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Transcript
2015 BLOCK IMMUNE SYSTEM & DISSORDERS FACULTY OF MEDICINE UDAYANA UNIVERSITY Study Guide Immune System and Disorders FOREWORD The Block “The Immune System and Disorders” is designed for students in order to serve health care professionals in the diagnosis and management of allergic and other immunological disorders. Our goals have been to present the basic and essential material clearly and to provide the knowledge and skills due to: - Diagnose and manage patient with inflammation - Diagnose and manage patient with hypersensitivity / allergic disease - Diagnose and manage patient with autoimmune disease - Diagnose and manage patient with immunodeficiency This block try to give the essential information to assist in clinical decision making and treatment planning on commonly allergic diseases in pediatric, internal medicine, ENT,and skin. We also give essential information on commonly autoimmune diseases in neurology, dermatology, pediatric and internal medicine, beside try to complete the essential information duo to immune deficiency focus on HIV / AIDS infection. Our overall goal is to transfer the basic essential information on commonly allergy – immunological diseases that are required for the primary health care. This block will be completed by case illustration, learning tasks to be discuss by the students in the small group discussions and individually in order to achieve the block objectives. The Block ″ The Immune System an Disorders ″ ( ISD ) is undertaken 19 days including skill lab, examinations. Student – centered learning as the primary approach in the teachinglearning activities with dynamic group discussions are facilitated by tutors. Individual learning in Campus and at home is also an important part of the learning process. To develop good understanding of the ISD, learning activities will also be carried out as lectures, practical and learning with the patients ( Skill Lab). Team of Planners ISD 2 Study Guide Immune System and Disorders CONTENTS Foreword ………………………………………………………………………………………. 2 Contents …………………………………………………………………………………………. 3 Curriculum Block Immune System and Disorders …………………………………………... 4 Planners and Lecturers ……………………………………………………………………….. 5 Facilitators ……………………………………………………………………………………….. 7 Time Table ...................... ……………………………………………………………………… 8 Meeting of student representatives and Facilitators ,Assessment Method ………………. 13 Learning Program ; Abstract Learning Tasks, Case illustrations ,Self Assessments …… 14 Student Project ………………………………………………………………………………... 49 Curriculum Mapping…………………………………………………………………………….. 50 References ……………………………………………………………………………………… 51 3 Study Guide Immune System and Disorders CURRICULUM Aims: 1. To comprehend the biology of the immune system in health and diseases 2. To diagnose and manage common immune-mediated disorders 3. To diagnose and manage common disorders of the joints and adjacent tissue Learning Outcomes: To be able to 1. Diagnose and manage patients with inflammation 2. Diagnose and manage patients with hypersensitivity / allergic diseases 3. Diagnose and manage patients with autoimmune diseases 4. Diagnose and manage patients with immunodeficiency Curriculum contents: 1. The biology and responses of the immune system in health and diseases 2. The common immune-mediated disorders 4 Study Guide Immune System and Disorders PLANNERS TEAM No Name Department Phone Internal Medicine 082145854167 ENT 081237874447 Internal Medicine 08123985811 Biochemistry 081338486589 Internal Medicine 08123960964 1 dr.Tjok Istri Anom S, SpPD (Head) 2 dr.Sari Wulan DS, SpTHT-KL (Secretary) 3 dr. Ketut (Member) 4 dr. I Wayan Surudarma, M.Si (Member) 5 Dr.dr. Ketut (Member) 6 dr. I Made Sudipta, Sp.THT (member) ENT 08123837063 7 dr. Made Wardana, Sp.KK (member) Dermatology 08563704591 8 dr. Dewi Kumarawati, Sp.A (member) Pediatrics 03617442593 9 dr. Putu Sri Widnyani, Sp.PA (member) Pathology Anatomy 081337115012 10 Dr.dr. Ni Made Linawati, M.Si (member) Histology 081337070077 11 dr. I Wayan Juli Sumadi, Sp.PA (Member) Pathology Anatomy 12 dr.Komang Suryawati, Sp.KK (Member) 13 dr. Henky, SpF (Member) Suardamana, SpPD-KAI Suryana, Sp.PD-KAI 081916262663 Dermatology 0817447279 Forensic 081916613459 LECTURERS No Name Department Phone Internal Medicine 08123960964 1 Dr.dr. Ketut Suryana, Sp.PD-KAI 2 Dr. dr. Ni Made Linawati, MSi Histology 081805629937 3 dr. Putu Sri Widnyani, Sp.PA Pathology Anatomy 081337115012 4 Dr.dr. I Wyn Putu Sutirta Yasa, Msi Clinical Pathology 03617428983 5 Dr.dr. I Made Jawi, M.Kes Pharmacology 08179787972 5 Study Guide Immune System and Disorders 6 Dr.dr. B. K. Satriyasa, M.Repro 7 Pharmacology 0818053689 dr. Dewi Kumarawati, Sp.A Pediatrics 03617442593 8 dr. Henky, Sp.F., M.BEth, FACLM Forensic 081916613459 9 dr.Komang Suryawati, Sp.KK Dermatology 0817447279 Pathology Anatomy 081916262663 11 dr. Ketut Suardamana, Sp.PD-KAI Internal Medicine 08123985811 12 Internal Medicine 08123806626 ENT 081237874447 081338466039 Neurology 08164710744 15 dr. Gede Kambayana, Sp.PD-KR Internal Medicine 08124683416 16 dr.Tjok Istri Anom S, SpPD (Head) Internal Medicine 82145854167 17 dr. Nyoman Wande, Sp.PK Clinical Pathology 08124686885 10 dr. I Wayan Juli Sumadi, Sp.PA Prof. Dr.dr. Tuti Parwati M, Sp.PD-KPTI 13 dr. Sari Wulan Dwi Sutanegara , Sp.THTKL (Secretary) 14 Prof.Dr. dr. AA Raka Sudewi, Sp.S 6 Study Guide Immune System and Disorders FACILITATORS (REGULAR CLASS) NO NAME GROUP DEPT 1 dr. I Made Dwijaputra Ayustha, Sp.Rad dr. Ida Ayu Putri Wirawati, Sp.PK dr. Nyoman Astika, Sp.PDKger-FINASIM dr. Ketut Agus Somia, Sp.PDKPTI dr. I Gde Haryo Ganesha, S.Ked dr. I Gede Sastra Winata, M.Biomed, Sp.OG dr. I Gusti Ngurah Wien Aryana , Sp.OT dr. Pontisomaya Parami, Sp.An, MARS dr. I Made Oka Adnyana, Sp.S (K) dr. Ketut Suardamana, Sp.PDKAI 1 Radiology 2 3 Clinical Pathology Interna 4 Interna 5 DME 6 Obgyn 7 Orthopaedi 8 Anasthesi 9 Neurology 10 Interna 2 3 4 5 6 7 8 9 10 PHONE 08123670195 082145723828 08123974128 08123989353 081805391039 081338713951 0811385263 08123661312 0817347697 08123985811 VENUE 3nd floor: R.3.09 3nd floor: R.3.10 3nd floor: R.3.11 3nd floor: R.3.12 3nd floor: R.3.13 3nd floor: R.3.14 3nd floor: R.3.15 3nd floor: R.3.16 3nd floor: R.3.17 3nd floor: R.3.19 FACILITATORS (ENGLISH CLASS) NO 1 2 3 4 5 6 7 8 9 10 NAME dr. I Made Susila Utama, Sp.PDKPTI dr. I Gusti Ngurah Purna Putra, Sp.S (K) Dr.dr I Nyoman Gede Budiana, Sp.OG (K) Prof.Dr.dr.I Putu Gede Adiatmika, M.Kes dr. Komang Andi Dwi Saputra, Sp.THT- KL Dr. dr. I Dewa Made Sukrama, MSi, Sp.MK(K) dr. I Gusti Ayu Sri Darmayani, Sp.OG Dr.dr. Yenny Kandarini, Sp.PDKGH-FINASIM dr. I Gede Budhi Setiawan, Sp.B(K)Onk dr. Henky, Sp.F., M.BEth, FACLM GROUP 1 DEPT Interna PHONE 08123815025 2 Neurology 08123915769 3 Obgyn 08123997401 4 Fisiology 08123811019 5 ENT 081338701878 6 Microbiology 081338291965 7 DME 081338644411 8 Interna 08123805344 9 Surgery 08123923956 10 Forensic 08123988486 VENUE 3nd floor: R.3.09 3nd floor: R.3.10 3nd floor: R.3.11 3nd floor: R.3.12 3nd floor: R.3.13 3nd floor: R.3.14 3nd floor: R.3.15 3nd floor: R.3.16 3nd floor: R.3.17 3nd floor: R.3.19 7 Study Guide Immune System and Disorders TIME TABLE OF THE BLOCK IMMUN SYSTEM & DISSODERS 2015 DAYS / TIME ACTIVITY CONVEYER VENUE • Class Room DATE 1 ENGLISH CLASS REG CLASS 08.00-09.00 (60’) 09.00-10.00 (60’) • 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) Student Project preparation paper - - 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • 08.00-08.30 (30’) 09.00-09.30 (30’) • • 08.30-09.00 (30’) 09.30-10.00 (30’) Friday, Oct 16, 2015 2 Monday, Oct 19, 2015 • • Introduction to The Immune System and disorders (SP): Comprehend The Microscopic Structure of Limphoid Organ,Immune Cells and MHC • Comprehend tissue repair 3 Dr. dr. Ketut Suryana, SpPD-KAI dr. Ni Made Linawati, MSi Class Room Class Room dr. Putu Sri Widyani, S.PA. Comprehend basic mechanism of autoimmunity 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - 10.30-12.00 (90’) 13.30-15.00 (90’) SGD • 12.00-12.30 (30’) 11.30-12.00 (30’) Break 12.30-14.00 (90’) 10.00-11.30 (90’) Student Project preparation 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session Library Discussion Room Fasilitator - (SP) : - paper - • • Tuesday , Dr. dr. Ketut Suryana, SpPD-KAI dr. Ni Made Linawati, Msi Class Room dr. Putu Sri Widyani, S.PA. 08.00-08.30 (30’) 09.00-09.30 (30’) • 08.30-09.00 (30’) 09.30-10.00 (30’) • 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - Oct 20, 2015 Comprehend acute and chronic inflammation Comprehend hypersensitivity • Library • Dr. I Wayan Sumadi, Sp.PA. Dr.Tjok Istri Saturti, SpPD Juli Class Room Anom 8 Study Guide Immune System and Disorders 12.30-14.00 (90’) 10.00-11.30 (90’) SP: paper preparation - 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • • 4 08.00-08.30 (30’) 09.00-09.30 (30’) Wednes day, 08.30-09.00 (30’) 09.30-10.00 (30’) Oct 21, 2015 • • Comprehend basic mechanism of drug allergy and immunopharmacology Forensic Laboratory • Juli Class Room Dr. I Wayan Sumadi, Sp.PA. Dr.Tjok Istri Saturti, SpPD Anom Dr. I Made Jawi, M.Kes Class Room • • dr Henky, SpF 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) SP: paper preparation - Library 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • • 5. Library 08.00-09.00 (60’) 09.00-10.00 (60’) Thursda y, • • Adverse drug reaction • Able to diagnose and manage anaphylaxis Dr. I Made Jawi, M.Kes Class Room dr. Henky, SpF Dr. Ketut Suardamana, SpPDKAI Class Room Oct 22, 2015 6. 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) SP: paper preparation - Library 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • 08.00-08.30 (30’) 09.00-09.30 (30’) • • 08.00-09.00 (30’) 09.30-10.00 (30’) • 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) SP paper Imunomodulator Friday, Oct 23, 2015 Comprehend laboratory test of immune system Antihistamine • Dr. Ketut Suardamana, SpPDKAI Class Room Dr. dr. I Wyn Putu Sutirta Yasa, Msi Class Room Dr.dr.B.K.Satriyasa,M .Repro presentation: dr. Made Jawi, M.Kes Class Room 9 Study Guide Immune System and Disorders 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • • 7. 08.00-08.30 (30’) 09.00-09.30 (30’) • 08.00-09.00 (30’) 09.30-10.00 (30’) • Monday, Oct 26, 2015 Able to diagnose and manage allergic diseases in ENT Able to diagnose and manage allergic diseases in dermatology • • 9. Dr. Sari Wulan Dwi Sutanegara , Sp THTKL Class Room -Dr.Nyoman Suryawati, SpKK Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) K Suardamana, Class Room SP paper presentation: Urtikaria dr. SpPD-KAI and Angiodema 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. Sari Wulan Dwi Sutanegara , Sp THTKL Class Room Dr.Nyoman Suryawati, SpKK 08.00-09.00 (60’) 09.00-10.00 (30’) • 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) SP paper presentation: Blood Dr.dr. Wy Putu Sutirta Class Room Group Incompatibility Yasa, M.Si. 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • 08.00-08.30 (30’) 09.00-09.30 (30’) • • 08.00-09.00 (30’) 09.30-10.00 (30’) • 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - Wednes day, Dr.dr.B.K.Satriyasa, M.Repro 12.00-13.30 (90’) Tuesday , Oct 27, 2015 Class Room 09.00-10.30 (90’) • 8. Dr. dr. I Wyn Putu Sutirta Yasa, Msi Able to diagnose and manage SLE, RA & Polimyalgia Rheumatica Able to diagnose and manage • autoimmune diseases in Neurology Oct 28, 2015 Able to diagnose and manage secondary immunodeficiency diseases (focus HIV) • Dr. Gede Kambayana, SpPDKR Dr. Gede Kambayana, SpPDKR Prof. Dr. dr AA Raka Sudewi, Sp S Class Room Class Room Class Room Prof. DR. Dr. Tuti Parwati M, SpPDKPTI 10 Study Guide Immune System and Disorders 12.30-14.00 (90’) 14.00-15.00 (60’) 10.00-11.30 (90’) 15.00-16.00 (60’) SP paper Limphadenitis TB presentation: dr. • Plenary Session • 10 08.00-08.30 (30’) 09.00-09.30 (30’) • Thursda y, 08.00-09.00 (30’) 09.30-10.00 (30’) • Oct 29, 2015 11. • Sriwidnyani, Class Room Able to diagnose and manage Rheumatic Disease of Childhood • Prof. Dr. dr AA Raka Sudewi, Sp S Class Room Prof. DR. Dr. Tuti Parwati M, SpPDKPTI Dr. Dewi Kumarawati, SpA Class Room Able to diagnose and manage Food allergy Able to diagnose and manage immunodeficiency diseases in childhood 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-12.00 (90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room 12.00-12.30 (30’) 11.30-12.00 (30’) Break - - 12.30-14.00 (90’) 10.00-11.30 (90’) SP paper presentation: Steven dr. Komang Suryawati, Class Room Johnson Syndrome Sp.KK. 14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session 08.00-09.00 (60’) 09.00-10.00 (60’) Soluble markers of inflammation (BCS) 09.00-10.30 (90’) 10.00-11.30 (90’) Independent Learning 10.30-13.00 (150’) 13.30-16.00 (150’) BCS Training 13.00-15.00 (120’) 11.30-13.30 Friday, Oct 30, 2015 Putu Sp.A BCS Discussion Dr. Dewi SpA Kumarawati, Class Room allergic dr. Wande, Sp.PK. Class Room - Library dr. Wande, Sp.PK & Skill Lab Team 12. 08.00-09.00 (60’) 09.00-10.00 (60’) Forensic Laboratory (BCS) Dr. Henky, SpF Class Room 09.00-10.30 (90’) 10.00-11.30 (90’) Independent Learning - Library 10.30-13.00 (150’) 13.30-16.00 (150’) BCS Training 13.00-15.00 (120’) 11.30-13.30 Monday, Nop 02, 2015 BCS Discussion Dr. Henky , SpF, & Team Skill Lab 13 08.00-09.00 (60’) 09.00-10.00 (60’) Anaphylactic syok (BCS) Dr. Tjok Istri Anom S, Class Room SpPD 09.00-10.30 (90’) 10.00-11.30 (90’) Independent Learning - Tuesday , Library 11 Study Guide Immune System and Disorders Nop 03, 2015 14 10.30-13.00 (150’) 13.30-16.00 (150’) 13.00-15.00 (120’) 11.30-13.30 08.00-09.00 (60’) 09.00-10.00 (60’) Morphology of Acute & Chronic Dr. Putu Sri Widyani , Class Room Imflamation (BCS) Sp.A 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning 10.30-13.00 (150’) 13.30-16.00 (150’) BCS Training 13.00-15.00 (120’) 11.30-13.30 08.00-09.00 (60’) 09.00-10.00 (60’) Skin Prick Test (BCS) Dr. Ketut Suryana, SpPD- Class Room KAI 09.00-10.30 (90’) 12.00-13.30 (90’) Independent Learning - Library 10.30-13.00 (150’) 13.30-16.00 (150’) BCS Training 11.30-13.30 Dr. Ketut Suryana, SpPD-KAI & Team Skill Lab 13.00-15.00 (120’) Wednes day Nop 04, 2015 15 BCS Training BCS Discussion BCS Discussion Thursda y, Nop 05, 2015 BCS Discussion Dr. Tjok Istri Anom S, Skill Lab SpPD & Team - Library Dr. Putu Sri Widyani , LAB Bersama Sp.A & Team Friday, Nop 06, 2015 Pre-evaluation Break Monday, Nop 9, 2015 Examination 12 Study Guide Immune System and Disorders Meeting of the student representatives The meeting between block planners team and the student group representatives will be held on Monday, October 12, 2015 at 09.00 until 10.00 a.m at HAPEQ discussion room. In this meeting, all of the student group representatives are expected to give suggestions or inputs or complaints to the team planners for improvement. For this purpose, every student group must choose one student as their representative to attend the meeting. Meeting of facilitators The meeting between block planners team and the facilitators will take place on, Monday, October 12, 2015 at 10.00 am until 12.00 pm at HAPEQ discussion room. In this meeting all the facilitators are expected to give suggestions and inputs as evaluation to improve the study guide and the educational process. Because of the importance of this meeting, all the facilitators are strongly expected to attend the meeting. Plenary session For each task of SGD, the students are requested to prepare a group report. The reports will be presented in a plenary session. The group will be chosen randomly by the lecturer in charge. The group report will be evaluated by respective facilitator. Assessment Methods Assessment will be performed at the end of the block on Nopember 9th 2015. There are 100 questions for the examination that consists of Multiple Choice Question (MCQ). The borderline to pass exam is 70. 13 Study Guide Immune System and Disorders LEARNING PROGRAMS Day 1 Topics : Introduct. to the immune system and disorders Lecturer : dr. Ketut Suryana, SpPD-KAI Abstract 1. The Immune system has evolved to protect us from pathogens. Some, such as viruses, infect individual cells; others, including many bacteria, divide extracellularly within tissues or body cavities. 2. The cells which mediate immunity include lymphocytes and phagocytes. Lymphocytes recognize antigens on pathogens. Phagocytes internalize pathogens and degrade them 3. An Immune response consists of two phases. In the first phase, antigen activates specific lymphocytes that recognize it; in the effector phase, these lymphocytes coordinate an immune response that eliminates that source of the antigens. 4. Specificity and memory are two essential features of adaptive immune responses. The Immune system mounts a more effective response on second and subsequent encounters with a particular antigen. 5. Lymphocytes have specialized functions. B cells make antibodies; cytotoxic T cells kill virally infected cells; helper T cell coordinate the immune response by direct cell-cell interactions and the release of cytokines, which help B cells to make antibody. 6. Antigens are molecules which are recognized by receptors on lymphocytes. B lymphocytes usually recognize intact antigen molecules, while T lymphocytes recognize antigen fragment on the surface of other cells. 7. Clonal selection involves recognition of antigen by a particular lymphocyte; this leads to clonal expansion and differentiation to effector and memory cells. 8. The immune system may break down. This can lead to immunodeficiency or hypersensitivity diseases or to autoimmune diseases. Learning task 1. 2. 3. 4. Comprehend of immune system with clinical implications Comprehend the lymphoid organs and describe of it’s microscopic organization Comprehend the cellular immunity Comprehend the mechanism of cellular and humoral immunity to infection 14 Study Guide Immune System and Disorders Day 2 Topic : The Microscopic Structure of Limphoid Organ, Immune Cells and Histocompatibility Molecule Lecturer : dr. Ni Made Linawati, M. Si. Abstract The limphoid systems is responsible for the immunological defense of the body. Some of its component organs ; lymph nodes, thymus and spleen are surrounded by connective tissue capsules, whereas its other components, member of the diffuse lymphoid system, are not encapsulated. The cells of the limphoid systems such as lymphocytes ( T, B and Natural Killer), Antigen Presenting Cells (Dendritic cells, Macrophages and B lymphocytes) and other (Neutrophils) protect the body against foreign macromolecules, viruses, bacteria, and other invasive microorganism, and they kill virally transformed cells. Major Histocompability Complex (MHC) molecule are important to permit APCs and cells under viral attact (or cells already virally transformed) to present the epitopes of the invading pathogen to the T cells. Learning Task Vignette A 65-year-old man had suffered from rectal bleeding during defecation for a few weeks. Laboratory findings were normal except a slight elevation in the level of alkaline phosphatase. Multiple polypoid lesions were observed in colonoscopic examination. The histological and immunochemical evaluation showed atypical lymphoid cell proliferation and lymphoepithelial lesions on the colonic mucosa, staining with CD20. After the diagnosis had been confirmed as low grade mucosa associated lymphoid tissue lymphoma. a. Please describe histological structure of the Mucosa associated lymphoid tissue. b. Why M cells has important roles in mucosa immune response? Self Assesment 1. What are primary and secondary lymphoid organ. Mention the of organ that has function as primary and secondary lymphoid organ 2. Describe about function and microscopic structure of thymus, lymph nodes; spleen; tonsils; and MALT 3. Describe about MHC class I and class II 15 Study Guide Immune System and Disorders Topic : INFLAMMATION AND TISSUE REPAIR Lecturer : dr. Ni Putu Sriwidyani, Sp.PA ABSTRACT Inflammation is fundamentally a protective response, designed to rid the organism of both the initial cause of cell injury and the consequences of such injury. Inflammation is a complex reaction in tissues that consists mainly of responses of blood vessels and inflammatory cells. The vascular and cellular reactions of inflammation are triggered by soluble factors that are produced by various cells or derived from plasma proteins and are generated or activated in response to the inflammatory stimulus. Inflammation may be acute or chronic, depending on the nature of the stimulus and the effectiveness of the initial reaction in eliminating the stimulus. Inflammation is terminated when the offending agent is eliminated. Outcomes of acute inflammation could be resolution, chronic inflammation, or fibrosis. Inflammation response is closely intertwined with the process of repair. Repair most often consists of a combination of regeneration and scar formation by deposition of collagen. Inflammation and repair may be harmful in some situations and may contribute to a variety of diseases. Understanding inflammation and repair can be applied as basic concept of patient management, diagnostic, therapy, and monitoring. LEARNING TASK Vignette A 20 year old female came to a doctor in private practice and complaint a right lower abdominal pain and fever since 3 days ago. On physical examination, BP: 120/80 mm Hg,T axilla: 400C. On lower right abdominal region revealed warm and pain in palpation. Complete blood count showed leucocytosis. Appendectomy performed. Histology examination showed oedematous, hypermi, and neutrophil infiltration extended from mucosal until serosal layer. The diagnosis was acute appendicitis. Task 1. Explain reactions of blood vessels and leukocyte in acute inflammation 2. Mention mediators of inflammation 3. Mention local effects and systemic effects of inflammation 4. Mention outcomes of acute inflammation 5. Mention role of macrophage and other inflammatory cells in chronic inflammation 6. Mention morphologic patterns of acute and chronic inflammation 7. Mention consequences of defective or excessive inflammation 8. Explain healing by fibrosis, scar formation, and fibrosis 16 Study Guide Immune System and Disorders SELF ASSESMENT 1. Inflammatory cells that have a major role in most acute inflammation are: A. Basophyl B. Eosinophyl C. Netrophyl D. Macrophage E. Mast cell 2. Mediators of increased vascular permeability in acute inflammation responses include all of the following, except: A. Histamine B. Bradykinin C. Leukotriene C4 D. Platelet Activating factor E. Complement complex C5-9 3. Mediators of neutrophyl chemotaxis in acute inflammation responses include all of the following, except: A. C3a B. C5a C. IL-1 D. TNF E. Bacterial product 4. Opsonization increases engulfment capability of macrophage in fagocytosis. Complement system component that involved as a potent opsonin is: A. C3a B. C3b C. C5a D. C5b E. C9 5. A 35 years old man with acute appendicitis and appendectomy performed. Pathologic examination shows marked neutrophyl infiltration in the wall of the appendix. Based on the morphological feature, the type of inflammation of this case is: A. Serous B. Suppurative C. Catharalis D. Fibrinous E. Granulomatous 6. A 5 years old boy hospitalize in intensive care unit cause by accidently expose to boiled water. All the skin of his body was red with blebs. Based on the morphological feature, the type of inflammation of this case is: A. Serous B. Suppurative C. Catharralis D. Fibrinous E. Granulomatous 7. Chronic inflammation are characterized by all of following morphologic feature, except: A. Mononuclear infiltration B. Tissue destruction C. Angiogenesis D. Fibrosis E. Vasodilatation 17 Study Guide Immune System and Disorders 8. Permanent tissue is a mature tissue without capability to divide. The following tissue is a permanent tissue: A. Skeletal muscle B. Hepar C. Skin D. Neuron E. Kidney 9. A large aggregate of epitelioid cells is seen in a microscopic section of an ovarial tumor. Your diagnosis is: A. Granulation tissue B. Granuloma pyogenicum C. Granulosa cell tumor D. Granuloma E. Granulocytosis 10. Local factor that retard wound healing is: A. Diabetes B. Malnutrition C. Foreign bodies D. Genetic E. Vitamin C deficiency Day 3 Topic : Basic mechanism of autoimmunity Lecturer : dr. I Wayan Juli Sumadi, Sp.PA. ABSTRACT Immunologic Tolerance: Is a state in which an individual is incapable of developing an immune response against a specific antigen. Self- tolerance: Specifically refers to a lack of immune responsiveness to one’s own tissue antigens. Two broad groups of mechanisms to explains the tolerant state: ▪ Central tolerance: This refers to deletion of self-reactive T and B lymphocytes during maturation in central lymphoid organs (i.e. in the thymus for T cells and the bone marrow for B cells) ▪ Peripheral tolerance: Self reactive T cells that escape negative selection in the thymus can potentially wreak havoc unless they are deleted or effectively muzzled. Several backmechanisms in the peripheral tissues that silence such potentially autoreactive T cells have been identified: - Anergy. - Activation-induced cell death - Peripheral suppression by T cells. Mechanisms of Autoimmune Disease Breakdown of one or more of the mechanisms of self-tolerance can unleash an immunologic attack on tissues that leads to the development of autoimmune disease. 18 Study Guide Immune System and Disorders Furthermore, the breakdown of tolerance and initiation of autoimmunity involves the interaction of complicated immunologic, genetic, and microbial factors. Learning task Trigger Case A 25-year-old woman has had increasing malaise, a skin rash of her face exacerbated by sunlight exposure, and arthtralgias and myalgias for the past month. On physical examination she has mild pedal edema. On auscultation a friction rub is audible over the chest. Laboratory findings include pancytopenia and serum creatinine 3 mg/dL. Urinalysis shows hematuria and proteinuria. A serologic test for shypilis yields a false positive result. A renal biopsy shows a slight increase of mesangial cells and granular deposit of IgG and complement in the mesangium and along basement membrane. The result of ANA test is positive. Finally, the patient is diagnosed as systemic lupus erythematosus (SLE). SLE is the best example of autoimmune disease. Does the autoimmunity result from the loss of self-tolerance, how this happen, and why they have a broad clinical spectrum as showed in that patient? Before you answer the question, please try to find out the following task. Task 1. Describe the mechanism of immunological tolerance to self antigent! 2. Explain the mechanism of autoimmunity, including the role of susceptibility genes and enviromental triggers! 3. Describe the general features of autoimmune diseases! 4. Describe the etiopathogenesis of SLE! 5. Describe the mechanism of tissue injury in SLE, and give some examples of morphological changes in SLE! 6. Mention other diseases that belong to autoimmune diseases group! Topic : Hypersensitivity Lecturer : dr. Tjok Istri Anom Saturti, SpPD ABSTRACT There are 4 types classifications according to Gel & Coombs 1. Type I : Immediate hypersensitivity 2. Type II : Cytotoxic hypersensitivity 3. Type III : Immune complex hypersensitivity 4. Type IV : Delayed (cell mediated) hypersensitivity Hypersensitivity the immune response results are harmful to the heart Type I : Antigen bind to IgE on the surface of mast cells à release of several mediators within minutes. Important mediators are: Histamin, SRS-A, ECF-A, serotonin, Prostaglandins and thromboxanes, etc. Clinical manifestations: 1. Anaphylaxis : severe bronconstriction, hypotension à shock 19 Study Guide Immune System and Disorders Type II Type III Type IV 2. Atopy: genetic factor to induce by exposure to spesific allergens (pollens, dust, shellfish, nuts, etc). Clinical manifestation: hay fever, asthma, eczema, and urticaria. Treatment and prevention: Avoidance of the responsible allergen, Hyposensitization (Desensitization) & Drug treatment. : Antibody is directed against antigen on an individual’s own cell (target cell) or foreign antigen, such as transfused red blood cell. This may lead to cytotoxic action by K Cells, or complement mediated lysis. : Immune Complexes are deposited in the tissue. Complement is activated and polymorphs are attracted to the site of deposition causing local tissue damage and inflammation : Antigen sensitized T cells release lymphokines following a secondary contact with the same antigen. Cytokines induced inflammatory reactions activate and attract macrophages, which release inflammatory mediators. Learning Task Hypersensitivity : 1. Make definition of the term hypersensitivity 2. Explain the biological roles of hypersensitivity 3. Make classification of hypersensitivity 4. Compare the hypersensitivity type I, II, III and IV 5. Explain principle treatment and prevention of hypersensitivity SELF ASSESSEMENT R. HIPERSENSITIFITAS 1. Hypersensitivity reaction is a general pathologic reaction which has following characteristics: A. Never happens on the first exposure B. Generally divided into 4 types C. Is an overreaction of immune system D. Occurred if humoral and cellular immunological status are increased E. All above are correct 2. The followings are the feature of hypersensitivity reaction type I, except: A. Occurs in few seconds or minutes B. Is an IgE mediated immune response C. IgE is bind by mast cell D. Ia a delayed hypersensitivity E. Histamine is a primary mediator produced 3. In hypersensitivity reaction type I, eosinophyl is activated by: A. IL-4 B. IL-2 C. IL-5 D. IL-6 E. IL-1 4. Histamine release effect of hypersensitivity reaction type I is: A. Vasoconstriction of blood vessels B. Vasodilation of blood vessels C. Capillary permeability decreased D. Bronchus dilated E. Hyposecretion of mucosa 5. Hypersensitivity reaction type II is a cytotoxic reaction which involves: A. IgG and IgM B. IgG and IgD C. IgG and IgA D. IgA and IgD E. IgD and IgE 20 Study Guide Immune System and Disorders Day 4 Topic : Immunopharmacology Lecturer : dr. I Made Jawi, M.Kes. ABSTRACT Immunopharmacology includes the characteristics of drugs that can suppress, modulate, or stimulate immune functions. It also includes the pharmacology of antibodies that have been developed for use in immune disorders. The drugs available comprise a wide variety of chemical and pharmacologic types. In this topic also will be discuss the ways in which drugs may activate the immune system and cause unwanted immunologic reactions. Drugs that modulate immune function and as a immune suppressants are: glucocorticoids (prednisone), immunophilin ligands (Cyclosporine), cytotoxic drugs (Cyclophosphamide), Anti-TNF-α agents (etanercept), enzyme inhibitors (mycophenolate mofetil) and Antibodies. Drugs that modulate immune function and as a immune potentiators are: Cytokines (Interleukin-2, Interferons), BCG vaccine and Thymosin. Learning Task A patient was treated with penicillin. Within a few minutes after penicillin injection, he developed severe bronchoconstriction, laryngeal odema and hypotension. 1. Explain the immunologic mechanism of those problems. 2. To manage that patient what medicine will you give for him immediately? 3. Explain your answer if you give him prednisone. Do you agree? Why? 4. How about antihistamine like dimenhydrinate for this patient? Self assessment Immunopharmacology 1. Cyclosporine is effective in organ transplantation. The immunosuppressant action of the drug appears to be due to A. Activation of natural killer (NK) cells B. Blockade of tissue responses to inflammatory mediators C. Increased catabolism of IgG antibodies D. Inhibition of the gene transcription of interleukins E. Interference with antigen recognition 2. Azathioprine A. Binds avidly to a cytoplasmic immunophillin B. Blocks formation of tetrahydrofolic acid C. Is a precursor of cytarabine D. Is markedly hematotoxic and has caused neoplasms E. Is a metabolite of mercaptopurine 3. Which of the following drugs is a widely used agent that suppresses cellular immunity, inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG antibodies? A. Cyclophosphamide B. Cyclosporine C. Infliximab D. Mercaptopurine E. Prednisone 21 Study Guide Immune System and Disorders 4. Which one of the following agents acts at the step of antigen recognition ? A. Cyclosporine B. Cyclophosphamide C. Methotrexate D. Rh0 (D) immune globulin E. Tacrolimus 5. An immunosuppressed patient was treated for a bacterial infection with parentral penicillin. Within a few minutes after penicillin injection, he developed severe bronchoconstriction, laryngeal edema, and hypotension. Due to the rapid administration of epinephrine, the patient survived. Unfortunately, a year later he was treated with an antipsychotic drug and developed agranulocytosis. The type of drug reaction that was caused by the penicillin is A. An autoimmune syndrome B. A cell-mediated reaction C. A type II drug allergy D. Mediated by IgE E. Serum sickness Topic : Forensic Laboratory Lecture : dr. Henky, SpF Abstract Forensic serology is the study of serology in relation to crimes and other legal matters by using a scientific approach. Doctors should have knowledge about forensic serology to assist investigators in revealing crime cases related with human’s body and health. Moreover, based on legislations, doctors have legal duty to carry out forensic examination when asked by the investigators. Mostly, investigators asked doctors to prove homicide, rape, assault or dispute paternity case. To prove it, the doctors need to do serological examination of biological evidence that found on the victim’s body, such as blood, semen, urine, and other body fluids. Principle of serological test is the use of specific antibodies to detect a target antigen. By doing a simple serological test, doctor can filter the type and origin of biological substances. If the screening test gives a positive result, biological substances must be processed for DNA testing to determine the owner of biological materials. Vignette 1 A woman, 22 years old was found dead and naked. She suffered bruises almost on her entire body. There were blood stains and fluid around her genital. Learning Task 1. In above case, discuss the role of forensic serology in examining biological evidence! 2. Discuss the steps to examine blood stain and fluid around the genital! 3. Discuss the concept of species determination and individualization of blood stain and biological fluid! 4. If in that case, there are 3 suspects, what the forensic serologist do to identify the suspect? 5. Discuss about DNA analysis for that case! 22 Study Guide Immune System and Disorders Vignette 2 A man, with blood type O, come to prove that his wife, with blood type AB, have an affair with her boss, with blood type A. He is not sure whether he is the biological father of his child, because his first child is male, with blood type O, and the second one is female, with blood type AB. Learning Task As a doctor, what would you explain to the man? Day 5 Topic : Adverse drugs reaction Lecture : dr. Ketut Suardamana, Sp. PD Introduction Drug allergy or hypersensitivity is a form of Adverse Drug Reaction (ADR) Definition An ADR is any undesirable effect of drug that is administered in standard doses by the proper route for the purpose of prophylaxis, diagnosis, or treatment. Drug allergy is an immunologically mediated reaction, occurs in a susceptible populations, characterized by specificity, transferability by antibodies or lymphocytes, and recurrence on re-exposure Pathophysiology Allergic drug reactions are usually defined as; 1. reaction caused by suspected immunologic mechanisms 2. result from the production of antibodies and / or cytotoxic T cells directed against the drug, 3. its metabolite, a soluble / cell-bound carrier protein as a responses to prior or continuous exposure to a drug Risk factors 1. Patient related : Age, sex, genetics, atopy, AIDS 2. Drug related : Macromolecular size ; bivalency, haptens, route, dose, duration of treatment 3. Aggravating factors : β Blockers, asthma, pregnancy Diagnosis 1. Diagnosis of drug allergy based on ; 2. Clinical history 3. Clinical manifestations 4. Diagnostic test 23 Study Guide Immune System and Disorders Diagnostic tests 1. SPT may be helpful for diagnosing IgE mediated drug reactions (in vivo) 2. RAST may detect serum IgE antibodies to certain drugs (e.g : penicillin and succinyl choline) (in vitro) 3. Provocation tests Oral provocation tests, may be as a gold standard They must be performed under strict medical supervision with resuscitative equipment available Management 1. Avoidance 2. Premedication 3. Desensitisation Learning Task ADVERSE DRUGS REACTION (ADR) Vignette Male 20 years old, was diagnosed with Pulmonary TB and taking the anti TB regimen (Category 1). On the second day treatment he felt an itchy – swollen redness on whole body. He had previous history of drug allergy but the allergen is unknown, his mother also had history of drugs allergy. The patient was fully alert, T 110/70 mmHg, pulse rate 92x per minute regular, RR 18x per minute. Task 1. Could you explore more to complete the anamnesis! 2. Describe any sign that you find on Physical examination? 3. How to manage this patient? Self assessment 1. Could you describe the adverse drugs reaction (ADR)! 2. Describe the immunopathophysiology of drugs allergy (due to Gell & Coombs Criteria)! 3. Comprehend the diagnostic approach of the drugs allergy! Topic : Anaphylaxis reaction Lecture : dr. Ketut Suardamana, Sp. PD. Definition Anaphylaxis is an acute severe, life-threatening, generalized or systemic hypersensitivity reactions Pathophysiology 1. Type I reaction (IgE mediated) 2. Anaphylactoid reaction (Non IgE mediated) : complement activation, physical factors, substance for Histamine release, idiopathic, arachidonic acid modulation 24 Study Guide Immune System and Disorders Clinical Criteria for Diagnosing Anaphylaxis (Sampson HA, et al. JACI 2006) 1. Acute onset of an illness ( minutes to several hours) with involvement of the skin, mucosal tissues, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING a. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) b. Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia /collapse, syncope, incontinence) 2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours) : a. Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen lips-tongue-uvula) b. Respiratory compromise (eg dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia) c. Reduced BP or associated symptoms (eg, hypotonia collapse, syncope, incontinence) d. Persistent gastrointestinal symptoms (eg cramp abdominal pain, vomiting) 3. Reduced BP after exposure to known allergen for that patient ( minutes to several hours) a. Infants and children: low systolic BP (age specific) or greater than 30% decrease in systolic BP b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that person's baseline Learning task ANAPHYLAXIS Vignette Female 30 years old, came to the Emergency Unit with chief complaint; edema on palpebra, itchy redness on the whole body skin after taking metampirone 500 mg tab. as a treatment for headache. She also complains; shortness of breath, fatique and warmth on the lower extremity. Task 1. 2. 3. 4. What should you do for the first? Could you complete your anamnesis! What do you find on physical examination? The laboratory plan? Or other diagnostic procedure? Self assessment 1. What are the differential diagnoses? 2. Could you describe the pathophysiology of anaphylaxis? 3. Could you describe the clinical manifestations? 4. The management in this case! 5. Describe the prevention! 6. Comprehend any prognostic factors! 25 Study Guide Immune System and Disorders Day 6 Topic : Laboratory test of immune system Lecture : Dr. dr. I Wyn Putu Sutirta Yasa, M.Si. Abstract Objective to comprehend laboratory test of immune system 1. Approach in the patient with immune system disease and disorders are evidence based in immunology, history and physical examination, laboratory studies to make diagnosis. Laboratory test of immune system (immunoassay) based on antigenantibody reactions. Immunoassay can be used for the detection of either antigens or antibodies. For antigen detection, the corresponding specific antibody should be prepared as one of reagents. The reverse is true for antibody detection. 2. The sensitivity of the immunoassays has been enhanced through the development of types of signal detection systems and solid-phase technology. Immunoassay has been optimized to detect less than 0.1 pg/mL of antigen in blood. 3. The can be applied to detection of haptens as small molecules, protein and protein complexes as macromolecules, as well as of any antibody to allergens, infectious agent, and autologous antigens. 4. Students to comprehend the overview of general principles and based of immunoassay. High concentration of such molecules and where antigen- antibodies are mixed in solution can be measured by precipitation techniques. Medium concentration of such molecules and where antigen- antibodies are on solid phase can be quantified by agglutination techniques. Very low concentration of such molecules can be quantified by radioimmunoassay techniques or enzyme linked immunosorbent assay techniques. Outcome of laboratory test of immunes system Students to comprehend the overview of general principles and based of immunoassay to purpose and function of laboratories are to assist students in (1) confirming or rejection a diagnosis, (2) providing guidelines for patient management, (3) establishing a prognosis, (4) detecting disease through case finding or screening and (5) monitoring follow up therapy. Learning Task Laboratoric test 1. Explain the precipitin reactions, what are antibody excess zone, equivalence zone and antigen excess zone 2. Explain the differential of haemagglutination and complement fixation. 3. Explain the differential of direct and indirect immunofluorescence 4. Mention the immunoassay using labeled reagents for detecting antigens and antibodies. 5. Explain the competitive assay and two-site capture assay techniques. Self assessment Laboratory test 1. Mention the principle of methods on immunoassay techniques? 2. What’s the meaning of equivalence zone? 3. Mention the reaction marked on haemagglutination methods? 4. Mention the reaction marked on complement fixation methods? 5. Mention the label used on the ELISA method? Topic : Antihistamine 26 Study Guide Immune System and Disorders Lecturer : Dr. dr. Bagus Komang Satriyasa, M.Repro. ABSTRACT Histamine receptor antagonists represent a third approach to the deduction of histamine-mediated responses. For over 60 years, compounds have been available that competitively antagonize many of the actions of histamine on the smooth muscle. Compounds that competitively block histamine at H1 receptor have been used clinically for many years, and many H1 antagonists are currently marketed. Many are available without prescription, both alone and in combination formulations such as “cold pills” and sleep aids. The H1 antagonists are conveniently divided into firs generations and second generation agents. These groups are distinguished by relatively strong sedative effect of most of the generation drugs. The first generation agents are also more likely to block autonomic receptors. The relatively less sedating characteristic of the second generation H1 blockers is due in part to their less complete distribution into the central nervous system. H1 receptor antagonists block the actions of histamine by reversible competitive antagonism at the H1 receptor; these drugs have no effect on histamine release from storage sites. They are more effective if given before histamine release occurs. The first generation are often the first drugs used to prevent or treat the symptoms of allergic reactions, and the second generation H1 antagonists are used mainly for treatment of allergic rhinitis and chronic urticaria. The drugs adverse effect are sometimes exploited therapeutically. Learning Task 1. 2. 3. 4. 5. Explain two classification of H1 blockers List two drugs the older members of the first generation agent List three drugs the second generation of H1 blockers. Describe mechanism and effect of H1 blockers Describe clinical use of H1 blockers Self assessment Antihistamine 1. Many H1 blocker have additional nonhistamine-related effect, these are likely to include all of the following. EXPECT: A. Antimuscarinic reduction in bladder tone B. Local anesthetic effect if the drug is injected C. Anti-motion sickness effect D. Increase in total peripheral resistance E. Sedation 2. Which of the following drugs will result from blockade of H1 receptor? A. Decreased cAMP in smooth muscle B. Decrease channel opening in enteric nerves C. Decrease IP3 in smooth muscle D. Increase IP3 in smooth muscle E. Increase in total peripheral resistance 27 Study Guide Immune System and Disorders 3. Which of the following drugs are used as anti-motion sickness and also for management of chemotherapy-induced vomiting? A. Diphenhydramine B. Dimenhydrinate C. Meclizine D. Cyclizine E. Loratadine 4. Toxicities of H1 blocker include which one of the following A. Sedation B. Dry mouth C. Blurry vision D. Vomiting E. Hypotension Day 7 Topic : Lecturer : Rhinitis Alergy Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL ABSTRACT Allergic rhinitis is an inflammation of the nasal passages, usually associated with watery nasal discharge and itching of the nose and eyes. Allergic rhinitis affects about 20 percent of population and ranks as one of the most common illnesses. The symptoms occur in the nose and eyes and usually occur after exposure to dust, danders, or certain seasonal pollens in people that are allergic to these substances. There is strong genetic predisposition to allergic rhinitis. One parent with a history of allergic rhinitis has about a 30 percent chance of producing offspring with the disorder. Tthe risk increases to 50 percent if both parents have a history of allergies. Characteristic symptoms include repetitive sneezing, rhinorrhea (runny nose), postnasal drip, nasal congestion, pruritic (itchy) eyes, ears, nose or throat, and generalized fatigue. Symptoms can also include wheezing, eye tearing, sore throat, and impaired smell. A chronic cough may be secondary to postnasal drip, but should not be mistaken for asthma. Sinus headaches and ear plugging are also common. Diagnosis of Allergic Rhinitis. After a medical history, physician will perform a physical exam. Often, the nasal mucosa (lining of the nose) is pale or violaceous because of the engorged veins. Nasal polyps may be seen. Classic signs of allergic rhinitis may include swelling of the eyelids, injected sclerae (the whites of the eyes may be red), allergic shiners (darkened areas under the lower eyelids thought to result from venous pooling of blood), and extra skin folds in the lower eyelids. Skin testing may confirm the diagnosis of allergic rhinitis. Initial skin testing is performed by the prick method. Intradermal testing is performed if results of prick testing are negative. 28 Study Guide Immune System and Disorders The goal of treatment is to reduce the allergy symptoms. Avoidance of the allergen or minimization of contact with it is the best treatment, but some relief may be found with the following medications: antihistamines and decongestants, nasal sprays and immunotherapy. LEARNING TASK ENT. CASE: A 25 years old man complained of sneezing 5 to 10 times and watery nose everytime he wakes up in the morning. Task: 1. 2. 3. 4. 5. Please do further anamnesis in this case! If in the anamnesis his mother had asthma, what is the possible diagnosis of this case? What is/are the differential/s diagnosis of this case? What is/are the complication/s of this case? How is the management of this case? Self Assessment 1. 2. 3. 4. What is the definition of allergy rhinitis? What are the symptom and sign of allergy rhinitis? How is the classification of allergy rhinitis? When immunotherapy can be applied to allergy rhinitis patient? Topic : Allergic Dise ase in Dermatology Lecturer : Dr.Nyoman Suryawati, SpKK Atopic Dermatitis Absract Atopic dermatitis (AD) or atopic eczema is a chronically relapsing, pruritic, exanthematous dermatosis of uncertain etiology that is characterized primarily by an allergic diathesis as well as erythema, oozing, crusting, excoriations, lichenification, and dehydration of involved skin surfaces (Figs 1 and 2). Affected infants typically are fussy from sleep deprivation because of pruritus and often are uncomfortable, are fretful, and may not eat well. Older children who have severe atopic eczema frequently are asthenic and may have difficulties at school. Onset occurs at approximately 2 to 3 months of age, and the disease may persist, with periodic exacerbations and remissions, into adulthood. Sites predisposed to rash change with growth and development. Spread to other areas may occur in severe cases. Pathophysiology of AD by Hyperactive Th2 subset T helper cells (associated with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, stimulation of proliferation, and differentiation of B lymphocytes), Increased levels of serum IgE, Upregulation of interleukin-4, Downregulation of interferon gamma, Increased eosinophils, Elevated levels of IgEactivated mast cells. Clinical feature of AD, there are three stages under the different age groups: 29 Study Guide Immune System and Disorders Infancy, In infancy, at between two months to two years of age, a child may develop an itchy erythemathous rash on the cheeks. The rash may develop into minute epidermal vesicles which can rupture and produce moist crusted areas. Childhood, In the childhood phase, the rashes are usually less acute, less exudative, drier and more papular. The lesions occur at classical locations like the antecubital and popliteal fossae, wrists, eyelids, face and collar regions. Lichenified, slightly scaly or infiltrated patches may intermingle with isolated, excoriated papules over the exposed parts. Adolescence, In the adolescent and adult stage, the lesions may appear as localised erythematous, scaly, papular or vesicular patches. Or they may appear in the form of pruritic, lichenified patches. They usually involve the antecubital and popliteal fossae, the front and sides of the neck, the forehead, and around the eyes. The hands and wrists are frequently involved. Hyperlinearity of the palm is a manifestation of ichthyosis vulgaris which accompanies 30-40% of cases. Diagnostic of AD according the diagnostic criteria of Haniffin & Rajka (1980) is with at least 3 of Major criteria and at least 3 Minor Criteria. Management of AD is basically according the form of skin lesion, severity of itching and inflammation, secondary infection. Contact Dermatitis Abstract Dermatitis or eczema is an inflammation of the skin with characteristic morphology but varied cause caused by skin contact with an environmental agent. Most occupational dermatoses are eczematous reactions to an environmental contactant, characterized by redness, swelling, small fluid filled blisters, and oozing in the acute state and as a scaly lichenified, thickened, fissured with pigmentary changes in the chronic stage. Contact dermatitis (CD) is an altered state of skin reactivity induced by exposure to an external agent. "Eczema" and "dermatitis" are often used synonymously to denote a polymorphic pattern of inflammation of the skin characterized, at least in its acute phase, by erythema, vesiculation and pruritus. Substances that induce CD after single or multiple exposures may be irritant or allergic in nature. The clinical presentation may vary depending on the identity of the triggering agent and the reactivity of the subject, but in all cases the lesions are primarily confined to the site of contact. According to the mechanism of elicitation, the following types of contact reactions may be distinguished: 1. allergic contact dermatitis (ACD), immunopathology based on type IV hypersensitivity, 2. irritant contact dermatitis (ICD), due to primary irritant, acute and chronic cumulative, 3. phototoxic and photoallergic contact dermatitis, and 4. immediate type contact reactions. The present review will focus on allergic contact dermatitis. ACD is the clinical presentation of contact sensitivity in humans. Management of contact dermatitis, the only available etiologic treatment of ACD is elimination of the contact allergen. The patients should be informed about the identity of the offending agent and the possible sources of the sensitizer. Corticosteroids have antiinflammatory and immunosuppressive effects. In murine models of contact sensitivity they inhibit both the induction and elicitation phase. ACD is a major indication for topical corticosteroid treatment. Histamine is not involved in the pathogenesis of ACD, but need for reduce itching. Systemic corticosteroid is not absolute for treatment in the most common forms of ACD. However they may be indicated for a short period of time if ACD is widespread and severe. 30 Study Guide Immune System and Disorders LEARNING TASK Case 1 A 22-year-old waitress complained of a 5 to 6 months history of painful, pruritic lesions on her hands, arms, and legs. The itch often disturbed her sleep, and her quality of life was diminished by physical discomfort and feelings of embarrassment. Lesions on both palms showed minimal vesiculation, moderate papulation and scaling, moderate to severe erythema, and severe fissuring and lichenification. Lesions on her arms and legs were less severe, showing only slight erythema and papulation. She reported a continuous course of eczematous lesions, primarily on her hands, over the previous 6 to 7 years, with the onset coinciding with a tongue piercing received in late 1995. Immediately after the piercing, she developed a significant lingual hematoma, which resolved after approximately 3 months. She received 4 subsequent piercings over the next year: one in her lip, one in her nose (transseptum) and 2 in her right pinna. She also reluctantly removed her facial piercings soon afterward, assuming a correlation between the jewelry and the appearance of hand eczema, which had emerged almost simultaneously. The patient had a personal history of atopic dermatitis, chronic rhinitis, and allergic conjunctivitis since infancy; allergies to melons, latex, and animals since childhood; and depression since adolescence. Her surgical history included a tonsillectomy, correction of a deviated septum, and adenoid removal. Her father and all of her siblings had histories of rhinitis, allergic conjunctivitis, and episodes of urticaria and contact dermatitis. Case 2 A 13-year-old Caucasian male came with chronic-residive of pruritus and ithching on the fosa cubiti, his cheeks, back and leg for 9 years. The itch often disturbed her sleep, and her quality of life was diminished by physical discomfort and feelings of embarrassment. Her father also had a history of asthma, both parents had drug allergies, and one sibling had atopic dermatitis as a child. Serum IgE level was 6120 IU/mL, and increase of eosinophil count. Prior therapies included all of those topical cream for self medication, but no significant result, even getting worse if intake sea food and other foods. What is the most likely diagnosis, and what test would confirm it? 31 Study Guide Immune System and Disorders Day 8 Topic : - RHEUMATOID ARTHRITIS - SYSTEMIC LUPUS ERYTHEMATOSIS ( SLE ) - Polimyalgia Rheumatica Lecture : dr I Gede Kambayana, Sp PD-KR. RHEUMATOID ARTHRITIS Abstract Definition Rheumatoid Arthritis (RA) is a chronic multisystem disease of unknown cause. The characteristic feature of RA is persistent inflammatory synovitis, involving peripheral joints in a symmetric distribution. Etiology The cause of RA remains unknown. RA might be a manifestation of the response to an infectious agent in a genetically susceptible host. Causative agents is involved; Mycoplasma, Epstein-Barr Virus (EBV), Cytomegalovirus, parvovirus, and rubella virus. Pathology and pathogenesis Microvascular injury and an increase the number of synovial lining cells. Histology of rheumatoid synovitis; the characteristic feature of RA inflammation with hyperplasia of lining layer, a higher CD4+ T cell infiltrate around postcapillary venules. Immunoglobulin and the autoantibody rheumatoid factor are produced within the synovial tissue, which leads to the local formation of immune complexes. Autoantibodies to synovial tissue components contribute to inflammation. Clinical manifestation Onset of RA; Polyarthritis which begins insidiously with fatigue, anorexia, and generalized weakness. Specific symptoms usually appear gradually as several joints, especially those of the hands, wrists, knees, and feet, become affected in a symmetric fashion. Signs and symptoms of articular disease; pain, swelling, and tenderness may initially localized to the joints. Laboratory findings - Rheumatoid factors; are autoantibodies reactive with the Fc portion of IgG , are found in more than two-thirds of adults with the disease. - Anti CCP (Antibodies to citrulline-containing proteins); are found in most patients with RA Radiographic evaluation Loss of articular cartilage and existence of bone erosions. 32 Study Guide Immune System and Disorders Diagnosis Revised Criteria for the classification of RA (1987 ); 1. Morning stiffness ( > 1 jam ) 2. Arthritis (³ 3 joints) 3. Arthritis of hand joints; wrists, MP jont or proximal interphalangeal join 4. Symmetric arthritis. 5. Rheumatoid nodule. 6. Serum rheumatoid factor 7. Radiographic changes 2 or more clinical diagnoses→ RA Learning Task Case A female 35 years old, married, has 4 children. She is a cleaning service. She came to Health Centre with chief complaint, problem on her wrist, fingers both side. She feels pain, swelling and tenderness, morning stiffness since a month. Learning task 1. 2. 3. 4. 5. 6. Could you complete the anamnesis! Describe the physical diagnostic! Base on the anamnesis and physical diagnostic, the working diagnosis of this patient? Describe the differential diagnosis! Describe other laboratory test Where should you reffer this patient? Self assessment 1. 2. 3. 4. 5. 6. 7. Describe the definition of rheumatoid arthritis! Describe the etiopathogenesis of AR! Describe the pathological aspect of AR! Describe the clinical manifestation of AR! Describe the laboratory test for AR! Describe the diagnostic criteria of AR! Comprehend the management of AR! Topic : SYSTEMIC LUPUS ERYTHEMATOSIS (SLE) Abstract Definition SLE is an autoimmune disease which involves multiorgan / multisystem damage, mediated by tissue-binding autoantibodies and immune complexes. Pathogenesis and etiology SLE is caused by interactions between susceptibility genes and environmental factors, resulting in abnormal immune responses. 33 Study Guide Immune System and Disorders Pathology In SLE biopsies of affected skin show deposition of Ig at the dermal-epidermal junction / DEJ , injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around blood vessels and dermal appendiges Diagnosis. Based on clinical features and auto antibodies. Classification criteria for the diagnosis of SLE; (specificity 95%, sensitivity 75%) : 1. Malar rash 2. Discoid rash 3. Photosensitivity 4. Oral ulcers (include oral, nasopharyngeal and observed by physician. 5. Arthritis 6. Serositis 7. Renal disorder (proteinuria > 0,5 g / d or ³ 3+, or cellular casts 8. Neurologic disorder 9. Hematologic disorder 10. Immunologic disorder 11. Antinuclear antibodies (ANA test ) If ³ 4 of these criteria ® SLE Laboratory test - ANA test : prevalence 98%, best screening, repeat test (-) → (-) - Anti ds-DNA : prevalence 70%, high titers are SLE specific, correlate with disease activity. Learning task A 17 years old female came to Health Centre with chief complaint; facial rash since 3 days ago. She had the rash since a year ago, and reduced after treatment. The rash is triggered by the UV. The patient also feels fatique since 3 months ago. Task 1. 2. 3. 4. 5. Please you complete the anamnesis! Describe the physical examination! If she also complains edema on whole body, what is the working diagnosis? Describe the differential diagnosis! Where should you reffer this patient? Self assessment 1. 2. 3. 4. 5. Describe the definition of SLE! Describe the etiopathophysiology of SLE! Describe the clinical manifestation of SLE! Describe the laboratory test for this patient! Comprehend the management of SLE! 34 Study Guide Immune System and Disorders Day 9 Topic : Autoimmune Disease in Neurology Lecturer : DR. Dr. A A Raka Sudewi, Sp.S. Guillain Barre Syndrome ABSTRACT This acute polyneuropathy, occurs in all parts of the world and in all seasons, its affects children and adults of all ages and both sexes. The major clinical manifestation is weakness, symmetrically, usually the lower extremities before the upper (Laundry’s ascending paralysis). The weakness can progress to total motor paralysis with death from respiratory failure within a few days. The clinical manifestations are suggesting the result of a cell-mediated immunology reaction directed at peripheral nerve. The most important laboratory aids are the electrodiagnostic studies and the CSF examination. LEARNING TASK CASE 1: Male 32 years old came to neurology clinic with chief complaint weakness of both legs since two days ago. The patients fully alert with normal: Blood pressure, pulse rate and respiratory rate. TASK 1. 2. 3. 4. 5. 6. 7. 8. Please explore another history to complete anamnesis! What kind of clinical examination will you do? What was the diagnosis of this patient? What kind of clinical manifestation based your diagnosed? Describe your plans of diagnosis for this patient? Describe your plans of therapy for this patient? Describe your plans of education for this patient or his family? Describe your monitoring plans for this patient? SELF ASSESMENT 1. What is the definition of GBS? 2. What is the differential diagnosis of GBS? 3. Describe the clinical manifestation of GBS? 4. Please describe the pathology feature of GBS! 5. Please describe the pathogenesis of GBS! 6. Please describe the prognosis of GBS! 35 Study Guide Immune System and Disorders Myasthenia Gravis Absract Myasthenia gravis is a disease affecting the neuromuscular junction. The main feature is a fluctuating weakness of certain voluntary muscles. Manifest weakening during continued activity, quick restoration of power with rest, and dramatic improvement in strength following the administration of anticholinesterase drugs. Reference has already been made to the involvement of the thymus gland in myasthenia gravis. The establishment of an immunologic mechanism, operative at the neuromuscular junction, has been the most significant development in our understanding of myasthenia gravis. LEARNING TASK CASE 2. Female 21 years old came to neurology clinic with chief complaint weakness of eyelid opening. The weakening manifests during continued activity in the afternoon, and improve in strength after rest, especially when she got up in the morning. TASK 1. 2. 3. 4. 5. 6. 7. 8. Please explore another history to complete anamnesis! What kind of clinical examination will you do? What was the diagnosis of this patient? What kind of clinical manifestation based your diagnosed? Describe your plans of diagnosis for this patient! Describe your plans of therapy for this patient! Describe your plans of education for this patient or his family! Describe your monitoring plan for this patient! Topic : Secondary Immunodeficiency Disease HIV Infection and AIDS Lecturer : Prof. DR. Dr. Tuti Parwati M, SpPD-KPTI Abstract SECONDARY IMMUNEDEFICIENCY DISEASES, (FOCUS ON HIV) Infeksi HIV merupakan infeksi kronik dengan beberapa stadium yang pada awalnya menimbulkan gangguan terutama pada sistem imunitas seluler tetapi kemudian disusul dengan terganggunya pengaturan sistem imunitas humoral dengan berbagai akibatnya. Pada infeksi akut atau infeksi Primer yang berlangsung sekitar 4-12 minggu pasca infeksi, akan terjadi serokonversi dari antibodi HIV negatif menjadi antibodi HIV positif. Setelah itu disusul dengan stadium kronik asimptomatik dan simptomatik, dimana fase ini berlangsung rata-rata sekitar 3-5 tahun setelah infeksi primer. Setelah itu penyakit masuk ke stadium lanjut yang disebut stadium AIDS, karena pada stadium ini terdapat sindroma penyakit akibat defisiensi imunitas sekunder yang berat. Pada era pra HAART (highly active antiretroviral therapy) stadium ini bertahan hanya sekitar 2-3 tahun kemudian penderita meninggal. Era HAART dimulai sekitar tahun 1995-1996 dimana diberikan setidaknya tiga jenis obat ARV dari kelas yang berbeda, dimana cara kerja obat dengan titik tangkap yang berbeda pada siklus hidup HIV dapat menekan pertambahan jumlah viurs, sehingga lama kelamaan jumlah HIV dalam 36 Study Guide Immune System and Disorders darah tidak dapat di deteksi lagi. Masa asimptomatik yang cukup lama disebut juga fase laten, namun istilah ini tidak memberikan arti yang sesungguhnya, karena dalam fase yang disebut laten sebenarnya berlangsung replikasi virus yang sangat aktif didalam kelenjar limfe dan organ RES (reticuloendothelial system). Proses yang terjadi sangat dinamik dan patologik baik dilihat dari aspek virologi maupun imunologi ini pada akhirnya dapat menimbulkan gejala klinik berupa sindroma defisiensi imun yang berat. Pengobatan terhadap infeksi HIV tergantung stadium penyakit dan sindroma gejala klinik infeksi oportunistik yang ada dan pengobatan dengan obat anti retroviral kombinasi. Tentukan derajat berat imunedeficiency dengan pemeriksaan jumlah limfosit CD4 dan viral load penderita. Menurut WHO ada 4 stadium infeksi HIV, yaitu stadium 1 – 4, dan stadium 3 dan 4 sudah termasuk stadium AIDS. Pengobatan infeksi oportunistik sama seperti pengobatan penyakit pada non HIV hanya saja diperlukan pemberian pengobatan yang lebih lama. Berdasarkan rekomendasi WHO sebelumnya, Obat ARV kombinasi mulai diberikan pada CD4=< 200 sel/mm3, tetapi rekomendasi WHO terbaru (2010) menyarankan pemberian ARV pada CD4 350 sel/mm3. Learning tasks Case 1: A 20-year-old man complained of cough and shortness of breath since a month earlier. He got dry cough and pain on his chest when inhale. He also lost weight until 15 kg in 1 month. He lost appetite and got dryness in his throat when eat or drink. He always takes medicine but the symptoms relapsed. Tasks 1. 2. 3. 4. 5. Complete history taking of this patient which can lead you closer to the case-diagnosis Describe physical examination to support diagnosis of this patient Describe laboratory and other examination to support diagnosis Describe principle management of this patient Define plan of therapy based on priority for this patient Self assessment 1. 2. 3. 4. 5. What is the definition of secondary immune deficiency? What is opportunistic infection? Named some example of opportunistic infection. What are the diagnosis criteria for HIV infection/AIDS? What kind of antiretroviral therapy (ART) does available for patient? What psycho-social problem of HIV infection/AIDS we should always remember at our duty as a doctor? 37 Study Guide Immune System and Disorders Day 10 Immunologic Dissorders in childhood Topic : Food Allergy Lecturer : Dr Ketut Dewi Kumara Wati, SpA ABSTRACT Food allergy (FA) is one of the earliest manifestations of allergic disease. It is a part of adverse reaction to food. FA is mediated either by IgE or other cells of the immune system, and could be mixed between IgE and cell mediated. The typical case of FA (IgE mediated), usually started during infancy in which most symptoms might be resolved over time, but the IgE allergies remain. Rather than genetic predisposition, every infant are prone to FA, especially Cow’s milk allergy (CMA), since the immaturity of the gastrointestinal tract will allow the allergen from CM to be absorbed and enter the circulation, enable for sensitization and clinical manifestation development. Diagnosis of FA is based on careful history, with reproducibility, timing, and response to elimination of food from the diet. The gold standard is the double blind placebo controlled food challenge (DBPCFC). Treatment consists of avoidance of the diet. Prevention for Food allergy is done by promoting breastfeeding and delayed exposure to food allergen. Other purpose of prevention is to avoid allergic march Learning tasks: A parent of 3 month-old baby girl complained about the rash in both cheeks of their baby, started 5 days before. It seemed that the rash was itchy so the baby seemed to be scratching her cheek intensely and became restless. Baby have been breastfed since she was 2 days old for only 7 days, while formula had been given since her first day of life, which then continued after breastfeeding cessation. Task: 1. What are other helpful informations you should get from the parent for complete management of this case? 2. When and how did the process of the diseases started? 3. Considering the onset of manifestation: please describe other clues you should find during physical examination on this baby! 4. Do you need laboratory investigation for diagnostic? 5. What are your suggestions for the parent? 6. Will you prescribe medication? If yes, please describe your plan. Self assessment: 1. What is FA 2. What are the types of FA? 3. How does FA develop? 4. What is (are) the cause(s) of FA in children? 5. What is the laboratory investigation of FA 6. How to make an assessment of FA? 7. What is the treatment for FA 8. What is allergic march? 9. How to prevent allergic march? 38 Study Guide Immune System and Disorders Topic : Manage Rheumatic disease in Childhood Lecturer : Dr. Dewi Kumarawati, SpA Abstract Henoch Schonlein Purpura is a systemic small vessel vasculitis. It usually begin with Upper Respiratory Tract Infection, although can be triggered by other factors. During infection, AgAb complex will activate complement, however, in HSP, C3a and C5a released during the process will increase vascular permeability results in plasma leakage, erythrocyte extravasation, recruitment of inflammatory cells, which will give clinical manifestation of palpable purpura, join inflammation, abdominal colic, and renal involvement. Treatment is conservative, using nonsteroid anti inflammation Drug (NSAID). Steroid used when there is complication. Recurrence can be developed. Juvenile Rheumatoid Arthritis Juvenile rheumatoid arthritis is arthritis that causes joint inflammation and stiffness for more than 6 weeks in a child of 16 years of age or less. Inflammation causes redness, swelling, warmth, and soreness in the joints, although many children with JRA do not complain of joint pain. Any joint can be affected and inflammation may limit the mobility of affected joints. Systemic JRA can also affect the internal organs. Classification of JRA into three types by the number of joints involved, the symptoms, and the presence or absence of certain antibodies found by a blood test. JRA is an autoimmune disorder, which means that the body mistakenly identifies some of its own cells and tissues as foreign. The main goals of treatment are to preserve a high level of physical and social functioning and maintain a good quality of life. Treatment consist of medication,: NSAID, DMARD, Anti TNF and physical treatment. Systemic Lupus Erythematosus in children. SLE is persistent nonspecific activation of the immune system that results in widespread tissue deposition of immune complexes. Thus most of the damage that occurs in SLE is ‘bystander’ damage. As a result of the deposition of immune complexes there is inflammation that damages the tissues where ever the immune complexes have landed. Nonspecific complaints of fatigue and malaise are the most common initial symptoms of SLE in children and adolescents. The typical 'butterfly' rash is present in less than one-third of affected children. Definitive diagnosis of SLE is done using The American College of Rheumatology. Treatment using corticosteroid soon after diagnosis confirmed. Learning tasks Case A 10-year-old boy complained of pain and warm on his left knee for the late 3 months. His right ankle had been pain and warm since two months, followed by left ankle since 6 weeks. Every morning he felt stiffness on those joints, particularly in the knee. No fever has been experienced, he ate well, and his body weight was in normal limit. Task: 1. 2. 3. 4. 5. What clues you may gather for JRA from the case above? What type of JRA is the case? Why? What laboratory investigation do you need? What are your planning for treatment of the case What is the prognosis? 39 Study Guide Immune System and Disorders Self assessment 1. What Is Arthritis? 2. What Is Juvenile Rheumatoid Arthritis? 3. What Causes Juvenile Rheumatoid Arthritis? 4. What Are the Symptoms and Signs of Juvenile Rheumatoid Arthritis? 5. How Is Juvenile Rheumatoid Arthritis Diagnosed? 6. Who Treats Juvenile Rheumatoid Arthritis? What Are the Treatments? 7. How Can the Family Help a Child Live Well With JRA? 8. Do Children With Juvenile Rheumatoid Arthritis Have To Limit Activities? 9. What is Purpura? 10. What Is Henoch Schonlein Purpura? 11. What Causes Henoch Schonlein Purpura? 12. What Are the Symptoms and Signs of Henoch Schonlein Purpura? 13. How Is Henoch Schonlein Purpura Diagnosed? 14. Who Treats Henoch Schonlein Purpura? What Are the Treatments? 15. Do Children With Henoch Schonlein Purpura Have To Limit Activities? Topic : Immunodeficiency in Childhood Lecturer : Dr Ketut Dewi Kumara Wati, SpA Absract When someone is born defected in one or more parts of the immune system, it is called primary immune deficiency. Recurrent infection or incomplete recovery from infections is among the clues from which we can suspect that the patient has immune deficiency. Thorough history taking and evaluation is needed to direct us to whether the immune deficiency is primary or secondary. Learning tasks 1. What is Primary Immune deficiency (PID)? 2. What are the types of PID? 40 Study Guide Immune System and Disorders BASIC CLINICAL SKILL Day 11 Topic : Soluble markers of allergic inflammation Lecture : Dr. dr. I Wayan Putu Sutirta Yasa, M.Si. Abstact The conventional way to assess and confirm an increased inflammatory activity in the body is to measure various acute-phase reactants. Of these, the erythrocyte sedimentation rate (ESR) is the most widely used, although there is a clear tendency today to replace the ESR by other more accurate methods such as measurement of the acute-phase proteins fibrinogen, haptoglobin, orosomucoid and C-reactive protein (CRP). Over 'the years, developed a number of assays for specific secretory proteins of various inflammatory cells such as the eosinophil, the neutrophil, and the monocyte/macrophage. Eosinophil markers The eosinophil granulocyte contains in its granules four major proteins. These proteins are all released in vitro to the extracellular environment upon stimulation of the eosinophil by various secretagogues. Neutrophil markers The neutrophil granulocyte contains several granule proteins, which are secreted in the extracellular environment and may therefore serve as markers of neutrophil activity in vivo. These proteins are contained in different subpopulations of granules and may therefore reflect slightly different aspects of neutrophil activation. Two proteins have been widely used as markers of primary granule protein secretion: elastase and MPO. Mast cell markers Histamine has been used in many studies to reflect mast cell activity. The mast cells contain in their secretory granules several proteins, some of which have been purified and characterized. One of these is tryptase. Other soluble markers of allergic inflammation Assays for most cytokines and soluble adhesion molecules have become available during 1992. The soluble receptor IL-2r has been assayed in BAE fluid and in blood in patients with asthma, as a reflection of T-cell activity. lL-4, which is believed to regulate IgE production, was shown to be raised in allergic asthma, as opposed to nonallergic. IL-5 is probably the most important cytokine in relation to eosinophil growth and activation. The molecules of particular interest to measure in patients with asthma and allergy are the adhesion molecules. are ELAM-1 (endothelial-leukocyte adhesion molecule) and VCAM-1 (vascular cell adhesion molecule) may be of interest, since ELAM-1 seems to be the only specific marker of 41 Study Guide Immune System and Disorders endothelial cell activity available, and VCAM-1 is involved in the selective accumulation of eosinophils at sites of inflammation. Vignette Women, 25 year old, come to the emergency room having shortness of breath, wheezing, tightness in the chest, and coughing Learning Task 1. What is the diagnosis 2. What various acute-phase reactants are you measure 3. Mention the a number of cells, the source of specific secretors proteins of various inflammatory cells 4. Mention the Eosinophil granule proteins, With once granule protein are particularly good, specific indicators of eosinophil activity? 5. What the granule protein secreted on patients with atopic dermatitis? 6. What cytokine are increasing in allergic diseases. 7. Mention the neutrophil granulocyte granule proteins, which are secreted in the extracellular environment and may therefore serve as markers of neutrophil activity 8. Mention the adhesion molecules of particular interest to measure in patients with asthma and allergy. Self Assessment : 1. Mention the soluble markers of eosinophil cells in blood 2. Mention the soluble markers of neutrophil cells in blood 3. Mention the soluble markers of Mast cell cells in blood 4. Mention the soluble markers of T lymphocyt cells in blood 5. Mention the soluble markers of endothelial cells in blood 42 Study Guide Immune System and Disorders Day 12 Topic : Forensic Laboratory Lecture : dr. Henky, Sp.F. Abstract In managing sexual assault cases, doctors must perform the examination to find signs of sexual intercourse. To prove that sexual intercourse has occurred, an ejaculate should be found inside the vagina. Ejaculate or seminal fluid contains a specific component of prostatespecific antigen (PSA). Formerly, the examination of PSA in seminal fluid quantitatively is difficult and quite expensive. But, nowadays, there is a rapid test for checking PSA, which is very practical, quick, easy to use, inexpensive, and quite sensitive and spesific. Task Perform a simple test to detect PSA in vulval swab / vaginal washing! Detection of Prostate-Specific Antigen (PSA) in Vulval Swab / Vaginal Washing Using Rapid Test Device Henky Department of Forensic Medicine Faculty of Medicine Udayana University Tools and Materials: 1. Female Genitalia Mannequin 2. Speculum 3. Labeled Sticker 4. Handschoen disposable 5. Cotton swab 6. Syringe 3 cc + Catheter 7. Test Tube 8. Pipette 9. Stopwatch 10. Camera 11. Distilled water 12. Seminal Fluid 13. PSA Rapid Test Device Step of Examinations: 1. Informed Consent. 2. Prepare a label which contains victim’s name, age, date, time, and doctor’s name. 3. Place the victim on gynecology table in lithotomy position. 4. Examine condition of the hymen, A. If the hymen is intact: 1) Take vulval swab using cotton swab around the vulva. Twist it for 5 – 10 times. 2) Insert the cotton swab into test tube containing 2 cc of distilled water. B. If the hymen is not intact: 1) Prepare a syringe containing 2 cc of distilled water. 43 Study Guide Immune System and Disorders 5. 6. 7. 8. 2) Insert a speculum into the vagina carefully. 3) Perform vaginal washing by using preloaded syringe and catheter. The fluid should be injected into upper vagina. 4) Agitated slightly with the speculum for 5 – 10 times. 5) Aspirate the fluid back into the syringe, and then place it into test tube. Take the fluid from test tube using pipette. Put 2 drops of samples on PSA rapid test device. Incubate for 5 minutes at room temperature. Interpret the result by observing the appearance of pink lines: (-) : The line only appears in the reference (R), and control (C) area. (+) : The line appears in the test (T), reference (R), and control (C) area. Invalid : The line does not appear in the reference (R), and/or control (C) area. 9. 10. Take photos of the result along with a label which already contain the victim’s data. 11. Attach the label to the test tube and store the tube in refrigerator. Day 13 BCS : Anaphylactic Shock Lecturer : dr. Tjok Istri Anom S, Sp PD ANAPHYLAXIS Anaphylaxis is defined as a rare, severe, and sudden allergic reaction. This acute hypersensitivity reaction is potentially fatal, and can occur within seconds to minutes to hours after exposure to an antigen. Anaphylaxis is a medical emergency; initial reactions can range from mild to severe. Common triggers for anaphylaxis are foods (e.g., peanuts, tree nuts, shellfish, fish, milk, or eggs), insect venoms (e.g., bees or wasps), medications (e.g., penicillin and other betalactam antibiotics, narcotics allergy extracts, vaccines, and other biologicals [e.g.,immune globulin and blood transfusions]), natural rubber latex exposure, and radiocontrast media. “New diagnostic criteria for anaphylaxis were published in 2006 to help health care professionals both recognize the spectrum of signs and symptoms that constitute anaphylaxis and establish a more systematic approach to its diagnosis and management. The following 3 criteria were established, and the presence of any 1 of these criteria indicates that anaphylaxis is highly likely: • Acute onset of an illness (over minutes to several hours) involving skin, mucosal tissue, or both (for example, generalized hives, pruritus or flushing, swollen lipstongue-uvula), and at least 1 of the following: o Respiratory compromise (for example, dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow rate, hypoxemia) o Reduced blood pressure (BP) or associated symptoms of end-organ dysfunction (for example, hypotonia (circulatory collapse), syncope, incontinence) OR 44 Study Guide Immune System and Disorders • Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours): o Involvement of the skin-mucosal tissue (for example, generalized hives, itchflush, swollen lips-tongue-uvula) o Respiratory compromise (for example, dyspnea, wheeze-bronchospasm, stridor, reduced peak expiratory flow rate, hypoxemia) o Reduced BP or associated symptoms of end-organ dysfunction (for example, hypotonia, syncope, incontinence) o Persistent GI symptoms (for example, crampy abdominal pain, vomiting) OR • Reduced BP after exposure to a known allergen for that patient (minutes to several hours). Reduced BP is defined: o In adults, as a systolic BP of less than 90 mm Hg or greater than 30% decrease from that person's baseline o In infants and children, as a low systolic BP (age-specific) or greater than 30% decrease in systolic BP. Low systolic BP is defined as: ▪ Less than 70 mm Hg for ages 1 month to 1 year ▪ Less than (70 mm Hg plus twice the age) for ages 1 to 10 years ▪ Less than 90 mm Hg for ages 11 to 17 years Note: In infants and young children, hypotension may be a late manifestation of hypovolemic shock. Tachycardia, in the absence of hypotension, also may indicate shock.” PROTOCOL FOR TREATMENT OF ANAPHYLAXIS Observation/ Condition MILD REACTION (May rapidly progress to a more severe reaction) Assessment • • • • • MODERATE REACTION Generalized flush Red, itchy, eyes Itching at the injection site or at other body sites Localized to generalized urticaria (hives) Vomiting, abdominal pain • Mild to moderate Intervention (Mild and Moderate Reactions) • • • • • • wheezing • Coughing • Complains of generalized itching, itching throat • Generalized urticaria (hives) • Swelling of lips, face, tongue, eyelids, • ABC’s. Call 911 or local EMS STAT (Preferably have someone not involved in direct patient care make the call). Place patient in supine position. Monitor vital signs. GIVE OXYGEN BY MASK, if any respiratory symptoms are present o Special instructions** for O2 administration, if given (O2 flow rate, lpm) ___________________ FIRST-LINE TREATMENT: GIVE AGE AND WEIGHT APPROPRIATE DOSES OF EPINEPHRINE, intramuscularly, preferably in the anterolateral thigh (See Table 1). Repeat every 5–15 minutes, up to 3 doses, depending on patient’s response SECONDARY TREATMENT: As an adjunct to epinephrine, give weight or age appropriate doses of diphenhydramine HCL orally or intramuscularly (See 45 Study Guide Immune System and Disorders Condition Observation/ Assessment Intervention (Mild and Moderate Reactions) hands, feet, or genitalia. • Vomiting, diarrhea, and/or abdominal pain • • • • • Table 2 or Table 3). DO NOT GIVE diphenhydramine HCL to infants aged less than 7 months Continue to observe for change in symptoms (lessening or worsening) Maintain accurate emergency flow sheet showing: o Date o Time of occurrence o Vital Signs o Medication(s) (time, dosage, response,, name of healthcare personnel who administered the medication) o Immediate therapy o Disposition of patient (transfer for further emergency care ASAP) Send summary of emergency treatment with patient with written assessment of patient’s condition at time of transfer. Document all measures taken in patient’s medical record and place allergy label on front of patient’s medical record. Advise patient (parent) about the drug or trigger that caused reaction. Advise patient (parent) to report reaction to their physician or primary care provider. Day 14 Topic : MORPHOLOGY OF INFLAMMATION Lecture : Dr. Ni Putu Sriwidyani, Sp.PA ABSTRACT The vascular and cellular reactions that characterize acute and chronic inflammation are reflected in the morphologic appearance of the reaction. The importance of recognizing these morphologic patterns is that they are often associated with different eliciting stimuli and clinical situations. In this topic, student will learn morphology of inflammation: acute inflammation, chronic inflammation, serous inflammation, fibrinous inflammation, abscess, granulomatous inflammation, and ulcer. 46 Study Guide Immune System and Disorders LEARNING TASK Describe macroscopic and microscopic features of following inflammation patterns: 1. Acute inflammation 2. Chronic inflammation 3. Serous inflammation 4. Fibrinous inflammation 5. Abscess 6. Granulomatous inflammation 7. Ulcer SELF ASSESMENT 1. Per definition, granuloma consists of: A. Cholesterol cleft B. Collagen C. Fibroblast D. Epitheloid cells E. Hemosiderophages 2. A pathologic cavity wich contain pus is: A. Granuloma B. Abscess C. Ulcer D. Scarr E. Fibrosis 3. Inflammation in varicella infection is: A. Granuloma B. Abscess C. Ulcer D. Serous inflammation E. Fibrinous inflammation 4. Constrictive pericarditis is a common complication of following condition in pericard cavity: A. Granuloma B. Abscess C. Ulcer D. Serous inflammation E. Fibrinous inflammation 5. Following is one of morphologic feature of chronic inflammation: A. Hyperemi B. Oedema C. Neutrophil infiltration D. Fibrosis E. Transudation 6. Necrosis that found in teberculosa infection is: A. Liquifactive necrosis B. Coagulative necrosis C. Caseous necrosis D. Fat necrosis E. Gangrenous necrosis 47 Study Guide Immune System and Disorders Day 15 BCS : Skin Prick Test Lecturer : Dr.dr. Ketut Suryana, Sp PD-KAI ABSTRACT Introduction The diagnosis of allergic diseases: a. A comprehensive history b. Physical examination c. Laboratory and other diagnostic testing: laboratory (eos. count, feces ex, IgE), roentgen, Skin test Methods of skin testing: Patch test, Scratch test, Prick test, Intradermal test Indications for SPT - An allergic patient / suspected allergy When SPT should be done : a. SPT should be undertaken during periods of free symptoms b. To prevent worsening of the clinical status Preparations of SPT : 1. Washout of any medication include ; antihistamines AH-1 (a 3-days washout), AH-2 (one day washout) antidepressants, codeine, long-term oral steroid (a 1-week washout) 2. A 1- week course of daily glucocorticosteroids was reported to have no effect on immediate skin tests. 3. High dose allergy immunotherapy results in a reduction in skin test reaction. 4. Emergency Kit Procedure of SPT 1. SPT was performed on volar region of antebrachium 2. Cleanse the skin with 70 % ethyl alcohol and allow it to dry by evaporation 3. Aseptically place a drop of a standardized allergen (2 cm apart, to prevent coalescence of positive results) 4. The vaccinostyle / a sterile needle no. 26 should not be inserted so deep (1mm) at about a 45° angle into the superficial skin 5. About 20 minutes, observe the test sites for erythema and wheal formation (WF reaction) 5. Grading and interpretation : based on the diameter WF Although many grading systems, consistency and familiarity with the system are most important. 1. Negative = no WF formation / diameter < 3 mm 2. +1 = WF formation with diameter ³ 3 mm 48 Study Guide Immune System and Disorders 3. +2 = WF formation with diameter 4-6 mm 4. +3 = WF formation with diameter > 6 mm A negative control: a test using deluent solution (coca solution) A positive control: a test using 0.1% histamine solution Learning task Famale 17 years old, suffers from shortness of breath recurrently especially in the midnight. Her mother has a history of asthma bronchiale. On the Skin Prick Test we found: + 4 for allergen house dust, + 2 for allergen nut, + 2 for allergen eggs. Task 1. Please describe completely the Skin Prick Test result! 2. Comprehend the clinical application! 3. How to manage and give some education! Self assessment 1. 2. 3. 4. 5. Describe the skin test type! Indication and preparation of the skin test (SPT) Comprehend the immunopathophysiology of the Skin test How to interpret the Skin test result Comprehend the clinical application of the skin test. STUDENT PROJECT SGD NO TOPICS SUPERVISORS ENG REG 1 Immunomodulator 1,2 1,2 Dr. dr. Made Jawi, M.Kes 2 Urtikaria and Angiodema 3,4 3,4 dr. Ketut Suardamana, Sp.PD-KAI. 3 Blood Group Incompatibility 5,6 5,6 Dr.dr. Wy Putu Sutirta Yasa, M.Si. 4 Limphadenitis TB 7,8 7,8 dr. Putu Sriwidnyani, Sp.A. 5 Steven Johnson Syndrome 9,10 9,10 dr. Komang Suryawati, Sp.KK. Regulation for Student Project 1. Each small group discussion must make a scientific writing from four topics has been given. 2. Each small group discussion must present their scientific writing. 3. Each small group discussion must collect their scientific writing after paper presentation. 4. Student project will be contribute 20% in to the final result. 49 Study Guide Immune System and Disorders ~ CURRICULUM MAP ~ Smstr Program or curriculum blocks 10 Senior Clerkship 9 Senior Clerkship 8 Senior clerksh ip 7 Medical Emergency (3 weeks) Special Topic: -Travel medicine (2 weeks) Elective Study III (6 weeks) Clinic Orientation (Clerkship) (6 weeks) 6 BCS (1 weeks) The Respiratory System and Disorders (4 weeks) The Cardiovascular System and Disorders (4 weeks) The Urinary System and Disorders (3 weeks) The Reproductive System and Disorders (3 weeks) BCS (1 weeks) Alimentary & hepatobiliary systems & disorders (4 Weeks) BCS (1 weeks) The Endocrine System, Metabolism and Disorders (4 weeks) BCS (1 weeks) Clinical Nutrition and Disorders (2 weeks) BCS (1 weeks) BCS (1 weeks) Musculoskeletal system & connective tissue disorders (4 weeks) Neuroscience and neurological disorders (4 weeks) Behavior Change and disorders (4 weeks) BCS (1 weeks) Hematologic system & disorders & clinical oncology (4 weeks) BCS (1 weeks) Immune system & disorders (2 weeks) BCS(1 weeks) Infection & infectious diseases (5 weeks) BCS (1 weeks) The skin & hearing system & disorders (3 weeks) BCS (1 weeks) Medical Professionalism (2 weeks) BCS(1 weeks) Evidence-based Medical Practice (2 weeks) BCS (1 weeks) Health Systembased Practice (3 weeks) BCS(1 weeks) Community-based practice (4 weeks) - Medical communication (3 weeks) BCS (1 weeks) The cell as biochemical machinery (3 weeks) Growth & development (4 weeks) BCS (1 weeks) BCS(1 weeks) BCS: (1 weeks) BCS (1 weeks) Elective Study II (1 weeks) 5 4 3 2 1 BCS (1 weeks) Studium Generale and Humaniora (3 weeks) BCS (1 weeks) Special Topic : - Palliative medicine -Compleme ntary & Alternative Medicine - Forensic (3 weeks) Elective Study II (1 weeks) Special Topic - Ergonomi - Geriatri (2 weeks) Elective Study I (2 weeks) The Visual system & disorders (2 weeks) Pendidikan Pancasila & Kewarganegaraan (3 weeks) 50 Study Guide Immune System and Disorders References 1. Fawcett DW, Jensh RP: Bloom & Fawcett’s CONCISE HISTOLOGY, 2nd ed. London, Arnold. 2002 2. Cotran RS, Kumar V, Collins: Robbins Pathologic Basis of Disease. Sixth ed. Philadelphia, WB Saunders Company. 2003. 3. Roitt IM, Brostoff J, Male D: Immunology 5th ed. Philadelphia, Mosby. 2000. 4. Fischbach F: A Manual of Laboratory & Diagnostic Test, 6th ed. Philadelphia, Lippincott, 2000 5. Trevor AJ, Katzung BG, Master SB: Katzung & Trevor’s Pharmacology. Sixth ed. New York, Lange Medical Books/Mc Graw-Hill, 2002. 6. Lange MD, PhD; Garry N. Holland MD,; Kirk R. Wihelmus, MD (Ocular Infection & Immunity) 7. Abbas AK, Lichtman AH: Immune BASIC IMMUNOLOGY Functions and disorders of the immune system. Second Eds. Philadelphia, Saunders, 2004. 8. Norton JA, Bollinger RR, Chang AE, Lowry SF, Mulvihil SJ, Pass HI, Thomson RW. Eds SURGERY Basic Science and Clinical Evidence, New York. Springer-Verlag, Inc. 2001. 9. Victor M, Ropper AH. Principles of Neurology. Seventh edition, New Tork. McGraw-Hill. 2001. 10. Bradly WG, Daroff RB, Fenichel GM, Marsden CD. Neurology in Clinical Practice. Second Edition. Boston. Butterworth-Heinemann 1995. 11. Marshal KG, Attia E. Disorders of The Nose and Paranasal Sinuses, Diagnosis and Management. USA. PSG Publishing Company, Inc. 1987. 12. Kasper DL, Fauci AS, Longe DL, Braunwald E, Hauser SL, Jameson JL. Harrison’s Principles of Internal Medicine. 16th edition, McGrwa-Hill, New York. 2005. 13. Lawlor GJ, Fischer TJ, Adelman DC. Manual of Allergy and Immunology. 4th edition/3th edition? 51 Study Guide Immune System and Disorders 52
