Académique Documents
Professionnel Documents
Culture Documents
CONTENTS
Contents ...1
Foreword
...
....2
Curriculum ........3
Block Team ......4
Facilitators Team .....6
Time Table .........................7
Meeting of student representatives 12
Meeting of facilitators 12
Assessment Method ..
12
Learning Program .13
Student Project ..43
References .44
Curriculum Mapping..45
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:
-
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
4. Diagnose and manage patients with immunodeficiency
Curriculum contents:
1. The biology and responses of the immune system in health and diseases
2. The common immune-mediated disorders
PLANNERS TEAM
No
Name
Department
Phone
Internal Medicine
082145854167
ENT
081237874447
dr.
Sari
(Secretary)
Internal Medicine
08123985811
Internal Medicine
08123960964
ENT
08123837063
Dermatology
08563704591
Pediatrics
03617442593
Pathology Anatomy
081337115012
10
Histology
081337222567
11
Dermatology
0817447279
Department
Phone
Internal Medicine
08123960964
Histology
081805629937
Pathology Anatomy
081337115012
Pediatrics
081239559559
Clinical Pathology
03617428983
Wulan
DS,
SpTHT-KL
LECTURERS
No
Name
Pharmacology
08179787972
Pharmacology
087777790064
Dermatology
0817447279
Internal Medicine
08123985811
10
Internal Medicine
08123806626
11
ENT
081237874447
081338466039
12
dr. Susilawathi,SpS
Neurology
08124690137
13
Internal Medicine
08124683416
14
Internal Medicine
82145854167
15
Clinical Pathology
08124686885
16
Internal Medicine
082146179796
17
Forensic
081916613459
18
Clinical Pathology
08123953344
FACILITATORS
(REGULAR CLASS)
NO
NAME
GROUP
DEPT
PHONE
VENUE
2nd floor:
R.2.01
2nd floor:
R.2.02
2nd floor:
R.2.03
2nd floor:
R.2.04
2nd floor:
R.2.05
2nd floor:
R.2.06
A1
Physiology
08123811019
A2
Biochemistry
081239990399
A3
Ophtalmology
081816513322
A4
Microbiology
08553711398
A5
Andrology
08123473593
A6
Microbiology
082236465801
A7
Ophtalmology
08123846995
A8
Physiology
08123989891
A9
Microbiology
089685415625
10
A10
Anatomy
087860405625
2nd floor:
R.2.07
2nd floor:
R.2.08
2nd floor:
R.2.21
2nd floor:
R.2.22
FACILITATORS
(ENGLISH CLASS)
NO
1
NAME
GROUP
DEPT
PHONE
B1
Farmacology
0812650481
B2
Histology
08164732743
B3
Pharmacology
087861030195
B4
Anatomy
085792652363
Biochemistry
081337141506
Fisiology
081337761299
2
3
4
5
B5
B6
7
Dr.dr. Ni Made Linawati, M.Si
Udayana University Faculty of Medicine, DME, 2016
B7
Histology
081337222567
VENUE
2nd floor:
R.2.01
2nd floor:
R.2.02
2nd floor:
R.2.03
2nd floor:
R.2.04
2nd floor:
R.2.05
2nd floor:
R.2.06
2nd floor:
R.2.07
6
B8
Cardiology
081289053234
B9
Public Health
08123816424
B10
Anatomy
085103043575
2nd floor:
R.2.08
2nd floor:
R.2.21
2nd floor:
R.2.22
9
10
TIME
ENGLISH
CLASS
Tuesday,
Nov 1, 2016
Wednes
day, Nov
2, 2015
ACTIVITY
CONVEYER
VENUE
REG CLASS
Introduction to The
Immune System and
disorders
Independent Learning
Library
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
Discussion
Room
14.00-15.00
(60)
08.00-08.30
(30)
15.00-16.00
(60)
09.00-09.30
(30)
Plenary Session
Class Room
Dr. dr. Ketut
Suryana, SpPD-KAI
Dr. dr. Ni Made
Class Room
Linawati,
MSi
08.30-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
10.30-12.00
(90)
12.00-12.30
(30)
12.30-14.00
(90)
12.00-13.30
(90)
13.30-15.00
(90)
11.30-12.00
(30)
10.00-11.30
(90)
Independent Learning
Library
SGD
Fasilitator
Discussion
Room
-
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
09.00-10.30
(90)
12.00-13.30
(90)
10.30-12.00
(90)
Comprehend The
Microscopic
Structure of Limphoid
Organ,Immune
Cells and MHC
Comprehend basic
mechanism of autoimmunity
Class Room
Dr. dr. Ketut
Suryana, SpPD-KAI
Break
Friday,
Nov 4,
2016
Comprehend basic
mechanism of drug
allergy
Immunopharmacology
Class Room
12.00-13.30
(90)
Independent Learning
Library
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
Discussion
Room
14.00-15.00
(60)
08.00-08.30
(30)
15.00-16.00
(60)
08.30-09.00
(30)
Plenary Session
Class Room
Dr. dr. I Made
Jawi,
Dr. dr. I Wayan Putu Class Room
Sutirta
Yasa, Msi
08.00-08.30
(30)
09.00-09.30
(30)
08.30-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
Monday,
Nov7,
2016
Comprehend
laboratory test of
immune system
08.30-10.00
(90)
09.00-10.30
(90)
Independent Learning
Library
10.00-11.30
(90)
10.30-12.00
(90)
SGD
Fasilitator
Discussion
Room
11.30-12.00
(30)
12.00-12.30
(30)
Break
12.00-13.30
(90)
12.30-14.00
(90)
SP paper preparation
Discussion
Room
13.30-14.30
(60)
14.30-15.30
(60)
Plenary Session
08.00-08.30
(30)
08.30-09.00
(30)
09.00-09.30
(30)
09.30-10.00
(30)
Comprehend hypersensifity
09.00-10.30
(90)
12.00-13.30
(90)
Independent Learning
Library
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
Class Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Antihistamin
Sutirta
Yasa, Msi
Wednes
day, Nov 9,
2016
Thursday,
Nov 10,
2016
08.00-09.00
(60)
09.00-10.00
(60)
dr. Ketut
Suardamana,
SpPD-KAI
Class Room
09.00-10.30
(90)
12.00-13.30
(90)
Independent Learning
Library
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-08.30
(30)
09.00-09.30
(30)
08.00-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
12.00-13.30
(90)
manage allergic
diseases in dermatology
Independent Learning
dr. Ketut
Suardamana,
SpPD-KAI
dr. Sari Wulan
Dwi
Sutanegara, Sp
THT (K)
dr.Nyoman
Suryawati,
SpKK
-
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
dr. Nyoman
Discussion
Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
dr.Gede
Kambayana,SpP
D-KR / dr.Pande
Ketut
Kurniari,SpPD
Class Room
09.00-10.30
(90)
12.00-13.30
(90)
Independent Learning
Library
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
SP paper presentation:
Urtikaria and Angiodema
Class Room
dr.Ketut
Suardamana,SpPDKAI
Class Room
Library
Suryawati,
SpKK
Friday,
Nov 11,
2016
Monday,
Nov14,
2016
dr.Gede
Kambayana,SpP
D_KR/dr.Pande
Ketut
Kurniari,SpPD
Prof. Dr. dr. Tuti
Parwati
M, SpPD-KPTI
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-08.30
(30)
09.00-09.30
(30)
08.00-09.00
(30)
09.30-10.00
(30)
09.00-10.30
(90)
12.00-13.30
(90)
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)
Class Room
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
08.00-08.30
(30)
09.00-09.30
(30)
08.00-09.00
(30)
09.30-10.00
(30)
Class Room
dr.Susilawathi,SpS
Class Room
Class Room
12.00-13.30
(90)
Independent Learning
Library
10.30-12.00
(90)
13.30-15.00
(90)
SGD
Fasilitator
Discussion
Room
12.00-12.30
(30)
11.30-12.00
(30)
Break
12.30-14.00
(90)
10.00-11.30
(90)
14.00-15.00
(60)
15.00-16.00
(60)
Plenary Session
Class Room
08.00-09.00
Tuesday,
Nov 15, 2016 (60)
09.00-10.00
(60)
Dr.dr. I Wayan
Wande, Sp.PK
Class Room
09.00-10.30
(90)
10.30-13.00
(150)
10.00-11.30
(90)
13.30-16.00
(150)
Independent Learning
Library
BCS Training
Dr.dr. I Wayan
Wande, Sp.PK
& Team
Skill Lab
10
11.30-13.30
BCS Discussion
09.00-10.00
(60)
09.00-10.30
(90)
10.00-11.30
(90)
Independent Learning
Library
10.30-12.00
(90)
Fasilitator
Discussion
Room
12.00-12.30
(30)
13.00-13.30
(30)
Break
12.30-13.30
(60)
13.30-15.00
(90)
Plenary Session
Class Room
08.00-09.00
(60)
09.00-10.00
(60)
09.00-10.30
(90)
10.00-11.30
(90)
Independent Learning
Library
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
13.00-15.00
(120)
11.30-13.30
BCS Discussion
08.00-09.00
(60)
09.00-10.00
(60)
dr.Gede
Kambayana,SpPDKR / dr.Pande Ketut
Kurniari,SpPD
09.00-10.30
(90)
10.00-11.30
(90)
Independent Learning
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
13.00-15.00
(120)
11.30-13.30
BCS Discussion
08.00-09.00
Monday,
Nov 21, 2016 (60)
09.00-10.00
(60)
Library
dr.Gede
Kambayana,SpPDKR / dr.Pande Ketut
Kurniari,SpPD
Skill Lab
dr.Gede
Kambayana,SpPDKR / dr.Pande Ketut
Kurniari,SpPD
Dr. dr. Ketut
Suryana, SpPD-KAI
09.00-10.30
(90)
10.00-11.30
(90)
Independent Learning
10.30-13.00
(150)
13.30-16.00
(150)
BCS Training
13.00-15.00
(120)
11.30-13.30
BCS Discussion
Wednes
day,
Nov 16,
2016
Thursday,
Nov 17,
2016
Friday,
Nov 18,
2016
Tuesday,
Nov 22, 2016
Class Room
Class Room
Class Room
Pre-evaluation Break
11
Wednes
day,
Nov 23,
2016
Meeting of facilitators
The meeting between block planners team and the facilitators will take place on, Monday,
Friday November 18 at 10.00 am until 12.00 pm at HPEQ discussion room. In this meeting all
the facilitators are expected to give suggestions and inputs as evaluation to improve the study
guide and the educational process. Because of the importance of this meeting, all the
facilitators are strongly expected to attend the meeting.
Plenary session
For each task of SGD, the students are requested to prepare a group report. The reports will
be presented in a plenary session. The group will be chosen randomly by the lecturer in
charge. The group report will be evaluated by respective facilitator.
Assessment Methods
Assessment will be performed at the end of the block on Nopember 9 th 2015. There are 100
questions for the examination that consists of Multiple Choice Question (MCQ). The borderline
to pass exam is 70.
12
LEARNING PROGRAMS
Day 1
Topics
Lecturer
1. The Immune system has evolved to protect us from pathogens. Some, such as viruses,
infect individual cells; others, including many bacteria, divide extracellularly within tissues
or body cavities.
2. The cells which mediate immunity include lymphocytes and phagocytes. Lymphocytes
recognize antigens on pathogens. Phagocytes internalize pathogens and degrade them
3. An Immune response consists of two phases. In the first phase, antigen activates specific
lymphocytes that recognize it; in the effector phase, these lymphocytes coordinate an
immune response that eliminates that source of the antigens.
4. Specificity and memory are two essential features of adaptive immune responses. The
Immune system mounts a more effective response on second and subsequent encounters
with a particular antigen.
5. Lymphocytes have specialized functions. B cells make antibodies; cytotoxic T cells kill
virally infected cells; helper T cell coordinate the immune response by direct cell-cell
interactions and the release of cytokines, which help B cells to make antibody.
6. Antigens are molecules which are recognized by receptors on lymphocytes. B lymphocytes
usually recognize intact antigen molecules, while T lymphocytes recognize antigen
fragment on the surface of other cells.
7. Clonal selection involves recognition of antigen by a particular lymphocyte; this leads to
clonal expansion and differentiation to effector and memory cells.
8. The immune system may break down. This can lead to immunodeficiency or
hypersensitivity diseases or to autoimmune diseases.
Learning task
1.
2.
3.
4.
13
Day 2
Topic
Lecturer
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
Lecturer
ABSTRACT
Immunologic Tolerance: Is a state in which an individual is incapable of developing an immune
response against a specific antigen.
Self- tolerance: Specifically refers to a lack of immune responsiveness to ones own tissue
antigens.
Udayana University Faculty of Medicine, DME, 2016
14
3.
4.
5.
6.
Describe the mechanism of tissue injury in SLE, and give some examples of
morphological changes in SLE!
Mention other diseases that belong to autoimmune diseases group!
15
Day 3
Topic
: Immunopharmacology
Lecturer
ABSTRACT
Immunopharmacology includes the characteristics of drugs that can suppress,
modulate, or stimulate immune functions. It also includes the pharmacology of antibodies that
have been developed for use in immune disorders. The drugs available comprise a wide
variety of chemical and pharmacologic types. In this topic also will be discuss the ways in
which drugs may activate the immune system and cause unwanted immunologic reactions.
Drugs that modulate immune function and as a immune suppressants are: glucocorticoids
(prednisone), immunophilin ligands (Cyclosporine), cytotoxic drugs (Cyclophosphamide), AntiTNF- agents (etanercept), enzyme inhibitors (mycophenolate mofetil) and Antibodies.
Drugs that modulate immune function and as a immune potentiators are: Cytokines
(Interleukin-2, Interferons), BCG vaccine and Thymosin.
Learning Task
A patient was treated with penicillin. Within a few minutes after penicillin injection, he
developed severe bronchoconstriction, laryngeal odema and hypotension.
Explain the immunologic mechanism of those problems.
To manage that patient what medicine will you give for him immediately?
Explain your answer if you give him prednisone. Do you agree? Why?
How about antihistamine like dimenhydrinate for this patient?
Self assessment
1. Cyclosporine is effective in organ transplantation. The immunosuppressant action of
the
drug appears to be due to
A. Activation of natural killer (NK) cells
B. Blockade of tissue responses to inflammatory mediators
C. Increased catabolism of IgG antibodies
D. Inhibition of the gene transcription of interleukins
E. Interference with antigen recognition
2. Azathioprine
A. Binds avidly to a cytoplasmic immunophillin
B. Blocks formation of tetrahydrofolic acid
C. Is a precursor of cytarabine
D. Is markedly hematotoxic and has caused neoplasms
E. Is a metabolite of mercaptopurine
3. Which of the following drugs is a widely used agent that suppresses cellular immunity,
inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG
antibodies?
A. Cyclophosphamide
B. Cyclosporine
C. Infliximab
D. Mercaptopurine
Udayana University Faculty of Medicine, DME, 2016
16
Day 4
Topic
Lecture
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.
Udayana University Faculty of Medicine, DME, 2016
17
Day 5
Topic
Lecturer
Hypersensitivity
dr. Tjok Istri Anom Saturti, SpPD
ABSTRACT
There are 4 types classifications according to
Gel & Coombs
1. Type I
: Immediate hypersensitivity
2. Type II
: Cytotoxic hypersensitivity
3. Type III
: Immune complex hypersensitivity
4. Type IV
: Delayed (cell mediated) hypersensitivity
Hypersensitivity the immune response results are harmful to the heart
Type I
: Antigen bind to IgE on the surface of mast cells release of several mediators
within minutes. Important mediators are: Histamin, SRS-A, ECF-A, serotonin,
Prostaglandins and thromboxanes, etc. Clinical manifestations:
1. Anaphylaxis : severe bronconstriction, hypotension shock
2. Atopy: genetic factor to induce by exposure to spesific allergens (pollens,
dust, shellfish, nuts, etc). Clinical manifestation: hay fever, asthma,
18
Type II
Type III
Type IV
Learning Task
1. Make definition of the term hypersensitivity
2. Explain the biological roles of hypersensitivity
3. Make classification of hypersensitivity
4. Compare the hypersensitivity type I, II, III and IV
5. Explain principle treatment and prevention of hypersensitivity
Self Assessement
1. Hypersensitivity reaction is a general pathologic reaction which has following characteristics:
A. Never happens on the first exposure
B. Generally divided into 4 types
C. Is an overreaction of immune system
D. Occurred if humoral and cellular immunological status are increased
E. All above are correct
2. The followings are the feature of hypersensitivity reaction type I, except:
A. Occurs in few seconds or minutes
B. Is an IgE mediated immune response
C. IgE is bind by mast cell
D. Ia a delayed hypersensitivity
E. Histamine is a primary mediator produced
3. In hypersensitivity reaction type I, eosinophyl is activated by:
A. IL-4
B. IL-2
C. IL-5
D. IL-6
E. IL-1
4. Histamine release effect of hypersensitivity reaction type I is:
A. Vasoconstriction of blood vessels
B. Vasodilation of blood vessels
C. Capillary permeability decreased
D. Bronchus dilated
E. Hyposecretion of mucosa
5. Hypersensitivity reaction type II is a cytotoxic reaction which involves:
A. IgG and IgM
B. IgG and IgD
C. IgG and IgA
D. IgA and IgD
E.
IgD and IgE
Udayana University Faculty of Medicine, DME, 2016
19
Topic
: Antihistamine
Lecturer
ABSTRACT
Histamine receptor antagonists represent a third approach to the deduction of
histamine-mediated responses. For over 60 years, compounds have been available that
competitively antagonize many of the actions of histamine on the smooth muscle. Compounds
that competitively block histamine at H1 receptor have been used clinically for many years,
and many H1 antagonists are currently marketed. Many are available without prescription, both
alone and in combination formulations such as cold pills and sleep aids. The H1 antagonists
are conveniently divided into firs generations and second generation agents. These groups are
distinguished by relatively strong sedative effect of most of the generation drugs. The first
generation agents are also more likely to block autonomic receptors. The relatively less
sedating characteristic of the second generation H1 blockers is due in part to their less
complete distribution into the central nervous system. H1 receptor antagonists block the
actions of histamine by reversible competitive antagonism at the H1 receptor; these drugs
have no effect on histamine release from storage sites. They are more effective if given before
histamine release occurs. The first generation are often the first drugs used to prevent or treat
the symptoms of allergic reactions, and the second generation H1 antagonists are used mainly
for treatment of allergic rhinitis and chronic urticaria. The drugs adverse effect are sometimes
exploited therapeutically.
Learning Task
1.
2.
3.
4.
5.
Self assessment
1. Many H1 blocker have additional nonhistamine-related effect, these are likely to include all
of the following. EXPECT:
A. Antimuscarinic reduction in bladder tone
B. Local anesthetic effect if the drug is injected
C. Anti-motion sickness effect
D. Increase in total peripheral resistance
E. Sedation
2. Which of the following drugs will result from blockade of H1 receptor?
A. Decreased cAMP in smooth muscle
B. Decrease channel opening in enteric nerves
C. Decrease IP3 in smooth muscle
D. Increase IP3 in smooth muscle
E. Increase in total peripheral resistance
20
3. Which of the following drugs are used as anti-motion sickness and also for management
of chemotherapy-induced vomiting?
A. Diphenhydramine
B. Dimenhydrinate
C. Meclizine
D. Cyclizine
E. Loratadine
4. Toxicities of H1 blocker include which one of the following
A. Sedation
B. Dry mouth
C. Blurry vision
D. Vomiting
E. Hypotension
Day 6
Topic
Lecture
Introduction
Drug allergy or hypersensitivity is a form of Adverse Drug Reaction (ADR)
Definition
An ADR is any undesirable effect of drug that is administered in standard doses by the
proper route for the purpose of prophylaxis, diagnosis, or treatment.
Drug allergy is an immunologically mediated reaction, occurs in a susceptible populations,
characterized by specificity, transferability by antibodies or lymphocytes, and recurrence on reexposure
Pathophysiology
Allergic drug reactions are usually defined as;
1. reaction caused by suspected immunologic mechanisms
2. result from the production of antibodies and / or cytotoxic T cells directed against the
drug,
3. its metabolite, a soluble / cell-bound carrier protein as a responses to prior or
continuous exposure to a drug
Risk factors
1. Patient related : Age, sex, genetics, atopy, AIDS
2. Drug related : Macromolecular size ; bivalency, haptens, route, dose, duration of
treatment
3. Aggravating factors : Blockers, asthma, pregnancy
Diagnosis
1.
Diagnosis of drug allergy based on ;
2.
Clinical history
Udayana University Faculty of Medicine, DME, 2016
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Clinical manifestations
Diagnostic test
Diagnostic tests
1. SPT may be helpful for diagnosing IgE mediated drug reactions (in vivo)
2. RAST may detect serum IgE antibodies to certain drugs (e.g : penicillin and succinyl
choline) (in vitro)
3. Provocation tests
Oral provocation tests, may be as a gold standard
They must be performed under strict medical supervision with resuscitative equipment
available
Management
1. Avoidance
2. Premedication
3. Desensitisation
Learning Task
Vignette
Male 20 years old, was diagnosed with Pulmonary TB and taking the anti TB regimen
(Category 1). On the second day treatment he felt an itchy swollen redness on whole body.
He had previous history of drug allergy but the allergen is unknown, his mother also had
history of drugs allergy. The patient was fully alert, T 110/70 mmHg, pulse rate 92x per minute
regular, RR 18x per minute.
Task
1. Could you explore more to complete the anamnesis!
2. Describe any sign that you find on Physical examination?
3. How to manage this patient?
Self assessment
1. Could you describe the adverse drugs reaction (ADR)!
2. Describe the immunopathophysiology of drugs allergy (due to Gell & Coombs Criteria)!
3. Comprehend the diagnostic approach of the drugs allergy!
Topic
Anaphylaxis reaction
Lecture
Definition
Anaphylaxis is an acute severe, life-threatening, generalized
reactions
or systemic hypersensitivity
Pathophysiology
1. Type I reaction (IgE mediated)
2. Anaphylactoid reaction (Non IgE mediated) : complement activation, physical factors,
substance for Histamine release, idiopathic, arachidonic acid modulation
Clinical Criteria for Diagnosing Anaphylaxis
(Sampson HA, et al. JACI 2006)
Udayana University Faculty of Medicine, DME, 2016
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Self assessment
1. What are the differential diagnoses?
2. Could you describe the pathophysiology of anaphylaxis?
3. Could you describe the clinical manifestations?
4. The management in this case!
5. Describe the prevention!
6. Comprehend any prognostic factors!
23
Day 7
Topic
: Rhinitis Alergy
Lecturer
ABSTRACT
Allergic rhinitis is an inflammation of the nasal passages, usually associated with
watery nasal discharge and itching of the nose and eyes.
Allergic rhinitis affects about 20 percent of population and ranks as one of the most
common illnesses. The symptoms occur in the nose and eyes and usually occur after
exposure to dust, danders, or certain seasonal pollens in people that are allergic to these
substances.
There is strong genetic predisposition to allergic rhinitis. One parent with a history of
allergic rhinitis has about a 30 percent chance of producing offspring with the disorder. Tthe
risk increases to 50 percent if both parents have a history of allergies.
Characteristic symptoms include repetitive sneezing, rhinorrhea (runny nose), postnasal drip, nasal congestion, pruritic (itchy) eyes, ears, nose or throat, and generalized
fatigue. Symptoms can also include wheezing, eye tearing, sore throat, and impaired smell. A
chronic cough may be secondary to postnasal drip, but should not be mistaken for asthma.
Sinus headaches and ear plugging are also common.
Diagnosis of Allergic Rhinitis. After a medical history, physician will perform a physical
exam. Often, the nasal mucosa (lining of the nose) is pale or violaceous because of the
engorged veins. Nasal polyps may be seen. Classic signs of allergic rhinitis may include
swelling of the eyelids, injected sclerae (the whites of the eyes may be red), allergic shiners
(darkened areas under the lower eyelids thought to result from venous pooling of blood), and
extra skin folds in the lower eyelids.
Skin testing may confirm the diagnosis of allergic rhinitis. Initial skin testing is
performed by the prick method. Intradermal testing is performed if results of prick testing are
negative.
The goal of treatment is to reduce the allergy symptoms. Avoidance of the allergen or
minimization of contact with it is the best treatment, but some relief may be found with the
following medications: antihistamines and decongestants, nasal sprays and immunotherapy.
LEARNING TASK
CASE:
A 25 years old man complained of sneezing 5 to 10 times and watery nose everytime he
wakes up in the morning.
Task:
1. Please do further anamnesis in this case!
2. If in the anamnesis his mother had asthma, what is the possible diagnosis of this case?
3. What is/are the differential/s diagnosis of this case?
Udayana University Faculty of Medicine, DME, 2016
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Topic
25
Contact Dermatitis
Abstract
Dermatitis or eczema is an inflammation of the skin with characteristic morphology but
varied cause caused by skin contact with an environmental agent. Most occupational
dermatoses are eczematous reactions to an environmental contactant, characterized by
redness, swelling, small fluid filled blisters, and oozing in the acute state and as a scaly
lichenified, thickened, fissured with pigmentary changes in the chronic stage.
Contact dermatitis (CD) is an altered state of skin reactivity induced by exposure to an
external agent. "Eczema" and "dermatitis" are often used synonymously to denote a
polymorphic pattern of inflammation of the skin characterized, at least in its acute phase, by
erythema, vesiculation and pruritus. Substances that induce CD after single or multiple
exposures may be irritant or allergic in nature. The clinical presentation may vary depending on
the identity of the triggering agent and the reactivity of the subject, but in all cases the lesions
are primarily confined to the site of contact.
According to the mechanism of elicitation, the following types of contact reactions may
be distinguished: 1. allergic contact dermatitis (ACD), immunopathology based on type IV
hypersensitivity, 2. irritant contact dermatitis (ICD), due to primary irritant, acute and chronic
cumulative, 3. phototoxic and photoallergic contact dermatitis, and 4. immediate type contact
reactions. The present review will focus on allergic contact dermatitis. ACD is the clinical
presentation of contact sensitivity in humans.
Management of contact dermatitis, the only available etiologic treatment of ACD is
elimination of the contact allergen. The patients should be informed about the identity of the
offending agent and the possible sources of the sensitizer. Corticosteroids have antiinflammatory and immunosuppressive effects. In murine models of contact sensitivity they
inhibit both the induction and elicitation phase. ACD is a major indication for topical
corticosteroid treatment. Histamine is not involved in the pathogenesis of ACD, but need for
reduce itching. Systemic corticosteroid is not absolute for treatment in the most common forms
of ACD. However they may be indicated for a short period of time if ACD is widespread and
severe.
LEARNING TASK
Case 1
A 22-year-old waitress complained of a 5 to 6 months history of painful, pruritic lesions
on her hands, arms, and legs. The itch often disturbed her sleep, and her quality of life was
diminished by physical discomfort and feelings of embarrassment. Lesions on both palms
showed minimal vesiculation, moderate papulation and scaling, moderate to severe erythema,
and severe fissuring and lichenification. Lesions on her arms and legs were less severe,
showing only slight erythema and papulation.
She reported a continuous course of eczematous lesions, primarily on her hands, over the
previous 6 to 7 years, with the onset coinciding with a tongue piercing received in late 1995.
Immediately after the piercing, she developed a significant lingual hematoma, which resolved
after approximately 3 months. She received 4 subsequent piercings over the next year: one in
her lip, one in her nose (transseptum) and 2 in her right pinna. She also reluctantly removed
Udayana University Faculty of Medicine, DME, 2016
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Day 8
Topic
Lecture
: - RHEUMATOID ARTHRITIS
- SYSTEMIC LUPUS ERYTHEMATOSIS ( SLE )
- Polimyalgia Rheumatica
:
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.
Udayana University Faculty of Medicine, DME, 2016
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Self assessment
28
Abstract
Definition
SLE is an autoimmune disease which involves multiorgan / multisystem damage, mediated by
tissue-binding autoantibodies and immune complexes.
Pathogenesis and etiology
SLE is caused by interactions between susceptibility genes and environmental factors,
resulting in abnormal immune responses.
Pathology
In SLE biopsies of affected skin show deposition of Ig at the dermal-epidermal junction / DEJ ,
injury to basal keratinocytes, and inflammation dominated by T lymphocytes in the DEJ and
around blood vessels and dermal appendiges
Diagnosis.
Based on clinical features and auto antibodies.
Classification criteria for the diagnosis of SLE; (specificity 95%, sensitivity 75%) :
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Oral ulcers (include oral, nasopharyngeal and observed by physician.
5. Arthritis
6. Serositis
7. Renal disorder (proteinuria > 0,5 g / d or 3+, or cellular casts
8. Neurologic disorder
9. Hematologic disorder
10. Immunologic disorder
11. Antinuclear antibodies (ANA test )
If 4 of these criteria SLE
Laboratory test
- ANA test
: prevalence 98%, best screening, repeat test (-) (-)
- Anti ds-DNA : prevalence 70%, high titers are SLE specific, correlate with
disease activity.
Learning task
A 17 years old female came to Health Centre with chief complaint; facial rash since 3
days ago. She had the rash since a year ago, and reduced after treatment. The rash is
triggered by the UV. The patient also feels fatique since 3 months ago.
Udayana University Faculty of Medicine, DME, 2016
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Task
1. Please you complete the anamnesis!
2. Describe the physical examination!
3. If she also complains edema on whole body, what is the working diagnosis?
4. Describe the differential diagnosis!
5. Where should you reffer this patient?
Self assessment
1.
2.
3.
4.
5.
Day 9
Topic
Lecturer
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.
Udayana University Faculty of Medicine, DME, 2016
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Complete history taking of this patient which can lead you closer to the case-diagnosis
Describe physical examination to support diagnosis of this patient
Describe laboratory and other examination to support diagnosis
Describe principle management of this patient
Define plan of therapy based on priority for this patient
Self assessment
1.
2.
3.
4.
5.
TOPIC
LECTURER
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
Udayana University Faculty of Medicine, DME, 2016
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32
Day 10
: Food Allergy
Lecturer
ABSTRACT
Food allergy (FA) is one of the earliest manifestations of allergic disease. It is a
part of adverse reaction to food. FA is mediated either by IgE or other cells of the immune
system, and could be mixed between IgE and cell mediated. The typical case of FA (IgE
mediated), usually started during infancy in which most symptoms might be resolved over time,
but the IgE allergies remain. Rather than genetic predisposition, every infant are prone to FA,
especially Cows milk allergy (CMA), since the immaturity of the gastrointestinal tract will allow
the allergen from CM to be absorbed and enter the circulation, enable for sensitization and
clinical manifestation development. Diagnosis of FA is based on careful history, with
reproducibility, timing, and response to elimination of food from the diet. The gold standard is
the double blind placebo controlled food challenge (DBPCFC). Treatment consists of
avoidance of the diet. Prevention for Food allergy is done by promoting breastfeeding and
delayed exposure to food allergen. Other purpose of prevention is to avoid allergic march
Learning tasks:
A parent of 3 month-old baby girl complained about the rash in both cheeks of their baby,
started 5 days before. It seemed that the rash was itchy so the baby seemed to be scratching
her cheek intensely and became restless. Baby have been breastfed since she was 2 days old
for only 7 days, while formula had been given since her first day of life, which then continued
after breastfeeding cessation.
Task:
1. What are other helpful informations you should get from the parent for complete
management of this case?
2. When and how did the process of the diseases started?
3. Considering the onset of manifestation: please describe other clues you should find
during physical examination on this baby!
4. Do you need laboratory investigation for diagnostic?
5. What are your suggestions for the parent?
6. Will you prescribe medication? If yes, please describe your plan.
Udayana University Faculty of Medicine, DME, 2016
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Self assessment:
1. What is FA
2. What are the types of FA?
3. How does FA develop?
4. What is (are) the cause(s) of FA in children?
5. What is the laboratory investigation of FA
6. How to make an assessment of FA?
7. What is the treatment for FA
8. What is allergic march?
9. How to prevent allergic march?
Topic : Manage Rheumatic disease in Childhood
Lecturer
Abstract
Henoch Schonlein Purpura is a systemic small vessel vasculitis. It usually begin with Upper
Respiratory Tract Infection, although can be triggered by other factors. During infection, Ag-Ab
complex will activate complement, however, in HSP, C3a and C5a released during the process
will increase vascular permeability results in plasma leakage, erythrocyte extravasation,
recruitment of inflammatory cells, which will give clinical manifestation of palpable purpura, join
inflammation, abdominal colic, and renal involvement. Treatment is conservative, using
nonsteroid anti inflammation Drug (NSAID). Steroid used when there is complication.
Recurrence can be developed.
Juvenile Rheumatoid Arthritis
Juvenile rheumatoid arthritis is arthritis that causes joint inflammation and stiffness for more
than 6 weeks in a child of 16 years of age or less. Inflammation causes redness, swelling,
warmth, and soreness in the joints, although many children with JRA do not complain of joint
pain. Any joint can be affected and inflammation may limit the mobility of affected joints.
Systemic JRA can also affect the internal organs. Classification of JRA into three types by the
number of joints involved, the symptoms, and the presence or absence of certain antibodies
found by a blood test. JRA is an autoimmune disorder, which means that the body mistakenly
identifies some of its own cells and tissues as foreign. The main goals of treatment are to
preserve a high level of physical and social functioning and maintain a good quality of life.
Treatment consist of medication,: NSAID, DMARD, Anti TNF and physical treatment.
Systemic Lupus Erythematosus in children.
SLE is persistent nonspecific activation of the immune system that results in widespread tissue
deposition of immune complexes. Thus most of the damage that occurs in SLE is bystander
damage. As a result of the deposition of immune complexes there is inflammation that
damages the tissues where ever the immune complexes have landed. Nonspecific complaints
of fatigue and malaise are the most common initial symptoms of SLE in children and
adolescents. The typical 'butterfly' rash is present in less than one-third of affected children.
Definitive diagnosis of SLE is done using The American College of Rheumatology. Treatment
using corticosteroid soon after diagnosis confirmed.
Learning tasks
Case
A 10-year-old boy complained of pain and warm on his left knee for the late 3 months.
His right ankle had been pain and warm since two months, followed by left ankle since 6
Udayana University Faculty of Medicine, DME, 2016
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What clues you may gather for JRA from the case above?
What type of JRA is the case? Why?
What laboratory investigation do you need?
What are your planning for treatment of the case
What is the prognosis?
Self assessment
1. What Is Arthritis?
2. What Is Juvenile Rheumatoid Arthritis?
3. What Causes Juvenile Rheumatoid Arthritis?
4. What Are the Symptoms and Signs of Juvenile Rheumatoid Arthritis?
5. How Is Juvenile Rheumatoid Arthritis Diagnosed?
6. Who Treats Juvenile Rheumatoid Arthritis? What Are the Treatments?
7. How Can the Family Help a Child Live Well With JRA?
8. Do Children With Juvenile Rheumatoid Arthritis Have To Limit Activities?
9. What is Purpura?
10. What Is Henoch Schonlein Purpura?
11. What Causes Henoch Schonlein Purpura?
12. What Are the Symptoms and Signs of Henoch Schonlein Purpura?
13. How Is Henoch Schonlein Purpura Diagnosed?
14. Who Treats Henoch Schonlein Purpura? What Are the Treatments?
15. Do Children With Henoch Schonlein Purpura Have To Limit Activities?
Absract
When someone is born defected in one or more parts of the immune system, it is called
primary immune deficiency. Recurrent infection or incomplete recovery from infections is
among the clues from which we can suspect that the patient has immune deficiency. Thorough
history taking and evaluation is needed to direct us to whether the immune deficiency is
primary or secondary.
Learning tasks
1. What is Primary Immune deficiency (PID)?
2. What are the types of PID?
Day 11
35
BCS
Lecturer
Abstract
Allergic diseases are the result of allergic inflammation that occurs as a result of an
interaction between the environment and the patient's immune system resulting in the release
of histamine and other proinflammatory mediators.
Commonly referred to as "RAST" tests ("Radio-AllergoSorbent Test" after technology
that has been superseded by enzyme and fluorescent-based assays), these tests detect
allergen-specific IgE in the serum. Patient's serum is incubated with allergen or allergen
mixtures bound to a solid material. Allergen-specific IgE is then detected using antibodies
specific for human IgE that are labeled with either enzyme or a fluorescent compound
Learning Task
1. Mentions of invitro test for allergic diease
2. Mentions of advantages and disadvantages RAST compared with skin test
Selft Assessment
1. To knows laboratory examination for diagnostif of allergic disease
2. To knows interpretation of RAST and other examination of allergic disease
Topic 2. Laboratory diagnostic in autoimmune disease
Abstract
Laboratory testing is of great value when evaluating a patient with a suspected
autoimmune disease. The results can confirm a diagnosis, estimate disease severity, aid in
assessing prognosis and are useful to follow disease activity. Components of the laboratory
exam include complete blood count with differential, comprehensive metabolic panel,
inflammatory markers, autoantibodies, and flow cytometry. This chapter discusses these
components and includes a discussion about organ-specific immunologic diseases where
immunological laboratory testing is employed. Comprehensive laboratory evaluation of a
suspected autoimmune illness in conjunction with a thorough clinical evaluation provides a
better understanding of a patient's immunologic disease.
Examining patients for potential autoimmune diseases is fraught with difficulty because
not one laboratory test establishes such a diagnosis. Typically, multiple laboratory tests are
needed and include basic studies like a complete blood count, comprehensive metabolic
panel, acute phase reactants, immunologic studies, serologies, flow cytometry, cytokine
analysis, and HLA typing. Although some tests may be non-specific, such as the erythrocyte
sedimentation rate (ESR), they are useful to assess disease activity. These tests can be useful
in the diagnosis and management of patients with autoimmune diseases and help in providing
a prognosis, or indicate the severity of organ involvement or damage.
Learning Task
1. Why are autoimmune diseases challenging to diagnose?
2. What is the first test to be considered for a patient suspected of having an autoimmune
disease?
3. What is the significance of ANA patterns?
4. How predictive are the specific antibodies? What is their sensitivity and specificity in
various autoimmune diseases?
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Day 12
Topic
Lecture
Abstract
Forensic serology is the study of serology in relation to crimes and other legal matters by using
a scientific approach.
Doctors should have knowledge about forensic serology to assist
investigators in revealing crime cases related with humans body and health. Moreover, based
on legislations, doctors have legal duty to carry out forensic examinationwhen asked by the
investigators.
Mostly, investigators asked doctors to prove homicide, rape, assault or dispute paternity case.
To prove it, the doctors need to do serological examination of biological evidence that found on
the victims body, such as blood, semen, urine, and other body fluids.
Principle of serological test is the use of specific antibodies to detect a target antigen. By doing
a simple serological test, doctor can filter the type and origin of biological substances. If the
screening test gives a positive result, biological substances must be processed for DNA testing
to determine the owner of biological materials.
Vignette 1
A woman, 22 years old was found dead and naked. She suffered bruises almost on her entire
body. There were blood stains and fluid around her genital.
Learning Task
1. In above case, discuss the role of forensic serology in examining biological evidence!
2. Discuss the steps to examine blood stain and fluid around the genital!
3. Discuss the concept of species determination and individualization of blood stain and
biological fluid!
4. If in that case, there are 3 suspects, what the forensic serologist do to identify the suspect?
5. Discuss about DNA analysis for that case!
Vignette 2
37
Day 13
BCS
: Anaphylactic Shock
Lecturer
ANAPHYLAXIS
Anaphylaxis is defined as a rare, severe, and sudden allergic reaction. This acute
hypersensitivity reaction is potentially fatal, and can occur within seconds to minutes to hours
after exposure to an antigen. Anaphylaxis is a medical emergency; initial reactions can range
from mild to severe.
Common triggers for anaphylaxis are foods (e.g., peanuts, tree nuts, shellfish, fish, milk, or
eggs), insect venoms (e.g., bees or wasps), medications (e.g., penicillin and other beta-lactam
antibiotics, narcotics allergy extracts, vaccines, and other biologicals [e.g.,immune globulin and
blood transfusions]), natural rubber latex exposure, and radiocontrast media.
New diagnostic criteria for anaphylaxis were published in 2006 to help health care
professionals both recognize the spectrum of signs and symptoms that constitute anaphylaxis
and establish a more systematic approach to its diagnosis and management. The following 3
criteria were established, and the presence of any 1 of these criteria indicates that
anaphylaxis is highly likely:
Acute onset of an illness (over minutes to several hours) involving skin, mucosal tissue,
or both (for example, generalized hives, pruritus or flushing, swollen lips-tongue-uvula), and at
least 1 of the following:
o Respiratory compromise (for example, dyspnea, wheeze-bronchospasm,
stridor, reduced peak expiratory flow rate, hypoxemia)
o Reduced blood pressure (BP) or associated symptoms of end-organ
dysfunction (for example, hypotonia (circulatory collapse), syncope,
incontinence) OR
Two or more of the following that occur rapidly after exposure to a likely allergen for
that patient (minutes to several hours):
o Involvement of the skin-mucosal tissue (for example, generalized hives, itchflush, swollen lips-tongue-uvula)
o Respiratory compromise (for example, dyspnea, wheeze-bronchospasm,
stridor, reduced peak expiratory flow rate, hypoxemia)
38
Reduced BP after exposure to a known allergen for that patient (minutes to several
hours). Reduced BP is defined:
o In adults, as a systolic BP of less than 90 mm Hg or greater than 30% decrease
from that person's baseline
o In infants and children, as a low systolic BP (age-specific) or greater than 30%
decrease in systolic BP. Low systolic BP is defined as:
Less than 70 mm Hg for ages 1 month to 1 year
Less than (70 mm Hg plus twice the age) for ages 1 to 10 years
Less than 90 mm Hg for ages 11 to 17 years
Note: In infants and young children, hypotension may be a late manifestation of hypovolemic
shock. Tachycardia, in the absence of hypotension, also may indicate shock.
Day 15
BCS
Lecturer
ABSTRACT
Introduction
The diagnosis of allergic diseases:
a. A comprehensive history
b. Physical examination
c. Laboratory and other diagnostic testing: laboratory (eos. count, feces ex, IgE),
roentgen, Skin test
Methods of skin testing: Patch test, Scratch test, Prick test, Intradermal test
Indications for SPT
- An allergic patient / suspected allergy
When SPT should be done :
a. SPT should be undertaken during periods of free symptoms
b. To prevent worsening of the clinical status
Preparations of SPT :
1. Washout of any medication include ;
antihistamines AH-1 (a 3-days washout), AH-2 (one day washout)
antidepressants, codeine, long-term oral steroid (a 1-week washout)
Udayana University Faculty of Medicine, DME, 2016
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40
Condition
MILD
REACTION
(May
rapidly
progress to
a
more
severe
reaction)
Observation/
Assessment
MODERAT
E
REACTION
Generalized
flush
Red, itchy,
eyes
Itching at the
injection site
or at other
body sites
Localized to
generalized
urticaria
(hives)
Vomiting,
abdominal
pain
Mild to moderate
wheezing
Coughing
Complains of
generalized
itching, itching
throat
Generalized
urticaria (hives)
Swelling of lips,
face, tongue,
eyelids, hands,
feet, or genitalia.
ABCs.
Call 911 or local EMS STAT
(Preferably have someone not
involved in direct patient care make
the call).
Place patient in supine position.
Monitor vital signs.
GIVE OXYGEN BY MASK, if any
respiratory symptoms are present
o Special instructions** for O2
administration, if given
(O2 flow rate, lpm)
___________________
FIRST-LINE TREATMENT: GIVE
AGE AND WEIGHT APPROPRIATE
DOSES OF EPINEPHRINE,
intramuscularly, preferably in the
anterolateral thigh (See Table 1).
Repeat every 515 minutes, up to
3 doses, depending on patients
response
SECONDARY TREATMENT: As an
adjunct to epinephrine, give weight or
age appropriate doses of
diphenhydramine HCL orally or
intramuscularly (See Table 2 or Table
3). DO NOT GIVE diphenhydramine
HCL to infants aged less than
7 months
41
Condition
Observation/
Assessment
Vomiting, diarrhea,
and/or abdominal
pain
42
STUDENT PROJECT
SGD
NO
TOPICS
SUPERVISORS
ENG
REG
Immunomodulator
1,2
1,2
3,4
3,4
5,6
5,6
Rhinitis Allergy
7,8
7,8
9,10
9,10
43
REFERENCES
1. Fawcett DW, Jensh RP: Bloom & Fawcetts CONCISE HISTOLOGY, 2 nd ed. London,
Arnold. 2002
2. Cotran RS, Kumar V, Collins: Robbins Pathologic Basis of Disease. Sixth ed. Philadelphia,
WB Saunders Company. 2003.
3. Roitt IM, Brostoff J, Male D: Immunology 5th ed. Philadelphia, Mosby. 2000.
4. Fischbach F: A Manual of Laboratory & Diagnostic Test, 6 th ed. Philadelphia, Lippincott,
2000
5. Trevor AJ, Katzung BG, Master SB: Katzung & Trevors Pharmacology. Sixth ed. New York,
Lange Medical Books/Mc Graw-Hill, 2002.
6. Lange MD, PhD; Garry N. Holland MD,; Kirk R. Wihelmus, MD (Ocular Infection &
Immunity)
7. Abbas AK, Lichtman AH: Immune BASIC IMMUNOLOGY Functions and disorders of the
immune system. Second Eds. Philadelphia, Saunders, 2004.
8. Norton JA, Bollinger RR, Chang AE, Lowry SF, Mulvihil SJ, Pass HI, Thomson RW. Eds
SURGERY Basic Science and Clinical Evidence, New York. Springer-Verlag, Inc. 2001.
9. Victor M, Ropper AH. Principles of Neurology. Seventh edition, New Tork. McGraw-Hill.
2001.
10. Bradly WG, Daroff RB, Fenichel GM, Marsden CD. Neurology in Clinical Practice. Second
Edition. Boston. Butterworth-Heinemann 1995.
11. Marshal KG, Attia E. Disorders of The Nose and Paranasal Sinuses, Diagnosis and
Management. USA. PSG Publishing Company, Inc. 1987.
12. Kasper DL, Fauci AS, Longe DL, Braunwald E, Hauser SL, Jameson JL. Harrisons
Principles of Internal Medicine. 16th edition, McGrwa-Hill, New York. 2005.
13. Lawlor GJ, Fischer TJ, Adelman DC. Manual of Allergy and Immunology. 4th edition/3th
edition?
44
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