The 360 Terms Named for 431 People in First Aid for the USMLE Step 11 (2019)
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Physical Esxam
Pearls in the Musculoskeletal Exam Frank Caruso MPS, PA-C, EMT-P Skin, Bones, Hearts & Private Parts 2019 Examination Key Points • Area that needs to be examined, gown your patients - well exposed • Understand normal functional anatomy • Observe normal activity • Palpation • Range of Motion • Strength/neuro-vascular assessment • Special Tests General Exam Musculoskeletal Overview Physical Exam Preview Watch Your Patients Walk!! Inspection • Posture – Erectness – Symmetry – Alignment • Skin and subcutaneous tissues – Swelling – Redness – Masses Inspection • Extremities – Size – Deformities – Enlargement – Alignment – Contour – Symmetry Inspection • Muscles – Bilateral symmetry – Hypertrophy – Atrophy – Fasciculations – Spasms Palpation • Palpate bones, joints, and surrounding muscles for the following: – Heat – Tenderness – Swelling – Fluctuation – Crepitus – Resistance to pressure – Muscle tone Muscles • Size and strength affected by the following: – Genetics – Exercise – Nutrition • Muscles move joints through range of motion (ROM). Muscle Strength • Compare bilateral muscles – Strength – Symmetry – Equality – Resistance End Feel Think About It!! • The sensation the examiner feels in the joint as it reaches the end of the range of motion of each passive movement • Bone to bone: This is hard, unyielding – normal would be elbow extension. • Soft–tissue approximation: yielding compression that stops further movement – elbow and knee flexion. End Feel • Tissue stretch: hard – springy type of movement with a slight give – toward the end of range of motion – most common type of normal end feel : knee extension and metacarpophalangeal joint extension. Abnormal End Feel • Muscle spasm: invoked by movement with a sudden dramatic arrest of movement often accompanied by pain - sudden hard – “vibrant twang” • Capsular: Similar to tissue stretch but it does not occur where one would expect – range of motion usually reduced. -
The Hematological Complications of Alcoholism
The Hematological Complications of Alcoholism HAROLD S. BALLARD, M.D. Alcohol has numerous adverse effects on the various types of blood cells and their functions. For example, heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker’s risk of suffering a stroke. KEY WORDS: adverse drug effect; AODE (alcohol and other drug effects); blood function; cell growth and differentiation; erythrocytes; leukocytes; platelets; plasma proteins; bone marrow; anemia; blood coagulation; thrombocytopenia; fibrinolysis; macrophage; monocyte; stroke; bacterial disease; literature review eople who abuse alcohol1 are at both direct and indirect. The direct in the number and function of WBC’s risk for numerous alcohol-related consequences of excessive alcohol increases the drinker’s risk of serious Pmedical complications, includ- consumption include toxic effects on infection, and impaired platelet produc- ing those affecting the blood (i.e., the the bone marrow; the blood cell pre- tion and function interfere with blood cursors; and the mature red blood blood cells as well as proteins present clotting, leading to symptoms ranging in the blood plasma) and the bone cells (RBC’s), white blood cells from a simple nosebleed to bleeding in marrow, where the blood cells are (WBC’s), and platelets. -
Hematology Unit Lab 1 Review Material
Hematology Unit Lab 1 Review Material Objectives Laboratory instructors: 1. Facilitate lab discussion and answer questions Students: 1. Review the introductory material below 2. Study and review the assigned cases and questions in small groups before the Lab. This includes the pathological material using Virtual Microscopy 3. Be prepared to present your cases, questions and answers to the rest of your Lab class during the Lab Erythropoiesis: The process of red blood cell (RBC) production • Characterized by: − Increasing hemoglobin synthesis Erythroid maturation stages (Below): − Decreasing cell size - Average of 4 cell divisions during maturation − Decreasing cytoplasmic basophilia [One pronormoblast gives rise to 16 red cells] (increasing pink color) - pronormoblast → reticulocyte = 7 days − Progressive chromatin condensation of the - reticulocytes → mature RBC =1-2 days nuclei − Extrusion of nucleus (orthochromatic stage) − Extruded nuclei are subsequently phagocytized − Loss of mitotic capability after the early stage of polychromatophilic normoblast • Picture below: Erythroid progenitors (normoblasts) cluster around macrophages (arrows) in the bone marrow and spleen • Macrophages store iron • Iron is transferred from macrophages to erythroid precursor cells • Iron is used by normoblasts for hemoglobin synthesis aka nucleated rbc aka reticulocyte 1 Mature Red Blood Cell 7-8 microns; round / ovoid biconcave disc with orange-red cytoplasm, no RNA, no nucleus; survives ~120 days in circulation Classification of Anemia by Morphology 1. -
Abdomen and Superficial Structures Including Introductory Pediatric and Musculoskeletal
National Education Curriculum Specialty Curricula Abdomen and Superficial Structures Including Introductory Pediatric and Musculoskeletal Abdomen and Superficial Structures Including Introductory Pediatric and Musculoskeletal Table of Contents Section I: Biliary ........................................................................................................................................................ 3 Section II: Liver ....................................................................................................................................................... 19 Section III: Pancreas ............................................................................................................................................... 35 Section IV: Renal and Lower Urinary Tract ........................................................................................................ 43 Section V: Spleen ..................................................................................................................................................... 67 Section VI: Adrenal ................................................................................................................................................. 75 Section VII: Abdominal Vasculature ..................................................................................................................... 81 Section VIII: Gastrointestinal Tract (GI) .............................................................................................................. 91 -
Complete Blood Count in Primary Care
Complete Blood Count in Primary Care bpac nz better medicine Editorial Team bpacnz Tony Fraser 10 George Street Professor Murray Tilyard PO Box 6032, Dunedin Clinical Advisory Group phone 03 477 5418 Dr Dave Colquhoun Michele Cray free fax 0800 bpac nz Dr Rosemary Ikram www.bpac.org.nz Dr Peter Jensen Dr Cam Kyle Dr Chris Leathart Dr Lynn McBain Associate Professor Jim Reid Dr David Reith Professor Murray Tilyard Programme Development Team Noni Allison Rachael Clarke Rebecca Didham Terry Ehau Peter Ellison Dr Malcolm Kendall-Smith Dr Anne Marie Tangney Dr Trevor Walker Dr Sharyn Willis Dave Woods Report Development Team Justine Broadley Todd Gillies Lana Johnson Web Gordon Smith Design Michael Crawford Management and Administration Kaye Baldwin Tony Fraser Kyla Letman Professor Murray Tilyard Distribution Zane Lindon Lyn Thomlinson Colleen Witchall All information is intended for use by competent health care professionals and should be utilised in conjunction with © May 2008 pertinent clinical data. Contents Key points/purpose 2 Introduction 2 Background ▪ Haematopoiesis - Cell development 3 ▪ Limitations of reference ranges for the CBC 4 ▪ Borderline abnormal results must be interpreted in clinical context 4 ▪ History and clinical examination 4 White Cells ▪ Neutrophils 5 ▪ Lymphocytes 9 ▪ Monocytes 11 ▪ Basophils 12 ▪ Eosinophils 12 ▪ Platelets 13 Haemoglobin and red cell indices ▪ Low haemoglobin 15 ▪ Microcytic anaemia 15 ▪ Normocytic anaemia 16 ▪ Macrocytic anaemia 17 ▪ High haemoglobin 17 ▪ Other red cell indices 18 Summary Table 19 Glossary 20 This resource is a consensus document, developed with haematology and general practice input. We would like to thank: Dr Liam Fernyhough, Haematologist, Canterbury Health Laboratories Dr Chris Leathart, GP, Christchurch Dr Edward Theakston, Haematologist, Diagnostic Medlab Ltd We would like to acknowledge their advice, expertise and valuable feedback on this document. -
Laboratory Diagnosis Review
Laboratory Diagnosis Review Hematology Definition: The study of the three cellular elements of blood: Red Blood Cells (RBCs), White Blood Cells (WBCs), and Platelets Hemoglobin (Hgb or Hb): The oxygen carrying compound in RBCs Reference Range: Men 14-18 g/dL, Women 12-16 g/dL, Boy and girl levels are equal till age 11 Smoking increases, Pregnancy decreases, Capillary levels in newborns are higher than venous levels, Race, Position, and Time of day have minor effects, High WBCs may falsely raise Hgb. Below normal Hgb = anemia Red Blood Cell Count Reference Range: Men 4l5-6 million / cubic ml, Women4.0-5.5 million / ml3. Hematocrit (Hct): The ratio of RBCs to plasma Reference Range, Men 40%-54%, Women 37%-47%, Depends mostly on the number of RBCs but is slightly effected by the average RBC size, Not measured directly, but is calculated from the RBC count and the mean corpuscular volume (MCV). Increased by smoking, Decrease = anemia Useful Relationships: Hb X 3 = Hct RBCs (millions) X 3 = Hgb RBCs (millions) X 9 = Hct Wintrobe Indices: These indices are only significant if the RBCs, Hgb, and/or Hct. is abnormal MCV: Mean Corpuscular Volume MCH: Mean Corpuscular Hemoglobin MCHC: Mean Corpuscular Hemoglobin Concentration RDW: Red blood cell Distribution Width MCV: Reference Ranges: Men 80-95 fl (femtoliters), Women 81-99 fl (femto = 1 quadrillionth) Increased MCV = Macrocytosis, Decreased = Microcytosis MCV is increased by smoking, by B12 and/or folic acid deficiency, chronic liver disease, chronic alcoholism, Cardiorespiratory problems… Some macrocytic patients will not have macrocytosis MCV is decreased by iron deficiency, thalassemia, and anemia of chronic disease MCH: Reference Range 27-31 pg MCH is increased by Macrocytic anemias. -
10 11 Cyto Slides 81-85
NEW YORK STATE CYTOHEMATOLOGY PROFICIENCY TESTING PROGRAM Glass Slide Critique ~ November 2010 Slide 081 Diagnosis: MDS to AML 9 WBC 51.0 x 10 /L 12 Available data: RBC 3.39 x 10 /L 72 year-old female Hemoglobin 9.6 g/dL Hematocrit 29.1 % MCV 86.0 fL Platelet count 16 x 109 /L The significant finding in this case of Acute Myelogenous Leukemia (AML) was the presence of many blast forms. The participant median for blasts, all types was 88. The blast cells in this case (Image 081) are large, irregular in shape and contain large prominent nucleoli. It is difficult to identify a blast cell as a myeloblast without the presence of an Auer rod in the cytoplasm. Auer rods were reported by three participants. Two systems are used to classify AML into subtypes, the French- American-British (FAB) and the World Health Organization (WHO). Most are familiar with the FAB classification. The WHO classification system takes into consideration prognostic factors in classifying AML. These factors include cytogenetic test results, patient’s age, white blood cell count, pre-existing blood disorders and a history of treatment with chemotherapy and/or radiation therapy for a prior cancer. The platelet count in this case was 16,000. Reduced number of platelets was correctly reported by 346 (94%) of participants. Approximately eight percent of participants commented that the red blood cells in this case were difficult to evaluate due to the presence of a bluish hue around the red blood cells. Comments received included, “On slide 081 the morphology was difficult to evaluate since there was a large amount of protein surrounding RBC’s”, “Slide 081 unable to distinguish red cell morphology due to protein” and “Unable to adequately assess morphology on slide 081 due to poor stain”. -
Advanced Blood Cell Id: Peripheral Blood Findings in Sickle Cell Anemia
ADVANCED BLOOD CELL ID: PERIPHERAL BLOOD FINDINGS IN SICKLE CELL ANEMIA Educational commentary is provided for participants enrolled in program #259- Advanced Blood Cell Identification. This virtual blood cell identification program includes case studies with more difficult challenges. To view the blood cell images in more detail, click on the sample identification numbers underlined in the paragraphs below. This will open a virtual image of the selected cell and the surrounding fields. If the image opens in the same window as the commentary, saving the commentary PDF and opening it outside your browser will allow you to switch between the commentary and the images more easily. Click on this link for the API ImageViewerTM Instructions. Learning Outcomes After completing this exercise, participants should be able to: • describe morphologic features of normal peripheral blood leukocytes. • identify morphologic characteristics distinctive of sickle cells. • distinguish selected RBC inclusions based on morphologic features. • describe significant morphologic characteristics of nucleated red blood cells. Case Study The CBC from a 30 year old African American male is as follows: WBC=9.5 x 109/L, RBC=1.66 x 1012/L, Hgb=5.0 g/dL, Hct=13.9%, MCV=83.7 fL, MCH=30.1 pg, MCHC=36.0 g/dL, RDW-CV=24.9%, MPV=9.6 fL, Platelet=326 x 109/L. Educational Commentary The cells and RBC inclusions chosen for identification in this testing event were seen in the peripheral blood of a man with a severe anemia resulting from sickle cell disease. The cell shown in ABI-08 contains a Howell-Jolly body. -
Screening for Developmental Dysplasia of the Hip
Screening for Developmental Dysplasia of the Hip: A Systematic Literature Review for the U.S. Preventive Services Task Force Scott A. Shipman, MD, MPH1 Mark Helfand, MD, MPH2 Virginia A. Moyer, MD, MPH3 Barbara P. Yawn, MD, MSc4 1Department of Pediatrics, and 2Oregon Evidence-based Practice Center, Oregon Health & Science University, Portland Ore 3Department of Pediatrics, University of Texas-Houston Health Science Center, Houston TX 4Department of Primary Care Research, Olmsted Medical Center, Rochester Minn Corresponding author: Scott A. Shipman, MD, MPH Department of Pediatrics Oregon Health & Science University 707 SW Gaines Rd., CDRC-P Portland, OR 97239 Phone: (503) 494-6542 FAX: (503) 494-4953 Email: [email protected] Abstract Background: Developmental dysplasia of the hip (DDH) represents a spectrum of anatomic abnormalities that can result in permanent disability. Objective: We sought to gather and synthesize the published evidence regarding screening for DDH by primary care providers. Methods: We performed a systematic review of the literature using a best evidence approach as used by the U.S. Preventive Services Task Force. The review focused on screening relevant to primary care in infants from birth to 6 months of age, and on interventions employed before 1 year of age. Results: The literature on screening and interventions for DDH suffers from significant methodological shortcomings. No published trials directly link screening to improved functional outcomes. Clinical examination and ultrasound identify somewhat different groups of newborns at risk for DDH. A significant proportion of hip abnormalities identified through clinical examination or ultrasound in the newborn period will spontaneously resolve. Very few studies examine the functional outcomes of patients who have undergone therapy for DDH. -
Morphologic Evaluation of Anemia – I Adewoyin S
nd M y a ed g ic lo i o n i e B Adewoyin and Ogbenna, Biol Med (Aligarh) 2016, 8:6 DOI: 10.4172/0974-8369.1000322 ISSN: 0974-8369 Biology and Medicine Review Article Open Access Morphologic Evaluation of Anemia – I Adewoyin S. Ademola1* and Ogbenna A. Abiola2 1Department of Haematology and Blood Transfusion, University of Benin Teaching Hospital, PMB 1111, Ugbowo, Benin City, Nigeria 2Department of Haematology and Blood Transfusion, Lagos University Teaching Hospital, Idi-Araba, Lagos, Nigeria *Corresponding author: Adewoyin S. Ademola, Department of Haematology and Blood Transfusion, University of Benin Teaching Hospital, PMB 1111, Ugbowo, Benin City, Nigeria, Tel: +2347033966347; E-mail: [email protected] Received date: June 20, 2016; Accepted date: July 15, 2016; Published date: July 22, 2016 Copyright: © 2016 Adewoyin AS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited. Abstract Anaemia is a feature of many tropical diseases. Anaemia diagnosis therefore remains a crucial intervention among physicians in developing countries. A barrage of laboratory test (anaemic work-up) is usually deployed in differentiating its underlying cause. However, central to anaemia evaluation is the morphology of the red cells and other cell lines. Conventionally, initial laboratory tests include full blood count, reticulocyte count and peripheral blood film (PBF). PBF is often a clinical request, performed by skilled technologist and reported by haematologist/ haematomorphologist. Findings from PBF are reviewed and reported in the light of patient’s clinical history and examination findings. -
Assessment of Splenic Function A
Assessment of splenic function A. P. N. A. Porto, A. J. J. Lammers, R. J. Bennink, I. J. M. Berge, P. Speelman, J. B. L. Hoekstra To cite this version: A. P. N. A. Porto, A. J. J. Lammers, R. J. Bennink, I. J. M. Berge, P. Speelman, et al.. Assessment of splenic function. European Journal of Clinical Microbiology and Infectious Diseases, Springer Verlag, 2010, 29 (12), pp.1465-1473. 10.1007/s10096-010-1049-1. hal-00624509 HAL Id: hal-00624509 https://hal.archives-ouvertes.fr/hal-00624509 Submitted on 19 Sep 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Manuscript Click here to download Manuscript: Review Assessment of Slenic Function.doc Click here to view linked References 1 2 3 4 Title-page. 5 6 7 8 Title: Assessment of splenic function 9 10 11 Authors: A.P.N.A. de Porto1, A.J.J. Lammers1, R.J. Bennink2, I.J.M. ten Berge3, P. Speelman1, 12 4 13 J.B.L. Hoekstra . 14 15 16 Affiliations 17 18 1: Department of Infectious Diseases, Tropical Medicine and AIDS, Academic Medical Center, 19 Meibergdreef 9, 1105 AZ, Amsterdam, Netherlands. -
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Maternal-Newborn Nursing Demystified Downloaded by [ Faculty of Nursing, Chiangmai University 5.62.156.86] at [07/18/16]
Downloaded by [ Faculty of Nursing, Chiangmai University 5.62.156.86] at [07/18/16]. Copyright © McGraw-Hill Global Education Holdings, LLC. Not to be redistributed or modified in any way without permission. Downloaded by [ Faculty of Nursing, Chiangmai University 5.62.156.86] at [07/18/16]. Copyright © McGraw-Hill Global Education Holdings, LLC. Not to be redistributed or modified in any way without permission. Maternal-Newborn Nursing Demystified Downloaded by [ Faculty of Nursing, Chiangmai University 5.62.156.86] at [07/18/16]. Copyright © McGraw-Hill Global Education Holdings, LLC. Not to be redistributed or modified in any way without permission. Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. The author and the publisher of this work have checked with sources believed to be reliable in their efforts to provide informa- tion that is complete and generally in accord with the standards accepted at the time of publication. However, in view of the possibility of human error or changes in medical sciences, neither the author nor the publisher nor any other party who has been involved in the preparation or publi- cation of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration.