2015
FACULTY OF
MEDICINE UDAYANA
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 teaching-learning 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
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
CURRICULUM
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
PLANNERS TEAM
No Name Department Phone
2 dr.Sari Wulan DS, SpTHT-KL (Secretary) ENT 081237874447
3 dr. Ketut Suardamana, SpPD-KAI (Member)
Internal Medicine 08123985811
4 dr. I Wayan Surudarma, M.Si (Member) Biochemistry 081338486589
5 Dr.dr. Ketut Suryana, Sp.PD-KAI (Member)
Internal Medicine 08123960964
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 081916262663
12 dr.Komang Suryawati, Sp.KK (Member) Dermatology 0817447279
13 dr. Henky, SpF (Member) Forensic 081916613459
LECTURERS
No Name Department Phone
1 Dr.dr. Ketut Suryana, Sp.PD-KAI Internal Medicine 08123960964
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
6 Dr.dr. B. K. Satriyasa, M.Repro Pharmacology 0818053689
7 dr. Dewi Kumarawati, Sp.A Pediatrics 03617442593
10 dr. I Wayan Juli Sumadi, Sp.PA Pathology Anatomy 081916262663
11 dr. Ketut Suardamana, Sp.PD-KAI Internal Medicine 08123985811
12 Prof. Dr.dr. Tuti Parwati M, Sp.PD-KPTI Internal Medicine 08123806626
13 dr. Sari Wulan Dwi Sutanegara , Sp.THT-KL (Secretary)
ENT 081237874447
081338466039
14 Prof.Dr. dr. AA Raka Sudewi, Sp.S 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
FACILITATORS
(REGULAR CLASS)
N
O
NAME
GROUP
DEPT
PHONE
VENUE
1 dr. I Made Dwijaputra Ayustha, Sp.Rad
1 Radiology 08123670195 3nd floor:
R.3.09
Sp.PK Pathology R.3.10 3 dr. Nyoman Astika,
Sp.PD-Kger-FINASIM
3 Interna 08123974128 3nd floor:
R.3.11 4 dr. Ketut Agus Somia,
Sp.PD-KPTI
4 Interna
08123989353 3nd floor:R.3.12 5 dr. I Gde Haryo Ganesha,
S.Ked
5 DME 081805391039 3nd floor:
R.3.13 6 dr. I Gede Sastra Winata,
M.Biomed, Sp.OG 6 Obgyn 081338713951 3nd floor:R.3.14
7 dr. I Gusti Ngurah Wien Aryana , Sp.OT
7 Orthopaedi 0811385263 3nd floor:
R.3.15 8 dr. Pontisomaya Parami, Sp.An,
MARS
8 Anasthesi 08123661312 3nd floor:
R.3.16 9 dr. I Made Oka Adnyana, Sp.S
(K)
9 Neurology
0817347697 3nd floor:R.3.17 10 dr. Ketut Suardamana,
Sp.PD-KAI
10 Interna 08123985811 3nd floor:
R.3.19
FACILITATORS (ENGLISH CLASS)
NO NAME GROUP DEPT PHONE VENUE
1 dr. I Made Susila Utama, Sp.PD-KPTI
1 Interna 08123815025 3nd floor:
R.3.09 2 dr. I Gusti Ngurah Purna Putra,
Sp.S (K)
2 Neurology 08123915769 3nd floor:
R.3.10 3 Dr.dr I Nyoman Gede Budiana,
Sp.OG (K)
3 Obgyn 08123997401 3nd floor:
R.3.11 4 Prof.Dr.dr.I Putu Gede
Adiatmika, M.Kes
4 Fisiology 08123811019 3nd floor:
R.3.12 5 dr. Komang Andi Dwi Saputra,
Sp.THT- KL
5 ENT 081338701878 3nd floor:
R.3.13 6 Dr. dr. I Dewa Made Sukrama,
MSi, Sp.MK(K)
6 Microbiology 081338291965 3nd floor: R.3.14 7 dr. I Gusti Ayu Sri Darmayani,
Sp.OG
7 DME 081338644411 3nd floor:
R.3.15 8 Dr.dr. Yenny Kandarini,
Sp.PD-KGH-FINASIM
8 Interna 08123805344 3nd floor:
R.3.16 9 dr. I Gede Budhi Setiawan,
Sp.B(K)Onk
9 Surgery 08123923956 3nd floor:
R.3.17 10 dr. Henky, Sp.F., M.BEth,
FACLM
10 Forensic 08123988486 3nd floor:
TIME TABLE OF THE BLOCK IMMUN SYSTEM & DISSODERS 2015
DAYS / DATE
TIME ACTIVITY CONVEYER VENUE
ENGLISH CLASS REG CLASS
1 Friday, Oct 16,
2015
08.00-09.00 (60’) 09.00-10.00 (60’) • Introduction to The Immune System and disorders
• Dr. dr. Ketut Suryana, SpPD-KAI
Class Room
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 (SP): paper preparation
-
-14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. dr. Ketut Suryana, SpPD-KAI
Class Room
2 Monday,
Oct 19, 2015
08.00-08.30 (30’)
08.30-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Comprehend The Microscopic Structure of Limphoid Organ,Immune Cells and MHC
• Comprehend tissue repair
• Comprehend basic mechanism of autoimmunity
• dr. Ni Made Linawati, MSi
• dr. Putu Sri Widyani, S.PA.
Class Room
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 (SP) : paper preparation
- Library
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • dr. Ni Made Linawati, Msi
• dr. Putu Sri Widyani, S.PA.
Class Room
3 Tuesday,
Oct 20, 2015
08.00-08.30 (30’)
08.30-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Comprehend acute and chronic inflammation
• Comprehend hypersensitivity
• Dr. I Wayan Juli Sumadi, Sp.PA.
• Dr.Tjok Istri Anom Saturti, SpPD
Class Room
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
-12.30-14.00 (90’) 10.00-11.30 (90’) SP: paper preparation - Library
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. I Wayan Juli Sumadi, Sp.PA.
• Dr.Tjok Istri Anom Saturti, SpPD
Class Room
4 Wednes
day, Oct 21,
2015
08.00-08.30 (30’)
08.30-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Comprehend basic mechanism of drug allergy and
immunopharmacology
• Forensic Laboratory
• Dr. I Made Jawi, M.Kes
•
• dr Henky, SpF
Class Room
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 • Dr. I Made Jawi, M.Kes
• dr. Henky, SpF
Class Room
5. Thursda
y, Oct 22,
2015
08.00-09.00 (60’) 09.00-10.00 (60’) • Adverse drug reaction
• Able to diagnose and manage anaphylaxis
• Dr. Ketut Suardamana, SpPD-KAI
Class Room
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 • Dr. Ketut Suardamana, SpPD-KAI
Class Room
6. Friday, Oct 23,
2015
08.00-08.30 (30’)
08.00-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Comprehend laboratory test of immune system
• Antihistamine
• Dr. dr. I Wyn Putu Sutirta Yasa, Msi
• Dr.dr.B.K.Satriyasa,M. Repro
Class Room
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 -
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. dr. I Wyn Putu Sutirta Yasa, Msi
• Dr.dr.B.K.Satriyasa, M.Repro
Class Room
7. Monday,
Oct 26, 2015
08.00-08.30 (30’)
08.00-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Able to diagnose and manage allergic diseases in ENT
• Able to diagnose and manage allergic diseases in dermatology
• Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL
• -Dr.Nyoman Suryawati, SpKK
Class Room
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: Urtikaria and Angiodema
dr. K Suardamana,
SpPD-KAI Class Room
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL
• Dr.Nyoman Suryawati, SpKK
Class Room
8. Tuesday,
Oct 27, 2015
08.00-09.00 (60’) 09.00-10.00 (30’) • Able to diagnose and manage SLE, RA & Polimyalgia Rheumatica
• Dr. Gede Kambayana, SpPD-KR
Class Room
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 Group Incompatibility
Dr.dr. Wy Putu Sutirta Yasa, M.Si.
Class Room
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Dr. Gede Kambayana, SpPD-KR
Class Room
9. Wednes
day, Oct 28,
2015
08.00-08.30 (30’)
08.00-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Able to diagnose and manage autoimmune diseases in Neurology
• Able to diagnose and manage secondary immunodeficiency diseases (focus HIV)
• Prof. Dr. dr AA Raka Sudewi, Sp S
• Prof. DR. Dr. Tuti Parwati M, SpPD-KPTI
Class Room
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
-12.30-14.00 (90’) 10.00-11.30 (90’) SP paper presentation: Limphadenitis TB
dr. Putu Sriwidnyani, Sp.A
Class Room
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session • Prof. Dr. dr AA Raka Sudewi, Sp S
• Prof. DR. Dr. Tuti Parwati M, SpPD-KPTI
Class Room
10 Thursda
y, Oct 29,
2015
08.00-08.30 (30’)
08.00-09.00 (30’)
09.00-09.30 (30’)
09.30-10.00 (30’)
• Able to diagnose and manage Rheumatic Disease of Childhood
• Able to diagnose and manage Food allergy
• Able to diagnose and manage immunodeficiency diseases in childhood
• Dr. Dewi Kumarawati, SpA
Class Room
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 Johnson Syndrome
dr. Komang Suryawati, Sp.KK
.
Class Room
14.00-15.00 (60’) 15.00-16.00 (60’) Plenary Session Dr. Dewi Kumarawati, SpA
Class Room
11. Friday, Oct 30,
2015
08.00-09.00 (60’) 09.00-10.00 (60’) Soluble markers of allergic inflammation (BCS)
dr. Wande, Sp.PK. 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
dr. Wande, Sp.PK & Team
Skill Lab 13.00-15.00 (120’) 11.30-13.30 BCS Discussion
12. Monday, Nop 02, 2015
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
Dr. Henky , SpF, & Team
Skill Lab 13.00-15.00 (120’) 11.30-13.30 BCS Discussion
Nop 03,
2015 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
Dr. Tjok Istri Anom S, SpPD & Team
Skill Lab 13.00-15.00 (120’) 11.30-13.30 BCS Discussion
14 Wednes
day Nop 04,
2015
08.00-09.00 (60’) 09.00-10.00 (60’) Morphology of Acute & Chronic Imflamation (BCS)
Dr. Putu Sri Widyani , Sp.A
Class Room
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
Dr. Putu Sri Widyani ,
Sp.A & Team LAB Bersama 13.00-15.00 (120’) 11.30-13.30 BCS Discussion
15 Thursda
y, Nop 05,
2015
08.00-09.00 (60’) 09.00-10.00 (60’) Skin Prick Test (BCS) Dr. Ketut Suryana, SpPD-KAI
Class Room
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
Dr. Ketut Suryana, SpPD-KAI & Team
Skill Lab 13.00-15.00 (120’) 11.30-13.30 BCS Discussion
Friday, Nop 06,
2015
Pre-evaluation Break
Monday, Nop 9,
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
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. Comprehend of immune system with clinical implications
2. Comprehend the lymphoid organs and describe of it’s microscopic organization 3. Comprehend the cellular immunity
4. Comprehend the mechanism of cellular and humoral immunity to infection
Day 1
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
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
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
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
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 back-mechanisms 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.
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
(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.
Type II : 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.
Type III : 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
Type IV : 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
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
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?
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?
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
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
. DefinitionAnaphylaxis is an acute severe, life-threatening, generalized or systemic hypersensitivity reactions
Pathophysiology
1. Type I reaction (IgE mediated)
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. What should you do for the first? 2. Could you complete your anamnesis! 3. What do you find on physical examination?
4. 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!
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 antigen-antibody 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
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. Explain two classification of H1 blockers
2. List two drugs the older members of the first generation agent 3. List three drugs the second generation of H1 blockers.
4. Describe mechanism and effect of H1 blockers 5. 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
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
Topic
:
Rhinitis Alergy
Lecturer
:
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), post-nasal drip, post-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.
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. Please do further anamnesis in this case!
2. If in the anamnesis his mother had asthma, what is the possible diagnosis of this case?
3. What is/are the differential/s diagnosis of this case? 4. What is/are the complication/s of this case?
5. How is the management of this case?
Self Assessment
1. What is the definition of allergy rhinitis?
2. What are the symptom and sign of allergy rhinitis? 3. How is the classification of allergy rhinitis?
4. 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.
of interferon gamma, Increased eosinophils, Elevated levels of IgEactivated mast cells. Clinical feature of AD, there are three stages under the different age groups:
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.
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.
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
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. Could you complete the anamnesis! 2. Describe the physical diagnostic!
3. Base on the anamnesis and physical diagnostic, the working diagnosis of this patient?
4. Describe the differential diagnosis! 5. Describe other laboratory test
6. Where should you reffer this patient?
Self assessment
1. Describe the definition of rheumatoid arthritis! 2. Describe the etiopathogenesis of AR!
3. Describe the pathological aspect of AR! 4. Describe the clinical manifestation of AR! 5. Describe the laboratory test for AR! 6. Describe the diagnostic criteria of AR! 7. 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.
resulting in abnormal immune responses.
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. Please you complete the anamnesis! 2. Describe the physical examination!
3. If she also complains edema on whole body, what is the working diagnosis? 4. Describe the differential diagnosis!
5. Where should you reffer this patient?
Self assessment
1. Describe the definition of SLE!
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. Please explore another history to complete anamnesis! 2. What kind of clinical examination will you do?
3. What was the diagnosis of this patient?
4. What kind of clinical manifestation based your diagnosed? 5. Describe your plans of diagnosis for this patient?
6. Describe your plans of therapy for this patient?
7. Describe your plans of education for this patient or his family? 8. 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!
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. Please explore another history to complete anamnesis! 2. What kind of clinical examination will you do?
3. What was the diagnosis of this patient?
4. What kind of clinical manifestation based your diagnosed? 5. Describe your plans of diagnosis for this patient!
6. Describe your plans of therapy for this patient!
7. Describe your plans of education for this patient or his family! 8. 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)
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 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. Complete history taking of this patient which can lead you closer to the case-diagnosis
2. Describe physical examination to support diagnosis of this patient 3. Describe laboratory and other examination to support diagnosis 4. Describe principle management of this patient
5. Define plan of therapy based on priority for this patient
Self assessment
1. What is the definition of secondary immune deficiency?
2. What is opportunistic infection? Named some example of opportunistic infection. 3. What are the diagnosis criteria for HIV infection/AIDS?
4. What kind of antiretroviral therapy (ART) does available for patient?
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 f
