Study Guide Immune Semester III 2017

CONTENTS

Contents ………...1

Foreword ………... ………....2

Curriculum ………..………...3

Block Team ………..………....4

Facilitators Team ……….………....6

Time Table ...……….………..7

Assessment Method ………..………19

Learning Program ……….20

Student Project ………..…50

References ……….51

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

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.

Our overall goal is to transfer the basic essential information on commonly allergy – immunological diseases that are required for the primary health care. This block will be completed by case illustration, learning tasks to be discuss by the students in the small group discussions and individually in order to achieve the block objectives.

The Block ″ The Immune System an Disorders ″ ( ISD ) is undertaken 19 days including skill lab, examinations. Student – centered learning as the primary approach in the teaching-learning activities with dynamic group discussions are facilitated by tutors. Individual learning in Campus and at home is also an important part of the learning process. To develop good understanding of the ISD, learning activities will also be carried out as lectures, practical and learning with the patients ( Skill Lab).

Team of Planners

CURRICULUM

Aims:

1. To comprehend the biology of the immune system in health and diseases 2. To diagnose and manage common immune-mediated disorders

3. To diagnose and manage common disorders of the joints and adjacent tissue

Learning Outcomes:

To be able to

1. Diagnose and manage patients with inflammation

2. Diagnose and manage patients with hypersensitivity / allergic diseases 3. Diagnose and manage patients with autoimmune diseases

Curriculum contents:

No Name Department Phone

1 dr. Tjok Istri Anom S, SpPD (Head) Internal Medicine 082145854167

2 dr. Sari Wulan DS, SpTHT-KL ENT 081237874447

3 dr. Ketut Suardamana, SpPD-KAI (Member)

Internal Medicine 08123985811

4 Dr. dr. Ketut Suryana, Sp.PD-KAI (Member)

Internal Medicine 08123960964

5 Dr. dr. Ni Putu Sriwidnyani, Sp.PA (member)

Pathology Anatomy 081337115012

6 Dr. dr. Ni Made Linawati, M.Si (member) Histology 081337222567 7 dr. Komang Suryawati, Sp.KK (Member) Dermatology 0817447279 9 dr. I Gusti Ayu Harry Sundariyati, S.Ked DME 081805380277

LECTURERS

No Name Department Phone

1 Dr. dr. Ketut Suryana, Sp.PD-KAI Internal Medicine 08123960964 2 Dr. dr. Ni Made Linawati, Msi Histology 081805629937 3 Dr. dr. Ni Putu Sriwidyani, Sp. PA Pathology Anatomy 081337115012 4 dr. Komang Ayu Witarini,SpA Pediatrics 081239559559 5 Dr. dr. I Wyn Putu Sutirta Yasa, Msi Clinical Pathology 03617428983 6 _{Dr. dr. I Made Jawi, M.Kes Pharmacology 08179787972} 7 _{Dr. dr. B. K. Satriyasa, M.Repro Pharmacology 087777790064} 8 _{dr. Nyoman Suryawati, Sp.KK Dermatology 0817447279} 9 _{dr. Ketut Suardamana, Sp.PD-KAI Internal Medicine 08123985811} 11 dr. Sari Wulan Dwi Sutanegara ,

Sp.THT-KL

FACILITATORS

No Name Group Departement Phone ₍₃Venuerd _floor)

1 Prof. Dr.dr. I Putu Gede Adiatmika, _M.Kes A1 Physiology 08123811019 3rd floor:_R.3.01

2 dr. I Kadek Swastika, M.Kes A2 Parasitology 08124649002 3rd floor:_R.3.02

3 dr. I Wayan Surudarma, Msi A3 Biochemistry 081338486589 3rd floor:_R.3.03

4 dr. Anak Agung Ayu Ngurah Susraini, _Sp.PA(K) A4 _PhatologyAnatomy 0811398913 3rd floor:_R.3.04

5 Dr. dr. Ni Made Linawati, M.Si A5 Histology 081337222567 3rd floor:_R.3.05

6 dr. I Gusti Ayu Harry Sundariyati, _S.Ked A6 DME 081805380277 3rd floor:_R.3.06

7 dr. Yukhi Kurniawan, Sp.And A7 Andrology 08123473593 3rd floor:_R.3.07

8 dr. Ni Nengah Dwi Fatmawati, Sp.MK, _Ph.D A8 Microbiology 087862200814 3rd floor:_R.3.08

9 dr. Dewa Gde Mahiswara Suadiatmika,_Sp.Rad A9 Radiology 08123846307 3rd floor:_R.3.21

No Name Group Departement Phone Venue(3rd floor)

1 dr. I Wayan Sugiritama, M.Kes B1 Histology 08164732743 3rd floor: _R.3.01

2 Dr. dr. I Made Muliarta, M.Kes B2 Physiology 081338505350 3rd floor: _R.3.02

3 dr. Muliani, M.Biomed B3 Anatomy 085103043575 3rd floor: _R.3.03

4 dr. Putu Cintya D.Y, MPH B4 Public Health 081353380666 3rd floor: _R.3.04

5 Dr. dr. I Dewa Made Sukrama, Msi, _{Sp.MK (K)} B5 Microbiology 081338291965 3rd floor: _R.3.05

6 Dr. dr. Gde Ngurah Indraguna Pinatih. _{M.Sc, Sp.GK} B6 Public Health 08123816424 3rd floor: _R.3.06

7 dr. Tjokorda Gde Dharmayuda, _Sp.PD-KHOM B7 Internal _Medicine 0811394108 3rd floor: _R.3.07

8 Dr. dr. Susy Purnawati, M.KK B8 Physiology 08123989891 3rd floor: _R.3.08

9 Prof. dr. I G M. Aman, Sp.FK B9 Pharmacology 081338770650 3rd floor: _R.3.21

10 Dr.dr. Luh Putu Ratna Sundari, _M.Biomed B10 Physiology 081933070077 3rd floor: _R.3.22

(ENGLISH CLASS)

TIME TABLE OF THE BLOCK IMMUNE SYSTEM & DISSODERS 2017

Regular Class

Days/Date

Activity

Conveyer

Venue

Monday,N

ov 13,

2017

08.00-09.00

(60’)

· Introduction to The

Immune System and

disorders

· Dr. dr. Ketut

Suryana, SpPD-KAI

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

Student Project (SP):

paper preparation

-

Discussio

n Room

14.00-15.00

Tuesday,

Nov 14,

2017

08.00-08.30

(30’)

08.30-09.00

(30’)

· Comprehend The

Microscopic Structure of

Limphoid Organ,Immune

Cells and MHC

· Comprehend basic

mechanism of

autoimmunity

· Dr. dr. Ni Made

Linawati,Msi

· Dr. dr. Ni Putu

Sriwidyani, Sp. PA

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

Student Project (SP) :

paper preparation

-

Discussio

n Room

14.00-15.00

(60’)

Plenary Session

· Dr. dr. Ni Made

Linawati, Msi

Class

Room

· Dr. dr. Ni Putu

Sriwidyani, Sp. PA

Wednesda

y, Nov 15,

2017

08.00-08.30

(30’)

08.30-09.00

(30’)

Forensic Serology &

Molecular

· Antihistamin

- dr. IB Putu Alit,

SpF, DFM

· Dr.dr.B.K.Satriyas

a,M.Repro

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP: paper preparation

-

Discussio

14.00-15.00

(60’)

Plenary Session

· dr. IB Putu Alit,

SpF, DFM

· Dr.dr.B.K.Satriyas

a,M.Repro

Class

Room

Thursday,

Nov 16,

2017

08.00-09.00

(60’)

· Comprehend laboratory

test of immune system

· Dr. dr. I Wayan

Putu Sutirta Yasa,

Msi

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP paper preparation

-

Discussio

n Room

14.00-15.00

(60’)

Plenary Session

· Dr. dr. I Wayan

Putu Sutirta Yasa,

Msi

Class

Room

Friday,

Nov 17,

2017

08.00-09.00

(60’)

· Able to Diagnose and

Manage Autoimmune

Disease in Neurology

· Dr. dr. Made Oka

Adnyana, Sp.S (K)

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP: paper preparation

-

Class

Room

14.00-15.00

(60’)

Plenary Session

Dr. dr. Made Oka

Adnyana, Sp.S (K)

Class

Room

Monday,

Nov 20,

2017

08.00-09.00

(60’)

· Able to diagnose and

manage allergic

diseases in ENT

· Comprehend

Hypersensitivity

· dr. Sari Wulan Dwi

Sutanegara, Sp THT

(K)

· dr.Tjokorda Istri

Anom Saturti,SpPD

Class

Room

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

· SP paper presentation:

Rinitis Allergy

· Rheumatic Fever

· dr. Sari Wulan Dwi

Sutanegara, Sp THT

(K)

· dr.Tjokorda Istri

Anom Saturti,SpPD

Discussio

n Room

14.00-15.00

(60’)

Plenary Session

· dr. Sari Wulan Dwi

Sutanegara, Sp THT

(K)

Class

Room

Tuesday,

Nov 21,

2017

08.00-09.00

(60’)

· Adverse drug reaction

· dr. Ketut

Suardamana,

SpPD-KAI

Class

Room

· Able to diagnose and

manageanaphylaxis

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP: paper presentation :

· Poliarthritis Nodusa

· Immunomodulator

-· dr. Ketut

Suardamana,

SpPD-KAI

· Dr. dr. I Made

Jawi, M.Kes

Discussio

n Room

14.00-15.00

(60’)

Plenary Session

· dr. Ketut

Suardamana,

SpPD-KAI

Class

Room

Wednesda

y, Nov 22,

2017

08.00-09.00

(60’)

Able to diagnose and

manage SLE,

Rheumatoid Arthritis &

Polimyalgia Rheumatica

· dr.Gede

Kambayana,SpPD-KR / dr.Pande Ketut

Kurniari,SpPD

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

Fasilitator

Discussio

n Room

12.00-12.30

(30’)

-12.30-14.00

(90’)

SP paper presentation:

Polimialgia Rheumatyca

· Blood Group

Incompatibility

· dr.Gede

Kambayana,SpPD-KR/dr.Pande Ketut

Kurniari,SpPD

· Dr. dr. I Wayan

Putu Sutirta Yasa,

Msi

Class

Room

14.00-15.00

(60’)

Plenary Session

· dr.Gede

Kambayana,SpPD-KR/dr.Pande Ketut

Kurniari,SpPD

Class

Room

Thursday,

Nov 23,

2017

08.00-09.00

(60’)

· Able to diagnose and

manage Allergy and

autoimmune diseases in

Dermatology

· Dr.Nyoman

Suryawati,SpKK

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP paper presentation:

HSP and Eritema

Multifornis

· Dr.Nyoman

Suryawati,SpKK

Class

Room

14.00-15.00

(60’)

Plenary Session

Dr.Nyoman

Suryawati,SpKK

Class

Room

Friday,

Nov 24,

2017

08.00-09.00

(60’)

· Able to diagnose and

manage Rheumatic

Disease of Childhood

· dr. Komang Ayu

Witarini,SpA

Class

Room

· Able to diagnose and

manage Food allergy

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP paper presentation :

Juvenile Chronic Arthritis

and Milk Allergy

· dr. Komang Ayu

Witarini,SpA

14.00-15.00

(60’)

Plenary Session

· dr. Komang Ayu

Witarini,SpA

Class

Room

Monday,

Nov 27,

2017

08.00-09.00

(60’)

 Comprehend basic

mechanism of drug

allergy

 Immunopharmacology

·  Dr. dr. I Made

Jawi,M.Kes

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-12.00

(90’)

SGD

· Fasilitator

Discussio

n Room

12.00-12.30

(30’)

Break

-

-12.30-14.00

(90’)

SP: paper preparation

-

-14.00-15.00

(60’)

Plenary Session

· Dr. dr. I Made

Jawi,M.Kes

Class

Room

Tuesday,

Nov 28,

2017

08.00-09.00

(60’)

Laboratory Test For

Allergy And Autoimune

Disease (BCS)

· Dr.dr. I Wayan

Wande, Sp.PK

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-13.00

(150’)

BCS Training

· Dr.dr. I Wayan

Wande, Sp.PK &

Team

Skill Lab

13.00-15.00

(120’)

BCS Discussion

Wednesda

y,Nov 29,

2017

08.00-09.00

(60’)

Anaphylactic Syok

(BCS)

· dr. Tjok Istri Anom

Saturti, SpPD

Class

Room

09.00-10.30

(90’)

Independent Learning

-

Library

10.30-13.00

(150’)

BCS Training

· dr. Tjok Istri

Anom Saturti, SpPD

Skill Lab

13.00-15.00

(120’)

BCS Discussion

08.00-09.00

(60’)

SLE, RA focus on

physical examination

(BCS)

· dr.Gede

Thursday,

Nov 30,

2017

09.00-10.30

(90’)

Independent Learning

-

Class

Room

10.30-13.00

(150’)

BCS Training

· dr.Gede

Kambayana,SpPD-KR / dr.Pande Ketut

Kurniari,SpPD

Library

13.00-15.00

(120’)

BCS Discussion

· dr.Gede

Kambayana,SpPD-KR / dr.Pande Ketut

Kurniari,SpPD

Skill Lab

Monday,D

ec 4, 2017

08.00-09.00

(60’)

Skin Prick Tes

· Dr. dr. Ketut

Suryana, SpPD-KAI

09.00-10.30

(90’)

Independent Learning

-

Class

Room

10.30-13.00

(150’)

BCS Training

· Dr. dr. Ketut

Suryana, SpPD-KAI

13.00-15.00

(120’)

BCS Discussion

· Dr. dr. Ketut

Suryana, SpPD-KAI

Tuesday,D

ec 5, 2017

Pre-Evaluation Break

Wednesda

y,Dec 6,

2017

Evaluation

TIME TABLE OF THE BLOCK IMMUN SYSTEM & DISSODERS 2017

English Class

Days/Date

Time

Activity

Conveyer

Venue

Monday,N

ov 13,

2017

09.00-10.00 (60’)

 Introduction to The

Immune System and

disorders

 Dr. dr. Ketut

Suryana,

SpPD-KAI

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

Discussion

Room

11.30-12.00 (90’)

Break

-

Discussion

Room

12.00-13.30 (30’)

Independent

Learning

-13.30-15.00 (90’)

SGD

Facilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 Dr. dr. Ketut

Suryana,

SpPD-KAI

Class Room

Tuesday,

Nov 14,

2017

09.00-09.30 (30’)

09.30-10.00 (30’)

 Comprehend The

Microscopic

Structure of

Limphoid

Organ,Immune Cells

and MHC

 Comprehend basic

mechanism of

autoimmunity

 Dr. dr. Ni Made

Linawati,Msi

 · Dr. dr. Ni

Putu Sriwidyani,

Sp. PA

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

Library

11.30-12.00 (90’)

Break

-

Discussion

Room

12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 Dr. dr. Ni Made

Linawati, Msi

Class Room

 · Dr. dr. Ni

Putu Sriwidyani,

Sp. PA

Wednesda

y, Nov 15,

2017

9.0.9.3030’)

09.30-10.00 (30’)

Forensic Serology &

Molecular

· Antihistamin

 dr. IB Putu Alit,

SpF, DFM

 Dr.dr.B.K.Satri

yasa,M.Repro

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

Library

11.30-12.00 (90’)

Break

-

Discussion

12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 dr. IB Putu Alit,

SpF, DFM

 Dr.dr.B.K.Satri

yasa,M.Repro

Class Room

Thursday,

Nov 16,

2017

09.00-10.00 (60’)

 Comprehend

laboratory test of

immune system

 Dr. dr. I Wayan

Putu Sutirta

Yasa, Msi

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

Library

11.30-12.00 (90’)

Break

-

Discussion

Room

12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 Dr. dr. I Wayan

Putu Sutirta

Yasa, Msi

Class Room

Friday,

Nov 17,

2017

09.00-10.00 (60’)

 Able to Diagnose

and Manage

Autoimmune

Disease in

Neurology

 Dr. dr. Made

Oka Adnyana,

Sp.S (K)

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

Library

11.30-12.00 (90’)

Break

-

Discussion

Room

12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Class Room

15.00-16.00 (60’)

Plenary Session

Dr. dr. Made Oka

Adnyana, Sp.S

(K)

Monday,

Nov 20,

2017

09.00-09.30 (30’)

09.30-10.00 (30’)

 Able to diagnose

and manage allergic

diseases in ENT

Comprehend

Hypersensitivity

 dr. Sari Wulan

Dwi Sutanegara,

Sp THT (K)

dr.Tjokorda Istri

Anom

Saturti,SpPD

Class Room

10.00-11.30 (90’)

 SP paper

presentation: Rinitis

Allergy

 Rheumatic Fever

 dr. Sari Wulan

Dwi Sutanegara,

Sp THT (K)

dr.Tjokorda Istri

Anom

Saturti,SpPD

Class Room

11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 dr. Sari Wulan

Dwi Sutanegara,

Sp THT (K)

Tuesday,

Nov 21,

2017

09.00-10.00 (60’)

 Adverse drug

reaction

 dr. Ketut

Suardamana,

SpPD-KAI

Class Room

 Able to diagnose

and

manageanaphylaxis

10.00-11.30 (90’)

SP: paper

presentation :

Poliarthritis

Nodusa

 Immunomodulator

-dr. Ketut

Suardamana,

SpPD-KAI

Dr. dr. I Made

Jawi, M.Kes

Class Room

11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 dr. Ketut

Suardamana,

SpPD-KAI

Wednesda

y, Nov 22,

2017

09.00-10.00 (60’)

Able to diagnose

and manage SLE,

Rheumatoid Arthritis

& Polimyalgia

Rheumatica

 dr.Gede

Kambayana,SpP

D-KR / dr.Pande

Ketut

Kurniari,SpPD

Class Room

10.00-11.30 (90’)

SP paper

presentation:

Polimialgia

Rheumatyca

 Blood Group

Incompatibility

 dr.Gede

Kambayana,SpP

D-KR/dr.Pande

Ketut

Kurniari,SpPD

Dr. dr. I Wayan

Putu Sutirta

Yasa, Msi

Class Room

11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 dr.Gede

Kambayana,SpP

D-KR/dr.Pande

Ketut

Kurniari,SpPD

Class Room

Thursday,

Nov 23,

2017

09.00-10.00 (60’)

 Able to diagnose

and manage Allergy

and autoimmune

diseases in

Dermatology

 Dr.Nyoman

Suryawati,SpKK

Class Room

10.00-11.30 (90’)

SP paper

presentation: HSP

and Eritema

Multifornis

 Dr.Nyoman

Suryawati,SpKK

Class Room

11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

Dr.Nyoman

Suryawati,SpKK

Friday,

Nov 24,

2017

09.00-10.00 (60’)

 Able to diagnose

and manage

Rheumatic Disease

of Childhood

 dr. Komang

Ayu Witarini,SpA

Class Room

 Able to diagnose

and manage Food

allergy

10.00-11.30 (90’)

SP paper

presentation :

Juvenile Chronic

Arthritis and Milk

Allergy

 dr. Komang

Ayu Witarini,SpA

Class Room

11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 dr. Komang

Ayu Witarini,SpA

Class Room

Monday,

Nov 27,

2017

09.00-10.00 (60’)

 Comprehend basic

mechanism of drug

allergy

 Immunopharmacol

ogy

 Dr. dr. I Made

Jawi,M.Kes

Class Room

10.00-11.30 (90’)

Student Project

(SP): paper

preparation

-

-11.30-12.00 (90’)

Break

-

-12.00-13.30 (30’)

Independent

Learning

-

-13.30-15.00 (90’)

SGD

 Fasilitator

Discussion

Room

15.00-16.00 (60’)

Plenary Session

 Dr. dr. I Made

Jawi,M.Kes

Class Room

Tuesday,

Nov 28,

2017

09.00-10.00 (60’)

Laboratory Test For

Allergy And

Autoimune Disease

(BCS)

 Dr.dr. I Wayan

Wande, Sp.PK

10.00-11.30 (90’)

Independent

Learning

-

Library

13.30-16.00 (150’)

BCS Training

 Dr.dr. I Wayan

Wande, Sp.PK &

Team

Skill Lab

16.00-17.00

BCS Discussion

Wednesda

y,Nov 29,

2017

09.00-10.00 (60’)

Anaphylactic Syok

(BCS)

 dr. Tjok Istri

Anom Saturti,

SpPD

Class Room

10.00-11.30 (90’)

Independent

Learning

-

Library

13.30-16.00 (150’)

BCS Training

 dr. Tjok Istri

Anom Saturti,

SpPD

Skill Lab

16.00-17.00

BCS Discussion

Thursday,

Nov 30,

2017

09.00-10.00 (60’)

SLE, RA focus on

physical examination

(BCS)

 dr.Gede

Kambayana,SpP

D-KR / dr.Pande

Ketut

Kurniari,SpPD

10.00-11.30 (90’)

Independent

Learning

-

Class Room

13.30-16.00 (150’)

BCS Training

 dr.Gede

Kambayana,SpP

D-KR / dr.Pande

Ketut

Kurniari,SpPD

Library

16.00-17.00

BCS Discussion

 dr.Gede

Kambayana,SpP

D-KR / dr.Pande

Ketut

Kurniari,SpPD

Skill Lab

Monday,D

ec 4, 2017

09.00-10.00 (60’)

Skin Prick Tes

 Dr. dr. Ketut

Suryana,

SpPD-KAI

10.00-11.30 (90’)

Independent

Learning

-

Class Room

13.30-16.00 (150’)

BCS Training

 Dr. dr. Ketut

Suryana,

SpPD-KAI

16.00-17.00

BCS Discussion

 Dr. dr. Ketut

Tuesday,D

ec 5, 2017

Pre-Evaluation Break

Wednesda

y,Dec 6,

2017

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 December 6th _{2017. There are 100}

Topics : Introduct. to the immune system and disorders

Lecturer : Dr.dr. Ketut Suryana, SpPD-KAI

Abstract

1. The Immune system has evolved to protect us from pathogens. Some, such as viruses, infect individual cells; others, including many bacteria, divide extracellularly within tissues or body cavities.

2. The cells which mediate immunity include lymphocytes and phagocytes. Lymphocytes recognize antigens on pathogens. Phagocytes internalize pathogens and degrade them 3. An Immune response consists of two phases. In the first phase, antigen activates specific

lymphocytes that recognize it; in the effector phase, these lymphocytes coordinate an immune response that eliminates that source of the antigens.

4. Specificity and memory are two essential features of adaptive immune responses. The Immune system mounts a more effective response on second and subsequent encounters with a particular antigen.

5. Lymphocytes have specialized functions. B cells make antibodies; cytotoxic T cells kill virally infected cells; helper T cell coordinate the immune response by direct cell-cell interactions and the release of cytokines, which help B cells to make antibody.

6. Antigens are molecules which are recognized by receptors on lymphocytes. B lymphocytes usually recognize intact antigen molecules, while T lymphocytes recognize antigen fragment on the surface of other cells.

7. Clonal selection involves recognition of antigen by a particular lymphocyte; this leads to clonal expansion and differentiation to effector and memory cells.

8. The immune system may break down. This can lead to immunodeficiency or hypersensitivity diseases or to autoimmune diseases.

Learning task

1. Comprehend of immune system with clinical implications

2. Comprehend the lymphoid organs and describe of it’s microscopic organization 3. Comprehend the cellular immunity

4. Comprehend the mechanism of cellular and humoral immunity to infection

Day 1

Topic :The Microscopic Structure of Limphoid Organ, Immune Cells and Histocompatibility Molecule

Lecturer : dr. Ni Made Linawati, M. Si.

Abstract

The limphoid systems is responsible for the immunological defense of the body. Some of its component organs ; lymph nodes, thymus and spleen are surrounded by connective tissue capsules, whereas its other components, member of the diffuse lymphoid system, are not encapsulated. The cells of the limphoid systems such as lymphocytes ( T, B and Natural Killer), Antigen Presenting Cells (Dendritic cells, Macrophages and B lymphocytes) and other (Neutrophils) protect the body against foreign macromolecules, viruses, bacteria, and other invasive microorganism, and they kill virally transformed cells. Major Histocompability Complex (MHC) molecule are important to permit APCs and cells under viral attact (or cells already virally transformed) to present the epitopes of the invading pathogen to the T cells.

Learning Task

Vignette

A 65-year-old man had suffered from rectal bleeding during defecation for a few weeks. Laboratory findings were normal except a slight elevation in the level of alkaline phosphatase. Multiple polypoid lesions were observed in colonoscopic examination. The histological and immunochemical evaluation showed atypical lymphoid cell proliferation and lymphoepithelial lesions on the colonic mucosa, staining with CD20. After the diagnosis had been confirmed as low grade mucosa associated lymphoid tissue lymphoma.

a. Please describe histological structure of the Mucosa associated lymphoid tissue. b. Why M cells has important roles in mucosa immune response?

Self Assesment

1. What are primary and secondary lymphoid organ. Mention the of organ that has function as primary and secondary lymphoid organ

2. Describe about function and microscopic structure of thymus, lymph nodes; spleen; tonsils; and MALT

3. Describe about MHC class I and class II

Topic : Basic mechanism of autoimmunity

Lecturer : Dr. dr. Putu Sri Widyani, SpPA

ABSTRACT

Immunologic Tolerance: Is a state in which an individual is incapable of developing an immune response against a specific antigen.

Self- tolerance: Specifically refers to a lack of immune responsiveness to one’s own tissue antigens.

• Central tolerance: This refers to deletion of self-reactive T and B lymphocytes during maturation in central lymphoid organs (i.e. in the thymus for T cells and the bone marrow for B cells)

• Peripheral tolerance: Self reactive T cells that escape negative selection in the thymus can potentially wreak havoc unless they are deleted or effectively muzzled. Several back-mechanisms in the peripheral tissues that silence such potentially autoreactive T cells have been identified:

- Anergy.

- Activation-induced cell death - Peripheral suppression by T cells. Mechanisms of Autoimmune Disease

Breakdown of one or more of the mechanisms of self-tolerance can unleash an immunologic attack on tissues that leads to the development of autoimmune disease. Furthermore, the breakdown of tolerance and initiation of autoimmunity involves the interaction of complicated immunologic, genetic, and microbial factors.

Learning task Trigger Case

A 25-year-old woman has had increasing malaise, a skin rash of her face exacerbated by sunlight exposure, and arthtralgias and myalgias for the past month. On physical examination she has mild pedal edema. On auscultation a friction rub is audible over the chest. Laboratory findings include pancytopenia and serum creatinine 3 mg/dL. Urinalysis shows hematuria and proteinuria. A serologic test for shypilis yields a false positive result. A renal biopsy shows a slight increase of mesangial cells and granular deposit of IgG and complement in the mesangium and along basement membrane. The result of ANA test is positive. Finally, the patient is diagnosed as systemic lupus erythematosus (SLE). SLE is the best example of autoimmune disease. Does the autoimmunity result from the loss of self-tolerance, how this happen, and why they have a broad clinical spectrum as showed in that patient? Before you answer the question, please try to find out the following task.

Task

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

2. Explain the mechanism of autoimmunity, including the role of susceptibility genes and enviromental triggers!

3. Describe the general features of autoimmune diseases! 4. Describe the etiopathogenesis of SLE!

5. Describe the mechanism of tissue injury in SLE, and give some examples of morphological changes in SLE!

Topic : Forensic Serology & Molecular

Lecture : dr. IB Putu Alit, SpF, DFM

Abstract

Forensic serology is the study of serology in relation to crimes and other legal matters by using a scientific approach. Doctors should have knowledge about forensic serology to assist investigators in revealing crime cases related with human’s body and health. Moreover, based on legislations, doctors have legal duty to carry out forensic examinationwhen asked by the investigators.

Mostly, investigators asked doctors to prove homicide, rape, assault or dispute paternity case. To prove it, the doctors need to do serological examination of biological evidence that found on the 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!

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

Topic : Antihistamine

Lecturer : Dr. dr. Bagus Komang Satriyasa, M.Repro.

ABSTRACT

Histamine receptor antagonists represent a third approach to the deduction of histamine-mediated responses. For over 60 years, compounds have been available that competitively antagonize many of the actions of histamine on the smooth muscle. Compounds that competitively block histamine at H1 receptor have been used clinically for many years, and many H1 antagonists are currently marketed. Many are available without prescription, both alone and in combination formulations such as “cold pills” and sleep aids. The H1 antagonists are conveniently divided into firs generations and second generation agents. These groups are distinguished by relatively strong sedative effect of most of the generation drugs. The first generation agents are also more likely to block autonomic receptors. The relatively less sedating characteristic of the second generation H1 blockers is due in part to their less complete distribution into the central nervous system. H1 receptor antagonists block the actions of histamine by reversible competitive antagonism at the H1 receptor; these drugs have no effect on histamine release from storage sites. They are more effective if given before histamine release occurs. The first generation are often the first drugs used to prevent or treat the symptoms of allergic reactions, and the second generation H1 antagonists are used mainly for treatment of allergic rhinitis and chronic urticaria. The drugs adverse effect are sometimes exploited therapeutically.

Learning Task

1. Explain two classification of H1 blockers

2. List two drugs the older members of the first generation agent 3. List three drugs the second generation of H1 blockers.

4. Describe mechanism and effect of H1 blockers 5. Describe clinical use of H1 blockers

Self assessment

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

3. Which of the following drugs are used as anti-motion sickness and also for management of chemotherapy-induced vomiting?

C. Meclizine D. Cyclizine E. Loratadine

4. Toxicities of H1 blocker include which one of the following A. Sedation

B. Dry mouth C. Blurry vision D. Vomiting E. Hypotension

Topic : Laboratory test of immune system

Lecture : Dr. dr. I Wyn Putu Sutirta Yasa, M.Si.

Abstract

Objective to comprehend laboratory test of immune system

1. Approach in the patient with immune system disease and disorders are evidence based in immunology, history and physical examination, laboratory studies to make diagnosis. Laboratory test of immune system (immunoassay) based on antigen-antibody reactions. Immunoassay can be used for the detection of either antigens or antibodies. For antigen detection, the corresponding specific antibody should be prepared as one of reagents. The reverse is true for antibody detection.

2. The sensitivity of the immunoassays has been enhanced through the development of types of signal detection systems and solid-phase technology. Immunoassay has been optimized to detect less than 0.1 pg/mL of antigen in blood.

3. The can be applied to detection of haptens as small molecules, protein and protein complexes as macromolecules, as well as of any antibody to allergens, infectious agent, and autologous antigens.

4. Students to comprehend the overview of general principles and based of immunoassay. High concentration of such molecules and where antigen- antibodies are mixed in solution can be measured by precipitation techniques. Medium concentration of such molecules and where antigen- antibodies are on solid phase can be quantified by agglutination techniques. Very low concentration of such molecules can be quantified by radioimmunoassay techniques or enzyme linked immunosorbent assay techniques. Outcome of laboratory test of immunes system

Students to comprehend the overview of general principles and based of immunoassay to purpose and function of laboratories are to assist students in (1) confirming or rejection a diagnosis, (2) providing guidelines for patient management, (3) establishing a prognosis, (4) detecting disease through case finding or screening and (5) monitoring follow up therapy.

1. Explain the precipitin reactions, what are antibody excess zone, equivalence zone and antigen excess zone

2. Explain the differential of haemagglutination and complement fixation. 3. Explain the differential of direct and indirect immunofluorescence

4. Mention the immunoassay using labeled reagents for detecting antigens and antibodies.

5. Explain the competitive assay and two-site capture assay techniques.

Self assessment

1. Mention the principle of methods on immunoassay techniques? 2. What’s the meaning of equivalence zone?

3. Mention the reaction marked on haemagglutination methods? 4. Mention the reaction marked on complement fixation methods? 5. Mention the label used on the ELISA method?

TOPIC : GUILLAIN BARRE SYNDROM, MYASTHENIA GRAVIS

MULTIPLE SCLEROSIS

LECTURER : Dr. dr. Made Oka Adnyana, Sp.S (K)

AUTOIMMUNE DISEASES IN NEUROLOGY

ABSTRACT

Autoimmunity is a misguided immune response to the body's own organs. The nervous and immune systems have many interactions that dictate overall body health. The nervous system is under constant monitoring from both the adaptive and innate immune system. Deregulation of both adaptive and acquired immune responses, impairment of crosstalk between these two systems as well as alterations in the deployment of innate immune mechanisms can predispose the central nervous system (CNS) to autoimmunity and neurodegeneration. Multiple sclerosis, myasthenia gravis and Guillain-Barre syndrome (GBS) are neurologic diseases induced by abnormal autoimmunity.

Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease of CNS. MS attack the myelinated axons in the CNS, destroying the myelin and the axons to varying degree. The course of MS is highly varied and unpredictable. In most patients, the disease is characterized initially by episodes of reversible neurological deficits, which is often followed by progressive neurological deterioration over time.

Myasthenia gravis (MG) is an autoimmune disease characterized by a fluctuating pathological weakness with remissions and exacerbations involving one or several skeletal muscle groups, mainly caused by antibodies to the acetylcholine receptor (AChR) at the post-synaptic site of the neuromuscular junction

Guillain-Barré syndrome (GBS) is a disorder in which the body's immune system attacks part of the peripheral nervous system. The first symptoms of this disorder include varying degrees of weakness or tingling sensations in the legs. In many instances the symmetrical weakness and abnormal sensations spread to the arms and upper body.

LEARNING TASK

CASE 1

A 29-year-old woman, complaining of double vision, was found to have ptosis on the right side. The ptosis was worse in the evening and almos absent in the morning. She admmitted to tiredness in the arms and legs, which recovered with resting.

CASE 2

A 18-year-old boy awoke one morning 2 weeks after an episode of influenza with a mild weakness in his legs and during the day he developed pain in his back and 'pins and needles' in his feet. He was considerably worse the next day and complained of weakness in his arms as well, and by the evening he was unable to stand.

Case 3

A 35 year old white female. She came to Neurology Clinic for evaluation of her long-term neurologic complaints. The patient relates that for many years she had noticed some significant changes in neurologic functions, particularly heat intolerance precipitating a stumbling gait and a tendency to fall. Her visual acuity also seemed to change periodically during several years. Two months ago the patient was working very hard and was under a lot of stress. She got sick with a flu and her neurologic condition worsened. At that time, she could not hold objects in her hands, had significant tremors and severe exhaustion. She also had several bad falls. The patient abruptly developed a right hemisensory deficit after several days of work..

TASK

1. What is the most likely diagnosis in Case 1,2 and 3

2. Describe the clinical symptoms of Myasthenia Gravis, GBS and Multiple sclerosis 3. Describe the spesific diagnostic examination and laboratory test for Myasthenia

Gravis, GBS and Multiple sclerosis

4. Describe principle management for Myasthenia Gravis, GBS and Multiple sclerosis

SELF ASSESSMENT

1. Describe the diagnosis criteria of Myasthenia gravis 2. Describe the diagnosis criteria of GBS

3. Describe the diagnosis criteria for Multiple Sclerosis

4. Describe the pathogenesis of Myasthenia Gravis, GBS and Multiple sclerosis 5. Describe imunologic finding in Myasthenia Gravis, GBS and Multiple sclerosis 6. Describe the prognosis of Myasthenia Gravis, GBS and Multiple sclerosis

REFFERENCE

1 Diagnostic Criteria in Autoimmune Diseases. 2008. Yehuda Shoenfeld, Ricard Cervera, M. Eric Gershwin editors. Humana Press.

Topic : Rhinitis Alergy

Lecturer : Dr. Sari Wulan Dwi Sutanegara , Sp THT-KL

ABSTRACT

Allergic rhinitis is an inflammation of the nasal passages, usually associated with watery nasal discharge and itching of the nose and eyes.

Allergic rhinitis affects about 20 percent of population and ranks as one of the most common illnesses. The symptoms occur in the nose and eyes and usually occur after exposure to dust, danders, or certain seasonal pollens in people that are allergic to these substances.

There is strong genetic predisposition to allergic rhinitis. One parent with a history of allergic rhinitis has about a 30 percent chance of producing offspring with the disorder. Tthe risk increases to 50 percent if both parents have a history of allergies.

Characteristic symptoms include repetitive sneezing, rhinorrhea (runny nose), post-nasal drip, post-nasal congestion, pruritic (itchy) eyes, ears, nose or throat, and generalized fatigue. Symptoms can also include wheezing, eye tearing, sore throat, and impaired smell. A chronic cough may be secondary to postnasal drip, but should not be mistaken for asthma. Sinus headaches and ear plugging are also common.

Diagnosis of Allergic Rhinitis. After a medical history, physician will perform a physical exam. Often, the nasal mucosa (lining of the nose) is pale or violaceous because of the engorged veins. Nasal polyps may be seen. Classic signs of allergic rhinitis may include swelling of the eyelids, injected sclerae (the whites of the eyes may be red), allergic shiners (darkened areas under the lower eyelids thought to result from venous pooling of blood), and extra skin folds in the lower eyelids.

Skin testing may confirm the diagnosis of allergic rhinitis. Initial skin testing is performed by the prick method. Intradermal testing is performed if results of prick testing are negative.

The goal of treatment is to reduce the allergy symptoms. Avoidance of the allergen or minimization of contact with it is the best treatment, but some relief may be found with the following medications: antihistamines and decongestants, nasal sprays and immunotherapy.

LEARNING TASK

CASE:

A 25 years old man complained of sneezing 5 to 10 times and watery nose everytime he wakes up in the morning.

Task:

1. Please do further anamnesis in this case!

2. If in the anamnesis his mother had asthma, what is the possible diagnosis of this case? 3. What is/are the differential/s diagnosis of this case?

4. What is/are the complication/s of this case? 5. How is the management of this case?

Self Assessment

1. What is the definition of allergy rhinitis?

2. What are the symptom and sign of allergy rhinitis? 3. How is the classification of allergy rhinitis?

4. When immunotherapy can be applied to allergy rhinitis patient?

Topic : Hypersensitivity

Lecturer : dr. Tjok Istri Anom Saturti, SpPD

ABSTRACT

There are 4 types classifications according to Gel & Coombs

1. Type I : Immediate hypersensitivity 2. Type II : Cytotoxic hypersensitivity

3. Type III : Immune complex hypersensitivity 4. Type IV : Delayed (cell mediated) hypersensitivity

Hypersensitivity the immune response results are harmful to the heart

Type I : Antigen bind to IgE on the surface of mast cells à release of several mediators within minutes. Important mediators are: Histamin, SRS-A, ECF-A, serotonin, Prostaglandins and thromboxanes, etc. Clinical manifestations:

1. Anaphylaxis : severe bronconstriction, hypotension à shock

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.

Type II : Antibody is directed against antigen on an individual’s own cell (target cell) or foreign antigen, such as transfused red blood cell. This may lead to cytotoxic action by K Cells, or complement mediated lysis.

Type III : Immune Complexes are deposited in the tissue. Complement is activated and polymorphs are attracted to the site of deposition causing local tissue damage and inflammation

Type IV : Antigen sensitized T cells release lymphokines following a secondary contact with the same antigen. Cytokines induced inflammatory reactions activate and attract macrophages, which release inflammatory mediators.

Learning Task

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

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

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;

2. result from the production of antibodies and / or cytotoxic T cells directed against the drug,

3. its metabolite, a soluble / cell-bound carrier protein as a responses to prior or continuous exposure to a drug

Risk factors

1. Patient related : Age, sex, genetics, atopy, AIDS

2. Drug related : Macromolecular size ; bivalency, haptens, route, dose, duration of treatment

3. Aggravating factors : β Blockers, asthma, pregnancy

Diagnosis

1. Diagnosis of drug allergy based on ; 2. Clinical history

3. Clinical manifestations 4. Diagnostic test

Diagnostic tests

1. SPT may be helpful for diagnosing IgE mediated drug reactions (in vivo)

2. RAST may detect serum IgE antibodies to certain drugs (e.g : penicillin and succinyl choline) (in vitro)

3. Provocation tests

Oral provocation tests, may be as a gold standard

They must be performed under strict medical supervision with resuscitative equipment available

Management

1. Avoidance 2. Premedication 3. Desensitisation

Learning Task 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!

Lecture : dr. Ketut Suardamana,SpPD-KAI

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

Clinical Criteria for Diagnosing Anaphylaxis

(Sampson HA, et al. JACI 2006)

1. Acute onset of an illness ( minutes to several hours) with involvement of the skin, mucosal tissues, or both (eg, generalized hives, pruritus or flushing, swollen lips-tongue-uvula) AND AT LEAST ONE OF THE FOLLOWING

a. Respiratory compromise (eg, dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)

b. Reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia /collapse, syncope, incontinence)

2. Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours) :

a. Involvement of the skin-mucosal tissue (eg, generalized hives, itch-flush, swollen lips-tongue-uvula)

b. Respiratory compromise (eg dyspnea, wheeze-bronchospasm, stridor, reduced PEF, hypoxemia)

c. Reduced BP or associated symptoms (eg, hypotonia collapse, syncope, incontinence)

d. Persistent gastrointestinal symptoms (eg cramp abdominal pain, vomiting)

3. Reduced BP after exposure to known allergen for that patient ( minutes to several hours) a. Infants and children: low systolic BP (age specific) or greater than 30% decrease in

systolic BP

b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that person's baseline

Learning task

Vignette

Female 30 years old, came to the Emergency Unit with chief complaint; edema on palpebra, itchy redness on the whole body skin after taking metampirone 500 mg tab. as a treatment for headache. She also complains; shortness of breath, fatique and warmth on the lower extremity.

Task

1. What should you do for the first? 2. Could you complete your anamnesis! 3. What do you find on physical examination?

4. The laboratory plan? Or other diagnostic procedure?

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!

Topic : - RHEUMATOID ARTHRITIS

- SYSTEMIC LUPUS ERYTHEMATOSIS ( SLE ) - Polimyalgia Rheumatica

Lecture : dr. Gede Kambayana, Sp PD-KR / dr. Pande Ketut Kurniari,SpPD

RHEUMATOID ARTHRITIS

Abstract

Definition

Rheumatoid Arthritis (RA) is a chronic multisystem disease of unknown cause. The characteristic feature of RA is persistent inflammatory synovitis, involving peripheral joints in a symmetric distribution.

Etiology

The cause of RA remains unknown. RA might be a manifestation of the response to an infectious agent in a genetically susceptible host. Causative agents is involved; Mycoplasma, Epstein-Barr Virus (EBV), Cytomegalovirus, parvovirus, and rubella virus.

Pathology and pathogenesis

Microvascular injury and an increase the number of synovial lining cells.

Histology of rheumatoid synovitis; the characteristic feature of RA inflammation with hyperplasia of lining layer, a higher CD4+ T cell infiltrate around postcapillary venules. Immunoglobulin and the autoantibody rheumatoid factor are produced within the synovial tissue, which leads to the local formation of immune complexes. Autoantibodies to synovial tissue components contribute to inflammation.

Clinical manifestation

Onset of RA; Polyarthritis which begins insidiously with fatigue, anorexia, and generalized weakness. Specific symptoms usually appear gradually as several joints, especially those of the hands, wrists, knees, and feet, become affected in a symmetric fashion.

Signs and symptoms of articular disease; pain, swelling, and tenderness may initially localized to the joints.

Laboratory findings

- Anti CCP (Antibodies to citrulline-containing proteins); are found in most patients with RA

Radiographic evaluation

Loss of articular cartilage and existence of bone erosions.

Diagnosis

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

2. Arthritis (³ 3 joints)

3. Arthritis of hand joints; wrists, MP jont or proximal interphalangeal join 4. Symmetric arthritis.

5. Rheumatoid nodule. 6. Serum rheumatoid factor 7. Radiographic changes 2 or more clinical diagnoses→ RA

Learning Task

Case

A female 35 years old, married, has 4 children. She is a cleaning service. She came to Health Centre with chief complaint, problem on her wrist, fingers both side. She feels pain, swelling and tenderness, morning stiffness since a month.

Learning task

1. Could you complete the anamnesis! 2. Describe the physical diagnostic!

3. Base on the anamnesis and physical diagnostic, the working diagnosis of this patient? 4. Describe the differential diagnosis!

5. Describe other laboratory test

6. Where should you reffer this patient?

Self assessment

1. Describe the definition of rheumatoid arthritis! 2. Describe the etiopathogenesis of AR!

Topic : SYSTEMIC LUPUS ERYTHEMATOSIS (SLE)

Abstract

Definition

SLE is an autoimmune disease which involves multiorgan / multisystem damage, mediated by tissue-binding autoantibodies and immune complexes.

Pathogenesis and etiology

SLE is caused by interactions between susceptibility genes and environmental factors, resulting in abnormal immune responses.

Pathology

In SLE biopsies of affected skin show deposition of Ig at the dermal-epidermal junction / DEJ , injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and around blood vessels and dermal appendiges

Diagnosis.

Based on clinical features and auto antibodies.

Classification criteria for the diagnosis of SLE; (specificity 95%, sensitivity 75%) : 1. Malar rash

2. Discoid rash 3. Photosensitivity

4. Oral ulcers (include oral, nasopharyngeal and observed by physician. 5. Arthritis

6. Serositis

7. Renal disorder (proteinuria > 0,5 g / d or ³ 3+, or cellular casts 8. Neurologic disorder

9. Hematologic disorder 10. Immunologic disorder

11. Antinuclear antibodies (ANA test ) If ³ 4 of these criteria ® SLE

Laboratory test

- ANA test : prevalence 98%, best screening, repeat test (-) → (-) - Anti ds-DNA : prevalence 70%, high titers are SLE specific, correlate with

disease activity.

Learning task

A 17 years old female came to Health Centre with chief complaint; facial rash since 3 days ago. She had the rash since a year ago, and reduced after treatment. The rash is triggered by the UV. The patient also feels fatique since 3 months ago.

Task

1. Please you complete the anamnesis! 2. Describe the physical examination!

5. Where should you reffer this patient?

Self assessment

1. Describe the definition of SLE!

2. Describe the etiopathophysiology of SLE! 3. Describe the clinical manifestation of SLE! 4. Describe the laboratory test for this patient! 5. Comprehend the management of SLE!

Topic : Allergic Disease in Dermatology Lecturer :Dr.NyomanSuryawati, SpKK

Atopic Dermatitis

Absract

Atopic dermatitis (AD) or atopic eczema is a chronically relapsing, pruritic, exanthematousdermatosis of uncertain etiology that is characterized primarily by an allergic diathesis as well as erythema, oozing, crusting, excoriations, lichenification, and dehydration of involved skin surfaces. Onset occurs at approximately 2 to 3 months of age, and the disease may persist, with periodic exacerbations and remissions, into adulthood. Sites predisposed to rash change with growth and development. Spread to other areas may occur in severe cases. Pathophysiology of AD by Hyperactive Th2 subset T helper cells (associated with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, stimulation of proliferation, and differentiation of B lymphocytes), increased levels of serum IgE, upregulation of interleukin-4, downregulation of interferon gamma, increased eosinophils, elevated levels of IgEactivated mast cells.

Clinical feature of AD, there are three stages under the different age groups: Infancy, in infancy, at between two months to two years of age, a child may develop an itchy erythemathous rash on the cheeks. The rash may develop into minute epidermal vesicles which can rupture and produce moist crusted areas. Childhood, in the childhood phase, the rashes are usually less acute, less exudative, drier and more papular. The lesions occur at classical locations like the antecubital and popliteal fossae, wrists, eyelids, face and collar regions. Lichenified, slightly scaly or infiltrated patches may intermingle with isolated, excoriated papules over the exposed parts. Adolescence, in the adolescent and adult stage, the lesions may appear as localised erythematous, scaly, papular or vesicular patches. Or they may appear in the form of pruritic, lichenified patches. They usually involve the antecubital and popliteal fossae, the front and sides of the neck, the forehead, and around the eyes. The hands and wrists are frequently involved. Hyperlinearity of the palm is a manifestation of ichthyosis vulgaris which accompanies 30-40% of cases.

Diagnostic of AD according the diagnostic criteria of Haniffin&Rajka (1980) is with at least 3 of Major criteria and at least 3 Minor Criteria.Management of AD is basically according the form of skin lesion, severity of itching and inflammation, secondary infection.

Contact Dermatitis

Abstract

Dermatitis or eczema is an inflammation of the skin with characteristic morphology but varied cause caused by skin contact with an environmental agent. Most occupational dermatoses are eczematous reactions to an environmental contactant, characterized by redness, swelling, small fluid filled blisters, and oozing in the acute state and as a scaly lichenified, thickened, fissured with pigmentary changes in the chronic stage.

Contact dermatitis (CD) is an altered state of skin reactivity induced by exposure to an external agent. "Eczema" and "dermatitis" are often used synonymously to denote a polymorphic pattern of inflammation of the skin characterized, at least in its acute phase, by erythema, vesiculation and pruritus. Substances that induce CD after single or multiple exposures may be irritant or allergic in nature. The clinical presentation may vary depending on the identity of the triggering agent and the reactivity of the subject, but in all cases the lesions are primarily confined to the site of contact.

According to the mechanism of elicitation, the following types of contact reactions may be distinguished: 1. allergic contact dermatitis (ACD), immunopathology based on type IV hypersensitivity, 2. irritant contact dermatitis (ICD), due to primary irritant, acute and chronic cumulative, 3. phototoxic and photoallergic contact dermatitis, and 4. immediate type contact reactions. The present review will focus on allergic contact dermatitis. ACD is the clinical presentation of contact sensitivity in humans.

Management of contact dermatitis, the only available etiologic treatment of ACD is elimination of the contact allergen. The patients should be informed about the identity of the offending agent and the possible sources of the sensitizer. Corticosteroids have anti-inflammatory and immunosuppressive effects. In murine models of contact sensitivity they inhibit both the induction and elicitation phase. ACD is a major indication for topical corticosteroid treatment. Histamine is not involved in the pathogenesis of ACD, but need for reduce itching. Systemic corticosteroid is not absolute for treatment in the most common forms of ACD. However they may be indicated for a short period of time if ACD is widespread and severe.

Cutaneous Lupus Erythematosus (CLE)

The inflammatory disorders of connective tissue often affect several organs, as in systemic lupus erythematosus (SLE), but they may also involve the skin alone (cutaneous lupus erythematosus/ CLE). Auto antibodies and cell-mediated immunity against normal cellular components (e.g. nuclei) are a feature of these diseases, which c