High Altitude Medical Problems (Medi- Medical Progress Cal Progress)
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X-Ray Interpretation
Objectives Describe a systematic method for interpretation of chest and abdomen x-rays List findings to accurately identify common X-ray Interpretation pathology in chest & abdomen x-rays Describe a systematic method to approach the Denise Ramponi, DNP, FNP-C, ENP-BC, FAANP, FAEN important components in interpretation of upper & lower extremity x-rays Chest X-ray: Standard Views Lateral Film Postero-anterior (PA): (LAT) view can determine th On inspiration – diaphragm descends to 10 rib the anterior-posterior posteriorly structures along the axis of the body Normal LAT film Counting Ribs AP View - Portable http://www.lumen.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr_f.htm When the patient is unable to tolerate routine views with pts sitting or supine No participation from the patient Film is against the patient's back (supine) 1 Consolidation, Atelectasis, Chest radiograph Interstitial involvement Consolidation - any pathologic process that fills the alveoli with Left and right heart fluid, pus, blood, cells or other borders well defined substances Interstitial - involvement of the Both hemidiaphragms supporting tissue of the lung visible to midline parenchyma resulting in fine or coarse reticular opacities Right - higher Atelectasis - collapse of a part of Heart less than 50% of the lung due to a decrease in the amount of air resulting in volume diameter of the chest loss and increased density. Infiltrate, Consolidation vs. Congestive Heart Failure Atelectasis Fluid leaking into interstitium Kerley B 2 Kerley B lines Prominent interstitial markings Kerley lines Magnified CXR Cardiomyopathy & interstitial pulmonary edema Short 1-2 cm white lines at lung periphery horizontal to pleural surface Distended interlobular septa - secondary to interstitial edema. -
Altitude Sickness in Nepal Is About 1 in 30,000 Trekkers, Or 2-3 Deaths Per Year
Shoreland Travax Medical Summary ALTITUDE ILLNESS INTRODUCTION Altitude illness occurs when one ascends more rapidly than the body can adjust ("acclimatize") to the reduced atmospheric pressure and decreased oxygen delivery to the body's cells at the higher altitude. Factors affecting acclimatization include the altitude attained, the rate of ascent, the duration of exposure, genetic predisposition, and certain preexisting conditions. (See "Acclimatization," "Risk," and "Effect of High Altitude on Preexisting Medical Conditions.") Altitude illness is generally divided into 3 syndromes: acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), and high altitude cerebral edema (HACE). See "Syndromes and Symptoms." Symptoms can range from mild to life-threatening. Although mild symptoms have been documented at relatively low altitudes of 1,200- 1,800 m (3,900-5,900 ft), serious syndromes are rarely seen below 2,500-3,000 m (8,200-9,800 ft). While death can occur from the more severe forms of altitude illness, most symptoms can be prevented or minimized by proper acclimatization and/or preventive medications. Risk and prevention strategies vary depending on the type of travel planned: travel to typical tourist destinations at relatively moderate heights or trekking in extreme high altitude situations. See "Risk of Altitude Illness" and "Prevention." ACCLIMATIZATION Acclimatization is a built-in adjustment mechanism that can optimize performance at higher altitudes. If a person ascends more rapidly than the body can adjust, symptoms occur that are referred to as altitude illness. Acclimatization seems to be determined by factors that are not known but may possibly be genetic. Some people adjust very easily to high altitude, while others cannot go above relatively moderate heights of 3,000 m (9,800 ft) without experiencing symptoms. -
A Randomized, Double-Blind, Placebo-Controlled Study
medRxiv preprint doi: https://doi.org/10.1101/2020.04.06.20055715; this version posted April 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . 1 Mo%on Sifnos: A randomized, double-blind, placebo-controlled study demonstra%ng the effec%veness of tradipitant in the treatment of mo%on sickness Vasilios M. Polymeropoulos*1, Mark É. Czeisler1#a, Mary M. Gibson1¶, Aus%n A. Anderson1¶, Jane Miglo1#b, Jingyuan Wang1, Changfu Xiao1, Christos M. Polymeropoulos1, Gunther Birznieks1, Mihael H. Polymeropoulos1 1 Vanda Pharmaceu%cals, Washington, District of Columbia, United States of America #a The Ins%tute for Breathing and Sleeping, Aus%n Health, Heidelberg, Victoria, Australia #b College of Pharmacy, University of Illinois at Chicago, Chicago, Illinois, United States of America *Corresponding author Email: [email protected] (VMP) ¶These authors contributed equally to this work. NOTE: This preprint reports new research that has not been certified by peer review and should not be used to guide clinical practice. medRxiv preprint doi: https://doi.org/10.1101/2020.04.06.20055715; this version posted April 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license . 2 Abstract Background Novel therapies are needed for the treatment of mo%on sickness given the inadequate relief, and bothersome and dangerous adverse effects of currently approved therapies. -
Adverse Drug Reactions Sample Chapter
Sample copyright Pharmaceutical Press www.pharmpress.com 5 Drug-induced skin reactions Anne Lee and John Thomson Introduction Cutaneous drug eruptions are one of the most common types of adverse reaction to drug therapy, with an overall incidence rate of 2–3% in hos- pitalised patients.1–3 Almost any medicine can induce skin reactions, and certain drug classes, such as non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics and antiepileptics, have drug eruption rates approaching 1–5%.4 Although most drug-related skin eruptions are not serious, some are severe and potentially life-threatening. Serious reac- tions include angio-oedema, erythroderma, Stevens–Johnson syndrome and toxic epidermal necrolysis. Drug eruptions can also occur as part of a spectrum of multiorgan involvement, for example in drug-induced sys- temic lupus erythematosus (see Chapter 11). As with other types of drug reaction, the pathogenesis of these eruptions may be either immunological or non-immunological. Healthcare professionals should carefully evalu- ate all drug-associated rashes. It is important that skin reactions are identified and documented in the patient record so that their recurrence can be avoided. This chapter describes common, serious and distinctive cutaneous reactions (excluding contact dermatitis, which may be due to any external irritant, including drugs and excipients), with guidance on diagnosis and management. A cutaneous drug reaction should be suspected in any patient who develops a rash during a course of drug therapy. The reaction may be due to any medicine the patient is currently taking or has recently been exposed to, including prescribed and over-the-counter medicines, herbal or homoeopathic preparations, vaccines or contrast media. -
Cardiothoracic Fellowship Program
Cardiothoracic Fellowship Program Table of Contents Program Contact ............................................................................................ 3 Other contact numbers .................................................................................. 4 Introduction ........................................................................................................... 5 Goals and Objectives of Fellowship: ..................................................................... 6 Rotation Schedule: ........................................................................................ 7 Core Curriculum .................................................................................................... 8 Fellow’s Responsibilities ..................................................................................... 22 Resources ........................................................................................................... 23 Facilities ....................................................................................................... 23 Educational Program .......................................................................................... 26 Duty Hours .......................................................................................................... 29 Evaluation ........................................................................................................... 30 Table of Appendices .................................................................................... 31 Appendix A -
Deadly High Altitude Pulmonary Disorders: Acute Mountain Sickness
Research Article Int J Pul & Res Sci Volume 1 Issue 1 - April 2016 Copyright © All rights are reserved by Michael Obrowski DOI : 10.19080/IJOPRS.2016.01.555553 Deadly High Altitude Pulmonary Disorders: Acute Mountain Sickness (AMS); High Altitude Pulmonary Edema (HAPE) and High Altitude Cerebral Edema (HACE): A Clinical Review Michael Obrowski1* and Stephanie Obrowski2 1Doctor of Medicine (M.D. – 2000); Assistant Professor of Anatomy; CEO, Chief Physician and Surgeon of Wilderness Physicians, European Union 2Doctor of Medicine (M.D. – 2019); Medical University of Łódź; President of Wilderness Physicians, European Union Submission: January 26, 2016; Published: April 15, 2016 *Corresponding author: Michael Obrowski, M.D., Doctor of Medicine (M.D. – 2000); Assistant Professor of Anatomy; CEO, Chief Physician and Surgeon of Wilderness Physicians, European Union, 43C Żeligowskiego Street, #45, Łódź, Poland 90-644, Email: Abstract Acute Mountain Sickness (AMS); High Altitude Pulmonary Edema (HAPE) and High Altitude Cerebral Edema (HACE). These three disorders, withMountain relatively Sickness, unimportant also smallcalled variationsHigh Altitude seen Sickness, in some isPulmonology specifically aTextbooks, triad of different because disorders, these are inso orderserious, of increasingthey are all seriousness: potentially deadly pulmonary disorders and we will discuss these three major, deadly disorders. Each one, starting with AMS, can progress rapidly to HAPE and then HACE. The two authors of this article have over half a century of high altitude mountaineering experience. They have also alsohad anddisaster still domedicine. have, for Since the lastspring twenty is rapidly years, approaching an NGO, Non-Profit and many Medical “weekend Organization backpackers” (Wilderness will start Physicians going into www.wildernessphysicians. -
Comparison of Health and Performance Risk for Accelerated Mars Mission Scenarios
NASA/TM-20210009779 Comparison of Health and Performance Risk for Accelerated Mars Mission Scenarios Erik Antonsen MD, PhD Baylor College of Medicine NASA Johnson Space Center, Houston, TX Mary Van Baalen, PhD; NASA Johnson Space Center, Houston, TX Integrated Medical Model Team Space Radiation Analysis Group Binaifer Kadwa, MS Lori Chappell, MS NASA Johnson Space Center, Houston, TX KBR NASA Johnson Space Center, Houston, TX Lynn Boley, RN, MS KBR Edward Semones, MS NASA Johnson Space Center, Houston, TX NASA Johnson Space Center, Houston, TX John Arellano, PhD Space Radiation Element MEI Technologies NASA Johnson Space Center, Houston, TX S. Robin Elgart, PhD University of Houston Eric Kerstman, MD NASA Johnson Space Center, Houston, TX University of Texas Medical Branch NASA Johnson Space Center, Houston, TX National Aeronautics and Space Administration Lyndon B. Johnson Space Center Houston, Texas 77058 February 2021 NASA STI Program…in Profile Since its founding, NASA has been dedicated to the CONFERENCE PUBLICATION. advancement of aeronautics and space science. The Collected papers from scientific and NASA scientific and technical information (STI) technical conferences, symposia, seminars program plays a key part in helping NASA or other meetings sponsored or co- maintain this important role. sponsored by NASA. The NASA STI program operates under the auspices of the Agency Chief Information Officer. SPECIAL PUBLICATION. Scientific, It collects, organizes, provides for archiving, and technical, or historical information from disseminates NASA’s STI. The NASA STI NASA programs, projects, and missions, program provides access to the NTRS Registered often concerned with subjects having and its public interface, the NASA Technical substantial public interest. -
12. Shortness of Breath
12. Shortness of breath Shortness of breath (dyspnea) is described as an intense tightening in the chest, air hunger, difficulty breathing, breathlessness or a feeling of suffocation. It is a subjective symptom of many diseases. The causes of shortness of breath can be various, but most often pulmonary or cardiac. The main causes of pulmonary or cardiac dyspnea include heart congestion, pulmonary embolism, emphysema, atelectasis, pneumothorax and interstitial lung processes. The basic imaging method in the diagnosis of dyspnea that follows clinical examination is a chest X- ray. It is used to evaluate heart congestion, fluid effusions, atelectasis, pneumothorax, and a rough assessment of interstitial lung processes. Only if there is a clinical suspicion of pulmonary embolization, the CT angiography (with intravenous contrast), perfusion lung scintigraphy or echocardiography are imaging methods of choice. If interstitial lung disease or pulmonary emphysema are suspected or there is uncertain finding on chest X-ray, high-resolution CT (HRCT) of the chest is recommended. HRCT allows detailed assessment of pulmonary parenchyma. Non-contrast CT is usually sufficient to assess interstitial changes. Heart congestion Heart congestion is the result of insufficient cardiac output due to heart failure or fluid overload. The most common cause of heart congestion is left heart failure with increased pressure in pulmonary veins and capillaries. On chest X- ray can be distinguished 3 degrees of heart congestion. Note: Right-sided heart failure most often occurs in long-term left-sided heart failure or lung disease, which leads to high pulmonary artery resistance (various etiologies of pulmonary hypertension, e.g. advanced COPD). -
Interstitial Lung Disease
Interstitial Lung Disease Camille Washowich, MSN, ACNP, CCRN Center for Advanced Lung Disease Stanford University Medical Center Lung Physiology ILD Classification Interstitial Lung Disease Connective Tissue Diseases Primary (unclassified) Idiopathic Fibrotic Disorders Drug and Treatment Induced Connective Tissue Diseases Scleroderma Systemic Lupus Erythematous (SLE) Rheumatoid Arthritis Mixed Connective Tissue Disease Primary (unclassified) Sarcoidosis Stage I-IV Neurofibromatosis Tuberous Sclerosis AIDS ARDS Bone Marrow Transplantation Post infectious Occupational & Environmental Exposures: Inorganic & Organic Agriculture Workers and Animal Handlers Construction: wood/metal Auto repair Military Chemicals (plastic, paint, polyurethane) Organisms: fungus/molds/bacterium Idiopathic Fibrotic Disorders Pulmonary fibrosis Familial pulmonary fibrosis Autoimmune pulmonary fibrosis Respiratory bronchiolitis Nonspecific interstitial pneumonitis (NSIP) Drug Induced Antibiotics Anti-arrhythmics Anti-inflammatory Anti-convulsant Radiation/Chemotherapy Oxygen toxicity Narcotics ILD Epidemiology in the US 100K admissions/year Occupation DILD Sarcoidosis 11% 15% pulmonologist patients 5% DAH 8% 4% CTD Incidence: 5/100K 9% Men (31%) versus Women (26%) Other 11% IPF 45% of all ILD patients Pulmonary Fibrosis 52% Age/Gender/Race Specifications to Assist in Diagnosis 20-40yrs: Inherited Interstitial Lung diseases Familial idiopathic pulmonary fibrosis Collagen vascular disease- associated ILD LAM Pulmonary Langerhans’ cell granulomatosis Sarcoidosis 50yrs: -
Chapter 5 Biological Effects of Ionizing Radiation Page I
CHAPTER 5 BIOLOGICAL EFFECTS OF IONIZING RADIATION PAGE I. Introduction ............................................................................................................................ 5-3 II. Mechanisms of Radiation Damage ........................................................................................ 5-3 A. Direct Action .............................................................................................................. 5-3 B. Indirect Action ........................................................................................................... 5-3 III. Determinants of Biological Effects ........................................................................................ 5-4 A. Rate of Absorption ..................................................................................................... 5-5 B. Area Exposed ............................................................................................................. 5-5 C. Variation in Species and Individual Sensitivity ......................................................... 5-5 D. Variation in Cell Sensitivity ....................................................................................... 5-5 IV. The Dose-Response Curve ..................................................................................................... 5-6 V. Pattern of Biological Effects .................................................................................................. 5-7 A. Prodromal Stage ........................................................................................................ -
Acute Radiation Syndrome (ARS) – Treatment of the Reduced Host Defense
International Journal of General Medicine Dovepress open access to scientific and medical research Open Access Full Text Article REVIEW Acute radiation syndrome (ARS) – treatment of the reduced host defense Lars Heslet1 Background: The current radiation threat from the Fukushima power plant accident has prompted Christiane Bay2 rethinking of the contingency plan for prophylaxis and treatment of the acute radiation syndrome Steen Nepper-Christensen3 (ARS). The well-documented effect of the growth factors (granulocyte colony-stimulating factor [G-CSF] and granulocyte-macrophage colony-stimulating factor [GM-CSF]) in acute radia- 1Serendex ApS, Gentofte; 2University of Copenhagen, tion injury has become standard treatment for ARS in the United States, based on the fact that Medical Faculty, Copenhagen; growth factors increase number and functions of both macrophages and granulocytes. 3 Department of Head and Neck Review of the current literature. Surgery, Otorhinolaryngology, Methods: Køge University Hospital, Køge, Results: The lungs have their own host defense system, based on alveolar macrophages. After Denmark radiation exposure to the lungs, resting macrophages can no longer be transformed, not even during systemic administration of growth factors because G-CSF/GM-CSF does not penetrate the alveoli. Under normal circumstances, locally-produced GM-CSF receptors transform resting macrophages into fully immunocompetent dendritic cells in the sealed-off pulmonary compartment. However, GM-CSF is not expressed in radiation injured tissue due to deferves- cence of the macrophages. In order to maintain the macrophage’s important role in host defense after radiation exposure, it is hypothesized that it is necessary to administer the drug exogenously in order to uphold the barrier against exogenous and endogenous infections and possibly prevent the potentially lethal systemic infection, which is the main cause of death in ARS. -
Angioedema After Long-Term Use of an Angiotensin-Converting Enzyme Inhibitor
J Am Board Fam Pract: first published as 10.3122/jabfm.10.5.370 on 1 September 1997. Downloaded from BRIEF REPORTS Angioedema After Long-Term Use of an Angiotensin-Converting Enzyme Inhibitor Adriana]. Pavietic, MD Angioedema is an uncommon adverse effect of cyclobenzaprine, her angioedema was initially be angiotensin-converting enzyme (ACE) inhib lieved to be an allergic reaction to this drug, and itors. Its frequency ranges from 0.1 percent in pa it was discontinued. She was also given 125 mg of tients on captopril, lisinopril, and quinapril to 0.5 methylprednisolone intramuscularly. Her an percent in patients on benazepril. l Most cases are gioedema did not improve, and she returned to mild and occur within the first week of treat the clinic the following day. She was seen by an ment. 2-4 Recent reports indicate that late-onset other physician, who discontinued lisinopril, and angioedema might be more prevalent than ini her symptoms resolved within 24 hours. Mter her tially thought, and fatal cases have been de ACE inhibitor was discontinued, she experienced scribed.5-11 Many physicians are not familiar with more symptoms and an increased frequency of late-onset angioedema associated with ACE in palpitations, but she had no change in exercise hibitors, and a delayed diagnosis can have poten tolerance. A cardiologist was consulted, who pre tially serious consequences.5,8-II scribed the angiotensin II receptor antagonist losartan (initially at dosages of 25 mg/d and then Case Report 50 mg/d). The patient was advised to report any A 57-year-old African-American woman with symptoms or signs of angioedema immediately copyright.