Pathology.Pre-Test.Pdf
Total Page:16
File Type:pdf, Size:1020Kb

Load more
Recommended publications
-
General Pathologic Anatomy
МІНІСТЕРСТВО ОХОРОНИ ЗДОРОВ'Я УКРАЇНИ Харківський національний медичний університет GENERAL PATHOLOGIC ANATOMY Manual for practical classes in pathomorphology for English-speaking teachers ЗАГАЛЬНА ПАТОЛОГІЧНА АНАТОМІЯ Методичні розробки до занять з патоморфології для англомовних викладачів медичних закладів Затверджено вченою радою ХНМУ. Протокол № 15 від 15.06.2017. Харків ХНМУ 2017 1 General pathologic anatomy : мanual for practical classes in patho- morphology for English-speaking teachers / comp. I. V. Sorokina, V. D. Markovskiy, I. V. Korneyko et al. – Kharkov : KNMU, 2017. – 64 p. Compilers I. V. Sorokina V. D. Markovskiy I. V. Korneyko G. I. Gubina-Vakulik V. V. Gargin O. N. Pliten M. S. Myroshnychenko S. N. Potapov T. V. Bocharova D. I. Galata O.V. Kaluzhina Загальна патологічна анатомія : метод. розроб. до занять з пато- морфології для англомовних викладачів мед. закладів / упоряд. І. В. Сорокіна, В. Д. Марковський, І. В. Корнейко та ін. – Харків : ХНМУ, 2017. – 64 с. Упорядники I. В. Сорокіна В. Д. Марковський І. В. Корнейко Г. І. Губіна-Вакулик В. В. Гаргін О. М. Плітень М. С. Мирошниченко С. М. Потапов Т. В. Бочарова Д. І. Галата О. В. Калужина 2 Foreword Pathomorphology, one of the most important medical subjects is aimed at teaching students understanding material basis and mechanisms of the development of main pathological processes and diseases. This manual published as separate booklets is devoted to general pathological processes as well as separate nosological forms. It is intended to the English-medium students of the medical and dentistry faculties. It can be used as additional material used for individual work in class. It can also be used to master the relevant terminology and its unified teaching. -
Cytomegalovirus Retinitis: a Manifestation of the Acquired Immune Deficiency Syndrome (AIDS)*
Br J Ophthalmol: first published as 10.1136/bjo.67.6.372 on 1 June 1983. Downloaded from British Journal ofOphthalmology, 1983, 67, 372-380 Cytomegalovirus retinitis: a manifestation of the acquired immune deficiency syndrome (AIDS)* ALAN H. FRIEDMAN,' JUAN ORELLANA,'2 WILLIAM R. FREEMAN,3 MAURICE H. LUNTZ,2 MICHAEL B. STARR,3 MICHAEL L. TAPPER,4 ILYA SPIGLAND,s HEIDRUN ROTTERDAM,' RICARDO MESA TEJADA,8 SUSAN BRAUNHUT,8 DONNA MILDVAN,6 AND USHA MATHUR6 From the 2Departments ofOphthalmology and 6Medicine (Infectious Disease), Beth Israel Medical Center; 3Ophthalmology, "Medicine (Infectious Disease), and 'Pathology, Lenox Hill Hospital; 'Ophthalmology, Mount Sinai School ofMedicine; 'Division of Virology, Montefiore Hospital and Medical Center; and the 8Institute for Cancer Research, Columbia University College ofPhysicians and Surgeons, New York, USA SUMMARY Two homosexual males with the 'gay bowel syndrome' experienced an acute unilateral loss of vision. Both patients had white intraretinal lesions, which became confluent. One of the cases had a depressed cell-mediated immunity; both patients ultimately died after a prolonged illness. In one patient cytomegalovirus was cultured from a vitreous biopsy. Autopsy revealed disseminated cytomegalovirus in both patients. Widespread retinal necrosis was evident, with typical nuclear and cytoplasmic inclusions of cytomegalovirus. Electron microscopy showed herpes virus, while immunoperoxidase techniques showed cytomegalovirus. The altered cell-mediated response present in homosexual patients may be responsible for the clinical syndromes of Kaposi's sarcoma and opportunistic infection by Pneumocystis carinii, herpes simplex, or cytomegalovirus. http://bjo.bmj.com/ Retinal involvement in adult cytomegalic inclusion manifestations of the syndrome include the 'gay disease (CID) is usually associated with the con- bowel syndrome9 and Kaposi's sarcoma. -
USMLE – What's It
Purpose of this handout Congratulations on making it to Year 2 of medical school! You are that much closer to having your Doctor of Medicine degree. If you want to PRACTICE medicine, however, you have to be licensed, and in order to be licensed you must first pass all four United States Medical Licensing Exams. This book is intended as a starting point in your preparation for getting past the first hurdle, Step 1. It contains study tips, suggestions, resources, and advice. Please remember, however, that no single approach to studying is right for everyone. USMLE – What is it for? In order to become a licensed physician in the United States, individuals must pass a series of examinations conducted by the National Board of Medical Examiners (NBME). These examinations are the United States Medical Licensing Examinations, or USMLE. Currently there are four separate exams which must be passed in order to be eligible for medical licensure: Step 1, usually taken after the completion of the second year of medical school; Step 2 Clinical Knowledge (CK), this is usually taken by December 31st of Year 4 Step 2 Clinical Skills (CS), this is usually be taken by December 31st of Year 4 Step 3, typically taken during the first (intern) year of post graduate training. Requirements other than passing all of the above mentioned steps for licensure in each state are set by each state’s medical licensing board. For example, each state board determines the maximum number of times that a person may take each Step exam and still remain eligible for licensure. -
© 2019 First Aid for the USMLE Step 1 732 INDEX INDEX
Index A Abnormal uterine bleeding (AUB), heart failure, 306 Achondroplasia, 454 A-a gradient 618, 619 hypertension, 312 chromosome disorder, 64 in elderly, 654 adenomyosis, 634 naming convention for, 253 endochondral ossification in, 450 with hypoxemia, 654, 655 anemia with, 410 preload/afterload effects, 282 inheritance, 60 restrictive lung disease, 661 Asherman syndrome, 634 teratogenicity, 600 AChR (acetylcholine receptor), 229 Abacavir, 201, 203 leiomyoma (fibroid), 634 Acetaldehyde, 72 Acid-base physiology, 580 Abciximab, 122 polyps (endometrial), 634 Acetaldehyde dehydrogenase, 70, 72 Acidemia, 580 Glycoprotein IIb/IIIa inhibitors, thecoma, 632 Acetaminophen, 474 diuretic effect on, 595 429 ABO blood classification, 397 vs. aspirin for pediatric patients, 474 Acid-fast oocysts, 177 thrombogenesis and, 403 newborn hemolysis, 397 free radical injury and, 210 Acid-fast organisms, 125, 140, 155 Abdominal aorta, 357 Abruptio placentae, 626 hepatic necrosis from, 249 Acidic amino acids, 81 atherosclerosis in, 300, 687 cocaine use, 600 N-acetylcysteine for overdose, 671 Acid maltase, 86 bifurcation of, 649 preeclampsia, 629 for osteoarthritis, 458 Acidosis, 578, 580 Abdominal aortic aneurysm, 300 Abscess, 470 toxicity effects, 474 contractility in, 282 Abdominal colic acute inflammation and, 215 toxicity treatment for, 247 hyperkalemia with, 578 lead poisoning, 411 lung, 670 Acetazolamide, 252, 539, 594 Acid phosphatase in neutrophils, 398 Abdominal pain Absence seizures idiopathic intracranial Acid reflux bacterial peritonitis, 384 characteristics -
High B1a0d Pressure and Its Treatment in General
HIGH B1A0D PRESSURE AND ITS TREATMENT IN GENERAL PRACTICE WITH PARTICULAR REFERENCE TO A SERIES OF 100 CASES TREATED BY THE AUTHOR By HAROLD WILSON B01YBR IB.ffh.B. ProQuest Number: 13849841 All rights reserved INFORMATION TO ALL USERS The quality of this reproduction is dependent upon the quality of the copy submitted. In the unlikely event that the author did not send a com plete manuscript and there are missing pages, these will be noted. Also, if material had to be removed, a note will indicate the deletion. uest ProQuest 13849841 Published by ProQuest LLC(2019). Copyright of the Dissertation is held by the Author. All rights reserved. This work is protected against unauthorized copying under Title 17, United States C ode Microform Edition © ProQuest LLC. ProQuest LLC. 789 East Eisenhower Parkway P.O. Box 1346 Ann Arbor, Ml 48106- 1346 -CONTENTS SECTION 1. Introduction. SECTION 2. General Remarks. Definitions of General Interest. Present Views on Etiology. Pathology and Morbid Anatomy. Brief Historical Survey. SECTION 3. The Present Position. Prevalence. Clinical Manifestations. Prognosis. SECTION 4. Prevalence in Bolton. Summary of Cases. Symptomatology and Case Histories Prognosis. Treatment. SECTION 5. Conclusions. Bibliography. SECTION 1. INTRODUCTION. I think it can truthfully be said that the most interest ing problems in Medioine are those that are most baffling. Some years ago Ralph M a j o r ^ wrote these words, ”If our knowledge of the etiology of arterial hypertension is shrouded in a oertain haze, our knowledge of an effective therapy in this disease is enveloped in a dense fog.n A study of some of the vast literature on this subject does not greatly clarify the obscurity. -
DISEASES of ARTERIES ARTERIOSCLEROSIS (“Hardening of the Arteries”): General Term Reflecting Arterial Wall Thickening and Loss of Elasticity
DISEASES OF ARTERIES ARTERIOSCLEROSIS (“hardening of the arteries”): general term reflecting arterial wall thickening and loss of elasticity 3 patterns •Atherosclerosis: involves the the aorta and the large arteries •Mönckeberg sclerosis: calcific deposits in the media of middle-sized arteries in persons >age 50 •Arteriolosclerosis: involves the small arteries and arterioles in association with hypertension or diabetes ATHEROSCLEROSIS Multifactorial, slowly progressive chronic degenerative-inflammatory disease of the aorta and the large arteries, such as • coronary arteries • circle of Willis • popliteal and tibial arteries Significance: > 50% of all death is attributed to atherosclerosis in well-developed countries Morphology Gross • Atheromatous plaque (pathognomic) - raised white-yellow lesion in the intima, protruding into the lumen • Large plaques in the aorta (> 2 cm) contain a yellow, grumous debris (”atheroma” - Greek word for gruel) Atheromatous plaque in the middle cerebral artery: raised white-yellow lesion in the intima, protruding into the lumen (formol-fixed brain) Aorta: the plaques contain a yellow, grumous debris (arrow) Structure of atheroma on LM • Intimal lesion • Central lipid core • Fibrous ”cap” subendothelially Central lipid core composed of lipids, cholesterol clefts, necrotic debris + calcium-salts, surrounded by foamy macrophages, T-lymphocytes, fibroblasts, small capillaries, and collagens and proteoglycans Types of plaques • Vulnerable plaques have large atheromatous cores, increased inflammatory cell content and thin fibrous caps high risk of rupture thrombosis • Stable plaques have minimal atheromatous cores and inflammation and thick fibrous caps 70% stenosis (critical stenosis) chronic ischemia distally Vulnerable plaque in the coronary artery Inflammatory infiltrates and capillaries around the lipid core. Lumen Intima Media Pathogenesis Response to chronic endocardial injury hypothesis • Cholesterol can’t dissolve in the blood. -
DUKE UNIVERSITY School of Medicine Pathologists' Assistant
DUKE UNIVERSITY School of Medicine Pathologists’ Assistant Program Department of Pathology Academic Programs The Department of Pathology at Duke University offers a wide array of training programs to fit individual requirements and goals. The Residency Training program is an ACGME approved program and is available as an Anatomic Pathology/Clinical Pathology combined program, a shorter Anatomic Pathology only program, or an Anatomic Pathology/Neuropathology program. Subspecialty fellowships in Cytopathology, Dermatopathology, Hematopathology, Medical Microbiology, and Neuropathology are also ACGME approved. These programs provide the highest quality of graduate medical education by drawing on the depth and breadth of faculty expertise in the Department in all aspects of anatomic and clinical pathology and the availability of a wide variety of often complex clinical cases seen at Duke University Health System. For medical students interested in a career in Pathology pre-doctoral fellowships, internships and externships are available. Research Training in Experimental pathology can be obtained through Pre- and postdoctoral fellowships of one to five years. All pre-doctoral fellows are candidates for the Ph.D. degree in pathology. The Ph.D. is optional in postdoctoral programs, which provide didactic and research training in various aspects of modern experimental pathology. A two year NAACLS accredited Pathologists’ Assistant Program leads to a Master of Health Science degree, certifies graduates to sit for the ASCP Board of Certification examination, and leads to exciting career opportunities in a variety of anatomic pathology laboratory settings. Pathologists’ assistants are analogous to physician assistants, but with highly specialized training in autopsy and surgical pathology. This profession was pioneered in the Duke Department of Pathology 50 years ago, and is one of only twelve such programs in existence today. -
Università Degli Studi Di Milano
UNIVERSITÀ DEGLI STUDI DI MILANO SCUOLA DI DOTTORATO IN MEDICINA MOLECOLARE CICLO XXVIII Anno Accademico 2014/2015 TESI DI DOTTORATO DI RICERCA MED09 STUDIES OF HEME-REGULATED eIF2α KINASE STRESS SIGNALING ON MATURATION OF MACROPHAGES AND ERYTHROBLASTIC ISLAND FORMATION IN IRON RESTRICTIVE ERYTHROPOIESIS Dottorando : Elena PALTRINIERI Matricola N° R10203 TUTORE : Chiar.ma Prof.ssa Maria Domenica CAPPELLINI CO-TUTORE: Prof.ssa Jane-Jane CHEN DIRETTORE DEL DOTTORATO: Chiar.mo Prof. Mario CLERICI ABSTRACT Iron is the most important metal for the human body. Different states of iron deficiency have long existed and remain very common in today’s population. The vast majority of cases of iron deficiency are acquired as a result from blood loss. Any condition in which dietary iron intake does not meet the body’s demands will result in iron deficiency. Iron and heme are both fundamental in hemoglobin synthesis and erythroid cell differentiation. In addition to act as a prosthetic group for hemoglobin, heme regulates the transcription of globin genes and controls the translational activity in erythroid precursors through modulation of the kinase activity of the eIF2α kinase HRI which is regulated by heme. HRI, the heme-regulated inhibitor of translation, was first discovered in reticulocytes under the conditions of iron and heme deficiencies. During heme deficiency conditions, in the erythroid precursors protein synthesis is inhibited by phosphorylation of the α-subunit of the eukaryotic initiation factor 2 (eIF2α) as the result of the activation of HRI. The role of HRI is to control that the amount of globin chains synthesized are not in excess of what can be utilized for hemoglobin tetramers depending of heme available. -
Cytomegalovirus Infection of the Human Gastrointestinal Tract
Journal of Gastroenterology and Hepatology (1999) 14, 973–976 OESOPHAGOGASTRODUODENAL DISORDERS Cytomegalovirus infection of the human gastrointestinal tract SUSAMA PATRA, SUBASH C SAMAL, ASHOK CHACKO, VADAKENADAYIL I MATHAN1 AND MINNIE M MATHAN1 The Wellcome Trust Research Laboratory, Department of Gastrointestinal Sciences, Christian Medical College and Hospital,Vellore,India Abstract Background: Current interest in cytomegalovirus (CMV) is largely due to an increase in the number of cases of acquired immunodeficiency syndrome and organ transplantation in recent years.The proper recognition of CMV-infected cells in gastrointestinal mucosal biopsies is critical for effective treatment of this condition. Methods: A total of 6580 endoscopic mucosal biopsies from 6323 patients in the 8-year period (1989–1996) were examined for CMV inclusion bodies. The endoscopic appearance and particularly the presence of ulcers were also analysed. Results and Conclusions: The prevalence of cytomegalovirus (CMV) inclusions was 9 per thousand in the gastrointestinal mucosal biopsies from an unselected group of patients. Of the 54 patients with CMV infection, 37 were immunocompromised and 17 apparently immunocompetent. Typical Cowdry inclusions and atypical inclusions were present, the latter more frequently in immunocompromised patients. The maximum prevalence of inclusions was in the oesophageal mucosa in immunocompro- mised individuals. © 1999 Blackwell Science Asia Pty Ltd Key words: cytomegalovirus, gastrointestinal tract, immunocompetent, immunocompromised, inclu- sion bodies, mucosal biopsies. INTRODUCTION in haematoxylin and eosin (HE)-stained histological samples is regarded as being sensitive and specific for Cytomegalovirus (CMV), first described in 1956,1 is a CMV infection,6–9 especially for samples from the gas- double-stranded DNA virus belonging to the herpes trointestinal tract. -
DSM III and ICD 9 Codes 11-2004
Diagnoses and ICD-9 Codes: Alphabetical 918.1 Abrasion -Corneal 682 Abscess 372 Abscess Conjunctiva 566 Abscess Corneal 566 Abscess Rectal 682.9 Abscess, Unspecified Site (Cellulitis) 995.81 Abuse, Adult 436 Accident Cerebrovascular, Acute (Less than 8 weeks after Occurrence) 438 Accident, Cerebrovascular, Chronic (Healed or Old) 276.2 Acidosis (Keto-Acidosis) 706.1 Acne 255.4 Addisonian Crisis (Adrenal Cortical Deficiency Hypoadrenalism) 289.3 Adenitis 525.1 Adentia (Loss of Teeth d\Due to Accident, Extraction or Periodontal Diease) 309.89 Adjustment Reaction to Late Life 309.9 Adjustment Reaction-Unspcified 742.2 Agenesis-Cerebral 307.9 Agitation 307.9 Agitation 368.16 Agnosia-Visual 291.9 Alcholick Psychosis 303.9 Alcholism (Addiction, Chronic Dependence) 291.8 Alcohol Withdrawal 291.8 Alcohol Withdrawal 291.2 Alcoholic Dementia 303 Alcoholism 303 Alcoholism 276.3 Alkalosis 995.3 Allergies, Cause Unspecifed (Reaction) 335.2 ALS (A;myothophic Lateral Sclerosis) 331 Alzheimers 331 Alzheimers Disease 362.34 Amaurosis Fugax 305.7 Amphetamine Abuse (Meth Abuse) 897 Amputation (Legs) 736.89 Amputation, Leg, Status Post (Above Knee, Below Knee) 736.9 Amputee, Site Unspecified (Acquired Deformity) 285.9 Anemia 284.9 Anemia Aplastic (Hypoplastic Bone Morrow) 280 Anemia Due to loss of Blood 281 Anemia Pernicious 280.9 Anemia, Iron Deficiency, Unspecified 285.9 Anemia, Unspecified (Normocytic, Not due to blood loss) 281.9 Anemia, Unspecified Deficiency (Macrocytic, Nutritional 441.5 Aneurysm Aortic, Ruptured 441.1 Aneurysm, Abdominal 441.3 Aneurysm, -
General Pathology
Jordan University of Science and Technology Faculty of Medicine 2018-2019 COURSE TITLE : GENERAL PATHOLOGY. COURSE CODE : MED 231. CREDIT HOURS : 3 CREDIT HOURS SEQUENCE : YEAR 2, FIRST SEMESTER COURSE COORDINATOR: Dr. Alia AlMuhtaseb; Dr. Mohammad Orjani CONTACT: [email protected]; [email protected] Course Description: This course deals with the investigation of those pathological mechanisms common to all tissue-cell pathology. Attention is paid to the processes of cellular adaptation, inflammation, repair, immunology, cellular accumulation, and neoplasia. Lecture will attempt first to familiarize the student with our basic layers of defense. Next those vocabulary terms and concepts relevant to the disease process will be introduced. The terminology employed is both medical and chiropractic. Processes and concepts will be developed with the aid of Data show. An interactive format is employed in which the instructor poses questions to enable the student to self-test their knowledge prior to exams and develop skills in communicating these basic pathological concepts to others. During the course and whenever relevant the students are exposed to clinical problems to emphasize the explanations of symptoms, signs, investigations and forms of treatments. Practical sessions are planned to give students the opportunity to expose their knowledge for discussion and confirm concepts learned in lectures. Small group discussions of clinical cases are planned at the end of the course were students are divided into small groups and with the help of an instructor they analyze and discuss the problem. The course will be given through 28 lectures, 7 practical (laboratory) sessions, and one small group discussion activity over 15 weeks and for one whole semester. -
Mycobacterium Tuberculosis Scott M
© 2015. Published by The Company of Biologists Ltd | Disease Models & Mechanisms (2015) 8, 591-602 doi:10.1242/dmm.019570 RESEARCH ARTICLE Presence of multiple lesion types with vastly different microenvironments in C3HeB/FeJ mice following aerosol infection with Mycobacterium tuberculosis Scott M. Irwin1, Emily Driver1, Edward Lyon1, Christopher Schrupp1, Gavin Ryan1, Mercedes Gonzalez-Juarrero1, Randall J. Basaraba1, Eric L. Nuermberger2 and Anne J. Lenaerts1,* ABSTRACT reservoir (Lin and Flynn, 2010). Since 2008, the incidence of Cost-effective animal models that accurately reflect the pathological multiple-drug-resistant (MDR) tuberculosis (TB) in Africa has progression of pulmonary tuberculosis are needed to screen and almost doubled, while in southeast Asia the incidence has increased evaluate novel tuberculosis drugs and drug regimens. Pulmonary more than 11 times (World Health Organization, 2013). Globally, disease in humans is characterized by a number of heterogeneous the incidence of MDR TB increased 42% from 2011 to 2012, with lesion types that reflect differences in cellular composition and almost 10% of those cases being extensively drug-resistant (XDR) organization, extent of encapsulation, and degree of caseous TB. With the rise in MDR and XDR TB, new drugs and especially necrosis. C3HeB/FeJ mice have been increasingly used to model drugs with a novel mechanism of action or drugs that can shorten the tuberculosis infection because they produce hypoxic, well-defined duration of treatment are desperately needed. granulomas