Study Guide Immune Semester III Tayang 1 November 2016

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FOREWORD

The Block “The Immune System and Disorders” is designed for students in order to serve health care professionals in the diagnosis and management of allergic and other immunological disorders. Our goals have been to present the basic and essential material clearly and to provide the knowledge and skills due to:

- Diagnose and manage patient with inflammation

- Diagnose and manage patient with hypersensitivity / allergic disease

- Diagnose and manage patient with autoimmune disease

- Diagnose and manage patient with immunodeficiency

This block try to give the essential information to assist in clinical decision making and treatment planning on commonly allergic diseases in pediatric, internal medicine, ENT,and skin. We also give essential information on commonly autoimmune diseases in neurology, dermatology, pediatric and internal medicine, beside try to complete the essential information duo to immune deficiency focus on HIV / AIDS infection.

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

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

Team of Planners

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CURRICULUM

Aims:

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

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

Learning Outcomes:

To be able to

1. Diagnose and manage patients with inflammation

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

4. Diagnose and manage patients with immunodeficiency

Curriculum contents:

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PLANNERS TEAM

No Name Department Phone

1 dr. Tjok Istri Anom S, SpPD (Head) Internal Medicine 082145854167 2 dr. Sari Wulan DS, SpTHT-KL

(Secretary)

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. I Made Sudipta, Sp.THT (member) ENT 08123837063 6 dr. Made Wardana, Sp.KK (member) Dermatology 08563704591 7 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 081337222567 11 dr. Komang Suryawati, Sp.KK (Member) Dermatology 0817447279

LECTURERS

No Name Department Phone

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8 _{dr. Komang Suryawati, Sp.KK} _Dermatology _0817447279 9 _{dr. Ketut Suardamana, Sp.PD-KAI} _{Internal Medicine} _08123985811 10 Prof. Dr. dr. Tuti Parwati M, Sp.PD-KPTI Internal Medicine 08123806626 11 dr. Sari Wulan Dwi Sutanegara ,

Sp.THT-KL

ENT 081237874447

081338466039

12 dr. Susilawathi,SpS Neurology 08124690137

13 dr. Gede Kambayana, Sp.PD-KR Internal Medicine 08124683416 14 dr. Tjok Istri Anom S, SpPD Internal Medicine 82145854167 15 Dr. dr. Nyoman Wande, Sp.PK Clinical Pathology 08124686885 16 dr. Pande Ketut Kurniari,SpPD Internal Medicine 082146179796 17 dr. IB Putu Alit, SpF, DFM Forensic 081916613459 18 Dr. dr. I Wayan Putu Sutirta

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FACILITATORS

(REGULAR CLASS)

NO NAME GROUP DEPT PHONE VENUE

1 Prof.Dr.dr.I Putu Adiatmika M.Kes A1 Physiology 08123811019 2nd floor: R.2.01 2 dr.I A Dewi Wiryanthini M.Biomed A2 Biochemistry 081239990399 2nd floor:

R.2.02 3 dr. Ni Made Laksmi Utari,

M.Biomed, SpM A3 Ophtalmology 081816513322 2nd floor:R.2.03 4 Dr.dr. Ni Nyoman Sri Budayanti,

Sp.MK (K) A4 Microbiology 08553711398 2nd floor:R.2.04 5 dr.Yukhi Kurniawan, Sp.And A5 Andrology 08123473593 2nd floor: R.2.05 6 dr.I Putu Bayu Mayura, S.Ked A6 Microbiology 082236465801 2nd floor:

R.2.06 7 Dr.dr. AA Mas Putrawati T Sp.M (K) A7 Ophtalmology 08123846995 2nd floor:

R.2.07 8 Dr.dr. Susy Purnawati, M.KK A8 Physiology 08123989891 2nd floor:

R.2.08 9 dr. Putu Yuliandari, S.Ked A9 Microbiology 089685415625 2nd floor:

R.2.21 10 dr.I N Gede Wardana M.Biomed A10 Anatomy 087860405625 2nd floor:

R.2.22

FACILITATORS

(ENGLISH CLASS)

NO NAME GROUP DEPT PHONE VENUE

1

dr. I G A Artini M.Sc B1 Farmacology 0812650481

2nd floor: R.2.01 2

dr. I Wayan Sugiritama M.Kes B2 Histology 08164732743

2nd floor: R.2.02 3

dr. Agung Nova Mahendra, M.Sc B3 Pharmacology 087861030195

2nd floor: R.2.03 4

dr. Yuliana, M.Biomed B4 Anatomy 085792652363

2nd floor: R.2.04 5

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

M.Si B5 Biochemistry 081337141506

2nd floor: R.2.05 6 dr. I Dewa Ayu Inten Dwi

Primayanti, M.Biomed B6 Fisiology 081337761299 2nd floor:R.2.06 7

Dr.dr. Ni Made Linawati, M.Si B7 Histology 081337222567

2nd floor: R.2.07 8

dr. I Nyoman Wiryawan Sp.JP FIHA B8 Cardiology 081289053234

2nd floor: R.2.08 9

Dr. dr. G N Indraguna P B9 Public Health 08123816424

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10

dr. Muliani, M.Biomed B10 Anatomy 085103043575

2nd floor: R.2.22

TIME TABLE OF THE BLOCK IMMUNE SYSTEM & DISSODERS 2016

DAYS /

DATE TIME ACTIVITY CONVEYER VENUE

ENGLISH

(60’)  Introduction to The Immune System and disorders

(90’) 10.00-11.30 (90’) Student Project (SP): paper preparation - Discussion Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session  Dr. dr. Ketut _{Suryana, SpPD-KAI} Class Room Wednes

Independent Learning - Library 10.30-12.00

(90’) 13.30-15.00 (90’) SGD  Fasilitator Discussion Room 12.00-12.30

(30’) 11.30-12.00 (30’) Break -

-12.30-14.00

(90’) 10.00-11.30 (90’) Student Project (SP) : paper preparation - Discussion Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session _{Linawati, MSi}Dr. dr. Ni Made  Dr. dr. Putu Sri

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10.30-12.00 (90’)

13.30-15.00 (90’)

SGD _ Fasilitator Discussion

Room 12.00-12.30

(30’) 11.30-12.00 (30’) Break -

-12.30-14.00

(90’) 10.00-11.30 (90’) SP: paper preparation - Discussion Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session  Dr. dr. I Made Jawi,

Class Room Friday,

Nov 4, 2016

08.00-08.30

(30’) 08.30-09.00 (30’)  Comprehend laboratory test of immune system

(90’) 09.00-10.30 (90’) Independent Learning - Library 10.00-11.30

(30’) 12.00-12.30 (30’) Break -

-12.00-13.30

(90’) 12.30-14.00 (90’) SP paper preparation - Discussion Room 13.30-14.30

(60’) 14.30-15.30 (60’) Plenary Session

 Dr. dr. I Wayan Putu

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

Class Room

09.00-10.30

(60’) 15.00-16.00 (60’) Plenary Session dr. Tjok Istri Anom Saturti, SpPD Dr. dr. B. K. Satriyasa, M.Repro

Class Room

Tuesday, Nov 8, 2016

08.00-09.00

(60’) 09.00-10.00 (60’)  Adverse drug reactionAble to diagnose and manageanaphylaxis

(90’)

13.30-15.00 (90’)

Room 12.00-12.30

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-12.30-14.00 (90’)

10.00-11.30 (90’)

SP: paper preparation - Discussion Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session

 dr. Ketut

Room

SP paper presentation: Steven

Johnson Syndrome  dr. Nyoman Suryawati, SpKK

Discussion Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session

 dr. Sari Wulan

Able to diagnose and manage SLE, Rheumatoid Arthritis & Polimyalgia Rheumatica

(90’) 13.30-15.00 (90’) SGD Fasilitator Discussion Room

12.00-12.30

Urtikaria and Angiodema  dr.Ketut Suardamana,SpPD-KAI

Plenary Session  dr.Gede

Kambayana,SpP D_KR/dr.Pande Ketut

Kurniari,SpPD

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09.00-10.30

SP paper presentation: Rhinitis

Allergy  dr.Sari Wulan DwiSutanegara,SpTH T

Class Room 14.00-15.00

(60’) 15.00-16.00 (60’) Plenary Session

 Prof. Dr. dr. Tuti

(30’) 11.30-12.00 (30’) Break -

-12.30-14.00

(90’) 10.00-11.30 (90’)

SP paper presentation: Blood

Group Incompatibility  Dr. dr. I Wayan PutuSutirtaYasa, Msi Class Room 14.00-15.00

(60’)

15.00-16.00 (60’)

Plenary Session _ dr. Komang Ayu Witarini,SpA

(150’)

13.30-16.00 (150’)

BCS Training  Dr.dr. I Wayan Wande, Sp.PK

(60’) 09.00-10.00 (60’) Forensic Serology & Molecular  dr. IB Putu Alit, SpF, _DFM Class Room

09.00-10.30 (90’)

10.00-11.30 (90’)

Independent Learning - Library

10.30-12.00

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12.00-12.30

Plenary Session dr. IB Putu Alit, SpF, DFM

(60’) 09.00-10.00 (60’) Anaphylactic Syok (BCS)

 dr. Tjok Istri Anom

Saturti, SpPD Class Room 09.00-10.30

(60’) 09.00-10.00 (60’) SLE, RA focus on physical examination (BCS)

 dr.Gede

Independent Learning - Class Room 10.30-13.00

(150’)

13.30-16.00 (150’)

BCS Training _ dr.Gede

Kambayana,SpPD-KR / dr.Pande Ketut Kurniari,SpPD

Library

13.00-15.00

(120’) 11.30-13.30 BCS Discussion  dr.Gede Kambayana,SpPD-KR / dr.Pande Ketut

(60’) 09.00-10.00 (60’) Skin Prick Tes  Dr. dr. Ketut _{Suryana, SpPD-KAI} 09.00-10.30

(90’) 10.00-11.30 (90’) Independent Learning - Class Room 10.30-13.00

(150’) 13.30-16.00 (150’) BCS Training  Dr. dr. Ketut _{Suryana, SpPD-KAI} 13.00-15.00

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Meeting of the student representatives

The meeting between block planners team and the student group representatives will be held on Friday November 18, 2016 at 09.00 until 10.00 a.m at HAPEQ discussion room. In this meeting, all of the student group representatives are expected to give suggestions or inputs or complaints to the team planners for improvement. For this purpose, every student group must choose one student as their representative to attend the meeting.

Meeting of facilitators

The meeting between block planners team and the facilitators will take place on, Monday, Friday November 18 at 10.00 am until 12.00 pm at HPEQ discussion room. In this meeting all the facilitators are expected to give suggestions and inputs as evaluation to improve the study guide and the educational process. Because of the importance of this meeting, all the facilitators are strongly expected to attend the meeting.

Plenary session

For each task of SGD, the students are requested to prepare a group report. The reports will be presented in a plenary session. The group will be chosen randomly by the lecturer in charge. The group report will be evaluated by respective facilitator.

Assessment Methods

Assessment will be performed at the end of the block on Nopember 9th_{2015. There are 100}

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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

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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.

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• 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!

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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.

• Explain the immunologic mechanism of those problems.

• To manage that patient what medicine will you give for him immediately? • Explain your answer if you give him prednisone. Do you agree? Why? • How about antihistamine like dimenhydrinate for this patient?

Self assessment

1. Cyclosporine is effective in organ transplantation. The immunosuppressant action of the drug appears to be due to

A. Activation of natural killer (NK) cells

B. Blockade of tissue responses to inflammatory mediators C. Increased catabolism of IgG antibodies

D. Inhibition of the gene transcription of interleukins E. Interference with antigen recognition

2. Azathioprine

A. Binds avidly to a cytoplasmic immunophillin B. Blocks formation of tetrahydrofolic acid C. Is a precursor of cytarabine

D. Is markedly hematotoxic and has caused neoplasms E. Is a metabolite of mercaptopurine

3. Which of the following drugs is a widely used agent that suppresses cellular immunity, inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG antibodies?

A. Cyclophosphamide B. Cyclosporine C. Infliximab D. Mercaptopurine 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 : 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.

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

Learning Task

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

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

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

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

Self assessment

1. Mention the principle of methods on immunoassay techniques? 2. 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 : 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

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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

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

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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

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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

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

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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 Vignette

Male 20 years old, was diagnosed with Pulmonary TB and taking the anti TB regimen (Category 1). On the second day treatment he felt an itchy – swollen redness on whole body. He had previous history of drug allergy but the allergen is unknown, his mother also had history of drugs allergy. The patient was fully alert, T 110/70 mmHg, pulse rate 92x per minute regular, RR 18x per minute.

Task

1. Could you explore more to complete the anamnesis! 2. Describe any sign that you find on Physical examination? 3. How to manage this patient?

Self assessment

1. Could you describe the adverse drugs reaction (ADR)!

2. Describe the immunopathophysiology of drugs allergy (due to Gell & Coombs Criteria)! 3. Comprehend the diagnostic approach of the drugs allergy!

Topic : Anaphylaxis reaction

Lecture : dr. Ketut Suardamana,SpPD-KAI

Definition

Anaphylaxis is an acute severe, life-threatening, generalized 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)

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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?

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!

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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

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1. What is the definition of allergy rhinitis?

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

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

Topic : Allergic Disease in Dermatology Lecturer : Dr.Nyoman Suryawati, SpKK

Atopic Dermatitis

Absract

Atopic dermatitis (AD) or atopic eczema is a chronically relapsing, pruritic, exanthematous dermatosis of uncertain etiology that is characterized primarily by an allergic diathesis as well as erythema, oozing, crusting, excoriations, lichenification, and dehydration of involved skin surfaces (Figs 1 and 2). Affected infants typically are fussy from sleep deprivation because of pruritus and often are uncomfortable, are fretful, and may not eat well. Older children who have severe atopic eczema frequently are asthenic and may have difficulties at school.

Onset occurs at approximately 2 to 3 months of age, and the disease may persist, with periodic exacerbations and remissions, into adulthood. Sites predisposed to rash change with growth and development. Spread to other areas may occur in severe cases.

Pathophysiology of AD by Hyperactive Th2 subset T helper cells (associated with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, stimulation of proliferation, and differentiation of B lymphocytes), Increased levels of serum IgE, Upregulation of interleukin-4, Downregulation of interferon gamma, Increased eosinophils, Elevated levels of IgEactivated mast cells.

Clinical feature of AD, there are three stages under the different age groups:

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

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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.

LEARNING TASK

Case 1

A 22-year-old waitress complained of a 5 to 6 months history of painful, pruritic lesions on her hands, arms, and legs. The itch often disturbed her sleep, and her quality of life was diminished by physical discomfort and feelings of embarrassment. Lesions on both palms showed minimal vesiculation, moderate papulation and scaling, moderate to severe erythema, and severe fissuring and lichenification. Lesions on her arms and legs were less severe, showing only slight erythema and papulation.

She reported a continuous course of eczematous lesions, primarily on her hands, over the previous 6 to 7 years, with the onset coinciding with a tongue piercing received in late 1995. Immediately after the piercing, she developed a significant lingual hematoma, which resolved after approximately 3 months. She received 4 subsequent piercings over the next year: one in her lip, one in her nose (transseptum) and 2 in her right pinna. She also reluctantly removed her facial piercings soon afterward, assuming a correlation between the jewelry and the appearance of hand eczema, which had emerged almost simultaneously.

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Case 2

A 13-year-old Caucasian male came with chronic-residive of pruritus and ithching on the fosa cubiti, his cheeks, back and leg for 9 years. The itch often disturbed her sleep, and her quality of life was diminished by physical discomfort and feelings of embarrassment. Her father also had a history of asthma, both parents had drug allergies, and one sibling had atopic dermatitis as a child. Serum IgE level was 6120 IU/mL, and increase of eosinophil count. Prior therapies included all of those topical cream for self medication, but no significant result, even getting worse if intake sea food and other foods.

What is the most likely diagnosis, and what test would confirm it?

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

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

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

Laboratory findings

- Rheumatoid factors; are autoantibodies reactive with the Fc portion of IgG , are found in more than two-thirds of adults with the disease.

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

Radiographic evaluation

Loss of articular cartilage and existence of bone erosions.

Diagnosis

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

2. Arthritis (³ 3 joints)

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

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

Learning Task

Case

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

Learning task

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

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

5. Describe other laboratory test

6. Where should you reffer this patient?

Self assessment

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

3. Describe the pathological aspect of AR! 4. Describe the clinical manifestation of AR! 5. Describe the laboratory test for AR! 6. Describe the diagnostic criteria of AR! 7. Comprehend the management of AR!

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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

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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 : Secondary Immunodeficiency Disease

HIV Infection and AIDS

Lecturer : Prof. DR. Dr. Tuti Parwati M, SpPD-KPTI

Abstract

SECONDARY IMMUNEDEFICIENCY DISEASES, (FOCUS ON HIV)

Infeksi HIV merupakan infeksi kronik dengan beberapa stadium yang pada awalnya menimbulkan gangguan terutama pada sistem imunitas seluler tetapi kemudian disusul dengan terganggunya pengaturan sistem imunitas humoral dengan berbagai akibatnya. Pada infeksi akut atau infeksi Primer yang berlangsung sekitar 4-12 minggu pasca infeksi, akan terjadi serokonversi dari antibodi HIV negatif menjadi antibodi HIV positif. Setelah itu disusul dengan stadium kronik asimptomatik dan simptomatik, dimana fase ini berlangsung rata-rata sekitar 3-5 tahun setelah infeksi primer. Setelah itu penyakit masuk ke stadium lanjut yang disebut stadium AIDS, karena pada stadium ini terdapat sindroma penyakit akibat defisiensi imunitas sekunder yang berat. Pada era pra HAART (highly active antiretroviral therapy) stadium ini bertahan hanya sekitar 2-3 tahun kemudian penderita meninggal. Era HAART dimulai sekitar tahun 1995-1996 dimana diberikan setidaknya tiga jenis obat ARV dari kelas yang berbeda, dimana cara kerja obat dengan titik tangkap yang berbeda pada siklus hidup HIV dapat menekan pertambahan jumlah viurs, sehingga lama kelamaan jumlah HIV dalam darah tidak dapat di deteksi lagi. Masa asimptomatik yang cukup lama disebut juga fase laten, namun istilah ini tidak memberikan arti yang sesungguhnya, karena dalam fase yang disebut laten sebenarnya berlangsung replikasi virus yang sangat aktif didalam kelenjar limfe dan organ RES (reticuloendothelial system). Proses yang terjadi sangat dinamik dan patologik baik dilihat dari aspek virologi maupun imunologi ini pada akhirnya dapat menimbulkan gejala klinik berupa sindroma defisiensi imun yang berat.

Pengobatan terhadap infeksi HIV tergantung stadium penyakit dan sindroma gejala klinik infeksi oportunistik yang ada dan pengobatan dengan obat anti retroviral kombinasi. Tentukan derajat berat imunedeficiency dengan pemeriksaan jumlah limfosit CD4 dan viral load penderita. Menurut WHO ada 4 stadium infeksi HIV, yaitu stadium 1 – 4, dan stadium 3 dan 4 sudah termasuk stadium AIDS. Pengobatan infeksi oportunistik sama seperti pengobatan penyakit pada non HIV hanya saja diperlukan pemberian pengobatan yang lebih lama. Berdasarkan rekomendasi WHO sebelumnya, Obat ARV kombinasi mulai diberikan pada CD4=< 200 sel/mm3, tetapi rekomendasi WHO terbaru (2010) menyarankan pemberian ARV pada CD4 350 sel/mm3.

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Learning tasks

Case 1:

A 20-year-old man complained of cough and shortness of breath since a month earlier. He got dry cough and pain on his chest when inhale. He also lost weight until 15 kg in 1 month. He lost appetite and got dryness in his throat when eat or drink. He always takes medicine but the symptoms relapsed.

Tasks

1. Complete history taking of this patient which can lead you closer to the case-diagnosis 2. Describe physical examination to support diagnosis of this patient

3. Describe laboratory and other examination to support diagnosis 4. Describe principle management of this patient

5. Define plan of therapy based on priority for this patient

Self assessment

1. What is the definition of secondary immune deficiency?

2. What is opportunistic infection? Named some example of opportunistic infection. 3. What are the diagnosis criteria for HIV infection/AIDS?

4. What kind of antiretroviral therapy (ART) does available for patient?

5. What psycho-social problem of HIV infection/AIDS we should always remember at our duty as a doctor?

TOPIC : GUILLAIN BARRE SYNDROM, MYASTHENIA GRAVIS

MULTIPLE SCLEROSIS

LECTURER : dr. NI MADE SUSILAWATHI, Sp.S

AUTOIMMUNE DISEASES IN NEUROLOGY

ABSTRACT

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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.

2 Neuroimmunology In Clinical Practice.2008.Bernadette Kalman and Thomas H Brannagan III editors. Blackwell Publishing

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Immunologic Dissorders in childhood

Topic : Food Allergy

Lecturer : dr. Komang Ayu Witarini,SpA

ABSTRACT

Food allergy (FA) is one of the earliest manifestations of allergic disease. It is a part of adverse reaction to food. FA is mediated either by IgE or other cells of the immune system, and could be mixed between IgE and cell mediated. The typical case of FA (IgE mediated), usually started during infancy in which most symptoms might be resolved over time, but the IgE allergies remain. Rather than genetic predisposition, every infant are prone to FA, especially Cow’s milk allergy (CMA), since the immaturity of the gastrointestinal tract will allow the allergen from CM to be absorbed and enter the circulation, enable for sensitization and clinical manifestation development. Diagnosis of FA is based on careful history, with reproducibility, timing, and response to elimination of food from the diet. The gold standard is the double blind placebo controlled food challenge (DBPCFC). Treatment consists of avoidance of the diet. Prevention for Food allergy is done by promoting breastfeeding and delayed exposure to food allergen. Other purpose of prevention is to avoid allergic march

Learning tasks:

A parent of 3 month-old baby girl complained about the rash in both cheeks of their baby, started 5 days before. It seemed that the rash was itchy so the baby seemed to be scratching her cheek intensely and became restless. Baby have been breastfed since she was 2 days old for only 7 days, while formula had been given since her first day of life, which then continued after breastfeeding cessation.

Task:

1. What are other helpful informations you should get from the parent for complete management of this case?

2. When and how did the process of the diseases started?

3. Considering the onset of manifestation: please describe other clues you should find during physical examination on this baby!

4. Do you need laboratory investigation for diagnostic? 5. What are your suggestions for the parent?

6. Will you prescribe medication? If yes, please describe your plan.

Self assessment:

1. What is FA

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Lecturer : dr. Komang Ayu Witarini,SpA

Abstract

Henoch Schonlein Purpura is a systemic small vessel vasculitis. It usually begin with Upper Respiratory Tract Infection, although can be triggered by other factors. During infection, Ag-Ab complex will activate complement, however, in HSP, C3a and C5a released during the process will increase vascular permeability results in plasma leakage, erythrocyte extravasation, recruitment of inflammatory cells, which will give clinical manifestation of palpable purpura, join inflammation, abdominal colic, and renal involvement. Treatment is conservative, using nonsteroid anti inflammation Drug (NSAID). Steroid used when there is complication. Recurrence can be developed.

Juvenile Rheumatoid Arthritis

Juvenile rheumatoid arthritis is arthritis that causes joint inflammation and stiffness for more than 6 weeks in a child of 16 years of age or less. Inflammation causes redness, swelling, warmth, and soreness in the joints, although many children with JRA do not complain of joint pain. Any joint can be affected and inflammation may limit the mobility of affected joints. Systemic JRA can also affect the internal organs. Classification of JRA into three types by the number of joints involved, the symptoms, and the presence or absence of certain antibodies found by a blood test. JRA is an autoimmune disorder, which means that the body mistakenly identifies some of its own cells and tissues as foreign. The main goals of treatment are to preserve a high level of physical and social functioning and maintain a good quality of life. Treatment consist of medication,: NSAID, DMARD, Anti TNF and physical treatment.

Systemic Lupus Erythematosus in children.

SLE is persistent nonspecific activation of the immune system that results in widespread tissue deposition of immune complexes. Thus most of the damage that occurs in SLE is ‘bystander’ damage. As a result of the deposition of immune complexes there is inflammation that damages the tissues where ever the immune complexes have landed. Nonspecific complaints of fatigue and malaise are the most common initial symptoms of SLE in children and adolescents. The typical 'butterfly' rash is present in less than one-third of affected children. Definitive diagnosis of SLE is done using The American College of Rheumatology. Treatment using corticosteroid soon after diagnosis confirmed.

Learning tasks

Case

A 10-year-old boy complained of pain and warm on his left knee for the late 3 months. His right ankle had been pain and warm since two months, followed by left ankle since 6 weeks. Every morning he felt stiffness on those joints, particularly in the knee. No fever has been experienced, he ate well, and his body weight was in normal limit.

Task:

1. What clues you may gather for JRA from the case above? 2. What type of JRA is the case? Why?

3. What laboratory investigation do you need? 4. What are your planning for treatment of the case 5. What is the prognosis?

Self assessment

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2. What Is Juvenile Rheumatoid Arthritis? 3. What Causes Juvenile Rheumatoid Arthritis?

4. What Are the Symptoms and Signs of Juvenile Rheumatoid Arthritis? 5. How Is Juvenile Rheumatoid Arthritis Diagnosed?

6. Who Treats Juvenile Rheumatoid Arthritis? What Are the Treatments? 7. How Can the Family Help a Child Live Well With JRA?

8. Do Children With Juvenile Rheumatoid Arthritis Have To Limit Activities? 9. What is Purpura?

10. What Is Henoch Schonlein Purpura? 11. What Causes Henoch Schonlein Purpura?

12. What Are the Symptoms and Signs of Henoch Schonlein Purpura? 13. How Is Henoch Schonlein Purpura Diagnosed?

14. Who Treats Henoch Schonlein Purpura? What Are the Treatments? 15. Do Children With Henoch Schonlein Purpura Have To Limit Activities?

Topic : Immunodeficiency in Childhood

Lecturer :dr. Komang Ayu Witarini,SpA

Absract

When someone is born defected in one or more parts of the immune system, it is called primary immune deficiency. Recurrent infection or incomplete recovery from infections is among the clues from which we can suspect that the patient has immune deficiency. Thorough history taking and evaluation is needed to direct us to whether the immune deficiency is primary or secondary.

Learning tasks

1. What is Primary Immune deficiency (PID)? 2. What are the types of PID?

BCS : Laboratory diagnostic in allergic disease

Lecturer : Dr.dr. I Wayan Wande, Sp.PK

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mixtures bound to a solid material. Allergen-specific IgE is then detected using antibodies specific for human IgE that are labeled with either enzyme or a fluorescent compound

Learning Task

1. Mentions of invitro test for allergic diease

2. Mentions of advantages and disadvantages RAST compared with skin test Selft Assessment

1. To knows laboratory examination for diagnostif of allergic disease

2. To knows interpretation of RAST and other examination of allergic disease

Topic 2. Laboratory diagnostic in autoimmune disease Abstract

Laboratory testing is of great value when evaluating a patient with a suspected autoimmune disease. The results can confirm a diagnosis, estimate disease severity, aid in assessing prognosis and are useful to follow disease activity. Components of the laboratory exam include complete blood count with differential, comprehensive metabolic panel, inflammatory markers, autoantibodies, and flow cytometry. This chapter discusses these components and includes a discussion about organ-specific immunologic diseases where immunological laboratory testing is employed. Comprehensive laboratory evaluation of a suspected autoimmune illness in conjunction with a thorough clinical evaluation provides a better understanding of a patient's immunologic disease.

Examining patients for potential autoimmune diseases is fraught with difficulty because not one laboratory test establishes such a diagnosis. Typically, multiple laboratory tests are needed and include basic studies like a complete blood count, comprehensive metabolic panel, acute phase reactants, immunologic studies, serologies, flow cytometry, cytokine analysis, and HLA typing. Although some tests may be non-specific, such as the erythrocyte sedimentation rate (ESR), they are useful to assess disease activity. These tests can be useful in the diagnosis and management of patients with autoimmune diseases and help in providing a prognosis, or indicate the severity of organ involvement or damage.

Learning Task

1. Why are autoimmune diseases challenging to diagnose?

2. What is the first test to be considered for a patient suspected of having an autoimmune disease?

3. What is the significance of ANA patterns?

4. How predictive are the specific antibodies? What is their sensitivity and specificity in various autoimmune diseases?

Self assessment

1. To know Initial laboratory evaluation for autoimmune diseases 2. Mentions of Inflammatory markers in autoimmune diseases

3. Mentions of Autoantibodies and Immunologic Studies in autoimmune diseases

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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.

Study Guide Immune Semester III Tayang 1 November 2016

CONTENTS

FOREWORD

CURRICULUM

PLANNERS TEAM

FACILITATORS

(REGULAR CLASS)

FACILITATORS

(ENGLISH CLASS)

Meeting of the student representatives

Meeting of facilitators

Plenary session

Assessment Methods

Day 1