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HEENT EXAMINIATION ______HEENT Exam Exam Overview
HEENT EXAMINIATION ____________________________________________________________ HEENT Exam Exam Overview I. Head A. Visual inspection B. Palpation of scalp II. Eyes A. Visual Acuity B. Visual Fields C. Extraocular Movements/Near Response D. Inspection of sclera & conjunctiva E. Pupils F. Ophthalmoscopy III. Ears A. External Inspection B. Otoscopy C. Hearing Acuity D. Weber/Rinne IV. Nose A. External Inspection B. Speculum/otoscope C. Sinus areas V. Throat/Mouth A. Mouth Examination B. Pharynx Examination C. Bimanual Palpation VI. Neck A. Lymph nodes B. Thyroid gland 29 HEENT EXAMINIATION ____________________________________________________________ HEENT Terms Acuity – (ehk-yu-eh-tee) sharpness, clearness, and distinctness of perception or vision. Accommodation - adjustment, especially of the eye for seeing objects at various distances. Miosis – (mi-o-siss) constriction of the pupil of the eye, resulting from a normal response to an increase in light or caused by certain drugs or pathological conditions. Conjunctiva – (kon-junk-ti-veh) the mucous membrane lining the inner surfaces of the eyelids and anterior part of the sclera. Sclera – (sklehr-eh) the tough fibrous tunic forming the outer envelope of the eye and covering all of the eyeball except the cornea. Cornea – (kor-nee-eh) clear, bowl-shaped structure at the front of the eye. It is located in front of the colored part of the eye (iris). The cornea lets light into the eye and partially focuses it. Glaucoma – (glaw-ko-ma) any of a group of eye diseases characterized by abnormally high intraocular fluid pressure, damaged optic disk, hardening of the eyeball, and partial to complete loss of vision. Conductive hearing loss - a hearing impairment of the outer or middle ear, which is due to abnormalities or damage within the conductive pathways leading to the inner ear. -
Advanced Interpretation of Adult Vital Signs in Trauma William D
Advanced Interpretation of Adult Vital Signs in Trauma William D. Hampton, DO Emergency Physician 26 March 2015 Learning Objectives 1. Better understand vital signs for what they can tell you (and what they can’t) in the assessment of a trauma patient. 2. Appreciate best practices in obtaining accurate vital signs in trauma patients. 3. Learn what teaching about vital signs is evidence-based and what is not. 4. Explain the importance of vital signs to more accurately triage, diagnose, and confidently disposition our trauma patients. 5. Apply the monitoring (and manipulation of) vital signs to better resuscitate trauma patients. Disclosure Statement • Faculty/Presenters/Authors/Content Reviewers/Planners disclose no conflict of interest relative to this educational activity. Successful Completion • To successfully complete this course, participants must attend the entire event and complete/submit the evaluation at the end of the session. • Society of Trauma Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. Vital Signs Vital Signs Philosophy: “View vital signs as compensatory to the illness/complaint as opposed to primary.” Crowe, Donald MD. “Vital Sign Rant.” EMRAP: Emergency Medicine Reviews and Perspectives. February, 2010. Vital Signs Truth over Accuracy: • Document the true status of the patient: sick or not? • Complete vital signs on every patient, every time, regardless of the chief complaint. • If vital signs seem misleading or inaccurate, repeat them! • Beware sending a patient home with abnormal vitals (especially tachycardia)! •Treat vital signs the same as any other diagnostics— review them carefully prior to disposition. The Mother’s Vital Sign: Temperature Case #1 - 76-y/o homeless ♂ CC: 76-y/o homeless ♂ brought to the ED by police for eval. -
Organ Transplant Manual
Congratulations! ystem lth S Hea sity iver Un 013 y, 2 Ma t© igh pyr Co Dear Patient: Congratulations! You have been given the gift of life! Receiving a transplant is a marvelous gift and the Transplant Team members will meet with you Transplant Team is here to assist you in taking care during your hospitalization to help you learn this of that gift. information. Here are some suggestions that may help you learn: Transplant Team members include the surgeons, medicine physicians, nurses, discharge coordinator, • Listen to the Transplant Team and ask them questions patient educator, dietitian, transplant pharmacists about things you don’t understand. and social workers. • Study every day. This manual is designed to help you care for yourself • Ask a family member or friend to study with you. following your transplant. As you read the following We want you to be able to return to your home and information, feel free to ask questions of your family in the best possible health to enjoy an active Transplant Team. and productive life. Understanding the information in this manual You must take your prescribed medications, follow is important. your diet, exercise, and monitor yourself for signs and symptoms of infection and rejection. By working as a team, you will achieve the best possible outcome from your transplant. Tim Nevil Kidney Recipient, 2001 Tania S. Gonzales José David Aguirre Liver Transplant Recipient, 2002 Liver Transplant Recipient, 2001 Table of Contents Organ Transplant Manual Contacting the Transplant Team When to Call ...........................................3 -
Ehrlichiosis and Anaplasmosis Are Tick-Borne Diseases Caused by Obligate Anaplasmosis: Intracellular Bacteria in the Genera Ehrlichia and Anaplasma
Ehrlichiosis and Importance Ehrlichiosis and anaplasmosis are tick-borne diseases caused by obligate Anaplasmosis: intracellular bacteria in the genera Ehrlichia and Anaplasma. These organisms are widespread in nature; the reservoir hosts include numerous wild animals, as well as Zoonotic Species some domesticated species. For many years, Ehrlichia and Anaplasma species have been known to cause illness in pets and livestock. The consequences of exposure vary Canine Monocytic Ehrlichiosis, from asymptomatic infections to severe, potentially fatal illness. Some organisms Canine Hemorrhagic Fever, have also been recognized as human pathogens since the 1980s and 1990s. Tropical Canine Pancytopenia, Etiology Tracker Dog Disease, Ehrlichiosis and anaplasmosis are caused by members of the genera Ehrlichia Canine Tick Typhus, and Anaplasma, respectively. Both genera contain small, pleomorphic, Gram negative, Nairobi Bleeding Disorder, obligate intracellular organisms, and belong to the family Anaplasmataceae, order Canine Granulocytic Ehrlichiosis, Rickettsiales. They are classified as α-proteobacteria. A number of Ehrlichia and Canine Granulocytic Anaplasmosis, Anaplasma species affect animals. A limited number of these organisms have also Equine Granulocytic Ehrlichiosis, been identified in people. Equine Granulocytic Anaplasmosis, Recent changes in taxonomy can make the nomenclature of the Anaplasmataceae Tick-borne Fever, and their diseases somewhat confusing. At one time, ehrlichiosis was a group of Pasture Fever, diseases caused by organisms that mostly replicated in membrane-bound cytoplasmic Human Monocytic Ehrlichiosis, vacuoles of leukocytes, and belonged to the genus Ehrlichia, tribe Ehrlichieae and Human Granulocytic Anaplasmosis, family Rickettsiaceae. The names of the diseases were often based on the host Human Granulocytic Ehrlichiosis, species, together with type of leukocyte most often infected. -
(June 2000) I. INTRODUCTION WHAT IS DOCUMENTATION and WHY
DRAFT EVALUATION & MANAGEMENT DOCUMENTATION GUIDELINES (June 2000) I. INTRODUCTION WHAT IS DOCUMENTATION AND WHY IS IT IMPORTANT? Medical record documentation is required to record pertinent facts, findings, and observations about an individual's health history including past and present illnesses, examinations, tests, treatments, and outcomes. The medical record chronologically documents the care of the patient and is an important element contributing to high quality care. The medical record facilitates: · the ability of the physician and other health care professionals to evaluate and plan the patient's immediate treatment, and to monitor his/her health care over time. · communication and continuity of care among physicians and other health care professionals involved in the patient's care; · accurate and timely claims review and payment; · appropriate utilization review and quality of care evaluations; and · collection of data that may be useful for research and education. An appropriately documented medical record can reduce many of the "hassles" associated with claims processing and may serve as a legal document to verify the care provided, if necessary. WHAT DO PAYERS WANT AND WHY? Because payers have a contractual obligation to enrollees, they may require reasonable documentation that services are consistent with the insurance coverage provided. They may request information to validate: · the site of service; · the medical necessity and appropriateness of the diagnostic and/or therapeutic services provided; and/or · that services provided have been accurately reported. II. GENERAL PRINCIPLES OF MEDICAL RECORD DOCUMENTATION The principles of documentation listed below are applicable to all types of medical and surgical Pg. 1 services in all settings. For Evaluation and Management (E/M) services, the nature and amount of physician work and documentation varies by type of service, place of service and the patient's status. -
Blood Pressure Year 1 Year 2 Core Clinical/Year 3+
Blood Pressure Year 1 Year 2 Core Clinical/Year 3+ Do Do • Patient at rest for 5 minutes • Measure postural BP and pulse in patients with a • Arm at heart level history suggestive of volume depletion or • Correct size cuff- bladder encircles 80% of arm syncope • Center of cuff aligns with brachial artery -Measure BP and pulse in supine position • Cuff wrapped snugly on bare arm with lower -Slowly have patient rise and stand (lie them down edge 2-3 cm above antecubital fossa promptly if symptoms of lightheadedness occur) • Palpate radial artery, inflate cuff to 70 mmHg, -Measure BP and pulse after 1 minute of standing then increase in 10 mmHg increments to 30 mmHg above point where radial pulse disappears. Know Deflate slowly until pulse returns; this is the • Normally when a person stands fluid shifts to approximate systolic pressure. lower extremities causing a compensatory rise in • Auscultate the Korotkoff sounds pulse by up to 10 bpm with BP dropping slightly -place bell lightly in antecubital fossa • Positive postural vital signs are defined as -inflate BP to 20-30mmHg above SBP as determined symptoms of lightheadedness and/or a drop in by palpation SBP of 20 mmHg with standing -deflate cuff at rate 2mmHg/second while auscultating • Know variations in BP cuff sizes -first faint tapping (Phase I Korotkoff) = SBP; • A lack of rise in pulse in a patient with an Disappearance of sound (Phase V Korotkoff)=DBP orthostatic drop in pressure is a clue that the Know cause is neurologic or related or related to -Korotkoff sounds are lower pitch, better heard by bell medications (eg. -
Outcome and Assessment Information Set OASIS-D Guidance Manual Effective January 1, 2019
Outcome and Assessment Information Set OASIS-D Guidance Manual Effective January 1, 2019 Centers for Medicare & Medicaid Services PRA Disclosure Statement According to the Paperwork Reduction Act of 1995, no persons are required to respond to a collection of information unless it displays a valid OMB control number. The valid OMB control number for this information collection is x. The time required to complete this information collection is estimated to average 0.3 minutes per response, including the time to review instructions, search existing data resources, gather the data needed, and complete and review the information collection. This estimate does not include time for training. If you have comments concerning the accuracy of the time estimate(s) or suggestions for improving this form, please write to: CMS, 7500 Security Boulevard, Attn: PRA Reports Clearance Officer, Mail Stop C4-26-05, Baltimore, Maryland 21244-1850. *****CMS Disclaimer*****Please do not send applications, claims, payments, medical records or any documents containing sensitive information to the PRA Reports Clearance Office. Please note that any correspondence not pertaining to the information collection burden approved under the associated OMB control number listed on this form will not be reviewed, forwarded, or retained. If you have questions or concerns regarding where to submit your documents, please contact Joan Proctor National Coordinator, Home Health Quality Reporting Program Centers for Medicare & Medicaid. OASIS-D Guidance Manual Table of Contents Page -
Edema II, Clinical Significance
EDEMA II CLINICAL SIGNIFICANCE F. A. LeFEVRE, M.D., R. H. McDONALD, M.D., AND A. C. CORCORAN, M.D. It is the purpose of this paper to outline the clinical syndromes in which edema significantly appears, to discuss their differentiation, and to comment on the changes to which edema itself may give rise. The frequency with which edema occurs indicates the variety of its origins. Its physiologic bases have been reviewed in a former paper.1 Conditions in which edema commonly appears are summarized in Table 1. Although clinical edema usually involves more than one physiologic mechanism, it is not difficult to determine the predominant disturbance. Table 2 illustrates the physiologic mechanisms of clinical edema. Physiologically, edema is an excessive accumulation of interstitial fluid. Clinically, it may be latent or manifest, and, by its nature, localized or generalizing. These terms, with the exception of generalizing, have been defined, and may be accepted. By generalizing edema is meant a condi- tion in which edema is at first local in its appearance, but in which, as the process extends, edema will become general, causing anasarca. The degree of edema in any area is limited by tissue tension and the sites of its first appearance and later spread are partly determined by gravity. CARDIAC EDEMA Generalizing edema is an early manifestation of cardiac failure. It is usually considered to be evidence of inadequacy of the right ventricu- lar musculature (back pressure theory). Peripheral edema may be accompanied by pulmonary edema in cases where there is simultaneous left ventricular failure. Actually, the genesis of cardiac edema may depend more on sodium retention2,3'4 due to "forward cardiac failure" and renal constriction than on venous back pressure alone. -
Wilderness First Aid Reference Cards
Pulse/Pressure Points Wilderness First Aid Reference Cards Carotid Brachial Prepared by: Andrea Andraschko, W-EMT Radial October 2006 Femoral Posterior Dorsalis Tibial Pedis Abdominal Quadrants Airway Anatomy (Looking at Patient) RIGHT UPPER: LEFT UPPER: ANTERIOR: ANTERIOR: GALL BLADDER STOMACH LIVER SPLEEN POSTERIOR: POSTERIOR: R. KIDNEY PANCREAS L. KIDNEY RIGHT LOWER: ANTERIOR: APPENDIX CENTRAL AORTA BLADDER Tenderness in a quadrant suggests potential injury to the organ indicated in the chart. Patient Assessment System SOAP Note Information (Focused Exam) Scene Size-up BLS Pt. Information Physical (head to toe) exam: DCAP-BTLS, MOI Respiratory MOI OPQRST • Major trauma • Air in and out Environmental conditions • Environmental • Adequate Position pt. found Normal Vitals • Medical Nervous Initial Px: ABCs, AVPU Pulse: 60-90 Safety/Danger • AVPU Initial Tx Respiration: 12-20, easy Skin: Pink, warm, dry • Move/rescue patient • Protect spine/C-collar SAMPLE LOC: alert and oriented • Body substance isolation Circulatory Symptoms • Remove from heat/cold exposure • Pulse Allergies Possible Px: Trauma, Environmental, Medical • Consider safety of rescuers • Check for and Stop Severe Bleeding Current Px Medications Resources Anticipated Px → Past/pertinent Hx • # Patients STOP THINK: Field Tx ast oral intake • # Trained rescuers A – Continue with detailed exam L S/Sx to monitor VPU EVAC NOW Event leading to incident • Available equipment (incl. Pt’s) – Evac level Patient Level of Consciousness (LOC) Shock Assessment Reliable Pt: AVPU Hypovolemic – Low fluid (Tank) Calm A+ Awake and Cooperative Cardiogenic – heart problem (Pump) Comment: Cooperative A- Awake and lethargic or combative Vascular – vessel problem (Hose) If a pulse drops but does not return Sober V+ Responds with sound to verbal to ‘normal’ (60-90 bpm) within 5-25 Alert stimuli Volume Shock (VS) early/compensated minutes, an elevated pulse is likely caused by VS and not ASR. -
Livedoid Vasculopathy Associated with Peripheral Neuropathy: a Report of Two Cases* Vasculopatia Livedoide Associada a Neuropatia Periférica: Relato De Dois Casos
CASE REPORT 227 s Livedoid vasculopathy associated with peripheral neuropathy: a report of two cases* Vasculopatia livedoide associada a neuropatia periférica: relato de dois casos Mariana Quirino Tubone1 Gabriela Fortes Escobar1 Juliano Peruzzo1 Pedro Schestatsky2 Gabriela Maldonado3 DOI: http://dx.doi.org/10.1590/abd1806-4841.20132363 Abstract: Livedoid vasculopathy (LV) is a chronic and recurrent disease consisting of livedo reticularis and sym- metric ulcerations, primarily located on the lower extremities, which heal slowly and leave an atrophic white scar ("atrophie blanche"). Neurological involvment is rare and presumed to be secondary to the ischemia from vascu- lar thrombosis of the vasa nervorum. Laboratory evaluation is needed to exclude secondary causes such as hyper- coagulable states, autoimmune disorders and neoplasms. We present two patients with a rare association of peripheral neuropathy and LV, thereby highlighting the importance of a multidisciplinary approach to reach the correct diagnosis. Keywords: Livedo reticularis; Mononeuropathies; Polyneuropathies; Skin diseases, vascular Resumo: Vasculopatia livedoide é uma doença crônica e recorrente caracterizada por livedo reticular e úlceras simétricas nos membros inferiores, que cicatrizam e deixam uma cicatriz branca atrófica ("atrophie blanche"). Envolvimento neurológico é raro e está provavelmente associado a isquemia pela trombose dos vasa nervorum. Avaliação laboratorial é indicada com o intuito de excluir causas secundárias como estados de hipercoagulabili- dade, doenças autoimunes e neoplasias. Apresentamos dois pacientes com uma rara associação de vasculopatia livedoide com neuropatia periférica, enfatizando a importância de uma abordagem multidisciplinar na busca do diagnóstico correto. Palavras-chave: Dermatopatias vasculares; Livedo reticular; Mononeuropatias; Polineuropatias INTRODUCTION Livedoid vasculopathy (LV) is a chronic and resentation of the dermo-hypodermic junction, was recurrent disease, usually restricted to the skin, and compatible with LV. -
Phase 4 Medicine Intended Learning Outcomes (Ilos)
Phase 4 Medicine Intended Learning Outcomes (ILOs) This Phase 4 document outlines the listed ILOs for Medicine. This will be examined in the Year 4 and Year 5 summative written examinations. It is important that we impress upon you the limitation of any ILOs in their application to a vocational professional course such as medicine. ILOs may be useful in providing a ‘shopping list’ of conditions that you will be expected to describe and anticipate. The depth and extent of your knowledge of each condition will be a joint function of the condition’s frequency and its gravity. Please use the ILOs to make sure you are familiar with the common and important presentations and conditions. The list does not comprise of the entire coda for successful medical practice but will provide you with a solid platform from which to build upon. More detailed explanations and outlines will be available in the standard textbooks. Any elucidation or expansion can be obtained there. Even more important is the point that ILOs will point you in the correct direction to pass our written exam, but that this is only part of the story. ILOs will point you in the correct direction to pass our written exam, but that this is only part of the story. Final exams function as ‘objective proof’ for the general public that you have enough knowledge to function as a doctor. As you will see during your time on the wards, however, being a doctor requires much more than knowledge; as well as being able to imitate and build on the activities you witness in your clinical placements, it is imperative that you acquire skills, behaviours, specific attitudes, and commitment to your patients’ well being. -
Alpha Thalassemia
Alpha Thalassemia Alpha thalassemia is a genetic disorder called a hemoglobinopathy, or an inherited type of anemia. People who have alpha thalassemia make red blood cells that are not able to carry oxygen as well throughout the body, which can lead to anemia. This chronic anemia can include pale skin, fatigue, and weakness. In more severe cases, people with alpha thalassemia can also develop jaundice (yellowing of the eyes and skin), heart defects, and an enlarged liver and spleen (called hepatosplenomegaly). Alpha thalassemia is more common in people of African, Southeast Asian, Chinese, Middle Eastern, and Mediterranean ancestries. Causes We have over 20,000 different genes in the body. These genes are like instruction manuals for how to build a protein, and each protein has an important function that helps to keep our body working how it should. The HBA1 and HBA2 genes make a protein called alpha-globin. Two of the alpha-globin proteins combine with two other proteins called beta-globins (which are made by the HBB gene) to make a normal red blood cell. Most people have four copies of the genes that make the alpha-globin protein: two copies of the HBA1 gene (one from each parent), and two copies of the HBA2 gene (one from each parent). Having all four copies of these genes is symbolized by writing αα/αα. Whether or not someone has alpha thalassemia depends on how many working copies of the alpha- globin gene they have (if someone has a missing or nonworking alpha-globin gene, it is most frequently caused by a deletion): Silent alpha thalassemia carrier (also referred to as -α/αα): When there is one missing alpha-globin gene.