Study Guide Immune Semester III 16 Oktober 2015
2015
BLOCK IMMUNE SYSTEM &
DISSORDERS
FACULTY OF
MEDICINE UDAYANA
UNIVERSITY
Study Guide Immune System
and Disorders
FOREWORD
The Block “The Immune System and Disorders” is designed for students in order to
serve health care professionals in the diagnosis and management of allergic and other
immunological disorders. Our goals have been to present the basic and essential material
clearly and to provide the knowledge and skills due to:
-
Diagnose and manage patient with inflammation
-
Diagnose and manage patient with hypersensitivity / allergic disease
-
Diagnose and manage patient with autoimmune disease
-
Diagnose and manage patient with immunodeficiency
This block try to give the essential information to assist in clinical decision making and
treatment planning on commonly allergic diseases in pediatric, internal medicine, ENT,and
skin. We also give essential information on commonly autoimmune diseases in neurology,
dermatology, pediatric and internal medicine, beside try to complete the essential
information duo to immune deficiency focus on HIV / AIDS infection.
Our overall goal is to transfer the basic essential information on commonly allergy –
immunological diseases that are required for the primary health care. This block will be
completed by case illustration, learning tasks to be discuss by the students in the small
group discussions and individually in order to achieve the block objectives.
The Block ″ The Immune System an Disorders ″ ( ISD ) is undertaken 19 days including
skill lab, examinations. Student – centered learning as the primary approach in the teachinglearning activities with dynamic group discussions are facilitated by tutors. Individual
learning in Campus and at home is also an important part of the learning process. To
develop good understanding of the ISD, learning activities will also be carried out as
lectures, practical and learning with the patients ( Skill Lab).
Team of Planners
ISD
2
Study Guide Immune System
and Disorders
CONTENTS
Foreword ……………………………………………………………………………………….
2
Contents ………………………………………………………………………………………….
3
Curriculum Block Immune System and Disorders…………………………………………...
4
Planners and Lecturers ………………………………………………………………………..
5
Facilitators ………………………………………………………………………………………..
7
Time Table ...................... ………………………………………………………………………
8
Meeting of student representatives and Facilitators ,Assessment Method ………………. 13
Learning Program ; Abstract Learning Tasks, Case illustrations ,Self Assessments …… 14
Student Project ………………………………………………………………………………...
49
Curriculum Mapping……………………………………………………………………………..
50
References ………………………………………………………………………………………
51
CURRICULUM
Aims:
1. To comprehend the biology of the immune system in health and diseases
3
Study Guide Immune System
and Disorders
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
1
Name
dr.Tjok Istri Anom S, SpPD (Head)
Department
Phone
Internal Medicine
082145854167
4
Study Guide Immune System
and Disorders
2
dr.Sari Wulan DS, SpTHT-KL (Secretary)
ENT
081237874447
3
dr.
Ketut
(Member)
Internal Medicine
08123985811
4
dr. I Wayan Surudarma, M.Si (Member)
Biochemistry
081338486589
5
Dr.dr.
Ketut
(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
Suardamana,
SpPD-KAI
Suryana,
Sp.PD-KAI
LECTURERS
No
Name
Department
Phone
Internal Medicine
08123960964
1
Dr.dr. Ketut Suryana, Sp.PD-KAI
2
Dr. dr. Ni Made Linawati, MSi
Histology
081805629937
3
dr. Putu Sri Widnyani, Sp.PA
Pathology Anatomy
081337115012
4
Dr.dr. I Wyn Putu Sutirta Yasa, Msi
Clinical Pathology
03617428983
5
Dr.dr. I Made Jawi, M.Kes
Pharmacology
08179787972
6
Dr.dr. B. K. Satriyasa, M.Repro
Pharmacology
0818053689
7
dr. Dewi Kumarawati, Sp.A
Pediatrics
03617442593
8
dr. Henky, Sp.F., M.BEth, FACLM
Forensic
081916613459
9
dr.Komang Suryawati, Sp.KK
Dermatology
0817447279
5
Study Guide Immune System
and Disorders
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
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
13 dr. Sari Wulan Dwi Sutanegara , Sp.THTKL (Secretary)
FACILITATORS
(REGULAR CLASS)
N
O
1
2
NAME
dr. I Made Dwijaputra Ayustha,
Sp.Rad
dr. Ida Ayu Putri Wirawati,
GROUP
DEPT
1
Radiology
2
Clinical
PHONE
08123670195
082145723828
VENUE
3nd floor:
R.3.09
3nd floor:
6
Study Guide Immune System
and Disorders
3
4
5
6
7
8
9
10
Sp.PK
dr. Nyoman Astika, Sp.PD-KgerFINASIM
dr. Ketut Agus Somia, Sp.PDKPTI
dr. I Gde Haryo Ganesha,
S.Ked
dr. I Gede Sastra Winata,
M.Biomed, Sp.OG
dr. I Gusti Ngurah Wien
Aryana , Sp.OT
dr. Pontisomaya Parami, Sp.An,
MARS
dr. I Made Oka Adnyana, Sp.S
(K)
dr. Ketut Suardamana, Sp.PDKAI
3
Pathology
Interna
4
Interna
5
DME
6
Obgyn
7
Orthopaedi
8
Anasthesi
9
Neurology
10
Interna
08123974128
08123989353
081805391039
081338713951
0811385263
08123661312
0817347697
08123985811
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
FACILITATORS
(ENGLISH CLASS)
NO
1
2
3
4
5
6
7
8
9
10
NAME
dr. I Made Susila Utama, Sp.PDKPTI
dr. I Gusti Ngurah Purna Putra,
Sp.S (K)
Dr.dr I Nyoman Gede Budiana,
Sp.OG (K)
Prof.Dr.dr.I Putu Gede
Adiatmika, M.Kes
dr. Komang Andi Dwi Saputra,
Sp.THT- KL
Dr. dr. I Dewa Made Sukrama,
MSi, Sp.MK(K)
dr. I Gusti Ayu Sri Darmayani,
Sp.OG
Dr.dr. Yenny Kandarini, Sp.PDKGH-FINASIM
dr. I Gede Budhi Setiawan,
Sp.B(K)Onk
dr. Henky, Sp.F., M.BEth,
FACLM
GROUP
1
DEPT
Interna
PHONE
08123815025
2
Neurology
08123915769
3
Obgyn
08123997401
4
Fisiology
08123811019
5
ENT
081338701878
6
Microbiology
081338291965
7
DME
081338644411
8
Interna
08123805344
9
Surgery
08123923956
10
Forensic
08123988486
VENUE
3nd floor:
R.3.09
3nd floor:
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
7
Study Guide Immune System
and Disorders
TIME TABLE OF THE BLOCK IMMUN SYSTEM & DISSODERS 2015
DAYS /
TIME
ACTIVITY
CONVEYER
VENUE
•
Class Room
DATE
1
ENGLISH CLASS
REG CLASS
08.00-09.00 (60’)
09.00-10.00 (60’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
Student
Project
preparation
-
-
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. dr. Ketut Suryana,
SpPD-KAI
08.00-08.30 (30’)
09.00-09.30 (30’)
•
•
dr. Ni Made Linawati,
MSi
Friday,
Oct 16,
2015
2
Monday,
Oct 19,
2015
3
08.30-09.00 (30’)
09.30-10.00 (30’)
(SP):
paper
Comprehend The Microscopic
Structure of Limphoid
Organ,Immune Cells and MHC
•
Comprehend tissue repair
•
Comprehend basic mechanism of
autoimmunity
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
•
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
12.30-14.00 (90’)
10.00-11.30 (90’)
Student Project
preparation
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
Dr. dr. Ketut Suryana,
SpPD-KAI
:
paper
Class Room
dr. Putu Sri Widyani,
S.PA.
Library
Discussion Room
Fasilitator
-
(SP)
Class Room
-
-
Library
•
dr. Ni Made Linawati,
Msi
•
dr. Putu Sri Widyani,
S.PA.
Class Room
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Comprehend acute and chronic
inflammation
•
Dr. I Wayan
Sumadi, Sp.PA.
08.30-09.00 (30’)
09.30-10.00 (30’)
•
Comprehend hypersensitivity
•
Dr.Tjok Istri
Saturti, SpPD
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
-
-
Tuesday,
Oct 20,
2015
Introduction to The Immune
System and disorders
Juli
Class Room
Anom
8
Study Guide Immune System
and Disorders
12.30-14.00 (90’)
10.00-11.30 (90’)
SP: paper preparation
-
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. I Wayan
Sumadi, Sp.PA.
•
Dr.Tjok Istri
Saturti, SpPD
•
Dr. I Made Jawi, M.Kes
4
08.00-08.30 (30’)
09.00-09.30 (30’)
Wednes
day,
08.30-09.00 (30’)
09.30-10.00 (30’)
Oct 21,
2015
5.
•
•
Class Room
Anom
Class Room
•
Forensic Laboratory
•
dr Henky, SpF
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
•
Dr. Ketut Suardamana,
SpPD-KAI
08.00-09.00 (60’)
09.00-10.00 (60’)
•
Adverse drug reaction
•
Able to diagnose and manage
anaphylaxis
Oct 22,
2015
Class Room
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
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Comprehend laboratory test of
immune system
•
Dr. dr. I Wyn Putu
Sutirta Yasa, Msi
Class Room
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Antihistamine
•
Dr.dr.B.K.Satriyasa,M.
Repro
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
SP
paper
Imunomodulator
Friday,
Oct 23,
2015
Juli
09.00-10.30 (90’)
Thursda
y,
6.
Comprehend basic mechanism of
drug allergy and
immunopharmacology
Library
presentation: dr. Made Jawi, M.Kes
Class Room
9
Study Guide Immune System
and Disorders
14.00-15.00 (60’)
7.
15.00-16.00 (60’)
Plenary Session
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Able to diagnose and manage
allergic diseases in ENT
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Able to diagnose and manage
allergic diseases in dermatology
Monday,
Oct 26,
2015
8.
•
Dr.dr.B.K.Satriyasa,
M.Repro
•
Dr. Sari Wulan Dwi
Sutanegara , Sp THTKL
•
-Dr.Nyoman Suryawati,
SpKK
Class Room
Class Room
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’)
K
Suardamana, Class Room
SP paper presentation: Urtikaria dr.
SpPD-KAI
and Angiodema
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. Sari Wulan Dwi
Sutanegara , Sp THTKL
•
Dr.Nyoman Suryawati,
SpKK
•
Dr. Gede Kambayana,
SpPD-KR
Class Room
08.00-09.00 (60’)
09.00-10.00 (30’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
SP paper presentation: Blood Dr.dr. Wy Putu Sutirta Class Room
Group Incompatibility
Yasa, M.Si.
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. Gede Kambayana,
SpPD-KR
08.00-08.30 (30’)
09.00-09.30 (30’)
•
•
Prof. Dr. dr AA Raka
Sudewi, Sp S
Oct 27,
2015
Wednes
day,
Dr. dr. I Wyn Putu
Sutirta Yasa, Msi
09.00-10.30 (90’)
Tuesday,
9.
•
Able to diagnose and manage
SLE, RA & Polimyalgia
Rheumatica
Able to diagnose and manage
autoimmune diseases in Neurology
•
Class Room
Class Room
Class Room
08.00-09.00 (30’)
09.30-10.00 (30’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
Oct 28,
2015
Able to diagnose and manage
secondary immunodeficiency
diseases (focus HIV)
Prof. DR. Dr. Tuti
Parwati M, SpPDKPTI
10
Study Guide Immune System
and Disorders
12.30-14.00 (90’)
14.00-15.00 (60’)
10.00-11.30 (90’)
15.00-16.00 (60’)
SP
paper
Limphadenitis TB
presentation: dr.
Plenary Session
10
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Thursda
y,
Able to diagnose and manage
Rheumatic Disease of Childhood
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Able to diagnose and manage
Food allergy
•
Able to diagnose and manage
immunodeficiency diseases in
childhood
Oct 29,
2015
11.
Sriwidnyani,
Class Room
•
Prof. Dr. dr AA Raka
Sudewi, Sp S
•
Prof. DR. Dr. Tuti
Parwati M, SpPDKPTI
•
Dr. Dewi Kumarawati,
SpA
Class Room
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 dr. Komang Suryawati, Class Room
Johnson Syndrome
Sp.KK.
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
08.00-09.00 (60’)
09.00-10.00 (60’)
Soluble markers of
inflammation (BCS)
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
Friday,
Oct 30,
2015
Putu
Sp.A
BCS Discussion
Dr. Dewi
SpA
allergic
Kumarawati,
Class Room
dr. Wande, Sp.PK.
Class Room
-
Library
dr. Wande, Sp.PK &
Skill Lab
Team
12.
08.00-09.00 (60’)
09.00-10.00 (60’)
Forensic Laboratory (BCS)
Dr. Henky, SpF
Class Room
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
-
Library
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
Monday,
Nop 02,
2015
BCS Discussion
Dr. Henky , SpF, & Team
Skill Lab
13
Tuesday,
08.00-09.00 (60’)
09.00-10.00 (60’)
Anaphylactic syok (BCS)
Dr. Tjok Istri Anom S,
SpPD
Class Room
11
Study Guide Immune System
and Disorders
Nop 03,
2015
14
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
-
Library
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Dr. Tjok Istri Anom S,
SpPD & Team
Skill Lab
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
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Dr. Putu Sri Widyani ,
Sp.A & Team
LAB Bersama
08.00-09.00 (60’)
09.00-10.00 (60’)
Skin Prick Test (BCS)
Dr. Ketut Suryana, SpPDKAI
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
Wednes
day
Nop 04,
2015
15
Thursda
y,
Nop 05,
2015
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Friday,
Nop 06,
2015
Monday,
Nop 9,
2015
Pre-evaluation Break
Examination
12
Study Guide Immune System
and Disorders
Meeting of the student representatives
The meeting between block planners team and the student group representatives will be
held on Monday, October 12, 2015 at 09.00 until 10.00 a.m at HAPEQ discussion room. In
this meeting, all of the student group representatives are expected to give suggestions or
inputs or complaints to the team planners for improvement. For this purpose, every student
group must choose one student as their representative to attend the meeting.
Meeting of facilitators
The meeting between block planners team and the facilitators will take place on, Monday,
October 12, 2015 at 10.00 am until 12.00 pm at HAPEQ discussion room. In this meeting all
the facilitators are expected to give suggestions and inputs as evaluation to improve the
study guide and the educational process. Because of the importance of this meeting, all the
facilitators are strongly expected to attend the meeting.
Plenary session
For each task of SGD, the students are requested to prepare a group report. The reports will
be presented in a plenary session. The group will be chosen randomly by the lecturer in
charge. The group report will be evaluated by respective facilitator.
Assessment Methods
Assessment will be performed at the end of the block on Nopember 9th 2015. There are 100
questions for the examination that consists of Multiple Choice Question (MCQ). The
borderline to pass exam is 70.
13
Study Guide Immune System
and Disorders
LEARNING
PROGRAMS
Day 1
Topics
:
Introduct. to the immune system and disorders
Lecturer
:
dr. Ketut Suryana, SpPD-KAI
Abstract
1. The Immune system has evolved to protect us from pathogens. Some, such as viruses,
infect individual cells; others, including many bacteria, divide extracellularly within
tissues or body cavities.
2. The cells which mediate immunity include lymphocytes and phagocytes. Lymphocytes
recognize antigens on pathogens. Phagocytes internalize pathogens and degrade them
3. An Immune response consists of two phases. In the first phase, antigen activates
specific lymphocytes that recognize it; in the effector phase, these lymphocytes
coordinate an immune response that eliminates that source of the antigens.
4. Specificity and memory are two essential features of adaptive immune responses. The
Immune system mounts a more effective response on second and subsequent
encounters with a particular antigen.
5. Lymphocytes have specialized functions. B cells make antibodies; cytotoxic T cells kill
virally infected cells; helper T cell coordinate the immune response by direct cell-cell
interactions and the release of cytokines, which help B cells to make antibody.
6. Antigens are molecules which are recognized by receptors on lymphocytes. B
lymphocytes usually recognize intact antigen molecules, while T lymphocytes recognize
antigen fragment on the surface of other cells.
7. Clonal selection involves recognition of antigen by a particular lymphocyte; this leads to
clonal expansion and differentiation to effector and memory cells.
8. The immune system may break down. This can lead to immunodeficiency or
hypersensitivity diseases or to autoimmune diseases.
Learning task
1.
2.
3.
4.
Comprehend of immune system with clinical implications
Comprehend the lymphoid organs and describe of it’s microscopic organization
Comprehend the cellular immunity
Comprehend the mechanism of cellular and humoral immunity to infection
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Day 2
Topic
:
The Microscopic Structure of Limphoid Organ,
Immune Cells and Histocompatibility Molecule
Lecturer
:
dr. Ni Made Linawati, M. Si.
Abstract
The limphoid systems is responsible for the immunological defense of the body.
Some of its component organs ; lymph nodes, thymus and spleen are surrounded by
connective tissue capsules, whereas its other components, member of the diffuse lymphoid
system, are not encapsulated. The cells of the limphoid systems such as lymphocytes ( T, B
and Natural Killer), Antigen Presenting Cells (Dendritic cells, Macrophages and B
lymphocytes) and other (Neutrophils) protect the body against foreign macromolecules,
viruses, bacteria, and other invasive microorganism, and they kill virally transformed cells.
Major Histocompability Complex (MHC) molecule are important to permit APCs and cells
under viral attact (or cells already virally transformed) to present the epitopes of the invading
pathogen to the T cells.
Learning Task
Vignette
A 65-year-old man had suffered from rectal bleeding during defecation for a few weeks.
Laboratory findings were normal except a slight elevation in the level of alkaline
phosphatase. Multiple polypoid lesions were observed in colonoscopic examination. The
histological and immunochemical evaluation showed atypical lymphoid cell proliferation and
lymphoepithelial lesions on the colonic mucosa, staining with CD20. After the diagnosis had
been confirmed as low grade mucosa associated lymphoid tissue lymphoma.
a. Please describe histological structure of the Mucosa associated lymphoid tissue.
b. Why M cells has important roles in mucosa immune response?
Self Assesment
1. What are primary and secondary lymphoid organ. Mention the of organ that has
function as primary and secondary lymphoid organ
2. Describe about function and microscopic structure of thymus, lymph nodes; spleen;
tonsils; and MALT
3. Describe about MHC class I and class II
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Topic
:
INFLAMMATION AND TISSUE REPAIR
Lecturer
:
dr. Ni Putu Sriwidyani, Sp.PA
ABSTRACT
Inflammation is fundamentally a protective response, designed to rid the organism of
both the initial cause of cell injury and the consequences of such injury. Inflammation is a
complex reaction in tissues that consists mainly of responses of blood vessels and
inflammatory cells. The vascular and cellular reactions of inflammation are triggered by
soluble factors that are produced by various cells or derived from plasma proteins and are
generated or activated in response to the inflammatory stimulus. Inflammation may be acute
or chronic, depending on the nature of the stimulus and the effectiveness of the initial
reaction in eliminating the stimulus. Inflammation is terminated when the offending agent is
eliminated. Outcomes of acute inflammation could be resolution, chronic inflammation, or
fibrosis.
Inflammation response is closely intertwined with the process of repair. Repair most
often consists of a combination of regeneration and scar formation by deposition of
collagen. Inflammation and repair may be harmful in some situations and may contribute to
a variety of diseases.
Understanding inflammation and repair can be applied as basic concept of patient
management, diagnostic, therapy, and monitoring.
LEARNING TASK
Vignette
A 20 year old female came to a doctor in private practice and complaint a right lower
abdominal pain and fever since 3 days ago. On physical examination, BP: 120/80 mm Hg,T
axilla: 400C. On lower right abdominal region revealed warm and pain in palpation.
Complete blood count showed leucocytosis. Appendectomy performed. Histology
examination showed oedematous, hypermi, and neutrophil infiltration extended from
mucosal until serosal layer. The diagnosis was acute appendicitis.
Task
1. Explain reactions of blood vessels and leukocyte in acute inflammation
2. Mention mediators of inflammation
3. Mention local effects and systemic effects of inflammation
4. Mention outcomes of acute inflammation
5. Mention role of macrophage and other inflammatory cells in chronic inflammation
6. Mention morphologic patterns of acute and chronic inflammation
7. Mention consequences of defective or excessive inflammation
8. Explain healing by fibrosis, scar formation, and fibrosis
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SELF ASSESMENT
1. Inflammatory cells that have a major role in most acute inflammation are:
A. Basophyl
B. Eosinophyl
C. Netrophyl
D. Macrophage
E. Mast cell
2. Mediators of increased vascular permeability in acute inflammation responses include all
of the following, except:
A. Histamine
B. Bradykinin
C. Leukotriene C4
D. Platelet Activating factor
E. Complement complex C5-9
3. Mediators of neutrophyl chemotaxis in acute inflammation responses include all of the
following, except:
A. C3a
B. C5a
C. IL-1
D. TNF
E. Bacterial product
4. Opsonization increases engulfment capability of macrophage in fagocytosis.
Complement system component that involved as a potent opsonin is:
A. C3a
B. C3b
C. C5a
D. C5b
E. C9
5. A 35 years old man with acute appendicitis and appendectomy performed. Pathologic
examination shows marked neutrophyl infiltration in the wall of the appendix. Based on
the morphological feature, the type of inflammation of this case is:
A. Serous
B. Suppurative
C. Catharalis
D. Fibrinous
E. Granulomatous
6. A 5 years old boy hospitalize in intensive care unit cause by accidently expose to boiled
water. All the skin of his body was red with blebs. Based on the morphological feature,
the type of inflammation of this case is:
A. Serous
B. Suppurative
C. Catharralis
D. Fibrinous
E. Granulomatous
7. Chronic inflammation are characterized by all of following morphologic feature, except:
A. Mononuclear infiltration
B. Tissue destruction
C. Angiogenesis
D. Fibrosis
E. Vasodilatation
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8. Permanent tissue is a mature tissue without capability to divide. The following tissue is a
permanent tissue:
A. Skeletal muscle
B. Hepar
C. Skin
D. Neuron
E. Kidney
9. A large aggregate of epitelioid cells is seen in a microscopic section of an ovarial tumor.
Your diagnosis is:
A. Granulation tissue
B. Granuloma pyogenicum
C. Granulosa cell tumor
D. Granuloma
E. Granulocytosis
10. Local factor that retard wound healing is:
A. Diabetes
B. Malnutrition
C. Foreign bodies
D. Genetic
E. Vitamin C deficiency
Day 3
Topic
:
Basic mechanism of autoimmunity
Lecturer
:
dr. I Wayan Juli Sumadi, Sp.PA.
ABSTRACT
Immunologic Tolerance: Is a state in which an individual is incapable of developing an
immune response against a specific antigen.
Self- tolerance: Specifically refers to a lack of immune responsiveness to one’s own tissue
antigens.
Two broad groups of mechanisms to explains the tolerant state:
▪ Central tolerance: This refers to deletion of self-reactive T and B lymphocytes during
maturation in central lymphoid organs (i.e. in the thymus for T cells and the bone marrow
for B cells)
▪ Peripheral tolerance: Self reactive T cells that escape negative selection in the thymus
can potentially wreak havoc unless they are deleted or effectively muzzled. Several
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.
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Furthermore, the breakdown of tolerance and initiation of autoimmunity involves the
interaction of complicated immunologic, genetic, and microbial factors.
Learning task
Trigger Case
A 25-year-old woman has had increasing malaise, a skin rash of her face exacerbated by
sunlight exposure, and arthtralgias and myalgias for the past month. On physical
examination she has mild pedal edema. On auscultation a friction rub is audible over the
chest. Laboratory findings include pancytopenia and serum creatinine 3 mg/dL. Urinalysis
shows hematuria and proteinuria. A serologic test for shypilis yields a false positive result. A
renal biopsy shows a slight increase of mesangial cells and granular deposit of IgG and
complement in the mesangium and along basement membrane. The result of ANA test is
positive. Finally, the patient is diagnosed as systemic lupus erythematosus (SLE). SLE is
the best example of autoimmune disease. Does the autoimmunity result from the loss of
self-tolerance, how this happen, and why they have a broad clinical spectrum as showed in
that patient? Before you answer the question, please try to find out the following task.
Task
1. Describe the mechanism of immunological tolerance to self antigent!
2. Explain the mechanism of autoimmunity, including the role of susceptibility genes
and enviromental triggers!
3. Describe the general features of autoimmune diseases!
4. Describe the etiopathogenesis of SLE!
5. Describe the mechanism of tissue injury in SLE, and give some examples of
morphological changes in SLE!
6. Mention other diseases that belong to autoimmune diseases group!
Topic
:
Hypersensitivity
Lecturer
:
dr. Tjok Istri Anom Saturti, SpPD
ABSTRACT
There are 4 types classifications according to
Gel & Coombs
1. Type I
: Immediate hypersensitivity
2. Type II
: Cytotoxic hypersensitivity
3. Type III
: Immune complex hypersensitivity
4. Type IV
: Delayed (cell mediated) hypersensitivity
Hypersensitivity the immune response results are harmful to the heart
Type I
: Antigen bind to IgE on the surface of mast cells à release of several
mediators within minutes. Important mediators are: Histamin, SRS-A, ECFA, serotonin, Prostaglandins and thromboxanes, etc. Clinical
manifestations:
1. Anaphylaxis : severe bronconstriction, hypotension à shock
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Type II
Type III
Type IV
2. Atopy: genetic factor to induce by exposure to spesific allergens
(pollens, dust, shellfish, nuts, etc). Clinical manifestation: hay fever,
asthma, eczema, and urticaria. Treatment and prevention: Avoidance of
the responsible allergen, Hyposensitization (Desensitization) & Drug
treatment.
: Antibody is directed against antigen on an individual’s own cell (target cell)
or foreign antigen, such as transfused red blood cell. This may lead to
cytotoxic action by K Cells, or complement mediated lysis.
: Immune Complexes are deposited in the tissue. Complement is activated
and polymorphs are attracted to the site of deposition causing local tissue
damage and inflammation
: Antigen sensitized T cells release lymphokines following a secondary
contact with the same antigen. Cytokines induced inflammatory reactions
activate and attract macrophages, which release inflammatory mediators.
Learning Task Hypersensitivity :
1. Make definition of the term hypersensitivity
2. Explain the biological roles of hypersensitivity
3. Make classification of hypersensitivity
4. Compare the hypersensitivity type I, II, III and IV
5. Explain principle treatment and prevention of hypersensitivity
SELF ASSESSEMENT R. HIPERSENSITIFITAS
1. Hypersensitivity reaction is a general pathologic reaction which has following
characteristics:
A. Never happens on the first exposure
B. Generally divided into 4 types
C. Is an overreaction of immune system
D. Occurred if humoral and cellular immunological status are increased
E. All above are correct
2. The followings are the feature of hypersensitivity reaction type I, except:
A. Occurs in few seconds or minutes
B. Is an IgE mediated immune response
C. IgE is bind by mast cell
D. Ia a delayed hypersensitivity
E. Histamine is a primary mediator produced
3. In hypersensitivity reaction type I, eosinophyl is activated by:
A. IL-4
B. IL-2
C. IL-5
D. IL-6
E. IL-1
4. Histamine release effect of hypersensitivity reaction type I is:
A. Vasoconstriction of blood vessels
B. Vasodilation of blood vessels
C. Capillary permeability decreased
D. Bronchus dilated
E. Hyposecretion of mucosa
5. Hypersensitivity reaction type II is a cytotoxic reaction which involves:
A. IgG and IgM
B. IgG and IgD
C. IgG and IgA
D. IgA and IgD
E. IgD and IgE
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Day 4
Topic
:
Immunopharmacology
Lecturer
:
dr. I Made Jawi, M.Kes.
ABSTRACT
Immunopharmacology includes the characteristics of drugs that can suppress,
modulate, or stimulate immune functions. It also includes the pharmacology of antibodies
that have been developed for use in immune disorders. The drugs available comprise a
wide variety of chemical and pharmacologic types. In this topic also will be discuss the ways
in which drugs may activate the immune system and cause unwanted immunologic
reactions. Drugs that modulate immune function and as a immune suppressants are:
glucocorticoids (prednisone), immunophilin ligands (Cyclosporine), cytotoxic drugs
(Cyclophosphamide), Anti-TNF-α agents (etanercept), enzyme inhibitors (mycophenolate
mofetil) and Antibodies.
Drugs that modulate immune function and as a immune potentiators are: Cytokines
(Interleukin-2, Interferons), BCG vaccine and Thymosin.
Learning Task
A patient was treated with penicillin. Within a few minutes after penicillin injection, he
developed severe bronchoconstriction, laryngeal odema and hypotension.
1. Explain the immunologic mechanism of those problems.
2. To manage that patient what medicine will you give for him immediately?
3. Explain your answer if you give him prednisone. Do you agree? Why?
4. How about antihistamine like dimenhydrinate for this patient?
Self assessment Immunopharmacology
1. Cyclosporine is effective in organ transplantation. The immunosuppressant action of
the drug appears to be due to
A. Activation of natural killer (NK) cells
B. Blockade of tissue responses to inflammatory mediators
C. Increased catabolism of IgG antibodies
D. Inhibition of the gene transcription of interleukins
E. Interference with antigen recognition
2. Azathioprine
A. Binds avidly to a cytoplasmic immunophillin
B. Blocks formation of tetrahydrofolic acid
C. Is a precursor of cytarabine
D. Is markedly hematotoxic and has caused neoplasms
E. Is a metabolite of mercaptopurine
3. Which of the following drugs is a widely used agent that suppresses cellular immunity,
inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG
antibodies?
A. Cyclophosphamide
B. Cyclosporine
C. Infliximab
D. Mercaptopurine
E. Prednisone
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4. Which one of the following agents acts at the step of antigen recognition ?
A. Cyclosporine
B. Cyclophosphamide
C. Methotrexate
D. Rh0 (D) immune globulin
E. Tacrolimus
5. An immunosuppressed patient was treated for a bacterial infection with parentral
penicillin. Within a few minutes after penicillin injection, he developed severe
bronchoconstriction, laryngeal edema, and hypotension. Due to the rapid administration of
epinephrine, the patient survived. Unfortunately, a year later he was treated with an
antipsychotic drug and developed agranulocytosis.
The type of drug reaction that was caused by the penicillin is
A. An autoimmune syndrome
B. A cell-mediated reaction
C. A type II drug allergy
D. Mediated by IgE
E. Serum sickness
Topic
:
Forensic Laboratory
Lecture
:
dr. Henky, SpF
Abstract
Forensic serology is the study of serology in relation to crimes and other legal matters by
using a scientific approach.
Doctors should have knowledge about forensic serology to
assist investigators in revealing crime cases related with human’s body and health.
Moreover, based on legislations, doctors have legal duty to carry out forensic examination
when asked by the investigators.
Mostly, investigators asked doctors to prove homicide, rape, assault or dispute paternity
case. To prove it, the doctors need to do serological examination of biological evidence that
found on the victim’s body, such as blood, semen, urine, and other body fluids.
Principle of serological test is the use of specific antibodies to detect a target antigen. By
doing a simple serological test, doctor can filter the type and origin of biological substances.
If the screening test gives a positive result, biological substances must be processed for
DNA testing to determine the owner of biological materials.
Vignette 1
A woman, 22 years old was found dead and naked. She suffered bruises almost on her
entire body. There were blood stains and fluid around her genital.
Learning Task
1. In above case, discuss the role of forensic serology in examining biological evidence!
2. Discuss the steps to examine blood stain and fluid around the genital!
3. Discuss the concept of species determination and individualization of blood stain and
biological fluid!
4. If in that case, there are 3 suspects, what the forensic serologist do to identify the
suspect?
5. Discuss about DNA analysis for that case!
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Vignette 2
A man, with blood type O, come to prove that his wife, with blood type AB, have an affair
with her boss, with blood type A. He is not sure whether he is the biological father of his
child, because his first child is male, with blood type O, and the second one is female, with
blood type AB.
Learning Task
As a doctor, what would you explain to the man?
Day 5
Topic
:
Adverse drugs reaction
Lecture
:
dr. Ketut Suardamana, Sp. PD
Introduction
Drug allergy or hypersensitivity is a form of Adverse Drug Reaction (ADR)
Definition
An ADR is any undesirable effect of drug that is administered in standard doses by
the proper route for the purpose of prophylaxis, diagnosis, or treatment.
Drug allergy is an immunologically mediated reaction, occurs in a susceptible populations,
characterized by specificity, transferability by antibodies or lymphocytes, and recurrence on
re-exposure
Pathophysiology
Allergic drug reactions are usually defined as;
1. reaction caused by suspected immunologic mechanisms
2. result from the production of antibodies and / or cytotoxic T cells directed against the
drug,
3. its metabolite, a soluble / cell-bound carrier protein as a responses to prior or
continuous exposure to a drug
Risk factors
1. Patient related : Age, sex, genetics, atopy, AIDS
2. Drug related : Macromolecular size ; bivalency, haptens, route, dose, duration of
treatment
3. Aggravating factors : β Blockers, asthma, pregnancy
Diagnosis
1.
Diagnosis of drug allergy based on ;
2.
Clinical history
3.
Clinical manifestations
4.
Diagnostic test
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Diagnostic tests
1. SPT may be helpful for diagnosing IgE mediated drug reactions (in vivo)
2. RAST
may detect serum IgE antibodies to certain drugs (e.g : penicillin and
succinyl choline) (in vitro)
3. Provocation tests
Oral provocation tests, may be as a gold standard
They must be performed under strict medical supervision with resuscitative
equipment available
Management
1. Avoidance
2. Premedication
3. Desensitisation
Learning Task ADVERSE DRUGS REACTION (ADR)
Vignette
Male 20 years old, was diagnosed with Pulmonary TB and taking the anti TB regimen
(Category 1). On the second day treatment he felt an itchy – swollen redness on whole
body. He had previous history of drug allergy but the allergen is unknown, his mother also
had history of drugs allergy. The patient was fully alert, T 110/70 mmHg, pulse rate 92x per
minute regular, RR 18x per minute.
Task
1. Could you explore more to complete the anamnesis!
2. Describe any sign that you find on Physical examination?
3. How to manage this patient?
Self assessment
1. Could you describe the adverse drugs reaction (ADR)!
2. Describe the immunopathophysiology of drugs allergy (due to Gell & Coombs
Criteria)!
3. Comprehend the diagnostic approach of the drugs allergy!
Topic
:
Anaphylaxis reaction
Lecture
:
dr. Ketut Suardamana, Sp. PD.
Definition
Anaphylaxis is an acute severe, life-threatening, generalized or systemic hypersensitivity
reactions
Pathophysiology
1. Type I reaction (IgE mediated)
2. Anaphylactoid reaction (Non IgE mediated) : complement activation, physical
factors, substance for Histamine release, idiopathic, arachidonic acid modulation
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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 lipstongue-uvula) AND AT LEAST ONE OF THE FOLLOWING
a. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced
PEF, hypoxemia)
b. Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia
/collapse, syncope, incontinence)
2. Two or more of the following that occur rapidly after exposure to a likely allergen for that
patient (minutes to several hours) :
a. Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen
lips-tongue-uvula)
b. Respiratory compromise (eg dyspnea, wheeze-bronchospasm, stridor, reduced
PEF, hypoxemia)
c. Reduced BP or associated symptoms (eg, hypotonia collapse, syncope,
incontinence)
d. Persistent gastrointestinal symptoms (eg cramp abdominal pain, vomiting)
3. Reduced BP after exposure to known allergen for that patient ( minutes to several
hours)
a. Infants and children: low systolic BP (age specific) or greater than 30% decrease
in systolic BP
b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from
that person's baseline
Learning task ANAPHYLAXIS
Vignette
Female 30 years old, came to the Emergency Unit with chief complaint; edema on palpebra,
itchy redness on the whole body skin after taking metampirone 500 mg tab. as a treatment
for headache. She also complains; shortness of breath, fatique and warmth on the lower
extremity.
Task
1.
2.
3.
4.
What should you do for the first?
Could you complete your anamnesis!
What do you find on physical examination?
The laboratory plan? Or other diagnostic procedure?
Self assessment
1. What are the differential diagnoses?
2. Could you describe the pathophysiology of anaphylaxis?
3. Could you describe the clinical manifestations?
4. The management in this case!
5. Describe the prevention!
6. Comprehend any prognostic factors!
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Day 6
Topic
:
Laboratory test of immune system
Lecture
:
Dr. dr. I Wyn Putu Sutirta Yasa, M.Si.
Abstract
Objective to comprehend laboratory test of immune system
1. Approach in the patient with immune system disease and disorders are evidence
based in immunology, history and physical examination, laboratory studies to make
diagnosis. Laboratory test of immune system (immunoassay) based on antigenantibody reactions. Immunoassay can be used for the detection of either antigens or
antibodies. For antigen detection, the corresponding specific antibody should be
prepared as one of reagents. The reverse is true for antibody detection.
2. The sensitivity of the immunoassays has been enhanced through the development
of types of signal detection systems and solid-phase technology. Immunoassay has
been optimized to detect less than 0.1 pg/mL of antigen in blood.
3. The can be applied to detection of haptens as small molecules, protein and protein
complexes as macromolecules, as well as of any antibody to allergens, infectious
agent, and autologous antigens.
4. Students to comprehend the overview of general principles and based of
immunoassay. High concentration of such molecules and where antigen- antibodies
are mixed in solution can be measured by precipitation techniques. Medium
concentration of such molecules and where antigen- antibodies are on solid phase
can be quantified by agglutination techniques. Very low concentration of such
molecules can be quantified by radioimmunoassay techniques or enzyme linked
immunosorbent assay techniques.
Outcome of laboratory test of immunes system
Students to comprehend the overview of general principles and based
immunoassay to purpose and function of laboratories are to assist students in
confirming or rejection a diagnosis, (2) providing guidelines for patient management,
establishing a prognosis, (4) detecting disease through case finding or screening and
monitoring follow up therapy.
of
(1)
(3)
(5)
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?
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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.
2.
3.
4.
5.
Explain two classification of H1 blockers
List two drugs the older members of the first generation agent
List three drugs the second generation of H1 blockers.
Describe mechanism and effect of H1 blockers
Describe clinical use of H1 blockers
Self assessment Antihistamine
1. Many H1 blocker have additional nonhistamine-related effect, these are likely to include
all of the following. EXPECT:
A. Antimuscarinic reduction in bladder tone
B. Local anesthetic effect if the drug is injected
C. Anti-motion sickness effect
D. Increase in total peripheral resistance
E. Sedation
2. Which of the following drugs will result from blockade of H1 receptor?
A. Decreased cAMP in smooth muscle
B. Decrease channel opening in enteric nerves
C. Decrease IP3 in smooth muscle
D. Increase IP3 in smooth muscle
E. Increase in total peripheral resistance
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3. Which of the following drugs are used as anti-motion sickness and also for management
of chemotherapy-induced vomiting?
A. Diphenhydramine
B. Dimenhydrinate
C. Meclizine
D. Cyclizine
E. Loratadine
4. Toxicities of H1 blocker include which one of the following
A. Sedation
B. Dry mouth
C. Blurry vision
D. Vomiting
E. Hypotension
Day 7
Topic
:
Lecturer
:
Rhinitis Alergy
Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL
ABSTRACT
Allergic rhinitis is an inflammation of the nasal passages, usually associated with
watery nasal discharge and itching of the nose and eyes.
Allergic rhinitis affects about 20 percent of population and ranks as one of the most
common illnesses. The symptoms occur in the nose and eyes and usually occur after
exposure to dust, danders, or certain seasonal pollens in people that are allergic to these
substances.
There is strong genetic predisposition to allergic rhinitis. One parent with a history of
allergic rhinitis has about a 30 percent chance of producing offspring with the disorder. Tthe
risk increases to 50 percent if both parents have a history of allergies.
Characteristic symptoms include repetitive sneezing, rhinorrhea (runny nose), postnasal drip, nasal congestion, pruritic (itchy) eyes, ears, nose or throat, and generalized
fatigue. Symptoms can also include wheezing, eye tearing, sore throat, and impaired smell.
A chronic cough may be secondary to postna
BLOCK IMMUNE SYSTEM &
DISSORDERS
FACULTY OF
MEDICINE UDAYANA
UNIVERSITY
Study Guide Immune System
and Disorders
FOREWORD
The Block “The Immune System and Disorders” is designed for students in order to
serve health care professionals in the diagnosis and management of allergic and other
immunological disorders. Our goals have been to present the basic and essential material
clearly and to provide the knowledge and skills due to:
-
Diagnose and manage patient with inflammation
-
Diagnose and manage patient with hypersensitivity / allergic disease
-
Diagnose and manage patient with autoimmune disease
-
Diagnose and manage patient with immunodeficiency
This block try to give the essential information to assist in clinical decision making and
treatment planning on commonly allergic diseases in pediatric, internal medicine, ENT,and
skin. We also give essential information on commonly autoimmune diseases in neurology,
dermatology, pediatric and internal medicine, beside try to complete the essential
information duo to immune deficiency focus on HIV / AIDS infection.
Our overall goal is to transfer the basic essential information on commonly allergy –
immunological diseases that are required for the primary health care. This block will be
completed by case illustration, learning tasks to be discuss by the students in the small
group discussions and individually in order to achieve the block objectives.
The Block ″ The Immune System an Disorders ″ ( ISD ) is undertaken 19 days including
skill lab, examinations. Student – centered learning as the primary approach in the teachinglearning activities with dynamic group discussions are facilitated by tutors. Individual
learning in Campus and at home is also an important part of the learning process. To
develop good understanding of the ISD, learning activities will also be carried out as
lectures, practical and learning with the patients ( Skill Lab).
Team of Planners
ISD
2
Study Guide Immune System
and Disorders
CONTENTS
Foreword ……………………………………………………………………………………….
2
Contents ………………………………………………………………………………………….
3
Curriculum Block Immune System and Disorders…………………………………………...
4
Planners and Lecturers ………………………………………………………………………..
5
Facilitators ………………………………………………………………………………………..
7
Time Table ...................... ………………………………………………………………………
8
Meeting of student representatives and Facilitators ,Assessment Method ………………. 13
Learning Program ; Abstract Learning Tasks, Case illustrations ,Self Assessments …… 14
Student Project ………………………………………………………………………………...
49
Curriculum Mapping……………………………………………………………………………..
50
References ………………………………………………………………………………………
51
CURRICULUM
Aims:
1. To comprehend the biology of the immune system in health and diseases
3
Study Guide Immune System
and Disorders
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
1
Name
dr.Tjok Istri Anom S, SpPD (Head)
Department
Phone
Internal Medicine
082145854167
4
Study Guide Immune System
and Disorders
2
dr.Sari Wulan DS, SpTHT-KL (Secretary)
ENT
081237874447
3
dr.
Ketut
(Member)
Internal Medicine
08123985811
4
dr. I Wayan Surudarma, M.Si (Member)
Biochemistry
081338486589
5
Dr.dr.
Ketut
(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
Suardamana,
SpPD-KAI
Suryana,
Sp.PD-KAI
LECTURERS
No
Name
Department
Phone
Internal Medicine
08123960964
1
Dr.dr. Ketut Suryana, Sp.PD-KAI
2
Dr. dr. Ni Made Linawati, MSi
Histology
081805629937
3
dr. Putu Sri Widnyani, Sp.PA
Pathology Anatomy
081337115012
4
Dr.dr. I Wyn Putu Sutirta Yasa, Msi
Clinical Pathology
03617428983
5
Dr.dr. I Made Jawi, M.Kes
Pharmacology
08179787972
6
Dr.dr. B. K. Satriyasa, M.Repro
Pharmacology
0818053689
7
dr. Dewi Kumarawati, Sp.A
Pediatrics
03617442593
8
dr. Henky, Sp.F., M.BEth, FACLM
Forensic
081916613459
9
dr.Komang Suryawati, Sp.KK
Dermatology
0817447279
5
Study Guide Immune System
and Disorders
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
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
13 dr. Sari Wulan Dwi Sutanegara , Sp.THTKL (Secretary)
FACILITATORS
(REGULAR CLASS)
N
O
1
2
NAME
dr. I Made Dwijaputra Ayustha,
Sp.Rad
dr. Ida Ayu Putri Wirawati,
GROUP
DEPT
1
Radiology
2
Clinical
PHONE
08123670195
082145723828
VENUE
3nd floor:
R.3.09
3nd floor:
6
Study Guide Immune System
and Disorders
3
4
5
6
7
8
9
10
Sp.PK
dr. Nyoman Astika, Sp.PD-KgerFINASIM
dr. Ketut Agus Somia, Sp.PDKPTI
dr. I Gde Haryo Ganesha,
S.Ked
dr. I Gede Sastra Winata,
M.Biomed, Sp.OG
dr. I Gusti Ngurah Wien
Aryana , Sp.OT
dr. Pontisomaya Parami, Sp.An,
MARS
dr. I Made Oka Adnyana, Sp.S
(K)
dr. Ketut Suardamana, Sp.PDKAI
3
Pathology
Interna
4
Interna
5
DME
6
Obgyn
7
Orthopaedi
8
Anasthesi
9
Neurology
10
Interna
08123974128
08123989353
081805391039
081338713951
0811385263
08123661312
0817347697
08123985811
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
FACILITATORS
(ENGLISH CLASS)
NO
1
2
3
4
5
6
7
8
9
10
NAME
dr. I Made Susila Utama, Sp.PDKPTI
dr. I Gusti Ngurah Purna Putra,
Sp.S (K)
Dr.dr I Nyoman Gede Budiana,
Sp.OG (K)
Prof.Dr.dr.I Putu Gede
Adiatmika, M.Kes
dr. Komang Andi Dwi Saputra,
Sp.THT- KL
Dr. dr. I Dewa Made Sukrama,
MSi, Sp.MK(K)
dr. I Gusti Ayu Sri Darmayani,
Sp.OG
Dr.dr. Yenny Kandarini, Sp.PDKGH-FINASIM
dr. I Gede Budhi Setiawan,
Sp.B(K)Onk
dr. Henky, Sp.F., M.BEth,
FACLM
GROUP
1
DEPT
Interna
PHONE
08123815025
2
Neurology
08123915769
3
Obgyn
08123997401
4
Fisiology
08123811019
5
ENT
081338701878
6
Microbiology
081338291965
7
DME
081338644411
8
Interna
08123805344
9
Surgery
08123923956
10
Forensic
08123988486
VENUE
3nd floor:
R.3.09
3nd floor:
R.3.10
3nd floor:
R.3.11
3nd floor:
R.3.12
3nd floor:
R.3.13
3nd floor:
R.3.14
3nd floor:
R.3.15
3nd floor:
R.3.16
3nd floor:
R.3.17
3nd floor:
R.3.19
7
Study Guide Immune System
and Disorders
TIME TABLE OF THE BLOCK IMMUN SYSTEM & DISSODERS 2015
DAYS /
TIME
ACTIVITY
CONVEYER
VENUE
•
Class Room
DATE
1
ENGLISH CLASS
REG CLASS
08.00-09.00 (60’)
09.00-10.00 (60’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
Student
Project
preparation
-
-
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. dr. Ketut Suryana,
SpPD-KAI
08.00-08.30 (30’)
09.00-09.30 (30’)
•
•
dr. Ni Made Linawati,
MSi
Friday,
Oct 16,
2015
2
Monday,
Oct 19,
2015
3
08.30-09.00 (30’)
09.30-10.00 (30’)
(SP):
paper
Comprehend The Microscopic
Structure of Limphoid
Organ,Immune Cells and MHC
•
Comprehend tissue repair
•
Comprehend basic mechanism of
autoimmunity
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
•
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
12.30-14.00 (90’)
10.00-11.30 (90’)
Student Project
preparation
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
Dr. dr. Ketut Suryana,
SpPD-KAI
:
paper
Class Room
dr. Putu Sri Widyani,
S.PA.
Library
Discussion Room
Fasilitator
-
(SP)
Class Room
-
-
Library
•
dr. Ni Made Linawati,
Msi
•
dr. Putu Sri Widyani,
S.PA.
Class Room
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Comprehend acute and chronic
inflammation
•
Dr. I Wayan
Sumadi, Sp.PA.
08.30-09.00 (30’)
09.30-10.00 (30’)
•
Comprehend hypersensitivity
•
Dr.Tjok Istri
Saturti, SpPD
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
-
-
Tuesday,
Oct 20,
2015
Introduction to The Immune
System and disorders
Juli
Class Room
Anom
8
Study Guide Immune System
and Disorders
12.30-14.00 (90’)
10.00-11.30 (90’)
SP: paper preparation
-
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. I Wayan
Sumadi, Sp.PA.
•
Dr.Tjok Istri
Saturti, SpPD
•
Dr. I Made Jawi, M.Kes
4
08.00-08.30 (30’)
09.00-09.30 (30’)
Wednes
day,
08.30-09.00 (30’)
09.30-10.00 (30’)
Oct 21,
2015
5.
•
•
Class Room
Anom
Class Room
•
Forensic Laboratory
•
dr Henky, SpF
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
•
Dr. Ketut Suardamana,
SpPD-KAI
08.00-09.00 (60’)
09.00-10.00 (60’)
•
Adverse drug reaction
•
Able to diagnose and manage
anaphylaxis
Oct 22,
2015
Class Room
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
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Comprehend laboratory test of
immune system
•
Dr. dr. I Wyn Putu
Sutirta Yasa, Msi
Class Room
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Antihistamine
•
Dr.dr.B.K.Satriyasa,M.
Repro
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
SP
paper
Imunomodulator
Friday,
Oct 23,
2015
Juli
09.00-10.30 (90’)
Thursda
y,
6.
Comprehend basic mechanism of
drug allergy and
immunopharmacology
Library
presentation: dr. Made Jawi, M.Kes
Class Room
9
Study Guide Immune System
and Disorders
14.00-15.00 (60’)
7.
15.00-16.00 (60’)
Plenary Session
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Able to diagnose and manage
allergic diseases in ENT
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Able to diagnose and manage
allergic diseases in dermatology
Monday,
Oct 26,
2015
8.
•
Dr.dr.B.K.Satriyasa,
M.Repro
•
Dr. Sari Wulan Dwi
Sutanegara , Sp THTKL
•
-Dr.Nyoman Suryawati,
SpKK
Class Room
Class Room
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’)
K
Suardamana, Class Room
SP paper presentation: Urtikaria dr.
SpPD-KAI
and Angiodema
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. Sari Wulan Dwi
Sutanegara , Sp THTKL
•
Dr.Nyoman Suryawati,
SpKK
•
Dr. Gede Kambayana,
SpPD-KR
Class Room
08.00-09.00 (60’)
09.00-10.00 (30’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
12.30-14.00 (90’)
10.00-11.30 (90’)
SP paper presentation: Blood Dr.dr. Wy Putu Sutirta Class Room
Group Incompatibility
Yasa, M.Si.
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
•
Dr. Gede Kambayana,
SpPD-KR
08.00-08.30 (30’)
09.00-09.30 (30’)
•
•
Prof. Dr. dr AA Raka
Sudewi, Sp S
Oct 27,
2015
Wednes
day,
Dr. dr. I Wyn Putu
Sutirta Yasa, Msi
09.00-10.30 (90’)
Tuesday,
9.
•
Able to diagnose and manage
SLE, RA & Polimyalgia
Rheumatica
Able to diagnose and manage
autoimmune diseases in Neurology
•
Class Room
Class Room
Class Room
08.00-09.00 (30’)
09.30-10.00 (30’)
•
09.00-10.30 (90’)
12.00-13.30 (90’)
Independent Learning
-
Library
10.30-12.00 (90’)
13.30-15.00 (90’)
SGD
Fasilitator
Discussion Room
12.00-12.30 (30’)
11.30-12.00 (30’)
Break
-
-
Oct 28,
2015
Able to diagnose and manage
secondary immunodeficiency
diseases (focus HIV)
Prof. DR. Dr. Tuti
Parwati M, SpPDKPTI
10
Study Guide Immune System
and Disorders
12.30-14.00 (90’)
14.00-15.00 (60’)
10.00-11.30 (90’)
15.00-16.00 (60’)
SP
paper
Limphadenitis TB
presentation: dr.
Plenary Session
10
08.00-08.30 (30’)
09.00-09.30 (30’)
•
Thursda
y,
Able to diagnose and manage
Rheumatic Disease of Childhood
08.00-09.00 (30’)
09.30-10.00 (30’)
•
Able to diagnose and manage
Food allergy
•
Able to diagnose and manage
immunodeficiency diseases in
childhood
Oct 29,
2015
11.
Sriwidnyani,
Class Room
•
Prof. Dr. dr AA Raka
Sudewi, Sp S
•
Prof. DR. Dr. Tuti
Parwati M, SpPDKPTI
•
Dr. Dewi Kumarawati,
SpA
Class Room
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 dr. Komang Suryawati, Class Room
Johnson Syndrome
Sp.KK.
14.00-15.00 (60’)
15.00-16.00 (60’)
Plenary Session
08.00-09.00 (60’)
09.00-10.00 (60’)
Soluble markers of
inflammation (BCS)
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
Friday,
Oct 30,
2015
Putu
Sp.A
BCS Discussion
Dr. Dewi
SpA
allergic
Kumarawati,
Class Room
dr. Wande, Sp.PK.
Class Room
-
Library
dr. Wande, Sp.PK &
Skill Lab
Team
12.
08.00-09.00 (60’)
09.00-10.00 (60’)
Forensic Laboratory (BCS)
Dr. Henky, SpF
Class Room
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
-
Library
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
Monday,
Nop 02,
2015
BCS Discussion
Dr. Henky , SpF, & Team
Skill Lab
13
Tuesday,
08.00-09.00 (60’)
09.00-10.00 (60’)
Anaphylactic syok (BCS)
Dr. Tjok Istri Anom S,
SpPD
Class Room
11
Study Guide Immune System
and Disorders
Nop 03,
2015
14
09.00-10.30 (90’)
10.00-11.30 (90’)
Independent Learning
-
Library
10.30-13.00 (150’)
13.30-16.00 (150’)
BCS Training
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Dr. Tjok Istri Anom S,
SpPD & Team
Skill Lab
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
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Dr. Putu Sri Widyani ,
Sp.A & Team
LAB Bersama
08.00-09.00 (60’)
09.00-10.00 (60’)
Skin Prick Test (BCS)
Dr. Ketut Suryana, SpPDKAI
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
Wednes
day
Nop 04,
2015
15
Thursda
y,
Nop 05,
2015
13.00-15.00 (120’)
11.30-13.30
BCS Discussion
Friday,
Nop 06,
2015
Monday,
Nop 9,
2015
Pre-evaluation Break
Examination
12
Study Guide Immune System
and Disorders
Meeting of the student representatives
The meeting between block planners team and the student group representatives will be
held on Monday, October 12, 2015 at 09.00 until 10.00 a.m at HAPEQ discussion room. In
this meeting, all of the student group representatives are expected to give suggestions or
inputs or complaints to the team planners for improvement. For this purpose, every student
group must choose one student as their representative to attend the meeting.
Meeting of facilitators
The meeting between block planners team and the facilitators will take place on, Monday,
October 12, 2015 at 10.00 am until 12.00 pm at HAPEQ discussion room. In this meeting all
the facilitators are expected to give suggestions and inputs as evaluation to improve the
study guide and the educational process. Because of the importance of this meeting, all the
facilitators are strongly expected to attend the meeting.
Plenary session
For each task of SGD, the students are requested to prepare a group report. The reports will
be presented in a plenary session. The group will be chosen randomly by the lecturer in
charge. The group report will be evaluated by respective facilitator.
Assessment Methods
Assessment will be performed at the end of the block on Nopember 9th 2015. There are 100
questions for the examination that consists of Multiple Choice Question (MCQ). The
borderline to pass exam is 70.
13
Study Guide Immune System
and Disorders
LEARNING
PROGRAMS
Day 1
Topics
:
Introduct. to the immune system and disorders
Lecturer
:
dr. Ketut Suryana, SpPD-KAI
Abstract
1. The Immune system has evolved to protect us from pathogens. Some, such as viruses,
infect individual cells; others, including many bacteria, divide extracellularly within
tissues or body cavities.
2. The cells which mediate immunity include lymphocytes and phagocytes. Lymphocytes
recognize antigens on pathogens. Phagocytes internalize pathogens and degrade them
3. An Immune response consists of two phases. In the first phase, antigen activates
specific lymphocytes that recognize it; in the effector phase, these lymphocytes
coordinate an immune response that eliminates that source of the antigens.
4. Specificity and memory are two essential features of adaptive immune responses. The
Immune system mounts a more effective response on second and subsequent
encounters with a particular antigen.
5. Lymphocytes have specialized functions. B cells make antibodies; cytotoxic T cells kill
virally infected cells; helper T cell coordinate the immune response by direct cell-cell
interactions and the release of cytokines, which help B cells to make antibody.
6. Antigens are molecules which are recognized by receptors on lymphocytes. B
lymphocytes usually recognize intact antigen molecules, while T lymphocytes recognize
antigen fragment on the surface of other cells.
7. Clonal selection involves recognition of antigen by a particular lymphocyte; this leads to
clonal expansion and differentiation to effector and memory cells.
8. The immune system may break down. This can lead to immunodeficiency or
hypersensitivity diseases or to autoimmune diseases.
Learning task
1.
2.
3.
4.
Comprehend of immune system with clinical implications
Comprehend the lymphoid organs and describe of it’s microscopic organization
Comprehend the cellular immunity
Comprehend the mechanism of cellular and humoral immunity to infection
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Day 2
Topic
:
The Microscopic Structure of Limphoid Organ,
Immune Cells and Histocompatibility Molecule
Lecturer
:
dr. Ni Made Linawati, M. Si.
Abstract
The limphoid systems is responsible for the immunological defense of the body.
Some of its component organs ; lymph nodes, thymus and spleen are surrounded by
connective tissue capsules, whereas its other components, member of the diffuse lymphoid
system, are not encapsulated. The cells of the limphoid systems such as lymphocytes ( T, B
and Natural Killer), Antigen Presenting Cells (Dendritic cells, Macrophages and B
lymphocytes) and other (Neutrophils) protect the body against foreign macromolecules,
viruses, bacteria, and other invasive microorganism, and they kill virally transformed cells.
Major Histocompability Complex (MHC) molecule are important to permit APCs and cells
under viral attact (or cells already virally transformed) to present the epitopes of the invading
pathogen to the T cells.
Learning Task
Vignette
A 65-year-old man had suffered from rectal bleeding during defecation for a few weeks.
Laboratory findings were normal except a slight elevation in the level of alkaline
phosphatase. Multiple polypoid lesions were observed in colonoscopic examination. The
histological and immunochemical evaluation showed atypical lymphoid cell proliferation and
lymphoepithelial lesions on the colonic mucosa, staining with CD20. After the diagnosis had
been confirmed as low grade mucosa associated lymphoid tissue lymphoma.
a. Please describe histological structure of the Mucosa associated lymphoid tissue.
b. Why M cells has important roles in mucosa immune response?
Self Assesment
1. What are primary and secondary lymphoid organ. Mention the of organ that has
function as primary and secondary lymphoid organ
2. Describe about function and microscopic structure of thymus, lymph nodes; spleen;
tonsils; and MALT
3. Describe about MHC class I and class II
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Topic
:
INFLAMMATION AND TISSUE REPAIR
Lecturer
:
dr. Ni Putu Sriwidyani, Sp.PA
ABSTRACT
Inflammation is fundamentally a protective response, designed to rid the organism of
both the initial cause of cell injury and the consequences of such injury. Inflammation is a
complex reaction in tissues that consists mainly of responses of blood vessels and
inflammatory cells. The vascular and cellular reactions of inflammation are triggered by
soluble factors that are produced by various cells or derived from plasma proteins and are
generated or activated in response to the inflammatory stimulus. Inflammation may be acute
or chronic, depending on the nature of the stimulus and the effectiveness of the initial
reaction in eliminating the stimulus. Inflammation is terminated when the offending agent is
eliminated. Outcomes of acute inflammation could be resolution, chronic inflammation, or
fibrosis.
Inflammation response is closely intertwined with the process of repair. Repair most
often consists of a combination of regeneration and scar formation by deposition of
collagen. Inflammation and repair may be harmful in some situations and may contribute to
a variety of diseases.
Understanding inflammation and repair can be applied as basic concept of patient
management, diagnostic, therapy, and monitoring.
LEARNING TASK
Vignette
A 20 year old female came to a doctor in private practice and complaint a right lower
abdominal pain and fever since 3 days ago. On physical examination, BP: 120/80 mm Hg,T
axilla: 400C. On lower right abdominal region revealed warm and pain in palpation.
Complete blood count showed leucocytosis. Appendectomy performed. Histology
examination showed oedematous, hypermi, and neutrophil infiltration extended from
mucosal until serosal layer. The diagnosis was acute appendicitis.
Task
1. Explain reactions of blood vessels and leukocyte in acute inflammation
2. Mention mediators of inflammation
3. Mention local effects and systemic effects of inflammation
4. Mention outcomes of acute inflammation
5. Mention role of macrophage and other inflammatory cells in chronic inflammation
6. Mention morphologic patterns of acute and chronic inflammation
7. Mention consequences of defective or excessive inflammation
8. Explain healing by fibrosis, scar formation, and fibrosis
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SELF ASSESMENT
1. Inflammatory cells that have a major role in most acute inflammation are:
A. Basophyl
B. Eosinophyl
C. Netrophyl
D. Macrophage
E. Mast cell
2. Mediators of increased vascular permeability in acute inflammation responses include all
of the following, except:
A. Histamine
B. Bradykinin
C. Leukotriene C4
D. Platelet Activating factor
E. Complement complex C5-9
3. Mediators of neutrophyl chemotaxis in acute inflammation responses include all of the
following, except:
A. C3a
B. C5a
C. IL-1
D. TNF
E. Bacterial product
4. Opsonization increases engulfment capability of macrophage in fagocytosis.
Complement system component that involved as a potent opsonin is:
A. C3a
B. C3b
C. C5a
D. C5b
E. C9
5. A 35 years old man with acute appendicitis and appendectomy performed. Pathologic
examination shows marked neutrophyl infiltration in the wall of the appendix. Based on
the morphological feature, the type of inflammation of this case is:
A. Serous
B. Suppurative
C. Catharalis
D. Fibrinous
E. Granulomatous
6. A 5 years old boy hospitalize in intensive care unit cause by accidently expose to boiled
water. All the skin of his body was red with blebs. Based on the morphological feature,
the type of inflammation of this case is:
A. Serous
B. Suppurative
C. Catharralis
D. Fibrinous
E. Granulomatous
7. Chronic inflammation are characterized by all of following morphologic feature, except:
A. Mononuclear infiltration
B. Tissue destruction
C. Angiogenesis
D. Fibrosis
E. Vasodilatation
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8. Permanent tissue is a mature tissue without capability to divide. The following tissue is a
permanent tissue:
A. Skeletal muscle
B. Hepar
C. Skin
D. Neuron
E. Kidney
9. A large aggregate of epitelioid cells is seen in a microscopic section of an ovarial tumor.
Your diagnosis is:
A. Granulation tissue
B. Granuloma pyogenicum
C. Granulosa cell tumor
D. Granuloma
E. Granulocytosis
10. Local factor that retard wound healing is:
A. Diabetes
B. Malnutrition
C. Foreign bodies
D. Genetic
E. Vitamin C deficiency
Day 3
Topic
:
Basic mechanism of autoimmunity
Lecturer
:
dr. I Wayan Juli Sumadi, Sp.PA.
ABSTRACT
Immunologic Tolerance: Is a state in which an individual is incapable of developing an
immune response against a specific antigen.
Self- tolerance: Specifically refers to a lack of immune responsiveness to one’s own tissue
antigens.
Two broad groups of mechanisms to explains the tolerant state:
▪ Central tolerance: This refers to deletion of self-reactive T and B lymphocytes during
maturation in central lymphoid organs (i.e. in the thymus for T cells and the bone marrow
for B cells)
▪ Peripheral tolerance: Self reactive T cells that escape negative selection in the thymus
can potentially wreak havoc unless they are deleted or effectively muzzled. Several
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.
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Furthermore, the breakdown of tolerance and initiation of autoimmunity involves the
interaction of complicated immunologic, genetic, and microbial factors.
Learning task
Trigger Case
A 25-year-old woman has had increasing malaise, a skin rash of her face exacerbated by
sunlight exposure, and arthtralgias and myalgias for the past month. On physical
examination she has mild pedal edema. On auscultation a friction rub is audible over the
chest. Laboratory findings include pancytopenia and serum creatinine 3 mg/dL. Urinalysis
shows hematuria and proteinuria. A serologic test for shypilis yields a false positive result. A
renal biopsy shows a slight increase of mesangial cells and granular deposit of IgG and
complement in the mesangium and along basement membrane. The result of ANA test is
positive. Finally, the patient is diagnosed as systemic lupus erythematosus (SLE). SLE is
the best example of autoimmune disease. Does the autoimmunity result from the loss of
self-tolerance, how this happen, and why they have a broad clinical spectrum as showed in
that patient? Before you answer the question, please try to find out the following task.
Task
1. Describe the mechanism of immunological tolerance to self antigent!
2. Explain the mechanism of autoimmunity, including the role of susceptibility genes
and enviromental triggers!
3. Describe the general features of autoimmune diseases!
4. Describe the etiopathogenesis of SLE!
5. Describe the mechanism of tissue injury in SLE, and give some examples of
morphological changes in SLE!
6. Mention other diseases that belong to autoimmune diseases group!
Topic
:
Hypersensitivity
Lecturer
:
dr. Tjok Istri Anom Saturti, SpPD
ABSTRACT
There are 4 types classifications according to
Gel & Coombs
1. Type I
: Immediate hypersensitivity
2. Type II
: Cytotoxic hypersensitivity
3. Type III
: Immune complex hypersensitivity
4. Type IV
: Delayed (cell mediated) hypersensitivity
Hypersensitivity the immune response results are harmful to the heart
Type I
: Antigen bind to IgE on the surface of mast cells à release of several
mediators within minutes. Important mediators are: Histamin, SRS-A, ECFA, serotonin, Prostaglandins and thromboxanes, etc. Clinical
manifestations:
1. Anaphylaxis : severe bronconstriction, hypotension à shock
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Type II
Type III
Type IV
2. Atopy: genetic factor to induce by exposure to spesific allergens
(pollens, dust, shellfish, nuts, etc). Clinical manifestation: hay fever,
asthma, eczema, and urticaria. Treatment and prevention: Avoidance of
the responsible allergen, Hyposensitization (Desensitization) & Drug
treatment.
: Antibody is directed against antigen on an individual’s own cell (target cell)
or foreign antigen, such as transfused red blood cell. This may lead to
cytotoxic action by K Cells, or complement mediated lysis.
: Immune Complexes are deposited in the tissue. Complement is activated
and polymorphs are attracted to the site of deposition causing local tissue
damage and inflammation
: Antigen sensitized T cells release lymphokines following a secondary
contact with the same antigen. Cytokines induced inflammatory reactions
activate and attract macrophages, which release inflammatory mediators.
Learning Task Hypersensitivity :
1. Make definition of the term hypersensitivity
2. Explain the biological roles of hypersensitivity
3. Make classification of hypersensitivity
4. Compare the hypersensitivity type I, II, III and IV
5. Explain principle treatment and prevention of hypersensitivity
SELF ASSESSEMENT R. HIPERSENSITIFITAS
1. Hypersensitivity reaction is a general pathologic reaction which has following
characteristics:
A. Never happens on the first exposure
B. Generally divided into 4 types
C. Is an overreaction of immune system
D. Occurred if humoral and cellular immunological status are increased
E. All above are correct
2. The followings are the feature of hypersensitivity reaction type I, except:
A. Occurs in few seconds or minutes
B. Is an IgE mediated immune response
C. IgE is bind by mast cell
D. Ia a delayed hypersensitivity
E. Histamine is a primary mediator produced
3. In hypersensitivity reaction type I, eosinophyl is activated by:
A. IL-4
B. IL-2
C. IL-5
D. IL-6
E. IL-1
4. Histamine release effect of hypersensitivity reaction type I is:
A. Vasoconstriction of blood vessels
B. Vasodilation of blood vessels
C. Capillary permeability decreased
D. Bronchus dilated
E. Hyposecretion of mucosa
5. Hypersensitivity reaction type II is a cytotoxic reaction which involves:
A. IgG and IgM
B. IgG and IgD
C. IgG and IgA
D. IgA and IgD
E. IgD and IgE
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Day 4
Topic
:
Immunopharmacology
Lecturer
:
dr. I Made Jawi, M.Kes.
ABSTRACT
Immunopharmacology includes the characteristics of drugs that can suppress,
modulate, or stimulate immune functions. It also includes the pharmacology of antibodies
that have been developed for use in immune disorders. The drugs available comprise a
wide variety of chemical and pharmacologic types. In this topic also will be discuss the ways
in which drugs may activate the immune system and cause unwanted immunologic
reactions. Drugs that modulate immune function and as a immune suppressants are:
glucocorticoids (prednisone), immunophilin ligands (Cyclosporine), cytotoxic drugs
(Cyclophosphamide), Anti-TNF-α agents (etanercept), enzyme inhibitors (mycophenolate
mofetil) and Antibodies.
Drugs that modulate immune function and as a immune potentiators are: Cytokines
(Interleukin-2, Interferons), BCG vaccine and Thymosin.
Learning Task
A patient was treated with penicillin. Within a few minutes after penicillin injection, he
developed severe bronchoconstriction, laryngeal odema and hypotension.
1. Explain the immunologic mechanism of those problems.
2. To manage that patient what medicine will you give for him immediately?
3. Explain your answer if you give him prednisone. Do you agree? Why?
4. How about antihistamine like dimenhydrinate for this patient?
Self assessment Immunopharmacology
1. Cyclosporine is effective in organ transplantation. The immunosuppressant action of
the drug appears to be due to
A. Activation of natural killer (NK) cells
B. Blockade of tissue responses to inflammatory mediators
C. Increased catabolism of IgG antibodies
D. Inhibition of the gene transcription of interleukins
E. Interference with antigen recognition
2. Azathioprine
A. Binds avidly to a cytoplasmic immunophillin
B. Blocks formation of tetrahydrofolic acid
C. Is a precursor of cytarabine
D. Is markedly hematotoxic and has caused neoplasms
E. Is a metabolite of mercaptopurine
3. Which of the following drugs is a widely used agent that suppresses cellular immunity,
inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG
antibodies?
A. Cyclophosphamide
B. Cyclosporine
C. Infliximab
D. Mercaptopurine
E. Prednisone
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4. Which one of the following agents acts at the step of antigen recognition ?
A. Cyclosporine
B. Cyclophosphamide
C. Methotrexate
D. Rh0 (D) immune globulin
E. Tacrolimus
5. An immunosuppressed patient was treated for a bacterial infection with parentral
penicillin. Within a few minutes after penicillin injection, he developed severe
bronchoconstriction, laryngeal edema, and hypotension. Due to the rapid administration of
epinephrine, the patient survived. Unfortunately, a year later he was treated with an
antipsychotic drug and developed agranulocytosis.
The type of drug reaction that was caused by the penicillin is
A. An autoimmune syndrome
B. A cell-mediated reaction
C. A type II drug allergy
D. Mediated by IgE
E. Serum sickness
Topic
:
Forensic Laboratory
Lecture
:
dr. Henky, SpF
Abstract
Forensic serology is the study of serology in relation to crimes and other legal matters by
using a scientific approach.
Doctors should have knowledge about forensic serology to
assist investigators in revealing crime cases related with human’s body and health.
Moreover, based on legislations, doctors have legal duty to carry out forensic examination
when asked by the investigators.
Mostly, investigators asked doctors to prove homicide, rape, assault or dispute paternity
case. To prove it, the doctors need to do serological examination of biological evidence that
found on the victim’s body, such as blood, semen, urine, and other body fluids.
Principle of serological test is the use of specific antibodies to detect a target antigen. By
doing a simple serological test, doctor can filter the type and origin of biological substances.
If the screening test gives a positive result, biological substances must be processed for
DNA testing to determine the owner of biological materials.
Vignette 1
A woman, 22 years old was found dead and naked. She suffered bruises almost on her
entire body. There were blood stains and fluid around her genital.
Learning Task
1. In above case, discuss the role of forensic serology in examining biological evidence!
2. Discuss the steps to examine blood stain and fluid around the genital!
3. Discuss the concept of species determination and individualization of blood stain and
biological fluid!
4. If in that case, there are 3 suspects, what the forensic serologist do to identify the
suspect?
5. Discuss about DNA analysis for that case!
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Vignette 2
A man, with blood type O, come to prove that his wife, with blood type AB, have an affair
with her boss, with blood type A. He is not sure whether he is the biological father of his
child, because his first child is male, with blood type O, and the second one is female, with
blood type AB.
Learning Task
As a doctor, what would you explain to the man?
Day 5
Topic
:
Adverse drugs reaction
Lecture
:
dr. Ketut Suardamana, Sp. PD
Introduction
Drug allergy or hypersensitivity is a form of Adverse Drug Reaction (ADR)
Definition
An ADR is any undesirable effect of drug that is administered in standard doses by
the proper route for the purpose of prophylaxis, diagnosis, or treatment.
Drug allergy is an immunologically mediated reaction, occurs in a susceptible populations,
characterized by specificity, transferability by antibodies or lymphocytes, and recurrence on
re-exposure
Pathophysiology
Allergic drug reactions are usually defined as;
1. reaction caused by suspected immunologic mechanisms
2. result from the production of antibodies and / or cytotoxic T cells directed against the
drug,
3. its metabolite, a soluble / cell-bound carrier protein as a responses to prior or
continuous exposure to a drug
Risk factors
1. Patient related : Age, sex, genetics, atopy, AIDS
2. Drug related : Macromolecular size ; bivalency, haptens, route, dose, duration of
treatment
3. Aggravating factors : β Blockers, asthma, pregnancy
Diagnosis
1.
Diagnosis of drug allergy based on ;
2.
Clinical history
3.
Clinical manifestations
4.
Diagnostic test
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Diagnostic tests
1. SPT may be helpful for diagnosing IgE mediated drug reactions (in vivo)
2. RAST
may detect serum IgE antibodies to certain drugs (e.g : penicillin and
succinyl choline) (in vitro)
3. Provocation tests
Oral provocation tests, may be as a gold standard
They must be performed under strict medical supervision with resuscitative
equipment available
Management
1. Avoidance
2. Premedication
3. Desensitisation
Learning Task ADVERSE DRUGS REACTION (ADR)
Vignette
Male 20 years old, was diagnosed with Pulmonary TB and taking the anti TB regimen
(Category 1). On the second day treatment he felt an itchy – swollen redness on whole
body. He had previous history of drug allergy but the allergen is unknown, his mother also
had history of drugs allergy. The patient was fully alert, T 110/70 mmHg, pulse rate 92x per
minute regular, RR 18x per minute.
Task
1. Could you explore more to complete the anamnesis!
2. Describe any sign that you find on Physical examination?
3. How to manage this patient?
Self assessment
1. Could you describe the adverse drugs reaction (ADR)!
2. Describe the immunopathophysiology of drugs allergy (due to Gell & Coombs
Criteria)!
3. Comprehend the diagnostic approach of the drugs allergy!
Topic
:
Anaphylaxis reaction
Lecture
:
dr. Ketut Suardamana, Sp. PD.
Definition
Anaphylaxis is an acute severe, life-threatening, generalized or systemic hypersensitivity
reactions
Pathophysiology
1. Type I reaction (IgE mediated)
2. Anaphylactoid reaction (Non IgE mediated) : complement activation, physical
factors, substance for Histamine release, idiopathic, arachidonic acid modulation
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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 lipstongue-uvula) AND AT LEAST ONE OF THE FOLLOWING
a. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced
PEF, hypoxemia)
b. Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia
/collapse, syncope, incontinence)
2. Two or more of the following that occur rapidly after exposure to a likely allergen for that
patient (minutes to several hours) :
a. Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen
lips-tongue-uvula)
b. Respiratory compromise (eg dyspnea, wheeze-bronchospasm, stridor, reduced
PEF, hypoxemia)
c. Reduced BP or associated symptoms (eg, hypotonia collapse, syncope,
incontinence)
d. Persistent gastrointestinal symptoms (eg cramp abdominal pain, vomiting)
3. Reduced BP after exposure to known allergen for that patient ( minutes to several
hours)
a. Infants and children: low systolic BP (age specific) or greater than 30% decrease
in systolic BP
b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from
that person's baseline
Learning task ANAPHYLAXIS
Vignette
Female 30 years old, came to the Emergency Unit with chief complaint; edema on palpebra,
itchy redness on the whole body skin after taking metampirone 500 mg tab. as a treatment
for headache. She also complains; shortness of breath, fatique and warmth on the lower
extremity.
Task
1.
2.
3.
4.
What should you do for the first?
Could you complete your anamnesis!
What do you find on physical examination?
The laboratory plan? Or other diagnostic procedure?
Self assessment
1. What are the differential diagnoses?
2. Could you describe the pathophysiology of anaphylaxis?
3. Could you describe the clinical manifestations?
4. The management in this case!
5. Describe the prevention!
6. Comprehend any prognostic factors!
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Day 6
Topic
:
Laboratory test of immune system
Lecture
:
Dr. dr. I Wyn Putu Sutirta Yasa, M.Si.
Abstract
Objective to comprehend laboratory test of immune system
1. Approach in the patient with immune system disease and disorders are evidence
based in immunology, history and physical examination, laboratory studies to make
diagnosis. Laboratory test of immune system (immunoassay) based on antigenantibody reactions. Immunoassay can be used for the detection of either antigens or
antibodies. For antigen detection, the corresponding specific antibody should be
prepared as one of reagents. The reverse is true for antibody detection.
2. The sensitivity of the immunoassays has been enhanced through the development
of types of signal detection systems and solid-phase technology. Immunoassay has
been optimized to detect less than 0.1 pg/mL of antigen in blood.
3. The can be applied to detection of haptens as small molecules, protein and protein
complexes as macromolecules, as well as of any antibody to allergens, infectious
agent, and autologous antigens.
4. Students to comprehend the overview of general principles and based of
immunoassay. High concentration of such molecules and where antigen- antibodies
are mixed in solution can be measured by precipitation techniques. Medium
concentration of such molecules and where antigen- antibodies are on solid phase
can be quantified by agglutination techniques. Very low concentration of such
molecules can be quantified by radioimmunoassay techniques or enzyme linked
immunosorbent assay techniques.
Outcome of laboratory test of immunes system
Students to comprehend the overview of general principles and based
immunoassay to purpose and function of laboratories are to assist students in
confirming or rejection a diagnosis, (2) providing guidelines for patient management,
establishing a prognosis, (4) detecting disease through case finding or screening and
monitoring follow up therapy.
of
(1)
(3)
(5)
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?
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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.
2.
3.
4.
5.
Explain two classification of H1 blockers
List two drugs the older members of the first generation agent
List three drugs the second generation of H1 blockers.
Describe mechanism and effect of H1 blockers
Describe clinical use of H1 blockers
Self assessment Antihistamine
1. Many H1 blocker have additional nonhistamine-related effect, these are likely to include
all of the following. EXPECT:
A. Antimuscarinic reduction in bladder tone
B. Local anesthetic effect if the drug is injected
C. Anti-motion sickness effect
D. Increase in total peripheral resistance
E. Sedation
2. Which of the following drugs will result from blockade of H1 receptor?
A. Decreased cAMP in smooth muscle
B. Decrease channel opening in enteric nerves
C. Decrease IP3 in smooth muscle
D. Increase IP3 in smooth muscle
E. Increase in total peripheral resistance
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3. Which of the following drugs are used as anti-motion sickness and also for management
of chemotherapy-induced vomiting?
A. Diphenhydramine
B. Dimenhydrinate
C. Meclizine
D. Cyclizine
E. Loratadine
4. Toxicities of H1 blocker include which one of the following
A. Sedation
B. Dry mouth
C. Blurry vision
D. Vomiting
E. Hypotension
Day 7
Topic
:
Lecturer
:
Rhinitis Alergy
Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL
ABSTRACT
Allergic rhinitis is an inflammation of the nasal passages, usually associated with
watery nasal discharge and itching of the nose and eyes.
Allergic rhinitis affects about 20 percent of population and ranks as one of the most
common illnesses. The symptoms occur in the nose and eyes and usually occur after
exposure to dust, danders, or certain seasonal pollens in people that are allergic to these
substances.
There is strong genetic predisposition to allergic rhinitis. One parent with a history of
allergic rhinitis has about a 30 percent chance of producing offspring with the disorder. Tthe
risk increases to 50 percent if both parents have a history of allergies.
Characteristic symptoms include repetitive sneezing, rhinorrhea (runny nose), postnasal drip, nasal congestion, pruritic (itchy) eyes, ears, nose or throat, and generalized
fatigue. Symptoms can also include wheezing, eye tearing, sore throat, and impaired smell.
A chronic cough may be secondary to postna