form of congenital melanocytic nevus that occurs on opposing margins of upper and lower eyelids. A paucity of literature on this rare anomaly exists, with most being case reports and series. Moreover, regression of this lesion was rarely reported. Case Illustration: We present a rare case of congenital divided nevus of the eyelid that regressed after eight years, confirmed with dermoscopy. A siX-year-old boy presented to the Dharmais National Cancer Hospital with two pigmented macules on the upper and lower right eyelid since birth. A year ago, the lesions started gradually disappearing and were replaced by a hypopigmented area. We evaluated the clinical and dermoscopic findings for two consecutive years. The dermoscopy showed pseudopigment networks, surrounded by a hypopigmented area resembling a halo. The pigmented lesions cleared with no residual lesions. Discussion: The dermoscopic findings of the patient resemble a solar lentigo characterized by pseudopigment networks, a feature caused by the relatively flattened rete ridge on the face. The hypopigmented area reflects a regression process, like the halo nevus, and is accompanied by leukotrichia of the eyelashes, a feature usually found in patients with vitiligo. -
Cutaneous Manifestations of Systemic Disease
Cutaneous Manifestations of Systemic Disease Dr. Lloyd J. Cleaver D.O. FAOCD FAAD Northeast Regional Medical Center A.T.Still University/KCOM Assistant Vice President/Professor ACOI Board Review Disclosure I have no financial relationships to disclose I will not discuss off label use and/or investigational use in my presentation I do not have direct knowledge of AOBIM questions I have been granted approvial by the AOA to do this board review Dermatology on the AOBIM ”1-4%” of exam is Dermatology Table of Test Specifications is unavailable Review Syllabus for Internal Medicine Large amount of information Cutaneous Multisystem Cutaneous Connective Tissue Conditions Connective Tissue Diease Discoid Lupus Erythematosus Subacute Cutaneous LE Systemic Lupus Erythematosus Scleroderma CREST Syndrome Dermatomyositis Lupus Erythematosus Spectrum from cutaneous to severe systemic involvement Discoid LE (DLE) / Chronic Cutaneous Subacute Cutaneous LE (SCLE) Systemic LE (SLE) Cutaneous findings common in all forms Related to autoimmunity Discoid LE (Chronic Cutaneous LE) Primarily cutaneous Scaly, erythematous, atrophic plaques with sharp margins, telangiectasias and follicular plugging Possible elevated ESR, anemia or leukopenia Progression to SLE only 1-2% Heals with scarring, atrophy and dyspigmentation 5% ANA positive Discoid LE (Chronic Cutaneous LE) Scaly, atrophic plaques with defined margins Discoid LE (Chronic Cutaneous LE) Scaly, erythematous plaques with scarring, atrophy, dyspigmentation DISCOID LUPUS Subacute Cutaneous -
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1 Index Note: Page numbers in italics refer to figures, those in bold refer to tables and boxes. References are to pages within chapters, thus 58.10 is page 10 of Chapter 58. A definition 87.2 congenital ichthyoses 65.38–9 differential diagnosis 90.62 A fibres 85.1, 85.2 dermatomyositis association 88.21 discoid lupus erythematosus occupational 90.56–9 α-adrenoceptor agonists 106.8 differential diagnosis 87.5 treatment 89.41 chemical origin 130.10–12 abacavir disease course 87.5 hand eczema treatment 39.18 clinical features 90.58 drug eruptions 31.18 drug-induced 87.4 hidradenitis suppurativa management definition 90.56 HLA allele association 12.5 endocrine disorder skin signs 149.10, 92.10 differential diagnosis 90.57 hypersensitivity 119.6 149.11 keratitis–ichthyosis–deafness syndrome epidemiology 90.58 pharmacological hypersensitivity 31.10– epidemiology 87.3 treatment 65.32 investigations 90.58–9 11 familial 87.4 keratoacanthoma treatment 142.36 management 90.59 ABCA12 gene mutations 65.7 familial partial lipodystrophy neutral lipid storage disease with papular elastorrhexis differential ABCC6 gene mutations 72.27, 72.30 association 74.2 ichthyosis treatment 65.33 diagnosis 96.30 ABCC11 gene mutations 94.16 generalized 87.4 pityriasis rubra pilaris treatment 36.5, penile 111.19 abdominal wall, lymphoedema 105.20–1 genital 111.27 36.6 photodynamic therapy 22.7 ABHD5 gene mutations 65.32 HIV infection 31.12 psoriasis pomade 90.17 abrasions, sports injuries 123.16 investigations 87.5 generalized pustular 35.37 prepubertal 90.59–64 Abrikossoff -
Photo Diagnosis
Photo Diagnosis Illustrated quizzes on problems seen in everyday practice Case 1 An 11-year-old boy presents with pain over the left clavicle after falling from an eight-foot high ladder and landing on a outstretched left hand. Questions 1. What is the diagnosis? 2. What is the significance? Answers 1. Fractured left clavicle. 2. The majority of clavicular fractures heal spontaneously through callus formation. Immobilization of the affected arm for pain control can be easily and effectively accomplished by an arm sling. A figure-of-eight splint offers no advantage over the sling and can be uncomfortable for some children. Inappropriate use of the splint may occasionally even lead to edema of the ipsilateral upper limb, compression of axillary vessels and brachial plexopathy. Provided by Dr. Alexander K.C. Leung; and Dr. Justine H.S. Fong, Calgary, Alberta. Share your photos and diagnoses with us! Do you have a photo diagnosis? Send us your photo and a brief text explaining the presentation of the illness, your diagnosis and treatment, and receive $25 per item if it is published. The Canadian Journal of Diagnosis 955, boul. St. Jean, suite 306, Pointe-Claire (Quebec) H9R 5K3 E-mail: [email protected] Fax: (514) 695-8554 The Canadian Journal of Diagnosis / January 2005 47 Photo Diagnosis Case 2 A 32-year-old former soccer player presents with recurrent attacks of excruciating pain in the right first metatarsophalangeal joint. The attacks have been occurring for the past six months. Questions 1. What is the diagnosis? 2. What is the significance? 3. What is the treatment? Answers 1. -
Dermatological Indications of Disease - Part II This Patient on Dialysis Is Showing: A
“Cutaneous Manifestations of Disease” ACOI - Las Vegas FR Darrow, DO, MACOI Burrell College of Osteopathic Medicine This 56 year old man has a history of headaches, jaw claudication and recent onset of blindness in his left eye. Sed rate is 110. He has: A. Ergot poisoning. B. Cholesterol emboli. C. Temporal arteritis. D. Scleroderma. E. Mucormycosis. Varicella associated. GCA complex = Cranial arteritis; Aortic arch syndrome; Fever/wasting syndrome (FUO); Polymyalgia rheumatica. This patient missed his vaccine due at age: A. 45 B. 50 C. 55 D. 60 E. 65 He must see a (an): A. neurologist. B. opthalmologist. C. cardiologist. D. gastroenterologist. E. surgeon. Medscape This 60 y/o male patient would most likely have which of the following as a pathogen? A. Pseudomonas B. Group B streptococcus* C. Listeria D. Pneumococcus E. Staphylococcus epidermidis This skin condition, erysipelas, may rarely lead to septicemia, thrombophlebitis, septic arthritis, osteomyelitis, and endocarditis. Involves the lymphatics with scarring and chronic lymphedema. *more likely pyogenes/beta hemolytic Streptococcus This patient is susceptible to: A. psoriasis. B. rheumatic fever. C. vasculitis. D. Celiac disease E. membranoproliferative glomerulonephritis. Also susceptible to PSGN and scarlet fever and reactive arthritis. Culture if MRSA suspected. This patient has antithyroid antibodies. This is: • A. alopecia areata. • B. psoriasis. • C. tinea. • D. lichen planus. • E. syphilis. Search for Hashimoto’s or Addison’s or other B8, Q2, Q3, DRB1, DR3, DR4, DR8 diseases. This patient who works in the electronics industry presents with paresthesias, abdominal pain, fingernail changes, and the below findings. He may well have poisoning from : A. lead. B. -
Dermoscopy Patterns of Halo Nevi
OBSERVATION Dermoscopy Patterns of Halo Nevi Isabel Kolm, MD; Alessandro Di Stefani, MD; Rainer Hofmann-Wellenhof, MD; Regina Fink-Puches, MD; Ingrid H. Wolf, MD; Erika Richtig, MD; Josef Smolle, MD; Helmut Kerl, MD; H. Peter Soyer, MD; Iris Zalaudek, MD Background: Halo nevi (HN) are benign melanocytic globular and/or homogeneous patterns in more than 80% nevi surrounded by a depigmented area (halo). This study of HN. Follow-up of 33 HN revealed considerable size aims to evaluate the dermoscopic features of HN and their reduction of the nevus component, but this was not as- changes during digital dermoscopic follow-up and to in- sociated with significant structural changes. Of a total of vestigate the frequency of the halo phenomenon in a se- 475 melanomas, only 2 revealed an encircling halo, but ries of melanomas. both displayed clear-cut melanoma-specific patterns ac- cording to dermoscopy. Observations: In a retrospective study, digital dermo- scopic images of HN from patients who attended the Pig- Conclusions: Halo nevi exhibit the characteristic der- mented Skin Lesions Clinic of the Department of Der- moscopic features of benign melanocytic nevi, repre- matology, Medical University of Graz, between October sented by globular and/or homogeneous patterns that are 1, 1997, and March 31, 2004, were reviewed and classi- typically observed in children and young adults. Halo nevi fied by dermoscopic morphologic criteria. For HN that reveal considerable changes of area over time during digi- were followed up with digital dermoscopy, the percent- tal dermoscopic follow-up, albeit their structural pat- ages of changes in the size of the nevus and halo com- terns remain unchanged. -
Table I. Genodermatoses with Known Gene Defects 92 Pulkkinen
92 Pulkkinen, Ringpfeil, and Uitto JAM ACAD DERMATOL JULY 2002 Table I. Genodermatoses with known gene defects Reference Disease Mutated gene* Affected protein/function No.† Epidermal fragility disorders DEB COL7A1 Type VII collagen 6 Junctional EB LAMA3, LAMB3, ␣3, 3, and ␥2 chains of laminin 5, 6 LAMC2, COL17A1 type XVII collagen EB with pyloric atresia ITGA6, ITGB4 ␣64 Integrin 6 EB with muscular dystrophy PLEC1 Plectin 6 EB simplex KRT5, KRT14 Keratins 5 and 14 46 Ectodermal dysplasia with skin fragility PKP1 Plakophilin 1 47 Hailey-Hailey disease ATP2C1 ATP-dependent calcium transporter 13 Keratinization disorders Epidermolytic hyperkeratosis KRT1, KRT10 Keratins 1 and 10 46 Ichthyosis hystrix KRT1 Keratin 1 48 Epidermolytic PPK KRT9 Keratin 9 46 Nonepidermolytic PPK KRT1, KRT16 Keratins 1 and 16 46 Ichthyosis bullosa of Siemens KRT2e Keratin 2e 46 Pachyonychia congenita, types 1 and 2 KRT6a, KRT6b, KRT16, Keratins 6a, 6b, 16, and 17 46 KRT17 White sponge naevus KRT4, KRT13 Keratins 4 and 13 46 X-linked recessive ichthyosis STS Steroid sulfatase 49 Lamellar ichthyosis TGM1 Transglutaminase 1 50 Mutilating keratoderma with ichthyosis LOR Loricrin 10 Vohwinkel’s syndrome GJB2 Connexin 26 12 PPK with deafness GJB2 Connexin 26 12 Erythrokeratodermia variabilis GJB3, GJB4 Connexins 31 and 30.3 12 Darier disease ATP2A2 ATP-dependent calcium 14 transporter Striate PPK DSP, DSG1 Desmoplakin, desmoglein 1 51, 52 Conradi-Hu¨nermann-Happle syndrome EBP Delta 8-delta 7 sterol isomerase 53 (emopamil binding protein) Mal de Meleda ARS SLURP-1 -
B K B Ld I MD Brooke Baldwin, MD Private Practice, Lutz, Florida Chief
BBkrooke BBldialdwin, MD Private Practice, Lutz, Florida Chief of Dermatology James A Haley VA Hospital Adjunct Assistant Professor of Dermatology University of Florida What we are going to cover today Dermatologic Emergencies Common benign skin growths Malignant skin tumors Common Rashes Photoprotecti on and CiCosmetics Dermatologic Emergencies Erythroderma PlPustular psoriiiasis Pemphigus DRESS Syndrome SJS / TEN EEthdrythroderma Erythroderma Generalized redness and scaling of skin involving >90% BSA Systemic manifestations PihPeripheral edema & ffilacial edema Tachycardia Loss of fluids and proteins Disturbed thermoregulation Most common etiologies Atopic dermatitis, psoriasis, CTCL, drug reactions Despite intensive evaluation, the cause remains unknown in 25‐30% PPlustular psoriiiasis Pustular Psoriasis Generalized pustular psoriasis Unusual mani festation o f psoriasis Triggering factors Pregnancy (impetigo herpetiformis) Tapering of corticosteroids (Von Zumbusch reaction) HliHypocalcemia Infections Topical irritants Rarely treatment with TNF alpha blockers (palms and soles) Pemphigus Group of chronic autoimmune blistering diseases presenting with painful erosions IgG Autoantibodies are directed against the cell surface of keratinocytes Results in blistering in varying areas of the epidermis Diagnosi s is confirmed wihith direct iflimmunofluorescence on skin biopsy 3 ma jor forms P. vulgaris, P. foliaceus, paraneoplastic Do not confuse with Bullous pemphigoid which presents with tense bullae Pempgphigus -
(2) October 2011\Protocol Book\Program-Speaker Page-Oc
Chicago Dermatological Society October 2011 Monthly Educational Conference Program Information Continuing Medical Education Certification and Case Presentations Wednesday, October 12, 2011 David Fretzin Lecture Conference Host: Department of Dermatology University of Illinois at Chicago Chicago, Illinois University of Illinois at Chicago C UIC Student Center West (SCW) - 828 S. Wolcott Ave., 2nd Floor Registration, lectures, slide viewing, lunch and committee meetings C UIC Outpatient Care Center, Dermatology Clinic - 1801 W. Taylor, Suite 3E Patient viewing only (no registration at this location! Protocol books will be available.) UIC parking – Use the Wood Street Parking Structure, 1100 S. Wood at the intersection of (Wood & Grenshaw, just south of the UIC Outpatient Care Center) See reverse side for detailed campus map From the Eisenhower Expressway, exit at Ashland/Paulina. Proceed south on Ashland to Taylor. Turn west on Taylor approximately two blocks to Wood St. Turn south on Wood for the entrance to the parking lot. Program Conference Locations Student Center West (SCW) – 828 S. Wolcott, 2nd Floor Dermatology Clinic, 1801 W. Taylor St., Suite 3E 8:00 a.m. Registration Opens Student Center West, 2nd floor Foyer 9:00 a.m. - 10:00 a.m. Resident Lecture – SCW Chicago Room A-C "Spectrum of CD30+ Lymphoproliferative Diseases" Samuel Hwang, MD, PhD 9:30 a.m. - 10:45 a.m. Clinical Rounds Patient & Poster Viewing Dermatology Clinic, Suite 3E Slide Viewing Student Center West, Room 213 A/B 11:00 a.m. - 12:15 p.m. General Session - SCW Chicago Room A-C FRETZIN LECTURE: "An Update on Th17 Cells in Psoriasis" Samuel Hwang, MD, PhD 12:15 p.m.