Study Guide Immune Semester III Tayang 1 November 2016

Study Guide Immune System and Disorders
CONTENTS
Contents ...1
Foreword
...
....2
Curriculum ........3
Block Team ......4
Facilitators Team .....6
Time Table .........................7
Meeting of student representatives 12
Meeting of facilitators 12
Assessment Method ..
12
Learning Program .13
Student Project ..43
References .44
Curriculum Mapping..45
Udayana University Faculty of Medicine, DME, 2016
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

ISD
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
PLANNERS TEAM
No
Name
Department
Phone
Internal Medicine
082145854167
ENT
081237874447
dr. Tjok Istri Anom S, SpPD (Head)
dr.
Sari
(Secretary)
dr. Ketut Suardamana, SpPD-KAI

(Member)
Internal Medicine
08123985811
Dr. dr. Ketut Suryana, Sp.PD-KAI

(Member)
Internal Medicine
08123960964
dr. I Made Sudipta, Sp.THT (member)
ENT
08123837063
dr. Made Wardana, Sp.KK (member)
Dermatology
08563704591
dr. Dewi Kumarawati, Sp.A (member)
Pediatrics
03617442593
dr. Putu Sri Widnyani, Sp.PA (member)
Pathology Anatomy
081337115012
10
Dr. dr. Ni Made Linawati, M.Si (member)
Histology
081337222567
11
dr. Komang Suryawati, Sp.KK (Member)
Dermatology
0817447279
Department
Phone
Internal Medicine
08123960964
Histology
081805629937
Pathology Anatomy
081337115012
Pediatrics
081239559559
Clinical Pathology
03617428983
Wulan
DS,
SpTHT-KL
LECTURERS
No
Name
Dr. dr. Ketut Suryana, Sp.PD-KAI
Dr. dr. Ni Made Linawati, Msi
Dr. dr. Putu Sri Widnyani, Sp.PA
dr. Komang Ayu Witarini,SpA
Dr. dr. I Wyn Putu Sutirta Yasa, Msi

6
Dr. dr. I Made Jawi, M.Kes
Pharmacology
08179787972
Dr. dr. B. K. Satriyasa, M.Repro
Pharmacology
087777790064
dr. Komang Suryawati, Sp.KK
Dermatology
0817447279
dr. Ketut Suardamana, Sp.PD-KAI
Internal Medicine
08123985811
10
Prof. Dr. dr. Tuti Parwati M, Sp.PD-KPTI
Internal Medicine
08123806626
11
dr. Sari Wulan Dwi Sutanegara , Sp.THTKL
ENT
081237874447
081338466039
12
dr. Susilawathi,SpS
Neurology
08124690137
13
dr. Gede Kambayana, Sp.PD-KR
Internal Medicine
08124683416
14
dr. Tjok Istri Anom S, SpPD
Internal Medicine
82145854167
15
Dr. dr. Nyoman Wande, Sp.PK
Clinical Pathology
08124686885
16
dr. Pande Ketut Kurniari,SpPD
Internal Medicine
082146179796
17
dr. IB Putu Alit, SpF, DFM
Forensic
081916613459
18
Dr. dr. I Wayan Putu Sutirta

Yasa, Msi
Clinical Pathology
08123953344
FACILITATORS
(REGULAR CLASS)
NO
NAME
GROUP
DEPT
PHONE
VENUE
2nd floor:
R.2.01
2nd floor:
R.2.02
2nd floor:
R.2.03
2nd floor:
R.2.04
2nd floor:
R.2.05
2nd floor:
R.2.06
Prof.Dr.dr.I Putu Adiatmika M.Kes
A1
Physiology
08123811019
dr.I A Dewi Wiryanthini M.Biomed
A2
Biochemistry
081239990399
A3
Ophtalmology
081816513322
A4
Microbiology
08553711398
dr. Ni Made Laksmi Utari,

M.Biomed, SpM
Dr.dr. Ni Nyoman Sri Budayanti,
Sp.MK (K)
dr.Yukhi Kurniawan, Sp.And
A5
Andrology
08123473593
dr.I Putu Bayu Mayura, S.Ked
A6
Microbiology
082236465801
Dr.dr. AA Mas Putrawati T Sp.M (K)
A7
Ophtalmology
08123846995
Dr.dr. Susy Purnawati, M.KK
A8
Physiology
08123989891
dr. Putu Yuliandari, S.Ked
A9
Microbiology
089685415625
10
dr.I N Gede Wardana M.Biomed
A10
Anatomy
087860405625
2nd floor:
R.2.07
2nd floor:
R.2.08
2nd floor:
R.2.21
2nd floor:
R.2.22
FACILITATORS
(ENGLISH CLASS)
NO
1
NAME
GROUP
DEPT
PHONE
dr. I G A Artini M.Sc
B1
Farmacology
0812650481
dr. I Wayan Sugiritama M.Kes
B2
Histology
08164732743
dr. Agung Nova Mahendra, M.Sc
B3
Pharmacology
087861030195
dr. Yuliana, M.Biomed
B4
Anatomy
085792652363
Biochemistry
081337141506
Fisiology
081337761299
2
3
4
5
Dr.rer.Nat. dr. Ni Nyoman Ayu Dewi,

M.Si
dr. I Dewa Ayu Inten Dwi
Primayanti, M.Biomed
B5
B6
7
Dr.dr. Ni Made Linawati, M.Si
B7
Histology
081337222567
VENUE
2nd floor:
R.2.01
2nd floor:
R.2.02
2nd floor:
R.2.03
2nd floor:
R.2.04
2nd floor:
R.2.05
2nd floor:
R.2.06
2nd floor:
R.2.07
6

8
dr. I Nyoman Wiryawan Sp.JP FIHA
B8
Cardiology
081289053234
Dr. dr. G N Indraguna P
B9
Public Health
08123816424
dr. Muliani, M.Biomed
B10
Anatomy
085103043575
2nd floor:
R.2.08
2nd floor:
R.2.21
2nd floor:
R.2.22
9
10
TIME TABLE OF THE BLOCK IMMUNE SYSTEM & DISSODERS 2016

DAYS /
DATE
TIME
ENGLISH
CLASS
Tuesday,
Nov 1, 2016
Wednes
day, Nov
2, 2015
ACTIVITY
CONVEYER
VENUE
REG CLASS
Introduction to The
Immune System and
disorders
Independent Learning
Library
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
Discussion
Room
14.00-15.00
(60)
08.00-08.30
(30)
15.00-16.00
(60)
09.00-09.30
(30)
Plenary Session
Class Room
Dr. dr. Ketut
Suryana, SpPD-KAI
Dr. dr. Ni Made
Class Room
Linawati,
MSi
08.30-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
10.30-12.00
(90)
12.00-12.30
(30)
12.30-14.00
(90)
12.00-13.30
(90)
13.30-15.00
(90)
11.30-12.00
(30)
10.00-11.30
(90)
Library
SGD
Fasilitator
Discussion
Room
-
Student Project (SP) : paper

preparation
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Dr. dr. Ni Made

Linawati, MSi
Dr. dr. Putu Sri
Widyani, SpPA
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
09.00-10.30
(90)
12.00-13.30
(90)
10.30-12.00
(90)
Comprehend The
Microscopic
Structure of Limphoid
Organ,Immune
Cells and MHC
Comprehend basic
mechanism of autoimmunity
Class Room
Dr. dr. Ketut
Suryana, SpPD-KAI
Dr. dr. Putu Sri

Widyani, SpPA
Break

Thursday,
Nov3,
2016
Friday,
Nov 4,
2016
Comprehend basic
mechanism of drug
allergy
Immunopharmacology
Dr. dr. I Made

Jawi,M.Kes
Class Room
12.00-13.30
(90)
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
Discussion
Room
14.00-15.00
(60)
08.00-08.30
(30)
15.00-16.00
(60)
08.30-09.00
(30)
Plenary Session
Class Room
Dr. dr. I Made
Jawi,
Dr. dr. I Wayan Putu Class Room
Sutirta
Yasa, Msi
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)
Monday,
Nov7,
2016
Comprehend
laboratory test of
immune system
08.30-10.00
(90)
09.00-10.30
(90)
Library
10.00-11.30
(90)
10.30-12.00
(90)
SGD
Fasilitator
Discussion
Room
11.30-12.00
(30)
12.00-12.30
(30)
Break
12.00-13.30
(90)
12.30-14.00
(90)
SP paper preparation
Discussion
Room
13.30-14.30
(60)
14.30-15.30
(60)
Plenary Session
08.00-08.30
(30)
08.30-09.00
(30)
09.00-09.30
(30)
09.30-10.00
(30)
Comprehend hypersensifity
dr. Tjok Istri Anom

Class Room
Saturti, SpPD
Dr. dr. B. K. Satriyasa,
M.Repro
09.00-10.30
(90)
12.00-13.30
(90)
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

imunomodulator
Class Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
dr. Tjok Istri Anom

Class Room
Saturti, SpPD
Dr. dr. B. K. Satriyasa,
M.Repro
Antihistamin
Sutirta
Yasa, Msi

Tuesday,
Nov 8, 2016
Wednes
day, Nov 9,
2016
Thursday,
Nov 10,
2016
08.00-09.00
(60)
09.00-10.00
(60)
Adverse drug reaction

Able to diagnose and
manageanaphylaxis
dr. Ketut
Suardamana,
SpPD-KAI
Class Room
09.00-10.30
(90)
12.00-13.30
(90)
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
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-08.30
(30)
09.00-09.30
(30)

manage allergic
diseases in ENT
08.00-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
12.00-13.30
(90)
manage allergic
diseases in dermatology
dr. Ketut
Suardamana,
SpPD-KAI
dr. Sari Wulan
Dwi
Sutanegara, Sp
THT (K)
dr.Nyoman
Suryawati,
SpKK
-
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. Nyoman
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
dr. Sari Wulan

Dwi
Sutanegara, Sp
THT (K)
dr.Nyoman
Suryawati,
SpKK
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
Able to diagnose and manage

SLE, Rheumatoid Arthritis &
Polimyalgia Rheumatica
dr.Gede
Kambayana,SpP
D-KR / dr.Pande
Ketut
Kurniari,SpPD
Class Room
09.00-10.30
(90)
12.00-13.30
(90)
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
Class Room
dr.Ketut
Suardamana,SpPDKAI
Class Room
Library
Suryawati,
SpKK
Friday,
Nov 11,
2016
Monday,
Nov14,
2016
dr.Gede
Kambayana,SpP
D_KR/dr.Pande
Ketut
Kurniari,SpPD
Prof. Dr. dr. Tuti
Parwati
M, SpPD-KPTI
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
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)

manage
secondary
immunodeficiency diseases
(focus HIV)
manage
autoimmune
diseases in
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: Rhinitis

Allergy
Class Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
08.00-08.30
(30)
09.00-09.30
(30)

manage
Rheumatic Disease of
Childhood
dr.Sari Wulan Dwi

Sutanegara,SpTH
T
Prof. Dr. dr. Tuti
Parwati
M, SpPD-KPTI
dr. Komang Ayu
Witarini,SpA
08.00-09.00
(30)
09.30-10.00
(30)

manage Food
allergy
Class Room
dr.Susilawathi,SpS
Class Room
Class Room

manage
immunodeficiency
diseases in
childhood
09.00-10.30
(90)
12.00-13.30
(90)
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

SutirtaYasa, Msi
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
dr. Komang Ayu

Witarini,SpA
Class Room
08.00-09.00
Tuesday,
Nov 15, 2016 (60)
09.00-10.00
(60)
Laboratory Test For

Allergy And Autoimune
Disease (BCS)
Dr.dr. I Wayan
Wande, Sp.PK
Class Room
09.00-10.30
(90)
10.30-13.00
(150)
10.00-11.30
(90)
13.30-16.00
(150)
Library
BCS Training
Dr.dr. I Wayan
Wande, Sp.PK
& Team
Skill Lab
10

13.00-15.00
(120)
08.00-09.00
(60)
11.30-13.30
BCS Discussion
09.00-10.00
(60)
Forensic Serology & Molecular
dr. IB Putu Alit, SpF, Class Room

DFM
09.00-10.30
(90)
10.00-11.30
(90)
Library
10.30-12.00
(90)
11.30-13.00 (90) SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
13.00-13.30
(30)
Break
12.30-13.30
(60)
13.30-15.00
(90)
Plenary Session
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
Anaphylactic Syok (BCS)
dr. IB Putu Alit, SpF,

DFM
dr. Tjok Istri Anom
Saturti, SpPD
09.00-10.30
(90)
10.00-11.30
(90)
Library
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
dr. Tjok Istri Anom Skill Lab

Saturti, SpPD
13.00-15.00
(120)
11.30-13.30
BCS Discussion
08.00-09.00
(60)
09.00-10.00
(60)
SLE, RA focus on physical

examination (BCS)
dr.Gede
Kambayana,SpPDKR / dr.Pande Ketut
Kurniari,SpPD
09.00-10.30
(90)
10.00-11.30
(90)
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
13.00-15.00
(120)
11.30-13.30
BCS Discussion
08.00-09.00
Monday,
Nov 21, 2016 (60)
09.00-10.00
(60)
Skin Prick Tes
Library
dr.Gede
Kurniari,SpPD
Skill Lab
dr.Gede
Kurniari,SpPD
Dr. dr. Ketut
Suryana, SpPD-KAI
09.00-10.30
(90)
10.00-11.30
(90)
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
Dr. dr. Ketut

Suryana, SpPD-KAI
13.00-15.00
(120)
11.30-13.30
BCS Discussion
Dr. dr. Ketut

Suryana, SpPD-KAI
Wednes
day,
Nov 16,
2016
Thursday,
Nov 17,
2016
Friday,
Nov 18,
2016
Tuesday,
Nov 22, 2016
Class Room
Class Room
Class Room
Pre-evaluation Break
11

Examination
Wednes
day,
Nov 23,
2016
Meeting of the student representatives

The meeting between block planners team and the student group representatives will be held
on Friday November 18, 2016 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,
Friday November 18 at 10.00 am until 12.00 pm at HPEQ 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 9 th 2015. There are 100
questions for the examination that consists of Multiple Choice Question (MCQ). The borderline
to pass exam is 70.
12
LEARNING PROGRAMS
Day 1
Topics
Introduct. to the immune system and disorders
Lecturer
Dr.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 its microscopic organization
Comprehend the cellular immunity
Comprehend the mechanism of cellular and humoral immunity to infection
13
Day 2
Topic
Lecturer
:The Microscopic Structure of Limphoid Organ,

Immune Cells and Histocompatibility Molecule
: 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
Topic
Basic mechanism of autoimmunity
Lecturer
Dr. dr. Putu Sri Widyani, SpPA
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 ones own tissue
antigens.
14

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.
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.
2.
Describe the mechanism of immunological tolerance to self antigent!

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.
6.
Describe the mechanism of tissue injury in SLE, and give some examples of
morphological changes in SLE!
Mention other diseases that belong to autoimmune diseases group!
15
Day 3
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), AntiTNF- 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.
Explain the immunologic mechanism of those problems.
To manage that patient what medicine will you give for him immediately?
Explain your answer if you give him prednisone. Do you agree? Why?
How about antihistamine like dimenhydrinate for this patient?
Self assessment
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
16

E. Prednisone
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
Day 4
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.
17
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
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
1. Mention the principle of methods on immunoassay techniques?
2. Whats 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?
Day 5
Topic
Lecturer
Hypersensitivity
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 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 shock
2. Atopy: genetic factor to induce by exposure to spesific allergens (pollens,
dust, shellfish, nuts, etc). Clinical manifestation: hay fever, asthma,
18
Type II
Type III
Type IV
eczema, and urticaria. Treatment and prevention: Avoidance of the

responsible allergen, Hyposensitization (Desensitization) & Drug
treatment.
: Antibody is directed against antigen on an individuals 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
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
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
19
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.
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
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
20
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 6
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 reexposure
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 : Blockers, asthma, pregnancy
Diagnosis
1.
Diagnosis of drug allergy based on ;
2.
Clinical history
21

3.
4.
Clinical manifestations
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
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,SpPD-KAI
Definition
Anaphylaxis is an acute severe, life-threatening, generalized
reactions
or systemic hypersensitivity
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
Clinical Criteria for Diagnosing Anaphylaxis
(Sampson HA, et al. JACI 2006)
22

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
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!
23
Day 7
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), 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.
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
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?
24

4. What is/are the complication/s of this case?
5. 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 Disease 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:
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.
25
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.
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
26

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?
Day 8
Topic
Lecture
: - RHEUMATOID ARTHRITIS
- SYSTEMIC LUPUS ERYTHEMATOSIS ( SLE )
- Polimyalgia Rheumatica
:
dr. Gede Kambayana, Sp PD-KR / dr. Pande Ketut Kurniari,SpPD

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.
27

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.
Diagnosis
Revised Criteria for the classification of RA (1987 );
1. Morning stiffness ( > 1 jam )
2. Arthritis ( 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
28

1.
2.
3.
4.
5.
6.
7.
Topic
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!
:
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.
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+, or cellular casts
8. Neurologic disorder
9. Hematologic disorder
10. Immunologic disorder
11. Antinuclear antibodies (ANA test )
If 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.
29
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.
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!
Day 9
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
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.
30

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?
TOPIC
: GUILLAIN BARRE SYNDROM, MYASTHENIA GRAVIS

MULTIPLE SCLEROSIS
LECTURER
: dr. NI MADE SUSILAWATHI, Sp.S

AUTOIMMUNE DISEASES IN NEUROLOGY
ABSTRACT
Autoimmunity is a misguided immune response to the body's own organs. The
nervous and immune systems have many interactions that dictate overall body health. The
nervous system is under constant monitoring from both the adaptive and innate immune
system. Deregulation of both adaptive and acquired immune responses, impairment of
crosstalk between these two systems as well as alterations in the deployment of innate
immune mechanisms can predispose the central nervous system (CNS) to autoimmunity
31

and neurodegeneration. Multiple sclerosis, myasthenia gravis and Guillain-Barre syndrome
(GBS) are neurologic diseases induced by abnormal autoimmunity.
Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease of
CNS. MS attack the myelinated axons in the CNS, destroying the myelin and the axons to
varying degree. The course of MS is highly varied and unpredictable. In most patients, the
disease is characterized initially by episodes of reversible neurological deficits, which is
often followed by progressive neurological deterioration over time.
Myasthenia gravis (MG) is an autoimmune disease characterized by a fluctuating
pathological weakness with remissions and exacerbations involving one or several skeletal
muscle groups, mainly caused by antibodies to the acetylcholine receptor (AChR) at the
post-synaptic site of the neuromuscular junction
Guillain-Barr syndrome (GBS) is a disorder in which the body's immune system
attacks part of the peripheral nervous system. The first symptoms of this disorder include
varying degrees of weakness or tingling sensations in the legs. In many instances the
symmetrical weakness and abnormal sensations spread to the arms and upper body.
LEARNING TASK
CASE 1
A 29-year-old woman, complaining of double vision, was found to have ptosis on the right
side. The ptosis was worse in the evening and almos absent in the morning. She
admmitted to tiredness in the arms and legs, which recovered with resting.
CASE 2
A 18-year-old boy awoke one morning 2 weeks after an episode of influenza with a mild
weakness in his legs and during the day he developed pain in his back and 'pins and
needles' in his feet. He was considerably worse the next day and complained of weakness
in his arms as well, and by the evening he was unable to stand.
Case 3
A 35 year old white female. She came to Neurology Clinic for evaluation of her long-term
neurologic complaints. The patient relates that for many years she had noticed some
significant changes in neurologic functions, particularly heat intolerance precipitating a
stumbling gait and a tendency to fall. Her visual acuity also seemed to change periodically
during several years. Two months ago the patient was working very hard and was under a
lot of stress. She got sick with a flu and her neurologic condition worsened. At that time,
she could not hold objects in her hands, had significant tremors and severe exhaustion.
She also had several bad falls. The patient abruptly developed a right hemisensory deficit
after several days of work..
TASK
1. What is the most likely diagnosis in Case 1,2 and 3
2. Describe the clinical symptoms of Myasthenia Gravis, GBS and Multiple sclerosis
3. Describe the spesific diagnostic examination and laboratory test for Myasthenia
Gravis, GBS and Multiple sclerosis
4. Describe principle management for Myasthenia Gravis, GBS and Multiple sclerosis
SELF ASSESSMENT
1. Describe the diagnosis criteria of Myasthenia gravis
2. Describe the diagnosis criteria of GBS
3. Describe the diagnosis criteria for Multiple Sclerosis
4. Describe the pathogenesis of Myasthenia Gravis, GBS and Multiple sclerosis
32

5. Describe imunologic finding in Myasthenia Gravis, GBS and Multiple sclerosis
6. Describe the prognosis of Myasthenia Gravis, GBS and Multiple sclerosis
REFFERENCE
1 Diagnostic Criteria in Autoimmune Diseases. 2008. Yehuda Shoenfeld, Ricard Cervera,
M. Eric Gershwin editors. Humana Press.
2 Neuroimmunology In Clinical Practice.2008.Bernadette Kalman and Thomas H
Brannagan III editors. Blackwell Publishing
Day 10
Immunologic Dissorders in childhood

Topic
: Food Allergy
Lecturer
: dr. Komang Ayu Witarini,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 Cows 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.
33
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?
Topic : Manage Rheumatic disease in Childhood
Lecturer
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, Ag-Ab
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
34

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?
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
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?
Day 11
35
BCS
: Laboratory diagnostic in allergic disease
Lecturer
: Dr.dr. I Wayan Wande, Sp.PK
Abstract
Allergic diseases are the result of allergic inflammation that occurs as a result of an
interaction between the environment and the patient's immune system resulting in the release
of histamine and other proinflammatory mediators.
Commonly referred to as "RAST" tests ("Radio-AllergoSorbent Test" after technology
that has been superseded by enzyme and fluorescent-based assays), these tests detect
allergen-specific IgE in the serum. Patient's serum is incubated with allergen or allergen
mixtures bound to a solid material. Allergen-specific IgE is then detected using antibodies
specific for human IgE that are labeled with either enzyme or a fluorescent compound
Learning Task
1. Mentions of invitro test for allergic diease
2. Mentions of advantages and disadvantages RAST compared with skin test
Selft Assessment
1. To knows laboratory examination for diagnostif of allergic disease
2. To knows interpretation of RAST and other examination of allergic disease
Topic 2. Laboratory diagnostic in autoimmune disease
Abstract
Laboratory testing is of great value when evaluating a patient with a suspected
autoimmune disease. The results can confirm a diagnosis, estimate disease severity, aid in
assessing prognosis and are useful to follow disease activity. Components of the laboratory
exam include complete blood count with differential, comprehensive metabolic panel,
inflammatory markers, autoantibodies, and flow cytometry. This chapter discusses these
components and includes a discussion about organ-specific immunologic diseases where
immunological laboratory testing is employed. Comprehensive laboratory evaluation of a
suspected autoimmune illness in conjunction with a thorough clinical evaluation provides a
better understanding of a patient's immunologic disease.
Examining patients for potential autoimmune diseases is fraught with difficulty because
not one laboratory test establishes such a diagnosis. Typically, multiple laboratory tests are
needed and include basic studies like a complete blood count, comprehensive metabolic
panel, acute phase reactants, immunologic studies, serologies, flow cytometry, cytokine
analysis, and HLA typing. Although some tests may be non-specific, such as the erythrocyte
sedimentation rate (ESR), they are useful to assess disease activity. These tests can be useful
in the diagnosis and management of patients with autoimmune diseases and help in providing
a prognosis, or indicate the severity of organ involvement or damage.
Learning Task
1. Why are autoimmune diseases challenging to diagnose?
2. What is the first test to be considered for a patient suspected of having an autoimmune
disease?
3. What is the significance of ANA patterns?
4. How predictive are the specific antibodies? What is their sensitivity and specificity in
various autoimmune diseases?
36

Self assessment
1. To know Initial laboratory evaluation for autoimmune diseases
2. Mentions of Inflammatory markers in autoimmune diseases
3. Mentions of Autoantibodies and Immunologic Studies in autoimmune diseases
Day 12
Topic
: Forensic Serology & Molecular
Lecture
: dr. IB Putu Alit, SpF, DFM
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 humans body and health. Moreover, based
on legislations, doctors have legal duty to carry out forensic examinationwhen 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 victims 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!
Vignette 2
37

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 13
BCS
: Anaphylactic Shock
Lecturer
: dr. Tjok Istri Anom S, SpPD
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 beta-lactam
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 lips-tongue-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
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)
38

o
o
Reduced BP or associated symptoms of end-organ dysfunction (for example,

hypotonia, syncope, incontinence)
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.
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)
39

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 mm
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.
40
PROTOCOL FOR TREATMENT OF ANAPHYLAXIS
Condition
MILD
REACTION
(May
rapidly
progress to
a
more
severe
reaction)
Observation/
Assessment
MODERAT
E
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
wheezing
Coughing
Complains of
generalized
itching, itching
throat
Generalized
urticaria (hives)
Swelling of lips,
face, tongue,
eyelids, hands,
feet, or genitalia.
Intervention (Mild and Moderate Reactions)
ABCs.
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 515 minutes, up to
3 doses, depending on patients
response
SECONDARY TREATMENT: As an
adjunct to epinephrine, give weight or
age appropriate doses of
diphenhydramine HCL orally or
intramuscularly (See Table 2 or Table
3). DO NOT GIVE diphenhydramine
HCL to infants aged less than
7 months
41
Condition
Observation/
Assessment
Vomiting, diarrhea,
and/or abdominal
pain
Intervention (Mild and Moderate Reactions)
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 patients condition at time
of transfer.
Document all measures taken in patients medical
record and place allergy label on front of patients
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.
42
STUDENT PROJECT
SGD
NO
TOPICS
SUPERVISORS
ENG
REG
Immunomodulator
1,2
1,2
Dr. dr. Made Jawi, M.Kes
Urtikaria and Angiodema
3,4
3,4
dr. Ketut Suardamana, Sp.PD-KAI.
Blood Group Incompatibility
5,6
5,6
Dr. dr. Wy Putu Sutirta Yasa, M.Si.
Rhinitis Allergy
7,8
7,8
dr. Putu Sriwidnyani, Sp.A.
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.
43
REFERENCES
1. Fawcett DW, Jensh RP: Bloom & Fawcetts CONCISE HISTOLOGY, 2 nd 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, 6 th ed. Philadelphia, Lippincott,
2000
5. Trevor AJ, Katzung BG, Master SB: Katzung & Trevors 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. Harrisons
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?
44
Smst
r
10
9
8
7
Program or curriculum blocks
BCS (1 weeks)
Senior Clerkship
Senior Clerkship
Senior Clerkship
Evidence-based
Elective Study IV
Medical
(evaluation)
Practice
(2 weeks)
(3 weeks)
Special topics :
Health
Ergonomy &
Health
Environment
(2 weeks)
The Urinary
The Reproductive
System and
System and
Disorders
Disorders
(3 weeks)
(4 weeks)
BCS (1 weeks)
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The skin &

hearing system
& disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary
systems & disorders
(3 Weeks)
BCS (1 weeks)
The Endocrine
System,
Metabolism and
Disorders
(4 weeks)
BCS (1 weeks)
Health Systembased Practice

(3 weeks)
BCS (1 weeks)
Community-based
practice
(4 weeks)
The
Cardiovascular
System and
Disorders
(3 weeks)
BCS (1 weeks)
Neuroscience and
neurological
disorders
(3 weeks)
BCS (1 weeks)
Medical Emergency
(2 weeks)
Musculoskeletal
system &
connective tissue
disorders
(3 weeks)
BCS (1 weeks)
Basic
microbiology &
parasitology
(3 weeks)
Basic Infection
& infectious
diseases
(3 weeks)
BCS (1 weeks)
Medical
communication
(3 weeks)
Basic
pharmacology
(2 weeks)
BCS (1 weeks)
Studium Generale
and Humaniora
(2 weeks)
Basic Anatomy
( 4 weeks)
Pratikum Anatomy
(1 Weeks)
BCS (1 weeks)
Immune system &
disorders
(2 weeks)
Hematologic
system &
disorder &
clinical oncology
(3 weeks)
BCS (1 weeks)
BCS (1 weeks)
Special Topic :
- Palliative med
- Complemnt &
Alternative Med.
- Forensic
(3 weeks)
Clinical Nutrition
and Disorders
(2 weeks)
Comprehen
sive Clinic
Orientation
(Clerkship)
+ medical
ethic
(4 weeks)
19 weeks
Elective
Study III
19 weeks
(3 weeks)
Elective
Study II
(2 weeks)
18 weeks
The Visual
system &
disorders
(2 weeks)
19 weeks
BCS (1 weeks)
Special Topic
- Andro & aging
- Geriatri
-Travel medicine
(4 weeks)
BCS
(1weeks)
Basic
Pharmaceut
ical
medicine &
drug etics
19 weeks
(1 weeks)
Medical
Professionalism
(2 weeks) + medical
ethic (1 weeks)
Basic Anatomy
Pathology &
Clinical pathology (3
weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(2 weeks)
Behavior
Change
and disorders
(3 weeks)
Elective Study I
(2 weeks)
19 weeks
BCS (1 weeks)
Growth &
development
(2 weeks)
19 weeks
Basic
Biochemistry
(2 weeks)
BCS (1 weeks)
Basic Histology
(2 weeks) & Basic
Physiology
(2 weeks)
BCS (1 weeks)
Pendidikan Pancasila & Kewarganegaraan ( 3 weeks )
CURRICULUM MAP
45
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Study Guide Immune Semester III Tayang 1 November 2016

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Study Guide Immune System and Disorders

Udayana University Faculty of Medicine, DME, 2016

Study Guide Immune System and Disorders

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

treatment planning on commonly allergic diseases in pediatric, internal medicine, ENT,and

( ISD ) is undertaken 19 days

Udayana University Faculty of Medicine, DME, 2016

Study Guide Immune System and Disorders

Udayana University Faculty of Medicine, DME, 2016

Study Guide Immune System and Disorders

dr. Tjok Istri Anom S, SpPD (Head)

dr. Ketut Suardamana, SpPD-KAI

Dr. dr. Ketut Suryana, Sp.PD-KAI

dr. I Made Sudipta, Sp.THT (member)

dr. Made Wardana, Sp.KK (member)

dr. Dewi Kumarawati, Sp.A (member)

dr. Putu Sri Widnyani, Sp.PA (member)

Dr. dr. Ni Made Linawati, M.Si (member)

dr. Komang Suryawati, Sp.KK (Member)

Dr. dr. Ketut Suryana, Sp.PD-KAI

Dr. dr. Ni Made Linawati, Msi

Dr. dr. Putu Sri Widnyani, Sp.PA

dr. Komang Ayu Witarini,SpA

Dr. dr. I Wyn Putu Sutirta Yasa, Msi

Udayana University Faculty of Medicine, DME, 2016

Study Guide Immune System and Disorders

Dr. dr. I Made Jawi, M.Kes

Dr. dr. B. K. Satriyasa, M.Repro

dr. Komang Suryawati, Sp.KK

dr. Ketut Suardamana, Sp.PD-KAI

Prof. Dr. dr. Tuti Parwati M, Sp.PD-KPTI

dr. Sari Wulan Dwi Sutanegara , Sp.THTKL

dr. Gede Kambayana, Sp.PD-KR

dr. Tjok Istri Anom S, SpPD

Dr. dr. Nyoman Wande, Sp.PK

dr. Pande Ketut Kurniari,SpPD

dr. IB Putu Alit, SpF, DFM

Dr. dr. I Wayan Putu Sutirta

Udayana University Faculty of Medicine, DME, 2016

Study Guide Immune System and Disorders

Prof.Dr.dr.I Putu Adiatmika M.Kes

dr.I A Dewi Wiryanthini M.Biomed

dr. Ni Made Laksmi Utari,

dr.I Putu Bayu Mayura, S.Ked

Dr.dr. AA Mas Putrawati T Sp.M (K)

Dr.dr. Susy Purnawati, M.KK

dr. Putu Yuliandari, S.Ked

dr.I N Gede Wardana M.Biomed

dr. I G A Artini M.Sc

dr. I Wayan Sugiritama M.Kes

dr. Agung Nova Mahendra, M.Sc

dr. Yuliana, M.Biomed

Dr.rer.Nat. dr. Ni Nyoman Ayu Dewi,

Study Guide Immune System and Disorders

Dr. dr. G N Indraguna P

dr. Muliani, M.Biomed

TIME TABLE OF THE BLOCK IMMUNE SYSTEM & DISSODERS 2016

Student Project (SP): paper

Student Project (SP) : paper

Dr. dr. Ni Made