2017 LAB GUIDE TEST MENU March 2017Edition
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Handout Page 1 of 8
MLT 112: Principles of Phlebotomy Learning Unit 3: Handout Specimen Collection – Venipuncture Procedure I. Collecting and Processing of Specimens A. Blood 1. Venipuncture Procedure (arm + dorsal/hand) – vacutainer, syringe, butterfly a. Approaching the Patient Correct patient identification Wash hands Have patient recite his/her name Wrist identification – mandatory must match requisition check ankle on babies and peds Out-patients – ask patient to spell name In-patients – see wrist ID Unconscious patient – see wrist ID Unidentified patient – emergency – use temporary I.D. band non-emergency – wait for I.D. Explanation and Reassurance – Inspire confidence Conversation Ensure that patient has complied with test requirements, such as fasting (only water), NPO (nothing per oral), etc. Check for any allergies, such as to latex, adhesive bandages, etc. b. Positions Positioning the patient Vein accessibility Sitting vs. lying down Phlebotomist position – always in front in case of fainting. c. Applying the Tourniquet See previous lecture Page 1 of 8 MLT 112: Principles of Phlebotomy Learning Unit 3: Handout d. Veins Used - Antecubital Fossa Cephalic Median Cephalic Median Basilic Median Cubital Vein – vein of choice, anchored best Other Structures – avoid Brachial artery – apply pressure 5 minutes Cutaneous nerve – very painful Tendon for the biceps muscle – always draw below crease e. Other Vein Sites Wrist (never palm side) Hand Ankle Foot f. Preparing Equipment Syringes Assembly – always work plunger before procedure. Plunger position – must -
Anti-Thymocyte Globulin (Atg) and Ciclosporin (Csa)
Myeloid group ANTI-THYMOCYTE GLOBULIN (ATG) AND CICLOSPORIN (CSA) INDICATION ATG and CSA is indicated for patients who require treatment for aplastic anaemia (AA) but who are not eligible for sibling donor BMT. This includes (note references to severity are based on the modified Camitta criteria): Patients with non-severe aplastic anaemia who are dependent on red cell and/or platelet transfusions. Patients with severe aplastic anaemia (SAA) or very SAA who are > 35-50 years of age. Patients with SAA or very SAA disease who lack an HLA-compatible sibling donor. Protocol may be used in selected patients with hypoplastic marrow conditions. Patients with severe AA who are ≤ 35 years old and have a HLA identical sibling donor, should be treated with allogenic bone marrow transplantation as soon as possible after diagnosis. TREATMENT INTENT Prolong survival Provide a rapid (within 3 months) and sustained improvement in peripheral blood counts Restore haematopoiesis PRE-ASSESSMENT 1. ATG should only used by physicians familiar with administering ATG. Medical and nursing teams must be aware of the side effects and how to treat promptly and appropriately. 2. ATG is highly immunosuppressive - only use in centres with at least level 2 facilities. Patients should be nursed in a single or double isolation room, as an inpatient. 3. Risk of transfusion-associated GvHD following treatment with ATG is unclear, therefore irradiated blood components are currently recommended. It is not known how long the use of irradiated products This is a controlled document and therefore must not be changed Page 1 of 9 ML.2 ATG & CSA Authorised by Myeloid Lead Oct 2019 V.4.1 Prof Adam Mead Myeloid group should be continued, but it may be reasonable to continue while patients are still taking CSA following ATG therapy. -
Vacutainer Tubes
Vacutainer Tube Guide - Order of Draw for routine volumes See separate guide for micro-tainers Number of Tube Inversions at Label Blood Collection Volume Tubes/Bottles Abbrev. Additive (Do Not Shake) General Laboratory Use Draw 1 Aerobic and 1 5 Blood Culture / requires Adapter 20 mL Anaerobic Culture Note: A separate venipuncture for trace BLCLT Bottles metal analysis is required if blood cultures are ordered at the same time. NAYYP Clot activator 8 Trace Element serum tube for Copper 6 mL Royal Trace Element whole blood for Aluminum, NAVYE 2 Call 2-5002 Blue K EDTA Lead, Zinc, Selenium, Manganese, Mercury, 8 for tubes Cadmium, Arsenic Discard tube or secondary sterile specimen 6 mL Clear None 0 tube 3 mL 2.7 mL Light (Blue) BLUE Sodium Citrate (3.2%) Coagulation Testing on Plasma Blue 3-4 1.8 mL (Blue/clear) Serum determinations where a gel-barrier is 6 mL Red RED Clot Activator 5 contraindicated; Therapeutic Drug 4 mL Monitoring (TDM) Clot Activator and gel SST - Serum determinations in Chemistry, Gold SST 5 5 mL for serum separation Immunology, Serology; HLA Ab screen, DSA Light Lithium heparin and PST PST - Plasma determinations in Chemistry 4.5 mL Green gel - plasma separation 8 GLI Lithium heparin 8 Whole Blood Plasma: Troponin, Lactic Acid, Ion. Ca+ 6 mL Dark 4 mL Green GNA Sodium heparin 8 Whole Blood Plasma: Tissue typing, plasma hemoglobin, plasma catecholamine, chromosome analysis Pink PINK Dry K2EDTA 8 Blood Bank / Transfusion; HLA Typing 6 mL Tan TAN K2EDTA 8 Lead Testing only 3 mL LAV 4 Whole Blood Hematology; some Flow, 4 mL Lavender Dry K2EDTA 8 Molecular, and Genetic tests; HIV Viral 2 mL LAV6 Load Whole Blood tube with Glycolytic inhibitor Potassium Oxalate / for GTT, Gray 6 mL GRAY Sodium fluoride 8 Post-Prandial Glucose, D-Xylose, and Volatiles panel ACDA ACD Whole Blood tube for Flow Yellow (Acid Citrate Dextrose 8 immunophenotyping; HLA cross matching; 8.5 mL ACDB Solution A) genetic and other referred tests ALWAYS Check Expiration Dates before use! If unsure of use, refer to the on-line “Lab User’s Guide” or call the lab at 25002 . -
I Have Spots and My Skin Burns
I have spots and my skin burns Patient presentation History Differential diagnosis Examination Investigations Discussion Treatment Final Outcome References Evaluation - Questions & answers MCQs Patient presentation Peter, a 60 year-old Caucasian policeman, complains of a painful burning sensation in his lower extremities lasting for several months. Lower limbs petechiae (small purple/red hemorrhagic spots) appeared one week ago. Acknowledgement This case study was provided by Prof. Olivier Boyer (M.D., Ph.D., Head of the Department of Immunology and Biotherapy, Rouen University Hospital, France) and Dr. Maëlle Le Besnerais (M.D., Assistant Professor of Internal Medicine, Rouen University Hospital, France) of the Faculty of Medicine of Rouen, Normandy University, France. The authors would like to thank David Saadoun, Odile Goria, Lucie Guyant-Maréchal and Fabienne Jouen for their critical reading of this case study, Isabelle Duval for the development of pictures and Laetitia Demoulins for technical assistance. We are grateful to Nikki Sabourin-Gibbs, Rouen University Hospital, for her help in editing the manuscript. Immunopaedia.org.za History Peter complains of chronic fatigue and aching joints which started several months ago. He denies significant alcohol consumption and intravenous drug abuse. He received a blood transfusion after a gunshot injury to his arm 35 years ago. He reports distal paraesthesia (tingling or numbness) of both legs and painful burning in both feet which has progressed to the lower and upper limbs. Knee pain wakes him up at night. Past medical history None No allergies Surgical history Appendix removed at 10 years old Arm gunshot injury 35 years ago Family history His father has hypertension and type 2 diabetes Travel history He traveled to Thailand 25 years ago Social history Policeman, married, two children Medication None Differential diagnosis IgA vasculitis Polyarteritis nodosa ANCA-associated vasculitis (eg. -
Penicillin Allergy Guidance Document
Penicillin Allergy Guidance Document Key Points Background Careful evaluation of antibiotic allergy and prior tolerance history is essential to providing optimal treatment The true incidence of penicillin hypersensitivity amongst patients in the United States is less than 1% Alterations in antibiotic prescribing due to reported penicillin allergy has been shown to result in higher costs, increased risk of antibiotic resistance, and worse patient outcomes Cross-reactivity between truly penicillin allergic patients and later generation cephalosporins and/or carbapenems is rare Evaluation of Penicillin Allergy Obtain a detailed history of allergic reaction Classify the type and severity of the reaction paying particular attention to any IgE-mediated reactions (e.g., anaphylaxis, hives, angioedema, etc.) (Table 1) Evaluate prior tolerance of beta-lactam antibiotics utilizing patient interview or the electronic medical record Recommendations for Challenging Penicillin Allergic Patients See Figure 1 Follow-Up Document tolerance or intolerance in the patient’s allergy history Consider referring to allergy clinic for skin testing Created July 2017 by Macey Wolfe, PharmD; John Schoen, PharmD, BCPS; Scott Bergman, PharmD, BCPS; Sara May, MD; and Trevor Van Schooneveld, MD, FACP Disclaimer: This resource is intended for non-commercial educational and quality improvement purposes. Outside entities may utilize for these purposes, but must acknowledge the source. The guidance is intended to assist practitioners in managing a clinical situation but is not mandatory. The interprofessional group of authors have made considerable efforts to ensure the information upon which they are based is accurate and up to date. Any treatments have some inherent risk. Recommendations are meant to improve quality of patient care yet should not replace clinical judgment. -
Letters to the Editor
LETTERS TO THE EDITOR Complications of plasma exchange in after percutaneous insertion of a subclavian central ve- thrombotic thrombocytopenic nous catheter from pneumothorax and hemorrhage. Two purpura-hemolytic uremic syndrome: patients suffered cardiac arrest with pulseless electrical a study of 78 additional patients activity: one from an anaphylactic reaction to plasma and The frequency of patients treated with plasma exchange the other from pericardial hemorrhage and tamponade, (PE) for thrombotic thrombocytopenic purpura- presumably due to cardiac perforation by an internal hemolytic uremic syndrome (TTP-HUS) increased seven- jugular catheter insertion guidewire. fold from 1981 to 1997.1 Therefore, the morbidity and Other major catheter-related complications included mortality due to PE is an increasingly important consid- one patient with a retroperitoneal hemorrhage following eration in management decisions for patients with clini- femoral catheter insertion and seven patients with cath- cally suspected TTP-HUS. Some studies have described eter thrombosis that prevented PE and/or required place- few complications associated with PE,2 but our previous ment of a new central venous catheter; two of these seven report on 71 consecutive patients with clinically sus- patients had catheter-related venous thrombosis requir- pected TTP-HUS treated with PE from 1996 to 1999 dem- ing systemic anticoagulation. Ten patients developed sys- onstrated a major complication rate of 30 percent, in- temic infection: eight had blood cultures positive for the cluding two deaths.3 This report describes our experience presence of bacteria (Staphylococcus aureus [five], Staph- during the subsequent 3 years, 1999 to 2002, with 78 con- ylococcus epidermidis [three]); the two patients with secutive patients. -
Hypersensitivity Reactions (Types I, II, III, IV)
Hypersensitivity Reactions (Types I, II, III, IV) April 15, 2009 Inflammatory response - local, eliminates antigen without extensively damaging the host’s tissue. Hypersensitivity - immune & inflammatory responses that are harmful to the host (von Pirquet, 1906) - Type I Produce effector molecules Capable of ingesting foreign Particles Association with parasite infection Modified from Abbas, Lichtman & Pillai, Table 19-1 Type I hypersensitivity response IgE VH V L Cε1 CL Binds to mast cell Normal serum level = 0.0003 mg/ml Binds Fc region of IgE Link Intracellular signal trans. Initiation of degranulation Larche et al. Nat. Rev. Immunol 6:761-771, 2006 Abbas, Lichtman & Pillai,19-8 Factors in the development of allergic diseases • Geographical distribution • Environmental factors - climate, air pollution, socioeconomic status • Genetic risk factors • “Hygiene hypothesis” – Older siblings, day care – Exposure to certain foods, farm animals – Exposure to antibiotics during infancy • Cytokine milieu Adapted from Bach, JF. N Engl J Med 347:911, 2002. Upham & Holt. Curr Opin Allergy Clin Immunol 5:167, 2005 Also: Papadopoulos and Kalobatsou. Curr Op Allergy Clin Immunol 7:91-95, 2007 IgE-mediated diseases in humans • Systemic (anaphylactic shock) •Asthma – Classification by immunopathological phenotype can be used to determine management strategies • Hay fever (allergic rhinitis) • Allergic conjunctivitis • Skin reactions • Food allergies Diseases in Humans (I) • Systemic anaphylaxis - potentially fatal - due to food ingestion (eggs, shellfish, -
Unique Urticarial Presentation of Minocycline-Induced Lupus
Volume 23 Number 8 | August 2017 Dermatology Online Journal || Case Report DOJ 23 (8): Unique urticarial presentation of minocycline-induced lupus erythematosus Ashley K Clark1, Vivian Y Shi2 MD, Raja K Sivamani3,4 MD MS CAT Affiliations: 1School of Medicine, University of California, Davis, Sacramento, CA USA, 2Department of Medicine, Division of Dermatology, University of Arizona, Tucson, USA, 3Department of Dermatology, University of California, Davis, Sacramento, CA USA, 4Department of Biological Sciences, California State Univeristy, Sacramento, CA USA Corresponding Author: Raja Sivamani, MD MS CAT, Department of Dermatology, University of California, Davis, 3301 C Street, Suite 1400, Sacramento, CA 95816, Tel: 916-703-5145, Fax: 916-734-7183, Email: [email protected] Abstract with minocycline-induced lupus (MIL) typically present with fever and polyarthralgia, ANA positivity, We present a 17-year-old boy who developed a and elevated erythrocyte sedimentation rate, but generalized urticarial eruption, malar rash, fever, and negative levels of antihistone antibodies (AHAs) arthralgia within one week of initiating minocycline and anti-native DNA antibodies [4, 5]. Our report therapy for acne. His workup showed positive anti- highlights an unusual urticarial presentation of MIL nuclear and anti-histone antibodies. His symptoms with rapid resolution after oral prednisone. To the best quickly resolved after discontinuing minocycline and of our knowledge there is only one case of DIL with starting oral prednisone. We believe the constellation an urticarial presentation. The purpose of this report of his symptoms, laboratory findings, and temporal is to increase recognition of a unique presentation of association of minocycline initiation was suggestive DIL following minocycline treatment. -
Topic: Type II and Type III Hypersensitivity Reactions
Topic: Type II and Type III Hypersensitivity reactions SOS In Microbiology M.Sc 2nd Semester Paper code: 202 (Immunology) Unit 4 Antibody-Mediated Cytotoxic (Type II) Hypersensitivity • Type II hypersensitive reactions involve antibody-mediated • destruction of cells. Antibody can activate the complement • system, creating pores in the membrane of a foreign cell (see • Figure 13-5), or it can mediate cell destruction by antibodydependent cell-mediated cytotoxicity (ADCC). • In this process, • cytotoxic cells with Fc receptors bind to the Fc region of • antibodies on target cells and promote killing of the cells (see • Figure 14-12).Antibody bound to a foreign cell also can serve • as an opsonin, enabling phagocytic cells with Fc or C3b receptors • to bind and phagocytose the antibody-coated cell 1. Transfusion Reactions • A large number of proteins and glycoprotein on the membrane of red blood cells are called blood group antigen. In addition antibodies are also found in blood for these epitopes except from which are showing on our blood cells (Blood group A, antibody against B epitop). • An individual possessing one form of blood group antigen can recognize other antigen (present in transfused blood) as foreign and elicit immune response. • In some cases, the antibodies have already been induced by natural exposure to similar antigenic determinants on a variety of microorganisms present in the normal flora of the gut. This is the case with the ABO blood-group antigens. • Antibodies to the A, B, and O antigens, called isohemagglutinins ( usulayy of IgM class). A • An individual with blood type A, for example, recognizes B-like epitopes on intestinal microorganisms and produces isohemagglutinins to the B-like epitopes. -
Laboratory-General Specimen Collection and Handling Guidelines
Laboratory-General Specimen Collection and Handling Guidelines Contents: Microbiology continued. Orders/Requests Stool Patient Preparation Throat or Pharynx Specimen Containers Tuberculosis (TB) Specimen Quality Urine Order of Draw Viral Specimen Transport VRE Surveillance (Vancomycin- Resistant entercoccus) Specimen Rejection Wound General Lab Sample/Source: Whole Blood Cytology (Cytopathology) Plasma Aspiration, Fine Needle Serum Aspiration, Cyst Fluids Urine Submission of slide Fecal (Stool) Tips on making smears Body Fluid Body Cavity Fluids Cerebrospinal Spinal Fluid Breast Nipple Secretions Synovial Fluid Brushing Specimens Microbiology Cerebrospinal Fluid (CSF) Sample/Source: Ectocervix, Endocervical canal, Vaginal pool Abscess (Deep aspirate) Pap Smear, Conventional Abscess (superficial swab) Pap Smear, Liquid Base Acid Fast Bacillus (AFB) Sputum Specimens Anaerobic Surface Scrape Specimen (Tzanck Smear) Aspirate, drainage, cyst fluid, or pustule Vaginal Wall (Maturation Index) Biopsy, Bone, Tissue Washing Specimens Blood (Adult) Histology (Anatomic Pathology) Blood )Pediatric Routine Submission Blood for Acid Fast Bacillus (AFB) Fresh Specimen Body Fluids Surgical Specimen and Microbiology test(s) Bronchial Washing Lavage Breast Tissue Catheter Tip Brushing Specimens C. difficile Toxin B Bronchial Washing and Brushings Chlamydia/Gonorrhea Amplified Detection Muscle Biopsy Crytococcal Antigen Renal Biopsy (Kidney) Cerebral Spinal Fluid (CSF) Renal calculi (Kidney/Bladder Stones) Ear (outer) Bone Marrow Ear (inner) Cytogenics Eye -
Human Idiopathic Membranous Nephropathy — a Mystery Solved? Richard J
The new england journal of medicine editorials Human Idiopathic Membranous Nephropathy — A Mystery Solved? Richard J. Glassock, M.D. Just over 50 years ago, the late David Jones1 iden were fulfilled, defining the autoimmune nature tified (using the periodic acid–Schiff and meth of the disease in the rat model. enamine silver stains) the unique glomerular However, translation of the pathogenesis of pathologic features of membranous nephropathy, the rat model to idiopathic membranous nephrop thus distinguishing it from other causes of “ne athy in humans proved difficult. The target an phrotic glomerulonephritis.” Subsequent immuno tigen responsible for Heymann’s model appeared fluorescence and electronmicroscopical studies to be absent in human kidneys.6 Diligent search established that membranous nephropathy was es for the autoantibody against the “Heymann” also characterized by striking granular aggrega antigen (now known to be megalin [glycoprotein tions of IgG and electrondense deposits along 330]) were unrewarding.6 Thus, the true patho the outer (or subepithelial) aspect of the glomer genesis of human idiopathic membranous ne ular basement membrane. These glomerular IgG phropathy remained unresolved. deposits were initially believed to represent an Now, this longlasting mystery may well have accumulation of immune complexes arising from been solved by Beck et al.,7 as reported in this the circulation, as is found with glomerulonephri issue of the Journal. Autoantibodies against an tis in a rabbit model (chronic serum sickness). antigen normally expressed on the podocyte cell In 1959, Heymann et al.2 described a rat mod membrane in humans, the Mtype phospholipase el of membranous nephropathy, similar to the dis A2 receptor (PLA2R), appear to circulate and bind ease in humans, induced by active immunization to a conformational epitope (or epitopes) present with crude kidney extracts in complete Freund’s on PLA2R, producing in situ deposits character adjuvant. -
Another Brick in the Wall: Serum Sickness
Scholars Journal of Medical Case Reports ISSN 2347-6559 (Online) Sch J Med Case Rep 2017; 5(10):615-617 ISSN 2347-9507 (Print) ©Scholars Academic and Scientific Publishers (SAS Publishers) (An International Publisher for Academic and Scientific Resources) Does So Frequent Use Of It Make Innocent? Another Brick In The Wall: Serum Sickness Induced By Horse-Antithymocyte Globulin In A Patient With Bone Marrow Failure Gokhan Ozgur1, Adem Aydin2, Musa Baris Aykan3, Murat Yildirim4, Selim Sayin5, Cengiz Beyan6 1Gülhane Training and Research Hospital, Clinical of Hematology, Etlik, Ankara, Turkey 2Health Sciences University, Gulhane School of Medicine, Department of Internal Medicine, Etlik, Ankara, Turkey 3TOBB University of Economics and Technology Faculty of Medicine, Department of Internal Medicine, Çankaya, Ankara, Turkey Abstract: Aplastic anemia is a condition characterized by the absence or decrease *Corresponding author of hematopoietic progenitor cells in the bone marrow. The disease is considered to Adem Aydin occur as a result of immune response triggered by the environmental factors, infective agents or endogenous antigens. Cyclosporine and antithymocyte globulin Article History is recommended as first line therapy in patients have no unidentified suitable donor Received: 22.09.2017 or hematopoietic stem cell transplantation cannot be done. However, despite skin Accepted: 09.10.2017 testing for hypersensitivity and concomitant steroids, adverse effects are sometimes Published:30.10.2017 unavoidable. 30-year-old female patient, fallowed with aplastic anemia since 2012, was admitted to hospital with painful swelling in the neck, rash and joint pain DOI: began after ATG. Laboratory examination revealed pancytopenia, elevated 10.21276/sjmcr.2017.5.10.5 erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).