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Hematoimmunology Block Module

2013
Tutor Guide’s book
Held on 5th semester in 3rd year

Medical Faculty
University of Lampung
2013
Person In Charge (PIC):

dr.Agustyas Tjiptaningrum, SpPK


dr. Indri Windarti, Sp.PA

Programme’s implementers:
Dr. Agustyas Tjiptaningrum, Sp.PK
Dr. Fidha Rahmayani
Published by :
Internal Publishing of Medical Faculty
Lampung University

No part of this book are allowed to be copied or excerpted in any forms or by any means
without the prior written permission of the publisher.

Immersion programme, HPEQ University of Lampung 2013


Contributor
Departement of Clinical Pathology:
dr.Agustyas Tjiptaningrum, SpPK
dr. Putu Ristyaning Ayu, Sp.PK
dr.Fidha Rahmayani
Department of Internal Medicine
dr.Hotmen, Sp.PD
dr. Tehar Karo Karo, Sp.PD
Department of Pediatric
dr. Murdoyo Rahmanoe, Sp.A
dr. Rogatianus Bagus P, Sp.A
Department of Microbiology
Prof. Dr.dr. Efrida Waraganegara, M.Kes
dr. Ety Apriliana, M.Biomed
dr. Tri Umiana Soleha, M.Kes,
Department of Anatomical Pathology
dr.Muhartono, M.Kes, Sp.PA
dr. Indri Windarti, Sp.PA
dr. Dewi Nur Fiana
Department of Pharmacology
DR. dr. Asep Sukohar, M.Kes
dr. Novita Carolia, M.Sc
Department of Radiology
dr. Haryadi, Sp.Rad
Department of Medical Ethics
DR. dr. Asep Sukohar, M.Kes
dr Betta Kurniawan,M.Kes
Department of Public Health
Dr. Dian Isti Anggraini, MSi
Dr. Reni Zuraida, MPH

Immersion programme, HPEQ University of Lampung 2013


PREFACE

We give our biggest gratitude to Allah SWT for His grace, so that
we can complete the preparation of Hematoimmunology Module
Guidebook. The book is expected to be used as a guide for tutors and
students on the Block of Hematoimmunology which is conducted in the
fifth semester of the academic year 2013-2014.
This handbook contains the theme of learning that is expected to
help students learn Block of Hematoimmunologi. This guide comes with
the scope of subject matter, teaching methods, materials lab activities,
laboratory skills, scenarios, scheduling, evaluations and reference of
learning resources.
Thank you profusely for the contribution of our management KBK
Medical Faculty of Lampung University and all lecturers who contribute
more in the preparation of this book. We are unabashedly admitted that,
there are still many shortcomings in this book. Therefore, We are
expecting for more inputs to this guidebook . Hopefully this book could be
useful for teachers, tutors, students and those who involved in the learning
system of Medical Faculty of Lampung University.
Bandar Lampung, April 2013

Editors

2
TABLE OF CONTENTS

1. Cover
2. Preface
3. Contents
4. Introduction .............................................................................. 1
Block description ........................................................................ 1
Learning Objective of Block ....................................................... 1
Related Medical Science Disciplines .......................................... 5
Block Link .................................................................................. 7
5. Framework ................................................................................ 8
6. Learning Activity ...................................................................... 9
7. Assessment ................................................................................ 11
8. References................................................................................. 19
9. Learning Module....................................................................... 23
Module-1 Red Blood Cells.......................................................... 23
Module-2 Platelet, Blood Plasma, and Hemostasis System ....... 26
Module-3Leukocyte and Malignancy of Hematologic and Lymphoid. 29
Module-4 Hypersensitivity and Autoimmune ............................. 31
Module-5 Immunodeficiency ....................................................... 33
10. Scenario........................................................................................ 34
Scenario 1 Weak and Fatigue....................................................... 34
Scenario 2 Bleeding in Tooth Expulsion .................................... 36
Scenario 3 Leukositosis in Chemical Factory Worker ............... 38

Immersion programme, HPEQ University of Lampung 2013


Scenario 4 Mala Needs Injection ............................................... 40
Scenario 5 Frequent Diarrhea............................................... 42
11. Learning Schedule .................................................................... 44
12. Literature Review ..................................................................... 54

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Hematoimmunology Block Module, Student Guide’s Book

HEMATO-IMMUNOLOGY BLOCK
INTRODUCTION

1. Block Description
Hematoimmunology block will be held on 5th semester, for 3rd year
students.This block runs for6 weeks, 5 weeks for active studyandthe rest
for examination week. This block will discuss about health problems
related to hematoimunology. The learning process itself based on
problem-based learning strategyusing tutorial discussion with seven jump
method, lecture, Laboratory Practicum, clinical skill laboratory,and
individual study.

2.Learning Objective
General Learning Objectives
Students are able to manage health problems related to hematology and
immune system comprehensively, holistically, continuously,
coordinatively, and collaboratively.

Specific Learning Objectives


After studying this block using information and communication
technology, students are expected to be able to:

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
1. Explain about hematopoeisis, blood components function(plasma&
blood cells) and coagulation factors.
2. Know various erythrocyte abnormalities (erythrocyte morphology
defect,anemia, and hemoglobinopathy) and the underlying
diseases.
3. Explain anemia types based on erythrocyte morphology.
4. Explain the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of normocytic
normochromic anemia (hemorrhagic anemia, hemolytic anemia,
aplastic anemia, autoimmune hemolytic anemia/AIHA, and
hemorrhagic disease of newborn/HDN).
5. Explain the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of microcytic
hypochromicanemia (iron deficiency anemia, anemia of chronic
disease, and anemia of thalassemia).
6. Explain the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management ofmacrocytic anemia
(folate deficiency anemia and vit. B12 deficiency anemia).
7. Explain the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management ofhemoglobinopathy
(thalassemia and Hb variant).
8. Perform peripheral blood smear examination (using Wright’s stain,

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Hematoimmunology Block Module, Student Guide’s Book

peripheral blood morphology examination, and interpret the


result).
9. Observe normal and pathology of peripheral blood film and bone
marrow film.
10. Explain about nutrition aspect for anemia, hematologic
malignancy, autoimmune, hypersensitivity, and immunodeficiency
diseases.
11. Explain the platelet abnormalities (platelet morphology defect, and
platelet count abnormalities, such as thrombocytopenia and
thrombocytosis) and the underlying diseases.
12. Explain the hemostatic abnormalities (coagulation factors
deficiency, coagulation factors dysfunction, and fibrinolysis
defect) and diseases with hemostaticabnormality manifestation
(hemophilia, DIC).
13. Explain laboratory examination as diagnostic tools, follow-up and
monitoring of hemostatic diseases, and follow-up for therapy
management of hemostatic diseases.
14. Observe and interpret the hemostasis examination result.
15. Know various leukocyte abnormalities (leukocyte morphology
defect, and leukocyte count abnormalities, such asleukopeniaand
leukocytosis) and the underlying diseases.
16. Explain the etiology, pathogenesis, pathophysiology, diagnosis,

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
laboratory examination, and management ofhematologic
malignancy (myeloproliferative (AML and CML),
lymphoproliferative (ALL and CLL), myeloma,myelodysplastic
syndromes (MDS),non-hodgkins lymphoma andhodgkins
lymphoma).
17. Know about stem cell and the ethical aspect.
18. Know about radiation effect and radiotherapy of cancer.
19. Know about various hypersensitivity reactions (juvenil chronic
arthritis, Henoch-schonlein purpura, StevenJohnson syndrome).
20. Know about the various of autoimmune diseases.
21. Explain the etiology, pathophysiology,symptoms, diagnosis,
laboratory examination, and management ofuncomplicatedlupus
erythematosus syndrome (LES),polymyalgia rheumatica, and
rheumatoid arthritis.
22. Know about complicated LES, scleroderma, polyarthritis nodusa,
vasculitis lupus.
23. Explain the etiology, pathophysiology, diagnosis, laboratory
examination, treatment planning, and prevention ofHIV.
24. Explain about immunoglobulin examination (total Ig
concentration, specific Ig concentration, and
immunoelectrophoresis) and immunology examination of
autoimmune diseases (Anti Nuclear Antibody/ANA, Anti

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Hematoimmunology Block Module, Student Guide’s Book

Cardiolipin Antibody/ACA, beta 2 glikoprotein,and rheumathoid


faktor/RF), immunodeficiency (HIV testing pathwayand the
interpretation), and specific laboratory examination for
hematologic malignancy (flowcytometri).
25. Explain pharmacokinetics, pharmacodynamicsof anemia drugs,
anticoagulantdrugs, anti-allergy drugs, autoimmune drugs,and
chemotherapy drugs.
26. Perform clinical skills of hemato-immunology block (Resuscitation
of newborn, i.v. catheter insertion, peripheral blood circulation
examination, minor surgery).

3. Related Medical Science Disciplines


1. Clinical pathology
2. Internal medicine
3. Pediatric
4. Medical nutrition
5. Radiology
6. Anatomical Pathology
7. Microbiology
8. Pharmacology
9. Medical ethic

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Related Laboratory:
1. Clinical Pathology:
 Performing peripheral blood smear and differential count
examination.
 Performing examinations of blood film of anemia, other
various type of blood film and interpret the result.
 Performing and interpretation of bone marrow punction film
examinations for leukemia.
 Observing the result of haemoglobin analysis (electrophoresis
haemoglobin)
 Performing examination and interpretationof blood type (ABO
and rhesus system).
 Performing examination dan interpretation of hemostatic
examination (cloting time, bleeding time and trombocyte
count) and interpretation of hemostatic examination
(prothrombin time and activated partial thrombin time)
2. Anatomical Pathology: laboratory finding of various lymphoid
malignancies.

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Hematoimmunology Block Module, Student Guide’s Book

4. Block Link
Previous Block
1. Medical Basic Science 3 (MBS3) block: studied coagulation
factors, complete hematology examination, specific hematology
examination, hemostasis, immunology, and blood transfusion.
2. Neuro Behavior and Sensory System (NBSS) block: studied
allergic rhinitis and epistaxis.
3. Dermato Musculo Skeletal (DMS) block:studied dermatological
emergencies, dermatitis, atopy, and eritema multiforme.
4. Cardio Vascular System block: studied rheumatic heart diseases.

NextBlock
1. Tropical infection block: DHF, malaria, and HIV.
2. Respiration block: asthma, HIV with TB infection.
3. Gastrointestinal block: food allergy.
4. Genitourinaria block : glomerulonephritis acute, and nephrotic
syndrome.
5. Emergencyblock: hemorrhagic and anaphylactic shock.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
FRAMEWORK

HEMATO-IMMUNOLOGY

HEMATOLOGY IMMUNOLOGY

BLOOD PLASMA AND HEMATOLOGY AUTOIMMUNE HYPER IMMUNO-


CELLS HEMOSTASIS MALIGNANCIES DISEASES SENSITIVITY DEFICIENCY

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Hematoimmunology Block Module, Student Guide’s Book

LEARNING ACTIVITIES

Tutorial
Tutorial discussions in this block consist of 5 scenarios run for 5
weeks.Two meetings for each scenario, step 1 to 5 for the first
meeting, and step 7 for the second. Step 6 is for individual study.
Scenarios consist cases of health problem that are most common found
in general practice, hospital, and in community.

Lecture
Lecture is held in big class. Lecturer is an expert lecturers or experts in
their field. Lectures areadjusted to the modules each week.

Clinical Skill Laboratory


Clinical skill laboratory are given in order to train the psychomotor
skill or to complete what the students got from theories. Train students
to be more skilled in dealing with the cases found in general practice.

Pleno
Pleno are held every Friday in big class. The purpose of pleno is to
equalize the student's perception of thelearning bbjectivesfrom the
scenario. Attended by lecturer or experts related on the medical

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
discipline needed. Student can throw direct questions to the experts
about what they doubt or what they don't know or understand yet.

Individual Study
Students do individual study not only based on block objectives and
scenario objectives, but can be developed based on recommended
references or sources/literatures obtained on internet. Individual study
is the core of competency-based curriculum.

Laboratory Practicum
Laboratory Practicum supports the theories obtained by the students.
The laboratory activities regulations are depend on related medical
discipline. Laboratory Practicum attendance must be 100%.

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Hematoimmunology Block Module, Student Guide’s Book

ASSESSMENT

Final score for Hemato-immunology block is 100%, no compensation


between assessment points.The assessment points detail are :
1. Tutorial : 10 %
2. Laboratory Practicum : 15 %
3. Clinical Skill Laboratory : 20 %
4. Block Final Exam : 50 %
5. Attitude : 5%

Tutorial
Students are assessed based on verbal interaction during tutorial session,
including sharing activity, idea, concentration, argumentation, dominant,
behavior/politeness/attitude, and discipline. Tutorial attendance must be
100 %.

Laboratory Practicum
Assessments including Laboratory Practicum examination at the end of
block, students are assessed for affective, cognitive, and psychomotor.
Instructor will give the students pre-test or post-test and task. Laboratory
Practicum attendance must be 100 %.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Clinical Skill Laboratory
Clinical skill laboratory is held in 2 sessions for each topic/skill.There is
pre-test or task before this activity begin.Attendance must be 100%.
Assessment for clinical skill laboratory is OSCE, held at the end of
semester. Students are assessed for affective, cognitiveand psychomotor
skills.OSCE has 20 % of overall score.

Block Final Exam


Block final exam will be held in 1 day on 6th week at the end of block,
with total of 150 multiple choice questions. This exam has 55 % of overall
score.To take this final exam block is required attendance for lecture at
least 80%, tutorial must be 100 %, Clinical Skill Laboratory must be
100%, Laboratory Practicummust be 100%,and pleno must be 100%.

Attitude
The student must be honest, having good performance in everystep of the
study including tutorial, clinical skill laboratory, and laboratory practice.
At the end of the block we will ask the student to write down the five best
and the five worst of student, it will influence the total score of the five
best and the five worst student.

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Hematoimmunology Block Module, Student Guide’s Book

BLUEPRINT

Information:

No Objective DM LV PCT QTY MTD SECT


1. Explaining about hematopoeisis, Cognitive C2,3 4% 7 Mcq CP
blood components function (plasma
& blood cells) and coagulation
factors.
2. Knowing various erythrocyte Cognitive C2,3 4% 7 Mcq PED
abnormalities (erythrocyte INT
morphology defect,anemia, and
hemoglobinopathy) and the
underlying diseases.
3. Explaininganemia types based Cognitive C3 6% 8 Mcq PED
onerythrocyte morphology.
4. Explaining about normocytic Cognitive C3 5% 8 Mcq INT
normochromic anemia PED
(hemorrhagic anemia, hemolytic CP
anemia, aplastic anemia, AIHA,
and HDN):
 etiology, diagnosis, and
management
 pathogenesis, pathophysiology,
and laboratory examination
5. Explainingaboutmicrocytic Cognitive C3,5 5% 8 Mcq INT
hypochromicanemia (iron PED
deficiency anemia, anemia of CP
chronic disease, and anemia of

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
thalassemia):
 etiology, diagnosis, and
management
 pathogenesis, pathophysiology,
and laboratory examination
6. Explainingaboutmacrocytic anemia Cognitive C3 5% 8 Mcq PED
(folate deficiency anemia and vit. INT
B12 deficiency anemia): CP
 etiology, diagnosis, and
management
 pathogenesis, pathophysiology,
and laboratory examination
7. Explaining about Cognitive C3,5 2% 4 Mcq INT
hemoglobinopathy (thalassemia and PED
Hb variant): CP
 etiology, diagnosis, and
management
 pathogenesis, pathophysiology,
and laboratory examination
8. Performing peripheral blood smear Cognitive C3 2% 4 Mcq CP
examination (using Wright’s stain,
peripheral blood morphology
examination, and interpret the
result)
9. Observing normal and pathology of Cognitive C3 4% 6 Mcq CP
peripheral blood film and bone
marrow smear.

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Hematoimmunology Block Module, Student Guide’s Book

10. Explaining about nutrition aspect Cognitive C3 4% 6 Mcq MN


for anemia, hematologic
malignancy, autoimmune,
hypersensitivity, and
immunodeficiency diseases.

11.  Explaining the hemostatic Cognitive C3 5% 8 Mcq INT


abnormalities (coagulation CP
factors deficiency, coagulation PED
factors dysfunction, and
fibrinolysis defect) and diseases
with hemostaticabnormality
manifestation (hemophilia,
DIC)

 Explaining laboratory
examination as diagnostic tools,
follow-up and monitoring of
hemostatic diseases, and
follow-up for therapy
management of hemostatic
diseases.
12. Explaining the platelet Cognitive C3 4% 7 Mcq INT
abnormalities(platelet morphology PED
defect, and platelet count CP
abnormalities, such as
thrombocytopenia and
thrombocytosis) and the underlying
diseases.
13 Knowing various leukocyte Cognitive C3 4% 7 Mcq INT

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
abnormalities (leukocyte PED
morphology defect, and leukocyte CP
count abnormalities, such
asleukopeniaand leukocytosis) and
the underlying diseases.
14 Explaining about hematologic Cognitive C3 4% 7 Mcq INT
malignancy (myeloproliferative PED
(AML and CML), CP
lymphoproliferative (ALL and
CLL), and myeloma)
 etiology, diagnosis, and
management
 pathogenesis, pathophysiology,
and laboratory examination
15 Explaining about basic clinical Cognitive C3,5 3% 3 Mcq PED
immunology examination (IgG, INT
IgA, IgM,IgE, IgD).
16 Explaining about immunoglobulin Cognitive C3,5 2% 3 Mcq CP
examination (total Ig
concentration,specific Ig
concentration, and
immunoelectrophoresis) and
immunology examination of
autoimmune diseases (ANA, ACA,
beta 2 glikoprotein, and RF),
immunodeficiency (HIV testing
pathway and the interpretation), and
specific laboratory examination for
hematologic malignancy

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Hematoimmunology Block Module, Student Guide’s Book

(flowcytometri).
17 Knowing about various Cognitive C3 4% 6 Mcq INT
hypersensitivity reactions (juvenil PED
chronic arthritis, Henoch-schonlein DV
purpura, Steven Johnson syndrome) MIC
18 Explaining the etiology, Cognitive C3 4% 6 Mcq PED
pathophysiology, symptoms, INT
diagnosis, laboratory examination,
and management of uncomplicated
LES
19 Explaining the etiology, Cognitive C3 4% 6 Mcq PED
pathophysiology, symptoms, INT
diagnosis, laboratory examination,
and initialmanagement of
polymyalgia rheumatica, and
rheumatoid arthritis.
20 Knowing about complicated LES, Cognitive C3 4% 6 Mcq PED
scleroderma, polyarthritis nodusa, INT
vasculitis lupus.

21 Explaining the etiology, Cognitive C3,5 4% 6 Mcq PED


pathophysiology, diagnosis, INT
laboratory examination, treatment MIC
planning, and prevention of HIV. ME
22 Knowing about radiation effect and Cognitive C3 4% 6 Mcq RAD
radiotherapy of cancer.
23 Knowing various hemato- Cognitive C3 3% 5 Mcq INT
immunology malignancies (non- PED

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
hodgkins lymhoma and hodgkins AP
lymphoma)
24 Explaining pharmacokinetics, Cognitive C3,5 5% 8 Mcq PHAR
pharmacodynamicsof anemia drugs,
anticoagulantdrugs, anti-allergy
drugs, autoimmune drugs,and
chemotherapy drugs.
25 Tutorial Cognitive C3,5 5% Mcq CB
TOTAL 100% 150
Information:
DM = Domain
LVL = Level
MTD = Method
SECT = Section
PCT = Percentge
QTY = Quantity
CB = Chief of Block
CP = Clinical Pathology
INT = Internal Medicine
PED = Pediatrics
MN = Medical Nutrition
DV = Dermatovenerology
RAD = Radiology
PHAR = Pharmacology
AP = Anatomical Pathology
MIC = Microbiology
ME = Medical Ethic

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Hematoimmunology Block Module, Student Guide’s Book

Based on Bloom's taxonomy, the competencies to be achieved are :


 C1= knowledge, recalling/memorizing
 C2= understanding, interpreting,andinferring
 C3= applying, implementing, usingconcept, princip, procedureto solve problem
 C4= analizing, differentiating, organizing, attributing
 C5=evaluating, make judgments about value of idea, comparing method with Standard
Operational Procedure (SOP).
 C6= creating, diagnosis, putting elements together to form a coherent or functional new
pattern or structure.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
REFERENCES

Clinical Pathology
 Greer J.P., Foerster, J., Lukens, J.N., Rodgers, G.M., Paraskevas,
F., Glader, B. 2004. Wintrobe's Clinical Hematology 11thEdition.
Philadelphia: Lippincott Williams & Wilkins.
 Henry, J.B. 2001. Clinical Diagnosis and Management by
Laboratory Methods 20thEdition. Philadelphia: WB Saunders Co.
 Burtis, C.A., Ashwood, E.R., Bruns, D.E. 1999. Tietz Textbook of
Clinical Chemistry and Molecular Diagnostics 4thEdition. St.
Louis: Elsevier Saunders.
 Hoffbrand, A.V., Catovsky, D., Tuddenham, E.G.D. 2005.
Postgraduate Haematology 5th Edition. Massachusetts: Blackwell
Publishing.
 Weatherall, D.J., Cleg, J.B. 2001. The Thalassaemia Syndrome
4thEdition. London: Blackwell Science.
 Kasper, D.L., Fauci, A.S., Longo, D.L., Braunwald, E., Hauser,
S.L., Jameson, J.L. 2005. Harrison's Principle of Internal Medicine
16thEdition. New York: McGraw-Hill.

 Abbas AK, Lichtman AH, Pillai S. Cellular and molecular immunology.


6th ed. Philadelphia: Saunders Elsevier; 2007.

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Hematoimmunology Block Module, Student Guide’s Book

 Abbas AK, Lichtman AH. Basic immunology: functions and disorders of


the immune system. 2nd ed. Philadelphia: Saunders Elsevier; 2004.

Internal Medicine
 Kasper, D.L., Fauci, A.S., Longo, D.L., Braunwald, E., Hauser,
S.L., Jameson, J.L. 2005. Harrison's Principle of Internal Medicine
16thEdition. New York: McGraw-Hill.
 Sudoyo, et al. 2006. Buku Ajar: Ilmu Penyakit Dalam Edisi IV
Jilid III. Jakarta: FKUI.
 Swart, M.H. 1995. Buku Ajar: Diagnostik Fisik. Jakarta: EGC.
 Bates, B., Bickley, L.S., Hoekelman, R.A. 1995. Physical
Examination and History Taking 6th Edition. Philadelphia:
Lippincott Co.
 Graber, et al. 2006. Buku Saku: Dokter Keluarga. Jakarta: EGC.

Anatomical Pathology
 Buku ajar patologi anatomi UI. 2009.

 Robbins, Kumar. Pathology basic of disease. 7th edition.


Philadelphia: WB Saunders. 2009

Microbiology
 Jawetz, et al. 2004. Medical Microbiology 23th Edition. New York:
Mc Graw-Hill.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
 Abbas AK, Lichtman AH. Basic immunology: functions and disorders of
the immune system. 2nd ed. Philadelphia: Saunders Elsevier; 2004.

Pharmacology
 Farmakope Indonesia. Edisi IV. 1995. Depkes RI
 Katzong: Farmakologi dasar dan klinis . edisi VI. EGC
 Dipiro, J.T., Talbert R.L., Yee G.C., Matzke G.R., Wells B.G.,
Posey, L.M. 2005. Pharmacotherapy: a pathophysiological
approach. 6th ed.

Pediatrics
 Behrman, R.E. 2006. Nelson Text Book of Pediatrics 15th Edition.
Philadelphia: WB. Saunders CO.

 Nelson.2006. Ilmu Kesehatan Anak Terjemahan Volume 2 Edisi


15. Jakarta: EGC. Hal 1574-1669

 Buku ajar Hematologi. UKK hematologi UI

Radiology
 Radiologi diagnostik. UI. Edisi kedua

 R. Suswob : Radioterapi

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Hematoimmunology Block Module, Student Guide’s Book

 Dasar-dasar radioterapi

 Tatalaksana radioterapi pada penyakit kanker

Medical Nutrition
 Almatsier, S. 2004. Penuntun Diet: instalasi Gizi RSCM dan
Asosiasi Dietesien Indonesia. Jakarta: PT Gramedia Pustaka
Utama. Hal 157-164.

 Mahan, L.K., Stump, S.E. 2004. Krause’s Food, Nutrition, and


Diet Therapy. Michigan: W.B. Saunders.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
LEARNING MODULE

Module 1: Red Blood Cells


The first week
Learning Objectives
1. Explaining about hematopoeisis, blood components function
(plasmaand blood cells) and coagulation factors.
2. Knowing various erythrocyte abnormalities (erythrocyte
morphology defect,anemia, and hemoglobinopathy) and the
underlying diseases.
3. Explaining anemia types based onerythrocyte morphology.
4. Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management ofnormocytic
normochromic anemia (hemorrhagic anemia, hemolytic anemia,
aplastic anemia,AIHA, and HDN).
5. Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of microcytic
hypochromicanemia (iron deficiency anemia, anemia of chronic
disease, and anemia of thalassemia).
6. Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management ofmacrocytic anemia
(folate deficiency anemia and B12 deficiency anemia).

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Hematoimmunology Block Module, Student Guide’s Book

7. Explaining the etiology, pathogenesis, pathophysiology, diagnosis,


laboratory examination, and management of hemoglobinopathy
(thalassaemia and Hb variant).
8. Performing peripheral blood smear examination (using Wright’s
stain, peripheral blood morphology examination, and interpret the
result).
9. Observing normal and pathology of peripheral blood smear and
bone marrow smear.
10. Explaining about nutrition aspect for anemia, hematologic
malignancy, autoimmune, hypersensitivity, and immunodeficiency
diseases.

Learning Activities
Lecture:
1. Clinical Pathology:
 Explaining about hematopoeisis, blood components function
(plasma & blood cells) and coagulation factors.
 Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of normocytic
normochromic anemia (hemorrhagic anemia, hemolytic anemia,
aplastic anemia, AIHA, and HDN).

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
 Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of microcytic
hypochromic anemia (iron deficiency anemia, anemia of chronic
disease, and anemia of thalassemia).
 Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of macrocytic anemia
(folate deficiency anemia and B12 deficiency anemia).
 Explaining the etiology, pathogenesis, pathophysiology, diagnosis,
laboratory examination, and management of hemoglobinopathy
(thalassemia and Hb variant).
 Performing peripheral blood smear examination and interpret the
result.
2. Internal Medicine:
 Explaining the etiology, diagnosis, and management of normocytic
normochromic anemia (hemorrhagic anemia, aplastic anemia, and
AIHA).
 Explaining the etiology,diagnosis, and management of microcytic
hypochromicanemia (iron deficiency anemiaand anemia of chronic
disease).
 Explaining the etiology, diagnosis, and management ofmacrocytic
anemia (folate deficiency anemia and B12 deficiency anemia).
 Explaining the pathogenesis, pathophysiology, and laboratory

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Hematoimmunology Block Module, Student Guide’s Book

examination, and management of hemoglobinopathy (thalassemia


and Hb variant).
3. Pediatrics:
 Explaining the etiology, diagnosis, and management of
hemoglobinopathy (thalassemia and Hb variant).
 Explaining the etiology, diagnosis, and management of juvenile
iron deficiency anemia, juvenile AIHA, and HDN.
4. Pharmacology: anemia management anddrugs which depresses
hematopoiesis.
5. Medical Nutrition: nutrition aspect of anemia.

Tutorial : scenario 1
Laboratory Practicum:
Clinical Pathology:
 Performing peripheral blood smear and differential count
examination.
 Performing examination of anemia blood film and interpret the
result.
Plenary : Module 1
Individual Study

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Module 2: Platelet, Blood Plasma, and Hemostasis System
The second week
Learning Objectives
1. Explaining the platelet abnormalities(platelet morphology defect,
and platelet count abnormalities, such as thrombocytopenia and
thrombocytosis) and the underlying diseases.
2. Explaining the hemostatic abnormalities (coagulation factors
deficiency, coagulation factors dysfunction, and fibrinolysis
defect) and diseases with hemostatic abnormality manifestation
(hemophilia, DIC).
3. Explaining laboratory examination as diagnostic tools, follow-up
and monitoring of hemostatic diseases, and follow-up for therapy
management of hemostatic diseases.
4. Observing and interpreting the hemostasis examination result.
5. Explaining pharmacokinetics, pharmacodynamics of anticoagulant
drugs,and drugs which affect the hemostasis.

Learning Activities
Lecture:
1. Clinical Pathology:

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Hematoimmunology Block Module, Student Guide’s Book

 Explaining laboratory examination as diagnostic tools, follow-


up and monitoring of hemostatic diseases, and follow-up for
therapy management of hemostatic diseases.
 Interpretation of hemostasis examination.
2. Internal Medicine:
 Platelet abnormalities
 Platelet count abnormalities (thrombocytopenia (ITP) and
thrombocytosis) and the underlying diseases.
 Platelet function defect and the underlying diseases.
 Hemostatic abnormalities (coagulation factor s deficiency
(hemophiliaAand hemophilia B),coagulation factors dysfunction,
and fibrinolysis defect), and diseases with hemostatic abnormality
manifestation (DIC).
3. Pediatrics:
 Platelet abnormalities
 Platelet count abnormalities (thrombocytopenia (ITP)
andthrombocytosis) and the underlying diseases.
 Platelet function defect and the underlying diseases.
 Hemostatic abnormalities (coagulation factor s deficiency
(hemophiliaA and hemophilia B),coagulation factors dysfunction,
and fibrinolysis defect), and diseases with hemostatic abnormality
manifestation (DIC).

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
4. Pharmacology: explaining pharmacokinetics andpharmacodynamicsof
anticoagulantdrugs, and drugswhich affect the hemostasis.

Tutorial: scenario 2
Laboratory Practicum:
Clinical Pathology:Observing and interpreting the hemostasis examination
result.
Clinical Skill Laboratory
Individual Study
Plenary 2

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Hematoimmunology Block Module, Student Guide’s Book

Module 3: Leukocyte and Malignancy of Hematologic and Lymphoid


The Third week
Learning Objectives
1. Knowing all kinds of leukocyte abnormalities (morphology
abnormalities also countabnormalities such as leukopeniaand
leukocytosis) and theunderlying diseases.
2. Explainingetiology, pathogenesis, pathophysiology, diagnosis,
laboratory examinationandmanagementof hematologic
malignancy(myeloproliferative (AML and CML),
lymphoproliferative (ALL and CLL), and myeloma,
myelodysplastic syndrome (MDS), non-hodgkins lymphoma and
hodgkins lymphoma).
3. Knowing peripheral blood morphology in each blood cell
malignancies.
4. Knowing specific examination for malignancy diagnosis
(flowcytometri).
5. Knowing stem cell and theethical aspect.
6. Knowing radiation effectand radiotherapy in cancer.
7. Pharmacodynamic and pharmacokinetic of chemotheraphy drugs.

Learning Activities
Lecture:

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
1. Clinical Pathology:
 Explaining pathogenesis, pathophysiology, and laboratory
examination of hematologic malignancy (AML, CML,
ALL, CLL, MDS).
 Knowing peripheral blood morphology in each type of
blood cell malignancies.
 Knowingspecific examination to get the malignancy
diagnosis (flowcytometri).
2. Internal Medicine:explaining etiology, diagnosis, and management
of hematologic malignancy (AML, CML, MDS).
3. Pediatric:explaining etiology, diagnosis, and management of
hematologic malignancy (ALL and CLL).
4. Pharmacology: pharmacokinetic and pharmacodynamic
chemotheraphy drugs.
5. Medical Nutrition: nutrition aspect in malignancy.
6. Anatomical Pathology: histopathology of lymphoid malignancies
(non-hodgkins lymhoma and hodgkins lymphoma).
7. Radiology: radiationeffect and radiotheraphyincancer.
8. Medical Ethic: stem cell and the ethical aspect.

Tutorial: scenario 3
Laboratory Practicum:

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Hematoimmunology Block Module, Student Guide’s Book

 Clinical Pathology: observing and explaining the peripheral


blood smear and bone marrow in hematologic malignancy.

 Pathology Anatomy: observing and explaining histopathologic


morphology in limphoid malignancy.

Clinical Laboratory Skill


Plenary
Individual Learning

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Module 4: Hypersensitivity and Autoimmune
The fourth week
Learning Objectives
1. Knowingevery hypersensitivity reaction (juvenile chronic arthritis,
Henoch-schonlein purpura).
2. Knowing various type of autoimmunedisease.
3. Explainingetiology, pathophysiology, symptom, diagnosis,
supportive examination and managementof uncomplicated SLE,
polymyalgia rheumatica and rheumatoid arthritis.
4. Knowing complicated SLE, scleroderma, polyarthritis nodusa,
vasculitis lupus.
5. Explaining immunoglobulin examination (total Ig,spesific Ig, and
immunoelectrophoresis) also various immunologic examinations in
autoimmune diseases (ANA,ACA, beta 2 glycoprotein, and RF),
immunodeficiency (HIV testing pathway dan interpretation),
andspecific laboratory examination for hematologic malignancies
(flowcytometri).
Learning Activities
Lecture :
1. Clinical Pathology:

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Hematoimmunology Block Module, Student Guide’s Book

 Explaining pathophysiology, pathogenesis andlaboratory


examination in SLE, rheumatoid arthritis, and polimyalgia
rheumatica.

 Immunoglobulin examination (total Ig, spesific Ig, and


immunoelectrophoresis) also various autoimmune examination
(ANA, ACA, beta 2 glycoprotein, and RF).

2. Internal Medicine:
 hypersensitive reaction Henoch-schonlein purpura.
 autoimmune diseases.
 Etiology, diagnosis, andmanagementuncomplicated SLE,
polymyalgia rheumatica andrheumatoid arthritis, complicated
SLE, scleroderma, polyarthritis nodusa, vasculitis lupus.
3. Pharmacology: pharmacokinetic and pharmacodynamic
ofautoimmune drugs and hypersensitivity.
4. Pediatric: children autoimmune disease (juvenile rheumatic
arthitis, SLE, henoch- schonlein purpura).
5. Microbiology: hypersensitivity reactions.
Tutorial : scenario 4
Clinical Laboratory Skill
Plenary
Individual Learning

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Module 5: Immunodeficiency
The fifth week
Learning Objectives
1. Explainingetiology, pathophysiology, diagnosis, supportive
examination,management planning,and prevention of HIV.
2. Explaining pharmacokinetic and pharmacodynamic of
antiretroviral drugs.
Learning Activities
Lecture:
1. Clinical Pathology: HIV testing pathway and interpretation.
2. Microbiology: etiology, pathophysiology, and pathogenesis of
HIV-AIDS.
3. Internal Medicine: diagnosis and management of HIV-AIDS
4. Pediatric: diagnosis and management of HIV in children
5. Pharmacology:anti retroviral drugs.
6. Medical Ethic:HIV-AIDS from social point of view.

Tutorial: scenario 5
Laboratory Skill
Plenary
Individual Learning

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Hematoimmunology Block Module, Student Guide’s Book

Scenario 1

“Weak and Fatigue”

Mrs. Riyana, age 36 years old, come to the doctor with a feeling of
weakness. 1 month earlier, she felt weak, fatigue, and lose appetite. Mrs.
Riyana is suffering remittent chronic cough. Physical examinations show
her conjunctiva is pale. Laboratory examination result shows Hb 9,5
gr/dL, MCV 75 fl, MCH 26 pg, serum iron 28 µg/dL (refferal score 37-
145µg/dL) , TIBC 180 µg/dL (refferal score 228-428 µg/dL), and serum
ferritin 300 µg/L (refferal score 30-150µg/L).(add: about nutrition for
anemia)

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Scenario 2

“Bleeding in Tooth Expulsion”

Bimo, 9 years old, accompanied by his mother to put off his tooth. After
expulsion, the blood is not stopping. Then, Bimo is taken care in the
hospital to observe the bleeding. When he learned to walk, Bimo often got
knee swelling if he felt down, also he easily got bruise when he got minor
trauma. His uncle also have similar condition. In physical examination
there’s no organomegaly found. The laboratory findings result that aPTT
80 second (refferal score 31-47 second) and platelet count 200.000/µL
(referral score 150.000-400.000/µL)

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Hematoimmunology Block Module, Student Guide’s Book

Scenario 3
“Leukositosis in Chemical Factory Worker”
Ms. Sarah, 34 years old, chemical factory worker, complaining of fever,
weak, and easily fatigue. She visits the doctor because often get fever. One
month earlier her stomach was cramping, her body was weak and fatigue.
Two weeks before seeing the doctor, Sarah felt uncomfortable in her
stomach, and lose appetite but no vommiting. Patient also complaining of
having red spots under the skin and easily got bruise. In physical
examination, the liver palpable in about 4 fingers under arcus costae, hard,
flat surface, and no ache. Lien palpable in S-IV. Laboratory result shows
Hb 10 gr/dL, leukosit 125.000/µL, platelet 100.000/µL.What happened to
this patient?

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Scenario 4.

“ Mala Needs Injection”

Mrs.Mala, 30 years old, come to the doctor complaining about her joint
discomfort. She feels it every morning in her knees. She also feels that
her knee is swelling. Beside that, Maya also feel ache in her arm. After
following the historical diseases, Mala said that she often had cough,
flu, and sorethroat.
Because she’s already bored for consuming drugs, Mala wants to be
injected by analgetic. After the doctor asks about the history of drug
allergic and she hasn’t have it, Mala is injected with an analgetic. Few
times later, Mala feels dizzy, blurring eyes and hard to breath. What is
actually happened to Mala.

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Hematoimmunology Block Module, Student Guide’s Book

Scenario 5
“Frequent Diarrhea”

Mr. X, 35 years old, is taken by his wife to the emergency unit because
of weak and almost fainted. After being asked, Mr. X is having
diarrhea and vomittingfrom the day before. According to his wife, it’s
not the first time that her husband suffering from this condition. Her
wife -who is pregnant- says that her husband was a drug user too and
after being fired from his job in Jakarta and come back to his village,
her husband has often gotten sick. In last six months Mr. X has been
becoming thinner and easily getting cough and cold.

From the result of physical examinations, there is oral thrush inside his
mouth. Doctor suggests Mr.X to do some laboratory examination.

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
LEARNING SCHEDULE
TIME WEEK I. ERYTHROCYTE
(WIB) WEDNESDA THURSD FRIDA
MONDAY TUESDAY Y AY Y
3/9/2013 4/9/2013 5/9/2013 6/9/2013 7/9/2013
07.00 – PEDIATRIC-
07.50 2
07.50 –
08.40
08.40 – CASE-1 CLINICAL CLINICAL CASE-1
09.30 PATHOLOG PATHOLOGY -
09.30 – Y-1 2
10.20
10.20 – MEDICAL PHAR 1
11.10 NUTRITION INTERNAL
11.10 – MED-1
12.00
12.00 – BREAK
13.00
13.00 – Pleno
13.50
13.50 –
14.40
14.40 – CSL CSL
15.30
15.30 –
16.20

Note: Empty schedule is used for individual learning

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Hematoimmunology Block Module, Student Guide’s Book

WEEK II. Platelet, Blood Plasma, and Hemostasis System


TIME MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY
(WIB) 10/9/2013 11/9/2013 12/9/2013 13/9/2013 14/9/2013
07.00 PEDIATRIC-2

07.50
07.50 CLINICAL
– PATHOLO
GY-4
08.40
08.40 CASE-1 CLINICAL CASE-2
– PATHOLOGY-3
09.30
09.30

10.20
10.20 INT 2 PHAR 2 PLENO

11.10
11.10

12.00
12.00
– BREAK
13.00
13.00 CP-PRACT CP-PRACTI Pleno

13.50
13.50

14.40
14.40 CSL CSL

15.30
15.30

16.20

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
WEEK III. Leukosit and Malignancyof Hematology and Limfoid
TIME MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY
(WIB) 17/9/2013 18/9/2013 19/9/2013 20/9/2013 21/9/2013
07.00 PEDIATRIC
– -3
07.50
07.50 CLIN
– PATH-6
08.40
08.40 CASE-3 MEDICAL PHAR-3 CASE-3
– NUTRITION-2
09.30
09.30

10.20
10.20 AP-1 CLIN PATH-5 INTER MED-5 RAD

11.10
11.10

12.00
12.00 BREAK

13.00
13.00 AP-PRACT AP-PRACT Pleno

13.50
13.50

14.40
14.40 CSL-3 CSL-3

15.30
15.30

16.20

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Hematoimmunology Block Module, Student Guide’s Book

TIME WEEK IV. Hypersensitivity and Autoimmune


(WIB) MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY
24/9/2013 25/9/2013 26/9/2013 27/9/2013 28/9/2013
07.00 – PEDIATRI
07.50
CS-4
07.50 – DERMATO
08.40
VEN-1
08.40 – CASE-4 CLIN MEDICAL CASE-4
09.30
PATH-7 NUTRITION
09.30 –
-3
10.20
10.20 – INTERN-4 MICRO-1 PHAR 4 CLIN
11.10
PATH-8
11.10 –
12.00
12.00 – BREAK
13.00
13.00 – CP- CP-PRACT Pleno
13.50
PRACT
13.50 –
14.40
14.40 – CSL-4 CSL-4
15.30
15.30 –
16.20
Note: Empty schedule is used for individual learning

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
WEEKV. Immunodeficiency
TIME MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY
(WIB) 1/10/2013 2/10/2013 3/10/2013 4/10/2013 5/10/2013

07.00 – PEDIATRIC-
07.50
5
07.50 –
08.40
08.40 – CASE-5 INTERNAL CASE-5
09.30
MED-5
09.30 –
10.20
10.20 – Microbiology 2
11.10
11.10 –
12.00
12.00 – BREAK
13.00
13.00 – Med Ethic-1 PHAR 5 Pleno
13.50
13.50 –
14.40
14.40 – CSL-5 CSL-5
15.30
15.30 –
16.20
Note: Empty schedule is used for individual learning

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Hematoimmunology Block Module, Student Guide’s Book

WEEKVI. BLOCK FINAL EXAMINATION


TIME (WIB) MONDAY TUESDAY WEDNESDAY THURSDAY FRIDAY
8/10/2013 9/10/2013 10/10/2013 11/10/2013 12/10/2013
07.00 – 07.50
07.50 – 08.40
Final Exam
08.40 – 09.30
09.30 – 10.20 CP Pract.
10.20 – 11.20 Final Exam
11.20 – 12.00
12.00 – 13.00 BREAK
13.00 – 13.50 AP Pract.
13.50 – 14.40 Final Exam
14.40 – 15.30
15.30 – 16.20

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
LITERATURE REVIEW

1. MODULE 1 : RED BLOOD CELLS

Anemia
Anemia is functionally defines as an insufficient red blood cell (RBC)
mass to adequately deliver oxygen to peripheral tissues. The laboratory
test to establish the presence of anemia is hematology examination. For
practical purpose, we can evaluate the three concentration measurement
such as haemoglobin (Hb) level (g/dL), haematocrit (%), dan RBC number
(1012/L). Index of erythrocyte can be established by calculate that
parameter. Erythrocyte index are mean corpuscular volume (MCV), mean
corpuscular haemoglobin (MCV) and mean corpuscular haemoglobin
concentration (MCHC). They are used to determine the type of anemia
based on erythrocyte morphology. (Glader, 2003, Adamson and Longo,
2008)
Based on erythrocyte morphology, anemia is divided into 3 types :(Glader,
2003)
1. Normocytic normochromic anemia (i.e blood loss, hemolytic
anemia, aplastic anemia)
2. Microcytic hypochromic anemia (i.e iron deficiency anemia,
anemia of chronic disease, thalassaemia)

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Hematoimmunology Block Module, Student Guide’s Book

3. Macrocytic anemia (i.e megaloblastic anemia caused by deficiency


of folat or vitamin B12)
Based on the cause of anemia, it is divided into:(Adamson and Longo,
2008)
1. Anemia caused by decrease red survival (i.e blood loss, or
hemolytic disease)
2. Anemia caused by defects of bone marrow production
(hypoproliferative) i.e marrow damage, iron deficiency, decrease
of stimulation in inflammation, metabolic defect, or renal disease.
3. Anemia caused by defects of red blood cell maturation (ineffective
erythropoiesis) i.e cytoplasmic defects in iron deficiency,
thalassaemia, sideroblastic anemia, or nuclear defects in folate
deficiency, vitamin B12 deficiency, drug toxicity, and refractory
anemia

Figure 1. The physiologic regulation of red blood cell production by tissue oxygen tension
(Adamson and Longo, 2008)

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
A. Iron deficiency anemia

Iron deficiency anemia is the condition in which there is anemia and clear
evidence of iron lack. It is the most prevalent forms of malnutrition
anemia. The causes of iron deficiency are :(Andrews, 2003, Adamson,
2008)
1. Increased demand for iron and or hematopoiesis i.e in infancy or
adolescence, pregnancy, and erythropoietin therapy.

2. Increased of iron loss in chronic blood loss, menometrorhagia,or acute


blood loss

3. Decrease iron intake or absorption i.e inadequate diet, malabsorpsi


disease (sprue or Crohn’s disease), surgery (post gastrectomy), or
inflammation

The progression of iron deficiency are divided into three stages.There


are: (Adamson, 2008)
1. The first stage is negative iron balance. In this stages, the iron
demand is higher than the ability of iron absorption. Iron stores
(serum ferritine) decrease, Total Iron Binding Capacity (TIBC)
increases, but serum iron is normal. This stage can be found in
several number of physiologic mechanisms such as pregnancy,
rapid growth in children and adolescent.

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Hematoimmunology Block Module, Student Guide’s Book

2. The second stage is iron deficient erythropoiesis. In this stage,


iron stores become depleted, serum iron begins to fall and
TIBC increases. Haemoglobin synthesis become impaired and
it causes of anemia. The morphology of erythrocyte in this
stage is normocytic normochrome.

3. The third stage is iron deficiency anemia. The characteristic of


this stage are anemia moderate (Hb value 10-13 g/dL),
morphology of erythrocyte is microcytic hypochrome, serum
iron, transferrin saturation and ferritin is low and TIBC is high.

Figure 2. Laboratory studies in the evolution of iron deficiency (Adamson, 2008)

Signs and symptoms of iron deficiency anemia:


1. Impairs growth in infancy

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
2. Fatigue
3. Headache
4. Irritability and palpitation
5. Dizziness and breathlessness
6. Disorder of neuromuscular system

Laboratory findings of IDA:(Adamson, 2008, Andrews, 2003)


1. Hematology
 Microcytic hypochrom anemia (MCV <80 fL, MCH and
MCHC are low)
 Blood smear : morphology of erythrocyte are microcytic
hypochrom, anisopoikilositosis, pencil cell (+), and or sel target
(+). Morphology of leucocyte can be found granulocytopenia in
longterm iron deficiency. Thrombocyte increases
(thrombocytosis)

2. Iron status
 serum iron is low
 TIBC increases
 Serum ferritin is low. Ferritin is acute phase reactan and its
value will increase in inflammatory stage. In order to
eliminate inflammation stage it is suggested to check C
reactive protein (CRP). The marker of iron store that has

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Hematoimmunology Block Module, Student Guide’s Book

better specifity than serum ferritin is soluble transferrin


receptor (sTfR).

Figure 3. Normal blood smear (Wright’s stain)(Adamson, 2008)

Microcytic
hypochrome

Pencil cell

Figure 4. Iron deficiency anemia blood smear(Adamson, 2008)

Terapi IDA(Adamson, 2008)


1. Ferrous tablet
2. Ferrous injection
3. Blood transfusion

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
B. Anemia of Chronic Disease (ACD)
Anemia of chronic disease is anemia that is often observed in
patients with infectious, inflammatory, or neoplastic disease that persist
for more than 1-2 months. The syndrome does not include anemia caused
by marrow replacement, blood loss, hemolysis, renal insufficiency, hepatic
disease, or endocrinopathy. The characteristic of anemia of chronic
disease are hypoferremia (serum iron is low) and normal or high of serum
ferritin.
Conditions associated with anemia of chronic disease are chronic
infectious (i.e pulmonary infections, pelvic inflammatory disease,
osteomyelitis etc), chronic noninfectious disease (i.e rheumatoid arthritis,
rheumatoid fever, SLE), malignancy (i.e carcinoma, leukemia, multiple
myeloma etc), and miscellaneous (i.e alcoholic liver disease, congestive
heart failure, thrombophlebitis, Ischemic Heart Disease etc)
Laboratory findings in ACD are:
1. Hematology :
 Mild-moderate anemia (hemoglobin value is 1-2 lower than normal
hemoglobin value, it is rare lower than 9 g/dl)
 Microcytic hypochrom anemia (MCV 77-82 fl)
 Haematocrit is more than 27%
2. Iron status :
 Serum iron is low (10-70 ug/dL)

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Hematoimmunology Block Module, Student Guide’s Book

 TIBC decreases (100-300 ug/dL)


 Transferrin saturation is low (10-25%)
 Serum ferritin value is normal or high. Its examination can be used
to determine iron deficiency anemia from anemia of chronic disease
The specific of signs and symptoms in ACD are associated with the
underlying disease.
Therapy of ACD depent on the underlying disease.
Thalassaemia
Thalassaemia is genetic disorders that characterized by reduced rate
or lack of production on one or more of the globin chain. The reduced
supply of globin diminishes production of haemoglobin. Based on genetic,
thalassaemia is classified into αthalassaemia, βthalassaemia,
γthalassaemia, δβthalassaemia, δthalassaemia, ɛζγβthalassaemia, and
hereditary persistence of fetal haemoglobin (HPFH).(Weatherall, 2001)
 αThalassaemia
α Thalassaemia is inherited disorder in α globin chain synthesis. It
causes an excess of β globin chain.
This thalassaemia is classified based on the number of gen
deletion. It is divided into one gen deletion, two genes deletion, three
genes deletion (HbH disease), and four genes deletion (Hb Bart/hydrops
foetalis).
 β Thalassaemia

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
β Thalassaemia is genetic disorders in β globin synthesis.
Clinically, it divided into three groups, that are β Thalassaemia major
(need a routine transfusion, it is also called Cooley’s anaemia), β
Thalassaemia intermediate (need transfusion in a certain condition),
and β Thalassaemia minor/trait/silent/asymptomatic (only diagnosed by
laboratory examination).(Weatherall, 2001, Hoffbrand et al., 2005,
Pignatti and Galanello, 2003)

2. MODULE 2 : PLATELET, BLOOD PLASMA, AND HEMOSTASIS SYSTEM

A. Disorder of Platelet’s Number


Disorders of platelet’s number can be determined into
thrombocytopeni and thrombocytosis. Trombocytopeni is condition in
which the number of thrombocyte is low. It is the most common cause of
abnormal bleeding. The diseases that cause thrombocytopeni can be
determined into:
a. Decreased platelet production (aplasy/hypoplasy of
megakaryocytes, ineffective thrombopoiesis, hereditary
thrombocytopenia)
b. Increased platelet destruction (immunologic thrombocytopenia
purpura, infectious, drugs, thrombotic microangiopathies,
thrombotic thrombocytopenic purpura, hemolytic uremic
syndrome)

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Hematoimmunology Block Module, Student Guide’s Book

c. Abnormal platelet distribution or pooling (hypersplenisme)


d. Miscellaneous (infectious disease such as dengue haemorrhagic
fever)(Parker and Levine, 2003a)
Thrombocytosis is a condition in which the number of thrombocyte is
high. It may result from physiologic or pathologic process. The
physiologic processes of thrombocytosis are exercise, parturation, or
ephinephrine. The pathologic processes are divided into primary (i.e
myeloproliferative syndrome, essential thrombocythemia,
polycythemia vera, chronic myelocytic leukemia, or myelofibrosis),
and secondary (infectious disease, inflammatory diseases, neoplasms,
rebound after recovery thrombocytopenia, asplenia) (Parker and
Levine, 2003b)

B. Disorders of Coagulation
Disorders of coagulation is caused by deficiency of coagulation
factors or present inhibitor of coagulation factor activity. It is X-link
disease. This disease is characterized by recurrent bleeding episodes into
joint, muscles, and closed space, either spontaneously or following an
injury. The most common of inherited factor deficiency are the
hemophilias. The disease is caused by deficiency of Factor VIII
(hemophilia A) or Factor IX (hemophilia B). The other causes, although it
is rare, are deficiency of Factor II (prothrombin), Factor V, Factor VII,

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
Factor X, Factor XIII and fibrinogen. They are usually inherited in
autosomal recessive manner.
Clinical manifestations of hemophilia are bleeding episodes into
joints (hemarthrosis), soft tissue and muscles after minor injury or even
spontaneously.(Arruda and High, 2008)
Laboratory examinations to diagnoseof hemophilia are aPTT (activated
Partial Thrombin Time), PT (Prothrombin Time), assay of activity and
value of coagulation factor, and assay of inhibitor coagulation factor.
Laboratory findings is isolated prolonged of aPTT, platelet count is
normal, and normal bleeding time. In hemophilia A, there is a deficiency
of FVIII or present FVIII inhibitor. In hemophilia B, there is a deficiency
of FIX (Arruda and High, 2008)

3. MODULE 3 : Leukocyte and Malignancy of Hematologic andLymphoid

A. Leucocyte Disorders
The various forms of leucocyte are neutrophil, eosinophil,
basophil, lymphocyte, and monocyte. They are derived from a common
stem cell in the bone marrow. Their function is in inflammatory and
immune responses. The schema event in granulocytes production and their
function in inflammation can be saw in figure below.(Holland and Gallin,
2008)

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Hematoimmunology Block Module, Student Guide’s Book

Figure 5. Schematic events in granulocytes production, recruitment, and inflammation


(Holland and Gallin, 2008)

Leucocyte disorders are determined into morphological disorders


and leucocyte number disorders. The morphological disorders is an
abnormality of leucocyte form (i.e toxic granulation, hypersegmentation,
Pelger-Huet anomaly, Dohle body, etc). The leucocyte number disorders
are leucopenia and leucocytosis. The kind of leucopenia or leucocytosis
depends on the form of leucocyte that has number alteration. (Holland
and Gallin, 2008, Hoffbrand et al., 2005)
Neutropenia is a condition in which the absolute neutrophil
number is low. The causes of neutropenia are decreased production (i.e
drug induced, hematologic disease such as aplastic anemia, myelofibrosis,
tumor invasion etc), peripheral destruction (antineutrophil antibody,

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Immersion Programme, HPEQ Faculty of Medicine Lampung University 2013
autoimmune disorders, drugs), and peripheral pooling (i.e overwhelming
bacterial infection, hemodialysis).(Holland and Gallin, 2008)
Neutrophilia is a condition in which the absolute neutrophil
number is high. The causes of neutrophilia are increased production
(idiopathic, drug induced, infection bacterial, fungal, or sometimes viral,
inflammation, myeloproliferative disease), increased marrow release
(glucocorticoids, acute infection, inflammatory such as thermal injury),
decreased or defective margination ( drugs induced such as ephinephrin,
stress, or leucocyte adhesion deficiency), and miscellaneous (metabolic
disorder, metastatic carcinoma, acute haemorrhagic, or
haemolysis)(Holland and Gallin, 2008)

B. Hematology Malignancy
The hematology malignancy is determined based on the kind of
hematology cell in which has abnormal proliferation. Abnormal
proliferation in myeloid cell is called myeloid leukemia. It is divided
into acute myeloid leukemia and chronic myelocytic leukemia based on
the maturation stage of myeloid cell. Myeloid leukemias is
characterized by infiltration of blood, bone marrow, and other tissue by
neoplastic cells of the hematopoietic system. The malignancies of
lymphoid cells arise from cells of the immune system at different stages
of differentiation, resulting in wide range of morphologic,

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immunologic, and clinical findings. The form of lymphoid cell


malignancies are leukemia and lymphomas (solid tumor of the immune
system). Lymphoid leukemia is determined into acute lymphoblastic
leukemia and chronic lymphocytic leukemia.

B. 1 Acute Myeloblastic Leukemia


Incidence of AML is 3,7 per 100.000 people per year, the age
adjusted incidence is higher in men than women, the incidence of AML
increase with age. Etiologies of AML are radiation or chemical
exposure, drugs, or heredity. There are 2 systems of AML
classification. That are The World Health Organization (WHO)
classification and French-American British (FAB)
classification.(Wetzler et al., 2008)
The WHO classification includes different biologically distict
group based on immunophenotype, clinical feature, and cytogenetic
and molecular abnormalities in addition to morphology. But the FAB
system classifies AML based of morphological features. The major
difference between the WHO and the FAB systems is the blast cutoff
for AML diagnosis to determine with myelodysplastic syndrome
(MDS). The blast cutoff in WHO system is 20%, in other side the blast
cutoff in FAB is 30%. The Classification Systems of AML can be saw
table-1. (Wetzler et al., 2008)

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Symptoms of AML are often nonspecific. They are the
consequence of anemia, leucocytosis, leukopenia or leucocyte
dysfunction, or thrombocytopenia. The symptoms was usually present
≤ 3 months before leukemia was diagnosed. They are fatigue,
weakness, anorexia, weight loss, or fever. Signs are bleeding, easy
bruising, bone pain, lymphadenopathy, non specific cough, or
headache. The physical findings are fever, splenomegaly,
hepatomegaly, lymphadenopathy, sternal tenderness, and evidence of
infection and haemorrhagic.
Hematology findings are anemia (mild-severe), normocytic
normochromic, the leucocyte count increase up to more than
100.000/µL, the morphology of the malignant cell varies in difference
subsets, Auer Roads can be found, platelet count is sometime lower
than 100.000/µL. Chemistry test can be foud the increased of uric acid,
LDH, ureum, and hepatic enzymes.(Wetzler et al., 2008). The diagnosis
is established based on blood smear, bone marrow punction (BMP),
cytochemistry, and gene analyze.

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Table 1. Classification AML(Wetzler et al., 2008)

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Figure 6. Blood film of AML (Wetzler et al., 2008)

B. 2 Chronic Myelocytic Leukemia


Chronic Myelocytic Leukemia (CML) is diagnose by identifying a
clonal expansion of a hematopoietic stem cell possessing a reciprocal
translocation between chromosomes 9 and 22. This translocation results
in head to tail fusion of the breakpoint cluster region (BCR) gene on
chromosome 22q11 with ABL gene located on chromosome 9q34. It is
called BRC ABL gene.
Symtomps of CML are fatigue, malaise, weight loss, infectious,
thrombosis, or bleeding. The physical findings are hepatomegaly and or
splenomegaly. Hematologic findings are anemia normocytic

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normochromic, elevated of WBC’s count with increases both immature


and mature granulocyte. The majority cells are myelocyte and
neutrophil (two peaks form). The diagnosis is established by blood
smear and BMP.(Wetzler et al., 2008)
B. 3 Acute Lymphoblastic Leukemia
Acute lymphoblastic leukemia have been divided based on
immunologic and cytogenetic abnormalities. The FAB classification is
divided ALL into three types based on morphologic character. There are
L1 (small uniform blast), L2 (Larger cell and more variable size cell), and
L3 (uniform cells with basophilic and sometimes vacuolated cytoplasms,
we are called Burkitt’s lymphoma cells). ALL is most common found in
childhood.(Longo, 2008). Diagnosis is established base on blood smear,
BMP, and cytogenetic analyze.
Table 2. Classification of ALL based on FAB System(Longo, 2008)

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B.4 Chronic Myelocytic Leukemia
Chronic Myelocytic Leukemia (CML) is the most common
lymphoid leukemia. This leukemia has the similar clinical findings with
other kind of leukemia. Hematology findings are anemia normocytic
normochromic, increased of lymphocyte number in peripheral blood (the
count is up to >109/µL), and the peripheral blood smear shows smudge
cell/basket cell (it is nuclear remnant of cells damaged by the physical
shear stress of making the blood smear).(Longo, 2008)

Smudge
cells/basketcells

Figure 7. Chronic Lymphocytic Leukemia(Longo, 2008)

4. MODULE 4 : HYPERSENSITIVITY AND AUTOIMMUNE DISEASE

Disease caused by Immune Responses


Hypersensitivity disease is disorders caused by immune responses.
There are 4 types of hypersensitivity that are classified according to the
type of immune response and the effector mechanism responsible for cell
and tissue injury. Type 1 hypersensitivity is called Immediate

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hypersensitivity. It is caused by IgE antibody and mast cells and the most
prevalent type of hypersensitivity disease. The diseases caused by this
hypersensitivity are brochial asthma, anafilactic shock, and allergic.
Type 2 hypersensitivity is called antibody mediated
hypersensitivity. In this type, IgM or IgG against cell surface or
extracellular matrix antigen. The disease caused by type 2 hypersensitivity
are transfusion reaction, haemolytic anemia, and haemolytic in Newborne
Disease.
Type 3 hypersensitivity is called immune complex mediated
hypersensitivity. It is caused by present of immune complexes of
circulating antigens and IgM or IgG antibody. The disease are rheumatoid
fever, nephrotic syndrome, Rheumatoid Heart Disease.
Type 4 hypersensitivity is called T cell mediated hypersensitivity.
It is determined into CD4+ T cells (delayed type hypersensitivity) and
CD8+ CTLs (T cell mediated cytolysis).(Abbas et al., 2007)

5. MODULE 5 : IMMUNODEFICIENCY

Immunodeficiencies
Immunodeficiencies is defects in one or more component of
immune system. It is divided into primary or secondary
immunodeficiencies. Immunodeficiency diseases increase susceptibility to
infection.

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The secondary immunodeficiencies develop as consequence of
malnutrition, disseminated cancer, immunosuppresive agents, or infection
(such as HIV infection that causes AIDS). HIV attack the T lymphocyte
CD4 and make destruction in lymphoid tissue. It causes depletion of CD4
number. The depletion of T lymphocyte CD4 increases susceptibility to
infection.(Abbas et al., 2007)

REFERENCE

ABBAS, A. K., LICHTMAN, A. H. & PILLAI, S. (2007) Cellular and


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ADAMSON, J. W. & LONGO, D. L. (2008) Anemia and polycythemia. IN
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