Study Guide Hematologic Tayang 9 September 2014

Study Guide Hematologic System & Disorders &
Clinical Oncology
1. PREFACE
Hematology system & clinical oncology is an expanding science with new concepts and
ideas appearing in the literature almost daily.
In this block, we will learn about the basic of hematology, disorder of blood cell which
occurred in the hemopoiesis process, or during circulation process and during the
destruction process of the cell, and management therapy of blood disorder. In this block, we
also will learn about the basic of malignancy, epidemiology, early detection of cancer,
diagnosis of cancer and management therapy of cancer including surgery, radiotherapy, and
systemic therapy for better quality of life of patient with cancer.
This block will take 25 meeting to be completed, each meeting consist of introductory
lecture continued by individual learning, single group discussion and self assessment,
student project and ending with plenary session. In each topic there will be a list of tasks to
discuss which some of them are based on a case that commonly find in clinical practice.
There will also a simple clinical problem that you need to discuss and respond, each part
will be given a cut of clinical information for you to be responded.
Evaluation in this block will be formative and summative. The formative evaluation is
directive and will take as checklist and peer assessment, while summative will be conducted
at the end of this block.
We believe that the basic of hematology and clinical oncology that you will learn in this block
will impulse you to learn more about it to help you dealing with hematology problems in
patients.
Good luck,
Planner team
Udayana University Faculty of Medicine, MEU

Clinical Oncology
2. LIST OF CONTENT
1. Preface.
2. List of Contents......
3. Planners Team & Lecture
4. Facilitators
5. Seven General Core Competency
....
6. Curriculum Block: The Hematology System &Disorder & Clinical Oncology
...
- Regular class...
7. Time Table
- English class....
8. Meeting of student representatives..
14
9. Assessment method..
14
10. Student Project .
16
11. Content outline and learning task.....
19
12. Curriculum Mapping. 48

13. References..
49

Clinical Oncology
3. PLANNERS TEAM
No.
NAME
DEPARTEMENT
PHONE
1.
Internal Medicine
0811394108
Clinical Pathology
08123647413
Clinical pathology
Surgery
Dept. of Child Health
Internal Medicine
0818566411
0811398971
08123600792
081338728421
7.
8.
9.
Dr. dr. Ketut Suega, SpPD KHOM

(Head)
dr. Ni Kadek Mulyantari, SpPK(K)
(secretary)
dr. Sianny Herawati, SpPK
dr. Wayan Sudarsa, SpB Onk
dr. Ketut Ariawati, SpA (K)
dr. Tjokorda Gde Dharmayuda, SpPD
KHOM
Dr. dr. Bagus Komang Satriyasa, M.Repro
dr. Ni Wayan Winarti, SpPA
dr. Losen Adnyana, SpPD KHOM
081805368922
087862457438
08123995536
10.
dr. Ni Made Renny Anggreni Rena, Sp.PD
Pharmacology
Anatomy Pathology
Div HOM Lab.
Interna
Div HOM Lab.
Interna
2.
3.
4.
5.
6.
081803651656
LECTURERS
NAME
Prof. Dr. dr. I Made Bakta, SpPD KHOM
Prof.Dr. dr. I B Tjakra Manuaba, MPH SpBOnk
dr. Tjokorda Gde Dharmayuda, SpPD KHOM
Dr.dr. Ketut Suega, SpPD KHOM
dr. W Sudarsa SpBOnk
dr. I Wayan Sugiritama, M.Kes
Prof. dr. N Agus Bagiada, SpBiok
dr. Tjokorda Gde Oka, MS., SpPK
dr. N Wiadnyana Steven Christian, SpBOnk
Dr. dr. Elysanti SpRad,
dr. Ketut Ariawati, SpA (K)
dr.I Nyoman Lila,MS
dr. Ni Made Renny Anggreni Rena, Sp.PD
Drs. I Made Adioka , Apt, M.Si
dr. Ni Putu Ekawati,M.Repro, Sp.PA
dr. Ni Kadek Mulyantari, SpPK (K)
dr. AA Widnyana, SpA
DEPARTEMENT
PHONE
Div HOM Lab. Interna

Div Onkologi Lab
Bedah
Div Onkologi Lab
Bedah
Lab. Histologi
Lab. Biokimia
Lab. Farmakologi
Lab Patologi Klinik
Div Onkologi Lab
Bedah
Lab. Patologi Klinik
Lab Radiologi
Div HOM Lab Pediatri
Lab. Patologi Anatomi
Lab Patologi Klinik
Lab.Farmasi
Lab. Patologi Anatomi
Lab. Patologi Klinik
Div HOM Lab Pediatri
0811399625
08113937779
0811394108
081338728421
0811398971
08164732743
081338338611
081805368922
081338454245
08123801156
0818566411
081805673099
08123600792
08123995536
087862457438
08123950009
081803651656
0361 - 8000382
08113803933
08123647413
081338550049

Clinical Oncology
4. FACILITATORS
REGULAR CLASS
NO
1
2
3
4
5
6
7
8
9
10
11
12
NAME
dr. Ni Kadek Mulyantari , Sp.PK
dr. Ni Luh Ariwati
dr. Ni Luh Putu Ratih Vibriyanti
Karna, Sp.KK
dr. Putu Ayu Asri Damayanti , M.Kes
dr. Ni Made Dewi Dian Sukmawati,
Sp.PD
dr. Putri Ariani, Sp.KJ
dr. Ni Nengah Dwi Fatmawati ,
Sp.MK, Ph.D
dr. Ni Nyoman Margiani, Sp.Rad
dr. PutuYuliandari, S.Ked
dr. I Gusti Made Gde Surya Chandra
Trapika , M.Sc
dr. Anak Agung Wiradewi Lestari ,
Sp.PK
dr. Nyoman Paramita Ayu, Sp.PD
ENGLISH CLASS
NO
NAME
1
2
3
4
5
6
7
8
9
10
11
12
dr. Nyoman Suryawati , M.Kes,

Sp.KK
dr.Wayan Citra Wulan Sucipta
Putri
dr. A.A. Ngurah Subawa, Msi
Dr. dr. Bagus Komang Satriyasa,
M.Repro
dr. Ponti somaya Parami, Sp.An
dr. Pratihiwi Primadharsini,
M.Biomol, Sp.PD
dr. I G.A. Indah Ardani, Sp.KJ
dr. I Gusti Ayu Widianti ,
M.Biomed
dr. Ni Made Adi Tarini, Sp.MK
dr. Putu Budhiastra, Sp.M(K)
dr. Putu Patriawan, Sp.Rad, MSc
dr. Ni Putu Sri widyani , Sp.PA
GROUP
1
2
3
4
5
6
7
8
9
10
11
12
GROUP
1
2
3
4
5
6
7
8
9
10
11
12
DEPT
Clinical
Pathology
PHONE
08123647413
Parasitology
08123662311
Dermatology
081337808844
Parasitology
085338565783
Interna
081805656501
Psychiatry
08123806397
Mikrobiology
087862200814
Radiology
081337401240
Mikrobiology
089685415625
Pharmacology
081337991177
Clinical
Pathology
08155237937
Interna
08123837372
DEPT
PHONE
Dermatology
0817447279
Public Health
082140517310
Clinical Pathology
08155735034
Pharmacology
087777790064
Anasthesi
08123661312
Interna
081805530196
Psychiatry
0361 -8810404
Anatomy
081936005559
Microbiology
081338675344
Opthalmology
085238238999
Radiology
08123956636
Anatomy
Pathology
081337115012
VENUE
3nd floor:
R.3.01
3nd floor:
R.3.02
3nd floor:
R.3.03
3nd floor:
R.3.04
3nd floor:
R.3.05
3nd floor:
R.3.06
3nd floor:
R.3.07
3nd floor:
R.3.08
3nd floor:
R.3.20
3nd floor:
R.3.21
3nd floor:
R.3.22
3nd floor:
R.3.23
VENUE
3nd floor:
R.3.01
3nd floor:
R.3.02
3nd floor:
R.3.03
3nd floor:
R.3.04
3nd floor:
R.3.05
3nd floor:
R.3.06
3nd floor:
R.3.07
3nd floor:
R.3.08
3nd floor:
R.3.20
3nd floor:
R.3.21
3nd floor:
R.3.22
3nd floor:
R.3.23

Clinical Oncology
5. THE SEVEN GENERAL CORE COMPETENCY

1. . Patient care
Demonstrate capability to provide comprehensive patient care that is compassionate,
appropriate, and effective for the management of health problems, promotion of health
and prevention of disease in the primary health care settings.
2. Medical knowledge base
Mastery of a core medical knowledge which includes the biomedical sciences,
behavioral sciences, epidemiology and statistics, clinical sciences, the social aspect of
medicine and the principles of medical ethics, and apply them
3. Clinical skill
Demonstrate capability to effectively apply clinical skills and interpret the findings in the
investigation of patient.
4. Communication
Demonstrate capability to communicate effectively and interpersonally to establish
rapport with the patient, family, community at large, and professional associates, that
results in effective information exchange, the creation of a therapeutically and ethically
sound relationship.
5. Information management
Demonstrate capability to manager information which includes information access,
retrieval, interpretation, appraisal, and application to patients specific problem, and
maintaining records of his or her practice for analysis and improvement
6. Professionalism
Demonstrate a commitment to carrying out professional responsibilities and to personal
probity, adherence to ethical principles, sensitivity to a diverse patient population, and
commitment to carrying out continual self-evaluation of his or her professional standard
and competence
7. Community based and health systembased practice
Demonstrate awareness and responsiveness to larger context and system of health
care, and ability to effectively use system resources for optimal patient care

Clinical Oncology
6. CURRICULUM BLOCK:
THE HEMATOLOGIC SYSTEM AND DISORDERS AND
CLINICAL ONCOLOGY
Aims:
1.
2.
3.
4.
5.
6.
7.
Comprehend the erythropoiesis, granulopoiesis, thrombopoiesis, basic

principles of haemostasis and transfusion medicine
Apply and interpret physical examination, laboratory, and imaging diagnosis of
hematology system disorders.
Apply general principles of approach and management of patient with
malignancy.
Diagnose and manage patient with common forms of anemias and to recognize
or identify common forms of white blood cell disorders.
Diagnose and manage common forms of hemostatic or coagulation disorder.
Diagnose and refer special patients with hematology system disorders
Plan patient, family, and necessary community education about hematology
system disorders and clinical oncology.
Sub thema 1 : Hematologic system and disorders.

Sub thema 2 : General and clinical oncology.
Sub thema 1
LEARNING OUTCOMES
1. Describe the biology of the hemopoetic system and its clinical implications
2. Describe the general principles and mechanisms of hemostasis and coagulation
3. Apply the general principles of transfusion medicine
4. Recognize or identify common forms of thrombotic and thromboembolic disorders
5. Recognize or identify common forms of splenic disorders (hypersplenism,
splenomegaly, and spleen rupture)
6. Differentiate and diagnose common form anemia
7. Differentiate acute and chronic leukemias, and myelodysplastic syndrome
8. Differentiate Hodgkins and non Hodgkins lymphoma
Sub thema 2
LEARNING OUTCOMES
1. Describe the general principles of cancer genetic and cancer cell biology and
immunology of cancer
2. Apply general principles of prevention and early detection of cancer
3. Apply general principles Clinical and Pathological approach to patient with cancer
4. Describe general principles of cancer therapy
5. Apply general principles of follow up, rehabilitation, palliative care, ethic and
psychosocial to cancer patient.

Clinical Oncology
7. TIME TABLE
Day
1
Date
Topic
Tuesday
Sept, 9,
2014
General Information
The Hematology
system disorder
General Information
General Oncology
Wednesd
ay
Sept, 10
2014
Thursday
Sept, 11,
2014
Friday
Sept, 12,
2014
Learning
situation
Intro. Lect
Regular
Class
08.00-08.30
English
Class
09.00-09.30
Intro.Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-09.00
09.00-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Leukopoesis,
Intro. Lect
08.00-08.30
09.00-09.30
Thrombopoesis
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
08.30- 09.00
09.30-10.00
09.00-10.30
12.00-13.30
Laboratory picture of
patient with blood
cells disorder (BSC)
Erythropoesis
Synthesis of Hb,
function of blood
and blood cells
metabolism
Ind. Learning
PIC
Dr.dr. Ketut
Suega, SpPD
KHOM
dr. Wayan
Sudarsa, SpB
Onk
Facilitator
Dr.dr. Ketut
Suega, SpPD
KHOM &dr.
Wayan Sudarsa,
SpBOnk
dr. Sianny
Herawati, Sp.PK
Facilitator
dr. Sianny
Herawati, Sp.PK
dr. I Wayan
Sugiritama,
M.Kes
Dr. Sianny
Herawati, Sp.PK
Facilitator
dr. I Wayan
Sugiritama,
M.Kes & Dr.
Sianny Herawati,
Sp.PK
Dr. Ni Kadek
Mulyantari,
Sp.PK(K)
Prof. dr. N Agus
Bagiada, SpBiok

Clinical Oncology
Monday
Sept, 15,
2014
SGD
Break
Student Project
Pleno
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Information
Nutritional Anemia
Intro. Lect
08.00-08.30
09.00-09.30
Pathophysiology of
Iron Deficiency
Anemia
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-09.00
09.00-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.30-09.00
09.30-10.00
Anemia
Polycythemia
Tuesday
Sept, 16,
2014
Wednesd
ay
Sep, 17,
2014
Thursday
Sep, 18,
2014
The diagnostic of
iron deficiency
anemia
Pathophysiology
folic acid and B12
deficiency anemia
Facilitator
Dr. Kadek
Mulyantari,
Sp.PK(K)
Prof. dr. N Agus
Bagiada, SpBiok
dr. Ketut
Ariawati, SpA(K)
dr. Tjokorda Gde
Dharmayuda,
SpPD KHOM
Facilitator
dr. Ketut
Ariawati, SpA (K)
& dr. Tjokorda
Gde
Dharmayuda,
SpPD KHOM
Dr.dr. Ketut
Suega, SpPD
KHOM
Dr.dr. Ketut
Suega, SpPD
KHOM
Facilitator
Dr.dr. Ketut
Suega, SpPD
KHOM
Dr.dr. Ketut
Suega, SpPD
KHOM
Facilitator
Dr.dr. Ketut
Suega, SpPD
KHOM
dr. Ni Made
Renny Anggreni
Rena, Sp.PD
The diagnostic of
folic acid and B12

Clinical Oncology
deficiency anemia
10
11
Friday
Sep, 19,
2014
Monday
Sep, 22,
2014
Tuesday
Sep, 23,
2014
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
AML
Intro. Lect
08.00-08.30
09.00-09.30
ALL
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Management
therapy of iron
deficiency
Intro. Lect
08.00-08.30
09.00-09.30
Therapy Folic acid

and B12 anemia
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
-Anemia on chronic
disease
Intro. Lect
08.00-08.30
09.00-09.30
-Aplastic anemia
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Facilitator
dr. Ni Made
Renny Anggreni
Rena, Sp.PD
dr. Losen
Adnyana, SpPD
KHOM
Dr. AA
Widnyana, Sp.A
Facilitator
dr. Losen
Adnyana, SpPD
KHOM
Dr. AA
Widnyana, Sp.A
Dr. dr. Bagus
Komang
Satriyasa,
M.Repro
Drs. I Made
Adioka , Apt,
M.Si
Facilitator
Dr. dr. Bagus
Komang
Satriyasa,
M.Repro
Drs. I Made
Adioka , Apt,
M.Si
dr. Losen
Adnyana, SpPD
KHOM
dr. Losen
Adnyana, SpPD
KHOM
Facilitator
dr. Losen
Adnyana, SpPD
KHOM

Clinical Oncology
12
13
14
15
Wednesd
ay
Sep, 24,
2013
Thursday
Sep, 25,
2014
Friday,
Sep, 26,
2014
Monday,
Sep, 29,
2014
Thrombositosis
Intro. Lect
08.00-08.30
09.00-09.30
Thrombocytopenia
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Principle of
Hemostasis
Intro. Lect
08.00-08.30
09.00-09.30
DIC, APS,
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
Von
Willebrands Intro. Lect
disease
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Malignan lymphoma
Intro. Lect
08.00-08.30
09.00-09.30
Malignan lymphoma
(diagnostic
pathology)
Intro. Lect
08.30-09.00
09.30-10.00
Hemophilia
Dr.dr. Ketut
Suega, SpPD
KHOM
dr. Ni Made
Renny Anggreni
Rena, Sp.PD
Facilitator
Dr.dr. Ketut
Suega, SpPD
KHOM &dr. Ni
Made Renny
Anggreni Rena,
Sp.PD
Dr.dr. Ketut
Suega, SpPD
KHOM
dr. Ni Made
Renny Anggreni
Rena, Sp.PD
Facilitator
Dr.dr. Ketut
Suega, SpPD
KHOM &dr. Ni
Made Renny
Anggreni Rena,
Sp.PD
Dr. AA
Widnyana, Sp.A
dr. Ni Made
Renny Anggreni
Rena, Sp.PD
Facilitator
Dr. AA
Widnyana, Sp.A
& dr. Ni Made
Renny Anggreni
Rena, Sp.PD
dr. Tjokorda Gde
Dharmayuda,
SpPD KHOM
dr. Ni Putu
Ekawati,M.Repro
, Sp.A
10

Clinical Oncology
16
17
18
19
Tuesday,
Sep,30,
2014
Wednesd
ay
Oct, 1,
2014
Thursday
Oct, 2,
2014
Friday
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Blood transfusion
Intro. Lect
08.00-08.30
09.00-09.30
Blood banking
(BCS)
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Multiple Myeloma,
Intro. Lect
08.00-08.30
09.00-09.30
MDS Langerhans
cell tumor
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
Congenital
hemolytic anemia,
hemoglobinopati
Acquired hemolytic
anemia
Management
CLL
Facilitator
dr. Tjokorda Gde
Dharmayuda,
SpPD KHOM&
dr. Ni Putu
Ekawati,M.Repro
, Sp.A
Dr. Ketut
Ariawati, Sp.A(K)
dr. Tjokorda Gde
Dharmayuda,
SpPD KHOM
Facilitator
Dr. Ketut
Ariawati, Sp.A(K)
dr. Tjokorda Gde
Dharmayuda,
SpPD KHOM
Dr. Ni Kadek
Mulyantari,
Sp.PK(K)
Dr. Ni Kadek
Mulyantari,
Sp.PK(K)
Facilitator
Dr. Ni Kadek
Mulyantari,
Sp.PK(K)
dr. Losen
Adnyana, SpPD
KHOM
dr. Losen
Adnyana, SpPD
KHOM
Facilitator
dr. Losen
Adnyana, SpPD
KHOM
dr. Losen
11

Clinical Oncology
Oct, 3,
2014
CML
20
21
22
Monday
Oct, 6,
2014
Tuesday
Oct, 7,
2014
Thursday
Oct, 9,
2014
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Intro. Lect
08.00-08.30
09.00-09.30
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Molecular biology of
cancer
Intro. Lect
08.00-08.30
09.00-09.30
Immunology of
cancer
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Management
diagnostic of cancer
Intro. Lect
08.00-08.30
09.00-09.30
Management
therapy and referral
of cancer
Intro. Lect
08.30-09.00
09.30-10.00
Ind. Learning
SGD
Break
Student Project
Pleno
09.00-10.30
10.30-12.00
12.00-12.30
12.30-14.00
14.00-15.00
12.00-13.30
13.30-15.00
11.30-12.00
10.00-11.30
15.00-16.00
Epidemiology of
cancer
Screening of cancer
Adnyana, SpPD
KHOM
dr. Losen
Adnyana, SpPD
KHOM
Facilitator
dr. Losen
Adnyana, SpPD
KHOM
dr. W Sudarsa
SpBOnk
dr. W Sudarsa
SpBOnk
Facilitator
dr. W Sudarsa
SpBOnk
Prof.Dr. dr. I B
Tjakra Manuaba,
MPH SpBOnk
Prof.Dr. dr. I B
Tjakra Manuaba,
MPH SpBOnk
Facilitator
Prof.Dr. dr. I B
Tjakra Manuaba,
MPH SpBOnk
dr. N Wiadnyana
Steven Christian,
SpBOnk
dr. N Wiadnyana
Steven Christian,
SpBOnk
Facilitator
dr. N Wiadnyana
Steven Christian,
SpBOnk
12

Clinical Oncology
23
Friday
Oct, 10,
2014
Diagnostic
pathology, tumor
marker
Diagnostic Imaging
of cancer
24
Monday
Oct, 13,
2014
Basic Clinical Skill

(Clinical Pathology)
25.
Tuesday
Oct, 14,
2014
Wednesd
ay
Oct, 15
2014
Thursday
Oct, 16,
2014
Basic Clinical Skill

(Pathology
Anatomy)
26
27
Intro. Lect
08.00-08.30
09.00-09.30
dr. Winarti, SpPA
Intro. Lect
08.30-09.00
09.30-10.00
Dr.dr. Elysanti
SpRad,
Ind. Learning
SGD
Break
09.00-10.30
10.30-12.00
12.00-12.30
12.00-13.30
13.30-15.00
11.30-12.00
Student Project
Pleno
12.30-14.00
14.00-15.00
10.00-11.30
15.00-16.00
Facilitator
dr. Winarti,
SpPA& Dr. dr.
Elysanti SpRad
dr. Sianny
Herawati,
SpPK& dr. Ni
Kadek
Mulyantari,
Sp.PK(K)
dr. Winarti, SpPA
Silent Day
Evaluation
Team
8. MEETING OF STUDENT REPRESENTATIVES
13

Clinical Oncology
In the middle of each block curriculum, a meeting is held among the student
representatives, facilitators, and resource person of the block. The meeting is to discuss
about the effectiveness of on going teaching and learning processes, facilitators and
lectures as a feedback to improve process. This meeting is held on ( schedule to be
advise).
9. ASSESSMENT METHOD
Assessment in this thema consists of:
SGD
:5%
SP (review article)
: 15 %
Final exam
: 80 %.
10. STUDENT PROJECT

Format Paper (Article Review)
TITLE
(subject/topic: choose from compentency list)
Name
NIM
Faculty of Medicine
Udayana University
2014
1.
2.
3.
4.
Introduction (Pendahuluan)
Content (Isi, sesuai topik yang dibahas)
Summary (Ringkasan)
Refferences: (Daftar Pustaka, minimal 10, 5 tahun terakhir) VanCouver
style,
Example:
Journal
Punnonen K, Irjala K, Rajamaki A. Serum transferrin receptor and its ratio to
serum ferritin in the diagnosis of iron deficiency. Blood. 1997;89(3):1052-7.
Textbook
Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A,
Kasper D, Hoster S, Longo D, Jamason S (eds). Harrisons principles of
internal medicine. 15th ed. New York: McGraw Hill; 2001. p. 1977-82.
Internet
WHO. Clinical Use of Blood. Geneva: WHO 1998. [cited 2005 July]. Available
from: http://www.who.int/blood/publications/facts/ .
10-15 pages, 1.5 spasi, Times new romance 12

Subject/topic
REGULAR CLASS
NO
TOPIC
1
Patophisiology of Iron Deficiency Anemia
GROUP
1
14

Clinical Oncology
2
Acute Lympoblatic Leukemia
B12 Deficiency Anemia
Chronic Myeloblatic Leukemia
Aquired Hemolytic Anemia
Interpretation of Complete Blood Count Result
Polycytemia
Laboratory Screening for Hemostasis
Multiple Myeloma
10
Hemophilia B
10
11
Promotion and Prevention of Iron Deficiency Anemia
11
12
Transfusion Reaction
12
ENGLISH CLASS
TOPIC
NO
GROUP
Management of Iron Deficiency Anemia
Acute Myeloblatic Leukemia
Chronic Lympoblatic Leukemia
Folic Acid Deficiency Anemia
Epidemiologi, Screening and diagnositic Of Cancer
Congenital Hemolytic Anemia
Hemophilia A
Limphoma
Anemia on Chronic Disease
10
Idiopatic Thrombocytopenia Purpura (ITP)
10
11
Aplastic /Hypoplastic Anemia
11
12
Von Wilebrands Disease
12
The Schedule for Student Project Presentation

NO
Date
Topic
Learning
Situation
Regular Class
English
Class
Lecture
15

Clinical Oncology
1.
Wednesd
ay Oct, 1,
2014
Limfoma (English
class)
Student
Project
12.30 14.00
10.00 -11.30
Dr
Tjokorda
Gde
Dharmay
uda,
Sp.PD
KHOM
Student
Project
12.30 14.00
10.00 -11.30
Dr. Ni
Made
Renny
Anggreni
Rena,
Sp.PD
Student
Project
12.30 14.00
10.00 -11.30
Dr. AA
Widnyan
a, SpA
Student
Project
12.30 14.00
10.00 -11.30
Dr. Losen
Adnyana,
Sp.PD
KHOM
Student
Project
12.30 14.00
10.00 -11.30
Dr. Losen
Adnyana,
Sp.PD
KHOM
Acute Myeloblatic
Leukemia (English
class)
Aquired Hemolytic
Anemia (regular class)
Polycytemia (regular
class)
2.
Thursday Patophisiology of Iron

Oct, 2,
Deficiency Anemia
2014
(regular class)
B12 Deficiency
Anemia (regular class)
Management of Iron
Deficiency Anemia
(English class)
3.
Friday
Oct, 3,
2014
Folic Acid Deficiency

Anemia (English
class)
Congenital
Hemolytic Anemia
(english class)
Hemophilia A
(English class)
Hemophilia B (regular
class)
4.
5.
Monday,
Oct, 6,
2014
Tuesday
Oct, 7,
2014
Acute Lympoblatic
Leukemia (regular
class)
Chronic
Lympoblastic
Leukemia (english
class)
Chronic Myeloblatic
Leukemia (regular
class)
Multiple Myeloma
(regular class)
Anemia on Chronic
Disease (english
class)
16

Clinical Oncology
Idiopatic
Thrombocytopenia
Purpura (ITP)
(english class)
Aplastic
/Hypoplastic Anemia
(english class)
6.
Thursday
Oct, 9,
2014
Von Wilebrands
Disease (english
class)
Interpretation of
complete blood count
result (reguler class)
Student
Project
12.30 14.00
10.00 -11.30
Dr. Ni
Kadek
Mulyanta
ri,
Sp.PK(K)
Student
Project
12.30 14.00
10.00 -11.30
Dr.
Winarti,
SpA/dr.
Elysanti,
Sp.Rad
Laboratory screening
for hemostasis(reguler
class)
Promotion and
prevention of iron
deficiency anemia
(reguler class)
7.
Friday
Oct, 10,
2014
Transfusion reaction
(reguler class)
Epidemiologi,
Screening and
Diagnostic Of
Cancer (English
class)
NOTE : Presenter will be choosen by moderator on site
Article Review Assessment Form

Faculty of Medicine, Udayana University
17

Clinical Oncology
_________________________________________________________________________
__
Block
: Hematology systems & disorders and clinical oncology
Name
: ________________________________________
Student No. (NIM) : ________________________________________
Facilitator
: ________________________________________
Title
:__________________________________________________
__________________________________________________
__________________________________________________
Time table of consultation
Point of discussion
1. Title
2. Refferences
3. Outline of paper
4. Content
5. Final discussion
Assessment
A. Paper structure
B. Content
C. Discussion
Total point
Week
1
2
3
4
5
:
:
:
:
Date
7
7
7
8
8
8
Tutor sign
9
9
9
10
10
10
( A + B + C ) : 3 = _____________
Denpasar, ______________________
Facilitator,
Assessment will be carried out on (day, date). There will be 100 questions consisting mostly
of Multiple Choice Questions (MCQ) and some other types of questions. The minimal
passing score for the assessment is 70. Other than the examination score, your
performance and attitude during group discussions will be considered in the calculation of
your average final score.
11. CONTENT OUTLINE AND LEARNING TASKS
18

Clinical Oncology
DAY I (Tuesday, Sept, 9th 2014)

Lecture 1.Introduction of
Hematologic System and Disorders
and General Oncology
Sub topic : Introduction of Hematologic
System and Disorders
Prof.Dr. dr. Ketut Suega, SpPD KHOM
Abstract
Hematologic System and Disorders is the discipline that studies the normal and abnormal
conditions of the blood and is components. Plasma component of the blood consists of
several proteins which are instrumental in the process of coagulation, anti-coagulation, as
well as fibrinolytic reactions. One of the most particular characteristics of the hematopoietic
system is the perpetual regeneration process of blood cells throughout the lifespan of the
organism.
Pluripotent hematopoietic stem cell (HSC) is the precursor of blood cells. The components
of blood from HSC that actively circulate are erythrocytes, leukocytes, and thrombocytes.
Lymphocytes are among the components produced by HSC, and thus the field of
hematology also includes in it the studies of reticuloendothelial system and lymph nodes.
No individual organ can be specifically linked to hematology disorders; the problems could
manifest themselves at the bone marrows, lymphatic organs, intravascular compartments
where the red blood cells circulate, or endothelial cells along the blood vessels and the
proteins in the plasma component.
Sub theme General Oncology is the discipline that studies the general aspect of tumor /
malignancy / cancer describe epidemiology, cancer prevention, therapy of cancer
rehabilitation patient with cancer.
At the end of this program, medical students are expected to:
1. Understand medical doctors approaches toward anemia and several erythrocytes
disorders.
2. Be able to evaluate complete blood check (complete hematology check)
3. Understand how to design screening tests to detect bleeding disorders.
Be able to apply them to appropriately classify the patients with cellular or protein damage
related to bleeding.
1. Study clinical profiles, proteins, and genetic factors instrumental in the process of
thrombosis.
2. Capable to identify the patient with hematological disorders who should be
referred to the hematological expert for further assessments!
Learning task:
1. Learn how to understand what is hematology?
2. How to evaluate Blood Celluler Function?
3. What is the physical stage of blood?
4. Explain what are the hematology disorders?
Self assessment
1. Understand what is hematology consisting of.
2. Understand the physical stage of blood as well as cellular element of the blood.
19

Clinical Oncology
3. Understand in general hematology disorders.
Lecture 2.Introduction of Hematologic

System and Disorders and General
Oncology
Sub topic : Introduction of Clinical
Oncology
Dr. Wayan Sudarsa, SpBOnk
Abstract
Oncology is a study of Cancer. Cancer arises from a series of genetic alterations that
promote self sufficiency in growth, escape from cell cycle exit, resistance to apoptosis,
cellular immortalization, and ultimately the acquisition of properties that facilitate
angiogenesis, invasion, and metastasis.
The scope of Oncology are basic sciences of oncology and clinical oncology. Basic
science of oncology are mainly consist of molecular biology and immunology. Clinical
Oncology is a multidisciplinary area of medicine, which means that several medical
disciplines are involved in the prevention, screening and early detection of people with risk
of cancer, and diagnosis, staging and treatment of individual patients with cancer as well
Learning Task:
1. At the level of molecular biology point of view, what is the definition of
Cancer?
2. Would you elaborate what are the causes of Cancer?
3. Can you define the ten most common cancer that affected of the human body
according of Global Cancer Statistics ? (www.IARC.org).
4. On your opinion, is cancer can be prevented?
DAY 2 (Wednesday, Sept 10th 2014)
Laboratory picture of patient with blood cells

disorder
dr. Sianny Herawati, Sp.PK
The differential diagnosis of anemia is broad. The likely cause of anemia in an individual
patient can be narrowed by systematic evaluation. Critical information includes
measurements of the erythropoietic response and measurement ofRBC size. These data
provide a framework that guides the selection of more specific studies to establish
underlying diagnosis.
The complete blood count (CBC is a laboratory report of the cellular elements of the blood.
CBC is now routinely performed with an automated instrument.
Seven values relating to RBC are reported in CBC, including Hb, RBC count, MCV, MCH,
MCHC and RDW.
Hb is direct measure ofthe concentration of Hb in grams per deciliter.
20

Clinical Oncology
Hct is the volume RBCs expressed as a percentage of whole blood
volume. RBC count is direct measure of the numher ofRBC
MCV is direct measure of mean RBC volume in femtoliters (fl)
MCH is calculated by dividing the Hb by the RBC count and is
expressed in picograms (pg)
MCHC is value calculated by dividing the Hb by the Hct and is
expressed in grams per deciliter.
RDW is a statistical value describing the coefficient of variation ofthe
MCV
The way to measure erythropoietic response is doing the reticulocyte count. Reticulocyte
count provides a rapid method to differentiate between anemia due to defective production
of RBC and anemia due to decrease survival of RBCs from bleeding or hemolysis
Learning Task:
1. Describe preanalytical factors in hematology test!
2. Describe laboratory examination should be done in hematology disorder!
3. Explain about complete blood count interpretation!
Self assessment:
1. Describe source of biologic variation in hematology test!
2. Explain about the parameter in complete blood count examination!
3. Explain about reticulocyte count and interpretation of the result!
4. Describe interpretation of blood smear evaluation!
DAY 3 (Thursday, Sept 11th 2014)

Lecture 1. Hematopoesis
Sub topic : Leukopoesis
dr. I Wayan Sugiritama, M.Kes
Leukopoiesis is the process by which white blood cells form and develop. Leukopoiesis
result in the formation of cells belonging to the granulocyte and agranulocyte series.
Granulocyte includes neutrophil, basophil and eosinophil, whereas Agranulocytes include
lymphocytes and monocytes.
Granulocytopoiesis
Eosinophil, Basophil and Neutrophil are derive from unipotential stem cell ,respectively,
CFU-Eo, CFU-Ba, and CFU-G. Each of these stem cells is descendant of pluripotential
stem cell CFU-S. Thus, CFU-Eo, CFU-Ba and CFU-G undergo mitosis giving rise to
myoblasts. Myoblast undergo mitosis giving rise to promyelocytes, which in turn divide to
form myelocytes. On this step the specific granules are present and three granulocyte lines
may be recognized. The subsequent stage of maturation is metamylocyte then to the
granulocyte with a band-shaped nucleus, and finally to the mature granulocyte (neutrophil,
eosinophil, and basophil).
Monocytopoiesis
21

Clinical Oncology
Monocyte is derive from the bipotential stem cell, CFU-GM, whose undergoes mitosis and
gives rise to two unipotential stem cells, CFU-G and CFU-M (monoblasts). The next stage
of maturation is promonocytes and finally to the mature monocyte. Every day, the
average adult forms more than 1010 monocytes, most of which enter the circulation. Within a
day or two, the newly formed monocytes enter the connective tissue spaces of the body and
differentiate into macrophages.
Lymphopoiesis
The multipotential stem cell CFU-Ly divides in the bone marrow to form the two unipotential
progenitor cells, CFU-Ly B and CFU-Ly T, neither of which is immunocompetent. CFU-LyB
migrates to a bursa-equivalent location in the bone marrow, divides several times and
giving rise to immunocompetent B lymphocytes. CFU-lyT cells undergo mitosis, forming
immunocompetent T cells, which travel to the cortex of thymus. On thymus CFU-lyT
proliferate, mature and begin to express cell surface markers. As these surface markers
appear on T-cell plasmalemma, the cell become immunocompetent T lymphocytes.
Learning Tasks :
1. Explain the classification, structure and function of leucocyte !
2. Explain the formation of the leucocytes!
3. Explain the regulation of the leucocytes formation!
4. Explain the maturation of lymphocyte!
5. Discuss in your group the definition, sign and symptom, causes, diagnosis and
treatment of the agranulositosis!
6. Discuss in your group the abnormality of leucocyte formation!
Self Assessment :
1. Describe the structure of the leucocytes !
2. Describe the Granulocytopoiesis, Monocytopoiesis, and Lymphopoiesis !
Sub topic:Thrombopoesis
dr. Sianny Herawati, Sp.PK

Learning Task:
1. Describe about trombopoiesis
2. Describe about the mechanism of platelet release.
3. Describe about thrombocyte maturation
4. Describe regulation of trombopoiesis
Self assessment:
1. Explain the characteristics of the thrombocyte
2. Explain about thrombopoietin
3. Explain the ultrastructural of thrombocyte
4. Explain the characteristics of megakaryocyte
5. Explain role of the spleen in platelet production.
6. Explain platelet life span and turnover of platelet
DAY 4 (Friday, Sept 12th 2014
22

Clinical Oncology
Sub topic : Erythropoesis
dr. NI Kadek Mulyantari, Sp.PK(K)

ABSTRACT
Under physiologic condition, the red-cell mass is maintained in equilibrium by appropriate
adjustments of red-cell production. The erythropoiesis results from the action of
erythropoietin on colony-forming unit erythroid (CFUe). Erythropoietin is produce by the
action of renal erythropoietic factor (REF), which is derived from the kidneys under the
secondary influence of hypoxic condition.
In vivo, the mature erythrocyte is a biconcave disk with a surfact-to-volume ratio that
enables optimal gaseous interchange. The cells also is deformed easily and, consequently,
can pass through small vessels and capillary without rupture.
The re-cells membrane is composed of matrix formed from a double layer of phospholipids.
The main fuction of red-cells membrane are to maintain cell-shape deformability for osmotic
balance between plasma and cell cytoplasm, to help in the tranfostation of essential cellular
ions and gases.
Maturation entails changes in the nucleus and the cytoplasm of cells. As maturation
progress, the nuclei became smaller, and their structure becomes denser and more coarse.
Normal red-cell maturation : Pronormoblast (rubriblast)- Basophilic normoblast
Polychromatic normoblast Orthochromatic normoblast reticulocyte mature erythrocyte.
The average life of a red cell approximates 120 days, and fewer than 2 % of the circulating
cells are newly produce and released from the bone marrowas reticulocytes.
Learning Tasks :
1. Explain the erythropoesis process and normal red-cell maturation!
2. What is the erythrocyte function?
3. Mention the nutritional requirement of erythropoesis process !
4. In normal condition, what kind of erythrocytes series can we find in peripheral blood
and in bone marrow?
5. Describe the structure of erythrocyte if lack of this nutrient : vitamin B12 and iron
during the erythrocytopoesis!
Self Assesment :
1. Understand the erythropoesis process and normal red-cell maturation.
2. Understand the erythrocyte function
3. Understand about the factors that influence of erythropoesis process
Sub topic : Synthesis of hemoglobin, function of
blood and blood cells metabolism
Prof. dr. Nyoman Agus Bagiada,SpBiok
23

Clinical Oncology
Case 1.
Women patient 35 years old, visiting her family physician complaining tired and feeling weak
after delivery one week ago. The baby weight 4 kg. She got 5 stitches on perineum.
Physical examination showed that the heart rate 100 x/mint, and face pale. The breathing
frequency 30 x/mint. Blood examination found Hb 7 mg% and haematocrite 35 %
Learning task
1. What happenedin this patient?
2. What is the cause?
3. Why she feel weak and tired?
4. What is the normal value of women Hb and haematocrite?
5. Why the heart rate and breathing rate increase?
6. What is 2,3 BPG. What is the function?
7. What happen when some one come to high altitude?
8. How many kind of Hb do you know and what are difference?
Self Assessment
1. Define the normal value of whole blood in man and women
2. Define the complete blood function
3. How Hb are synthesize an degradation
4. What are the iron function in Hb
5. What is the similar and the difference of Hb and Mb
DAY 5 (Monday sept, 15th 2014)

Lecture 1. Anemia
Sub topic : Pathophysiologi and Classification
of anemia
Dr. Ketut Ariawati, SpA (K)
Anemia is extremely common medical condition that all physicians must address in clinical
practice. The diagnostic approach to anemia is based on an understanding of the disease
mechanisms that lead to it. Important clues to the cause of anemia may be obtained from
the patients history, laboratory studies, and an examination of the peripheral blood smear.
A. Anemia is best defined and monitored by measurement of the hemoglobin (Hb)
concentration. The normal range for Hb is established by measuring the values from a
large sample of healthy individuals and varies as a function of age and gender
1. Males and females have equivalent Hb values until puberty.
24

Clinical Oncology
2. The increase in Hb that occurs in men is largely attributed to the effect of
androgens on the release of erythropoietin (EPO) and the responsiveness of red
blood cell (RBC) precursors to EPO.
3. The gender disparity in the normal range for Hb concentration is less significant in
elderly individuals.
B. Anemia is defined as Hb concentration more than to standard deviations below the
normal range for age and gender. Using this definition, there is less than a 5% chance
that a Hb concentration below the normal range is a normal value for the individual.
Worldwide, almost one-third of the population is anemic.
The first step in diagnosis of anemia is to establish whether the abnormality is isolated to a
single cell line (red blood cells only) or whether it is part of a multiple cell line abnormality
(red cells, white cells and platelets). Abnormalities of to or three cell lines usually indicate
one of the following :
bone marrow involvement, (e.g., aplastic anemia, leukemia), or
an immunologic disorder (e.g., connective tissue disease or immunoneutropenia,
idiopathic thrombocytopenic purpura [ITP] or immune hemolytic anemia singly or in
combination) or
sequestration of cells (e.g., hypersplenism).
The blood smear is very helpful in the diagnosis of anemia. It establishes whether the
anemia is hypochromic, microcytic, normocytic, macrocytic or show spezcific morphologic
abnormalities suggestive of red cell membrane disorders (e.g., spherocytes, stomatocytosis
or elliptocytosis) or hemoglobinopathies (e.g., sickle cell disease, thalassemia).
The mean corpuscular volume (MCV) confirms the findings on the smear with reference to
the red cell size, e.g., microcytic (<70 fl), macrocytic (>85 fl) or normocytic (72-79 fl). The
mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration
(MCHC) are calculated values and generally of less diagnostic.
Learning task
Patient of 2 years, girl with pale since 2 month ago, without fever and bleeding. Hemoglobin
level is 6 g/dL, MCV is 68 fl.
Answer the following question :
1. Discuss what are steps you can perform on this patient (anamnesis, physical
examination, other laboratorium).
2. What the differential diagnosis of this patient ?
Self Assessment
a. Defined of anemia !
b. Describe the classification of anemia based on etiologi !
c. What is the differential diagnosis of patients microcytic anemia ?
d. What is the differential diagnosis of patients normocytic anemia ?
e. Give the differential diagnosis of macrocytic anemia !
f. Describe of historical factors of importance in evaluating patients with anemia
25

Clinical Oncology
Lecture 2. POLISITEMIA
Learning task
1. What is definition of polisitemia?
2. Explain the pathophysiology of polisitemia?
3. Mention the sign and symptom of polisitemia!
4. What are laboratory finding in polisitemia?
DAY 6 (Tuesday, Sept 16th 2014)

Nutritional Anemia
Sub topic General Information Nutritional Anemia
Sub topic Patofisiology of Iron Deficiency Anemia
Dr.dr. Ketut Suega, SpPD KHOM
Learning task
A 56 years old male, come with chief complain palpitation and feel very weak. Several days
ago, he frequently had his stool with black color. He also suffered from nausea, vomiting,
and pain on epigastrial. Laboratory findings are : Hb 7,6 gr/dl, MCV 72 fl, MCH 25 pg ,
MCHC 28%, SI< 50 ng/dl, TIBC 525 ng/ Dl. Physical examination found with angular
cheilitis, liver and spleen without any abnormality.
1. What is the type of anemia the patient suffered from?

2. Explain how is the patomechanism of the case above!
Self Asessment
1. Understand the iron metabolism in the body
2. Understand the absorbtion of the iron in the body
3. Understand the function and cycle of iron in the body
NutritionalSept
Anemia
DAY 7 (Wednesday,
17th 2014)
The diagnostic of iron deficiency anemia
Dr.dr. Ketut Suega, SpPD-KHOM
26

Clinical Oncology
Learning Task
A 56 years old male, come with chief complain palpitation and feel very weak. Several days
ago, he frequently had his stool with black color. He also suffered from nausea, vomiting,
and pain on epigastrial. Laboratory findings are : Hb 7,6 gr/dl, MCV 72 fl, MCH 25 pg ,
MCHC 28%, SI < 50 ng/dl, TIBC 525 ng/ Dl. Physical examination found with angular
cheilitis, liver and spleen without any abnormality.
1. What are the supporting examinations needed to confirm the dignosis above?
2. Explain the blood smear and bone marrow examinations finding will found at the
patient above!
3. What is the other possibility diagnosis of the case? Explain your answer!
4. What are the possible etiology caused the anemic condition of the case?
Self Asessment
1. Understand clinical manifestation of IDA
2. Understand the way to make diagnosis of IDA
3. Understand how to prevent the IDA
DAY 8 (Thursday, Sept 18th 2014)

Nutritional Anemia
Sub topic Pathophysiology and management diagnostic of
folic acid
and B12 deficiency anemia
Sub topic The diagnostic of folic acid and B12 deficiency
anemia
Dr. Ni Made Renny Anggreni Rena, SpPD
ABSTRACT
The macrocytic anemias are a morphological classification of anemias that have an
MCV of greater than 100 fL. Broadly defined, the macrocytic anemias are divided into two
categories megaloblastic and nonmegaloblastic processes. If the source of the anemia is a
vitamin B12 or folic acid deficiency, the anemia is termed megaloblastic. If the source of the
anemia is unrelated to a nutritional deficiency, the anemia is macrocytic but not
megaloblastic.
Vitamin B12 or folic acid deficiency leads to impaired DNA synthesis, a serious
condition, and will affect all readily dividing cells, skin cells, hematopoietic cells, and
epithelial cells. The effects on the bone marrow, peripheral smear, and the patients quality
of life are dramatic and substantive.
27

Clinical Oncology
The megaloblastic anemias show striking similarities in their clinical and
hematological presentations. Several tests are used to confirmed the diagnostic of B12 or
folic acid deficiency anemia. They include serum B12, folic acid, or red cell folate
determination by radioimmunoassay.
Learning Task
1. How is the metabolism of B12 and folic acid in the body?
2. Explain the possible etiology of B12 and folic acid deficiency anemia!
3. Explain the way of diagnostic B12 and folic acid deficiency anemia!
Self Assessment
1. Understand the metabolism of B12 and folic acid in the body.
2. Mention the etiology of B12 and folic acid deficiency anemia.
3. Mention the clinical presentation of B12 and folic acid deficiency anemia.
4. Understand the laboratorium examinations that supporting thr diagnostic of B12 and
folic acid deficiency anemia.
DAY 9 (Friday, Sept 19 th 2014)

Acute Leukemia
Subtopic AML, ALL
dr. AA Widnyana, SpA
Abstract
Acute leukemia is defined as the malignant accumulation of transformed hematopoietic
progenitor cells. Leukemic blast cells retain the capability of self renewal, but unlike normal
hematopoietic stem cells (HSCs), they have limited or no potential for terminal
differentiation. Leukemic infiltration of the marrow space ultimately leads to bone marrow
failure, so most patient present with consequences of cytopenias. The acute leukemias can
be classified by morphology, histochemical staining, and immunophenotype into two broad
category : acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL). The
distinction between the two acute leukemias in clinically important because the treatments
and prognoses are different.
Learning Task
Kadek, six years old girl came to pediatric emergency at Sanglah Hospital with cheap
complaint pale, hematoma at femur, gum bleeding, limfadenopati and hepatosplenomegali.
Doctors at hospital do examination CBC.
Lab data : Erythrocyte and hemoglobin count are below normal
Leucocyte total count 85 x 109 /L
Leucocyte distribution on differential count is as follows
Blast form
86 %
Prolymphocyte
5%
Lymphocyte
9%
Platelet count is very low
Answer the following questions
1. What diagnosis is most likely for this case ?
28

Clinical Oncology
2. What additional test can be performed ?
3. What is the prognosis of the case ?
Self Assessment
1. What are the symptoms and sign of acute leukemia ?
2. Do you know the general classification for leukemia ?
3. When would it be suitable to forward a leukemia patient?
Learning Task
1. How do you define malignant hematology?
2. Name the types of malignant hematology
3. What are the prognostic factors for acute myeloblastic leukemia?
4. Outline the classification for acute myeloblastic leukemia
5. Explain the principles for treating acute myeloblastic leukemia.
How would you educate an acute myeloblastic leukemia patient?
DAY 10 (Monday, Sept 22 th 2014)

Lecture 1. Nutritional Anemia
Sub topic :Management therapy of iron deficiency,
Sub topic : Management therapy of Folic acid and Vit B12 Deficiency
Drs. I Made Adioka , Apt, M.Si
Learning task:
1 Describe the normal mechanism of regulation of iron absorption in the body
2. Describe the normal mechanism of regulation of iron storage in the body
3. Describe the acute and chronic toxicity of iron
4. Sketch and explain the enzymatic reaction that use folates
5. Describe the clinical applications of vitamin B12 and folic acid
Self assessment
1. Explain role of iron in the body
2. Describe the clinical applications of iron
3. Whey iron should not given in hemolytic anemia?
4. Explain role of vitamin B12 and folic acid in the body
DAY 11 (Tuesday, Sept 23th, 2014)

Aplastic Anemia & Anemia of Chronic
Diseases
29

Clinical Oncology
Aplastic Anemia
Abstract
Aplastic anemia is one type of anemia with incidence worldwide is 2 to 5 cases/million
population per year in industrial countries. Characterized by pancytopenia and markedly
hypocelluler marrow. The pathogenesis underlying anemia aplastic could be an immune
suppression of marrow, toxic injury to stem and / or progenitor cells, and inherited instrinsic
stem cell defect. Clinical features of aplastic anemia shown anemic syndrome, bleeding or
infection as a consequences of cytopenias. Supporting examination recommended are
complete blood count, and bone marrow aspiration.
Learning Task
:
1. A 23 years old woman gives a 3 month history of progressively increasing tiredness
with bruising, malaise and menorrhagia. On examination she is anemic and has
multiple bruises. A full blood count shows HGB 6.9 g/dL, WBC 1.1 x 10 9/l (ANC 0.3 x
109/l), platelets 17 x 109/l). Her chest X ray shows pneumonia.
a. What further investigations should be undertaken?
b. What are the possibility diagnostic for this patient?
c. What seems to be the cause of this case?
Self Assessment
:
1. Explain about the principles of pathogenesis of aplastic anemias.
2. Mention the type of aplastic anemias.
3. Mention the clinical manifestation and laboratory findings in Aplastic Anemia
Anemia of Chronic Disease
Abstract
Anemia associated with chronic infection, inflammatory disease or neoplasma disease. One
or two months of sustained disease is required for anemia develop.
Anemia is moderate, with a hemoglobin level between 7 and 11 g/dl and rarely symtomatik.
Common feature include:
- Low level of iron level
- Low serum total iron-binding capacity
- Increased morrow iron stores
- Modestly shortened red cell life span
- Reduced rate of red cell production
The cause of the anemia of chronic disease is multifactorial and includes a mildly decreased
life span of erythrocytes coupled with deregulation iron absorption and transport, a direct
inhoibition of hematopoiesis and a relative deficiency of erythropoietin. Research over past
decade has delineated the important role of inflammatory cytokines in each of these causes
and the emerging role of the iron regulator hepcidin in the patogenesis of ACD.
No treatment my be necessary. Iron (by mouth or parenterally) is contraindicated. Paced red
cell transfusion my be given, if the anemia is symptomatic. Recambinant human
erythropoietin therapy is efeective if serum EPO is low.
Male, 40 years old come to clinic with complain: Cough since 1 years ago. There are
phlegm and blood cough. Cough companied by fever and decrease of body weight 5 kg in
30

Clinical Oncology
six months. Physical examination: Blood pressure 110/80 mmHg, Pulse rate 98 x/mint, T
37,50C. Chest x-ray: support lung tuberculosis. Laboratory result WBC 12.10 3/mm3, Hb 8,5
g/dl, MCV 75, MCH 26 dan PLT 440.103/mm3.
Learning task:
1. Explain the patient problema!
2. What are diagnosis?
3. Explain the mechanism of anemia in this case!
4. Explain the patient management!
Self assessment:
1. Describe the sign and symptom of ACD
2. Explain the pathophysiology of ACD
3. Mention the kinds of test for ACD
4. Explain the patient management
DAY 12 (Wednesday, Sep, 24th 2014)

Platelet function and disorder
Sub topic trombositosis
Sub topic trombositopenia
DR Dr Ketut Suega,SpPD-KHOM
Dr Ni Made Renny Anggreni Rena,SpPD
ABSTRACT
Platelets are produced in the bone marrow by fragmentation of the cytoplasm of
megakaryocytes, one of the largest cells in the body. The main function of platelets is the
formation of mechanical plugs during the normal haemostatic response to vascular injury. In
the absence of platelets, spontaneous leakage of blood through small vessels may occur.
Thrombocythemia or thrombocytosis is present if the platelets are constantly
elevated to more than 600,000/L. Thrombocytosis can occur as primary which is the rarest
part of myeloproliferative disease called Essential Thrombocytosis (ET), while the
secondary, occurs as a reactive thrombocytosis is, in most cases, self-limited and occurs
after a major blood loss, after surgery, after splenectomy, or it may be paraneoplastic in
some cases.
Thrombocytopenia, by definition, exists when the platelet count drops below normal
limit. It is possibly due either to decreased bone marrow production of platelets or increased
destruction and sequestration of the platelets from the circulation, or both.
Learning Task
1. Learn how to differentiate the primary and secondary thrombocytosis?
2. What are the possible etiology caused the primary and secondary thrombocytosis?
3. How to classify the thrombocytopenia due to its cause?
4. How to diagnose and to treat an ITP patient?
Self Assessment
1. Understand the primary and secondary thrombocytosis.
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Clinical Oncology
2. Understand the etiology of thrombocytopenia.
3. Describe the clinical manifestation and how to confirm diagnosis and to treat ITP.
DAY 13 (Thursday, Sep, 25th 2014llllll)

Hemostasis
Sub topic Principle of hemostasis
Sub topic DIC, APS
DR Dr Ketut Suega,SpPD-KHOM
ABSTRACT
Cellular systems and biochemical processes related to the bleeding prevention or
blood coagulation mechanism of humans are very complex. The syntheses of the influential
components (proteins, cells and blood vessels) constantly interact in balance so as to make
sure that neither bleeding nor coagulation happen within the blood vessels throughout life.
In this opportunity we will discuss approaches to patients with bleeding and those
with abnormal blood coagulation as well as several situations that may happen to the
patient as the result of the process disorders.
Learning Task
1. Learn how to make diagnosis and treat DIC patient
Case Study
A patient with decrease of consciousness after had snake bite. He got hematome in the
bitten area and abdomen. He also had red color of urine.
1.
2.
3.
4.
Explain what are clinical features supporting DIC on that case!

What kinds of laboratory test are needed for the diagnosis?
How to manage this patient? Explain your answer!
What is Consumptive coagulopathy? Explain your answer!
Self Assessment
1. Understand the principle of hemostasis
2. Describe the possible etiology, clinical features, laboratory findings of DIC
3. Mention the clinical features, laboratory findings of APS
DAY 14 (Friday, Sep 26th 2014)
32

Clinical Oncology
Lecture 1. Hemofilia
Dr AA Widnyana,SpA
Learning Task
Bayu, A seven years old man came to the pediatric emergrncy at Sanglah Hospital with
hematoma at hand and femur with diameter 7 cm x 5 cm , 4 cm x 4 cm. Hematoma
disappear after trauma four days ago. What do you do to diagnosis the patiens ?
( anamnesis, physical examination, laboratory evaluation )
Self Assessment
1. How the patterns of clinical bleeding in disorders of hemostasis ( primary hemostasis
and secondary hemostasis ) ?
2. What the bleeding manifestation in hemophilia ?
3. Classify hemophilia A and B according to the degree of severity ?
Lecture 2. Von Willebrands disease

ABSTRACT
Von Willebrands Disease (VWD) is a bleeding disorder inherited in an autosomal
dominant, characterized by an abnormal platelet adhesion with or without a low factor VIII
activity. VWF promotes platelet adhesion and is also the carrier for factor VIII, protecting the
latter from premature destruction. This explains the combination of defective platelet
adhesion and reduced levels of factor VIII. There are varies of VWD, from mild to severe
type. Several supporting examinations needed to confirmed the diagnostic of VWD.
Learning Task
1. Learn how the pathophysiology of VWD.
2. How is the clinical manifestation and type of VWD?
3. What are the laboratory evaluation needed as a diagnostic tools for VWD?
Self Assessment
1.
2.
3.
Describe the pathophysiology and classification of von Willebrand disease!

Describe the bleeding manifestation in von Willebrand diasease!
Understand the laboratory examination support the VWD.
DAY 15 (Monday, Sep 29th 2014)

Malignan Lymphoma and Diagnostic Pathology
33

Clinical Oncology

dr. Ni Putu Ekawati,M.Repro, Sp.A
Learning Task :
Case
An 8-year-old female with lymph node enlargement of right neck region. The nodes are
confluent, without tenderness or redness of the skin above the nodes. There are also fever,
weight loss, pruritus and pain. Complete blood test results are within normal limit. Chest xray shows enlargement of mediastinal nodes.
Answer the following questions:
1.
What diagnosis is most possible for this case?
2.
What additional test can be performed to support the diagnosis?
3.
What is the prognosis of the case?
Self assessment :
1. Mention the base of classification of lymphoid malignancies and what are the
purposes of the classification
2. Why Hodgkin lymphoma is a distinct entity
3. Mention the clinical differences between HL and NHL
4. Mention the Ann Arbor staging system of Lymphoma
5. Mention the grouping lymphomas by clinical behavior
DAY 16 ( Tuesday, Sept 30th 2014)

Lecture 1. Hemolytic Anemia
Sub topic Congenital hemolytic anemia, hemoglobinopati
Dr. Ketut Ariawati, SpA(K)
Abstract
Congenital hemolytic anemias result from mutations that quantitatively or qualitatively
influence the function of red vlood cell proteins. These mutations can be broadly grouped
into three categories : membrane defects, enzymatic defects, and hemoglobin defects.
While many mutations have been described in each category, only a small number are
commonly encountered in clinical practice.
Clinical findings and specialized laboratory studies are often required to precisely define the
underlying disease process. This general approach is true especially in the case of
congenital hemolyitic anemias :
In all patients with hemolytic anemia, a careful history and physical examination are
important.
1. The history should explore the chronicity of the problem, ethnic and racial
background, family history, underlying or associated medical conditions, and new
medications.
34

Clinical Oncology
2. Jaundice is a common finding. Splenomegaly may also be associated with a wide
variety of hemolytic disorders.
Various laboratory abnormalities are associated with hemolysis.
1. An elevated reticulocyte index is typical , consistent with a compensatory bone
marrow response to anemia. Bone marrow examination is not necessary for most
patients.
2. Increased lactate dehydrogenase, uncojugted bilirubin, and depressed or absent
haptoglobin are also observed with hemolysis.
3. The red blood cell (RBC) morphology is frequently abnormal and provides an
important clue to the underlying disease process.
4. The peripheral blood smear is rarely pathognomic.
Learning task
Patients of 2 years, male with pale since 2 month ago, not history of bleeding, and fever.
The abdominal became more bigger since 1 months. History of transfusion six month ago
because pale. Hemoglobin level is 3 g/dL, MCV is 68 fl, reticulocyte is 3%.
Answer the following questions :
1. Would you like to explain what kind the abnormalities in patient above.
2. What the laboratorium test you need to confirm this disease ?
3. What the differential diagnosis in patient above ?
Self assessment
1. Describe classification of congenital hemolytic anemia.
2. Explain clinical presentation and laboratory evaluation of congenital hemolytic
anemias
3. Explain the principle management of congenital hemolytic anemias
Lecture 2. Hemolytic Anemia

Sub topic Acquired hemolytic anemia
Abstract :
Hemolytic anemias result from a shortened red blood cells (RBC) survival rate as a
result of an increased rate of RBC destruction. Hemolytic disorders are generally limited to
conditions in which the rate of RBC destruction is increased while the ability of the bone
marrow to respond to the anemia remains intact. Bone marrow can increase its production
rate 6-8 times normal; therefore, hemolytic disordes can be present in the absence of
anemia. When bone marrow erythropoesis cannoyt keep up with the shortened length of
RBC survival, hemolytic anemia result.
Learning Task :
1. Young female come with complain of yellowish eyes, feeling weak and dizzy since
around 3 days before admitted to hospital. On physical examination found icteric on
eyes, and pale on hand and foot. Patient without history of bleeding before.
35

Clinical Oncology
Laboratory results HGB 8.3 mg/dL, Leukosit 5900/mm3, thrombocyte 410.000/mm3
Total bilirubin 4.5, Indirect Bilirubin 3.5, and Coombs test positive.
a. Mention the possibility diagnostic of the case above.
b. Mention the examination supporting diagnostic.
Self Assessment :
1. Explain about the principles of hemolytic anemias.
2. Mention the type of hemolytic anemias.
3. Mention the clinical manifestation and laboratory findings in Acquired Hemolytic
anemia
DAY 17 (Wednesday, Oct 1st 2014)

Blood transfusion and
Blood banking
Dr. Ni Kadek Mulyantari, Sp.PK(K)
Abstract
1. Criteria for acceptability of blood donors are established to protect the health of
donor and recipient
2. Blood donations are processed into components
3. Stored blood components undergo changes that can influence the efectiveness of
transfusion
4. Routine pretransfusion testing should be done before the transfusion
5. In unexpected RBC ab are found, the antigen specifisity is determined and antigen
neg RBC are provide
6. Transfusion is generally be safe but can result in adverse out come
7. The reactions can be mild clinical effects
8. More serious reaction wich are un common include, hemolysis, bacterial
contamination, anaphylaxis and TRALI
9. Serious transusion-transmitted diseases are now rare due to progress in donor
screening and testing how ever hepatitis and HIVare still possible
Learning task
1. Why the FDA establish the criteria for acceptability of the blood donor?
2. What are we doing to reduce the incidence of transfusion-transmitted diseases?
3. Although we are already make a good laboratory screening to the blood for
transfusion, but the blood is still not 100% safe, why?
4. What is the benefit of using blood component?
5. Is using whole blood really not good? Please give your explanations?
Self Assessment
1. Characteristic of blood donations
2. Components of blood
3. Indications of transfusion
4. Complications of transfusion
CASE STUDY
One patients foreigner was hospitalezed in sanglah. Hospitalized because of anemia, she
was bleeding while having a baby and need blood transfusion.
1. What kind of information you need before you ask some blood to the Blood Bank?
36

Clinical Oncology
2. If you work in the Blood Bank, what will you do?
3. If you know that the patients blood type was AB Rh positif and the AB blood is empty
in the Blood Bank, what will you do?
4. What is your advice to the clinician?
5. Two day latter the patient need some more blood and in the Blood Bank the AB
blood type was allready available. If you are clinician what is your decision use the
AB blood or still asking the same blood type as before? Give your explanation!
DAY 18 (Thursday, Oct 2nd 2014)

Lecture 1. Multiple myeloma
Dr. Losen Adnyana, SpPD KHOM
Multiple meyloma is characterized by the proliferation and accumulation of clonal plasma

cells. The presence of somatic mutations in the complementarity determining regions (the
antigen-binding portion) of the clonal immunoglobulin indicates the transforming event
occurred in a postgerminal center B cell or a plasma cell itself.
The commonest chromosomal abnormality involves the heavy chain locus on chromosome
14, but there is no single cytogenetic abnormality that is characteristic of the disease.
Chromosome 13 abnormalities are also common and are associated with poor prognosis.
At the gene-expression level, monoclonal gammopathy of unknown significance (MGUS)
cannot be distinguished from multiple myeloma. However, normal plasma cells can be
clearly distinguished from plasma cells of both MGUS and myeloma. The clinical features of
the disease result from bene marrow infiltration by the malignant clone, secretion of
osteoclast-activating factors and cytokines, high levels of circulating immunoglobulin and/
or free light chains, and depressed immunity.
The most common presenting symptom is bone pain, present in 60% of patients, especially
in the back or chest. Weakness and fatigue are common and are often associated with a
normochromic, normocytic anemia. Twenty-five percent of patients have renal insufficiency,
and 20% of patients have hypercalcemia. Less than 5% of patients have clinically significant
amyloidosis or hyperviscosity.
Not all patients who fulfill the minimal criteria for the diagnosis of multiple myeloma require
treatment. More specifically, patients with SMM or asymptomatic stage I multiple myeloma
often remain stable for many years, and treatment has not been shown to prolong survival
or to prevent progression in presymptomatic disease.
The main options include conventonal chemotherapy, high-dose corticosteroids, doseintensive chemotherapy with autologous hematopoietic cell rescue (6,7), allogeneic stem
cell transplantation, as well as never therapies such as thalidomide or its analogs and the
protesome inhibitor bortezomib. Bisphosphonate treatments can prevent or slow bone
destruction and may also have antitumor activity.
No treatment modality with the possible exception of allogeneic stem cell transplantation is
curative in multiple myeloma. However, event-freee survival and overall survival are
imporoved by approximately a year following autologous hematopoietic stem cell
transplantation (HSCT) as compared with conventional chemotherapy, and newer agents
such as thalidomide and bortezemib are effective in a significant percentage of patients with
this relapsed or refractory disease. The management of myeloma has become more
complicated with this expanding set of therapeutic alternatives, but the lack of overlapping
toxicities means that many patients even with advanced disease can be managed
effectively as outpatients with reasonable quality of life. Survival from diagnosis has
increased significantly over the past decade, particularly in patients under age 60, because
of the activity of these new treatment modalities.
37

Clinical Oncology
Case
Female 67 years old come with pain on vertebra since 2 years ago and she also complain
about body weakness and dizziness. Pyshical examination BP 150/90 mmHg, PR 108
x/menit, Tax 38 oC. Palpebra: Paleness. Laboratory result: WBC 15.10 3/mm3, Hb 8,4 gr/dl,
PLT 100.103/mm3, BUN 78 mg/dl, creatinin 4 mg/dl. Bone survey : lesi osteolitik multipel in
vertebre
Learning task
1. Make the problem list for the patient!
2. What is diagnose fo the patient?
3. What kind of test should we do?
4. Base on the data, Explain the stage of this disease?!
5. Explain the patient management!?
Self asessment
1. Understand the sign and symptom Multiple myeloma
2. Understand the pathogenesis of Multiple myeloma.
3. Understand about how to diagnose Multiple myeloma.
4. Understand about the management of Multiple myeloma.
Lecture 2. MDS, Langerhans cell tumor

dr. Losen Adnyana,SpPD
Abstract
Myelodysplasia is the term used to encompass a diverse group of neoplasms that have in
common their origin in somatic mutation in multipotential hematopoietic cell. Characterized
by ineffective hematopoiesis, cytopenias, qualitative disorders of blood cells and their
precursors and variable predilection to evolve into acute myelogenous leukemia. Spectrum
disease ranges from indolent mild to moderate anemia to more troublesome multycytopenia
with hypercelluler marrow.
The fundamental alteration is a somatic mutations in a multipotential hematopoietic
cell resulting in trilineage blood cell abnormalities in most cases. Exposure to benzene,
chemotherapeutic agents (especially alkylating agent) or high dose radiation can cause
myelodysplastic disoerder as well as acute myelogenous leukemia.
Onset is usually after age 50 years but it may be seen in children. In younger
adults, it is often preceded by chemotherapy or irradiation. May be asymptomatic if mild
anemia and small changes in platelet and white cell counts. If moderate or severe anemia
and or granulocytopenia and thrombocytopenia develop, pallor, dysneu on exertion, easy
bruising.
Anemia occur more than 85% and my be macrocytic with circulating nucleated blast.
Netropenia occurs in about 50%, coarse chromatin, nuclear hyposegmentation, and
decreased cytoplasmic granulation of neutrophils commonly occur. Morrow abnormalities
include hypercellularity, delayed nuclear maturation, pathologic sideroblast, megakaryocytes
with uni- or bolobed nuclei, mycromegakaryocytes and increased number of myeloblast.
Chromosomal abnormalities occur in up to 80% patients. Commonly abnormalities very
similar to those in AML.
Treatment of patient with MDS remains challenging fort several reason. First, patient
with this disorder are likely to be enderly, so comorbid disease and performance status are
critical components in deciding specific therapy. Second, the disease is heterogenous,
38

Clinical Oncology
marking therapies on one type of MDS less optimal than the others. Given lack of precise
pathophysiologic understanding of more than few MDS subtypes, designing truly targeted
therapies is impossible.
Female, 65 years old came with body weakness and headache. Pyshical examination BP
110/80 mmHg, PR 108 x/menut, T 38,5 0C, mild hepatosplenomegali +. Laboratory result:
WBC 2.103/mm3, Hb 8,5 g/dl, MCV 75, MCH 26 dan PLT 40.103/mm3.
Learning task
1. Make the problem list for the patient!
2. What is diagnose fo the patient?
3. What kind of test should we do?
4. Base on the data, Explain the stage of this disease?!
5. Explain the patient management!?
Self asessment
1. Understand the sign and symptom MDS
2. Understand the pathogenesis of MDS.
3. Understand about how to diagnose MDS
4. Understand about the management of MDS
.
DAY 19 (Friday, Oct 3th 2014)

Lecture 1. Chronic Leukemia
Subtopic CLL, CML
CLL
Abstract:
Chronic Lymphocytic Leukemia is a neoplastic disease characterized by
accumulation of small, mature lymphocytes in blood, marrow and lymphoid tissues. The
incidence of about 3 per 100.000 population in the United States and become most
commonly adult leukemia in Western societies. Hereditary factors, genetic and
immunoglobulin abnormalities play a role in CLL. Ninety percent of patients are over age 50
years. Twenty five percent are asymptomatic, and others with lymph node enlargement.
Examination supported the diagnosis are blood examination, marrow biopsy and lymph
node biopsy.
Learning Task :
1. A 40 yo Balinesse male has bilateral axillary lymphadenopathy. He has a 3-4
week history of gradually increasing weakness and stiffness of both legs, with
lack of sensation. His full blood count show : HGB 11.1 g/dL, WBC 39 x 10 9/,
platelets 91 x 109/l). Biochemical analysis shows : Urea 13 mmol/l, Na+ 142
mmol/l, K+ 5.5 mmol/l, Ca2+ 3.15 mmol/l.
a. What further tests would you do?
b. What is the diagnosis and treatment for this case?
Self Assessment
39

Clinical Oncology
1. Describe the clinical presentation of CLL
2. Describe the hematology manifestation of CLL
3. Mention how to diagnose CLL
CML
Abstract
CML is a hematopoietic malignancy originating from transformation of primitive
hematopoietic cell. CML progresses from an initial chronic phase characterized by marrow
hyperplasia and increased numbers of circulating differentiated myeloid cells followed by
advanced phases of disease (accelerated phase and blast crisis) marked by block in
differentiation, accumulation of blasts and depletion of normal hematopoietic cells,
especially white blood cell and platelets.
Exposure to high-dose ionizing radiation increases the incidence of CML with a
mode of increased incidence that ranges 4 to 11 year in different exposed population.
Chemical agents, including cytotoxic drugs have not been established as a couse.
CML is the result of an acquired genetic abnormality that induces a malignant
transformation of single pluripoten lymphohematopoietic cell. CML is generally believed to
develop from transformation of primitive hematopoietic stem cell by the BCR-ABL fusion
gen. The BCR-ABL gen that characterizes CML results from a chromosomal translocation
that results in the fusion of the ABL gene on chromosome 9 and the BCR gene from
chromosome 22.
Approximately 30% of the patients are asymptomatic at the time of diagnosis. The
disease is discovered coincidentally wwhen a blood count is done for medical evaluation.
Symtoms are gradual in onset and may include easy fatigability, malaise, anorexia,
abdominal discomfort and early satiety, weight loss, and excessive sweating. Physical signs
my include pallor, splenomegaly and sternal tenderness.
The hemoglobin concentration is decreased in most patient at the time diagnosis.
The leukocyte count is elevated, usually above 25,000/l and often above 100,000/l.
Platelet count is normal or increased at diagnosis but may increase during the course of
chronic phase. The morrow is markedly hypercelluler, primarily because of granulocytic
hyperplasia.
New treatment options have made it more important to individualize treatment
decision base on the risk category in which a patient reside as judged by patient age, blast
cell, platelet counts, spleen size, whether patient is eligible for allogenic stem cell transplant.
Most of patient have massive expansion and turnover of blood cells with accompanying
hyperuricemia or the risk of hyperuricemia with therapeutic cytoreduction.
Male, 45 years old come to sanglah hospital with complain abdominal enlargement since2
years ago. He also complain pain pressure. Physical examination : spleen S4, liver 3 fingers
below costa margin and 4 cm below procesus xipoideus. Laboratory result WBC
120.103/mm3 dominated by neutrophils, Hb 7,5 g/dl, dan PLT 78.103/mm3.
Learning task:
1. Mention what kind of test should we do?
2. What is the diagnose?
3. What are step to diagnose?
4. What kind of treatment should we give before the patient refer?
Self assessment:
1. Describe the sign and symptom af CML
2. Mention the CML Phase
3. Mention the kind of test for diagnose CML
4. Explain the general management of CML
40

Clinical Oncology
DAY 20 (Monday, Oct 6th 2014)

Epidemiology and screening of cancer
dr. Wayan Sudarsa, SpB Onk
Abstract
Cancer is a major public health problem in the developed countries. Currently, cancer is the
second leading of death after cardiovascular disease. WHO have had established priority
program for cancer control. One of these priority program is Cancer screening, whether
there is a individual or mass screening program.
Screening test is performed on asymptomatic individual to determine that cancer
might be present and that further evaluation is necessary. Many tests have both screening
and diagnostic uses, and it is only the context in which these are used that determines
whether they are screening or diagnostic. A screening test is done on individuals who
receive the test principally because they are of the age or sex at risk for the cancer. A
diagnostic test is done on an individual because of clinical suspicion of disease. Screening
must find disease earlier and lead to an efficacious treatment, so earlier use of the
efficacious treatment must offer better outcome.
The ultimate purpose of cancer screening is to reduce mortality. However, there are
several biases of cancer screening program that can suggest benefit to even the most
astute clinician when there is none. These biases are selection, lead-time, and length bias.
Epidemiology of Cancer
Learning task
a. Explain the main purpose of studying Cancer Epidemiology
b. Explain what you know about Cancer incidence rate, Cancer mortality rate, Relative
Risks and Odds Ratio of cancer
c. Explain why globally, cancer incidents tend to increase.
d. Name five types of cancer most common in the world for men and women
e. based on incidence rate.
f. Name the highest cancer mortality rate in the world for men and women.
g. Name and explain the cancer etiology factors
h. Name and explain the types of epidemiology studies intended to find out about
cancer etiology.
Cancer Screenig and Early Detection
Learning task
Explain what you know about Cancer Screening
a. Explain what is meant by Primary, Secondary, and Tertiary Cancer Preventions
b. What is the main purpose of performing screening for cancer?
c. What conditions are imperative to perform an effective cancer screening program?
d. Explain what is meant by Critical point, Lead Time Bias, and Length time bias
.
e. In cancer screenmg
f. Explain about Pap Test as the screening test for Cervical Cancer
g. Explain about Mammography as the screening test for Breast Cancer
h. Explain about screening program for Colorectal Cancer.
i. Explain about screening program for Prostate Cancer
j. Explain the relationship between smoking and Lung Cancer
k. Explain the relationship between breast cancer and colorectal
l. Explain the relationship between HPV infection and cervical uterine cancer.
m. Explain about Familial Breast Cancer and Familial Colorectal Cancer
41

Clinical Oncology
n. What is meant by Chemoprevention on Cancer, and name some examples.
Self Assessment
a.
b.
c.
d.
e.
f.
Screening for the cancers below have very strong evidence based, except:
Mammography to screen for breast cancer on women above 50.
Thorax: photo to screen for lung cancer
Pap smear to screen for uteri cervix cancer
FOBT to screen for Colorectal Cancer.
Sigmoidoscopy to screen for Colorectal Cancer.
DAY 21 (Tuesday, Oct 7th 2014)

Lecture 1. Molecular Biology and immunology of
cancer
Prof.Dr.dr. I B Tjakra Manuaba, MPH SpB Onk
Molecular Biology of Cancer:
Learning Task
Explain The Following Processes In Relation To Carcinogenesis And Cancer Progression:
1. Cell Signaling
2. Cell Cycle
3. Program Cell Death
4. Angiogenesis
5. Invasion And Metastasis
(Refer To: De Vita: Cancer. Principles And Practice Of Oncology 2008. Part I. Chapter 5-9.
available on CD)
Immunology of Cancer
Learning Task
1.
2.
3.
4.
How Do Tumors Differ From Self Tissues?

Whats The Tumor Associated Antigen And Tumor Specific Antigen?
How Important Is Immune Surveillance Of Cancer?
Whats The Role Of Innate Immunity, Epithelial Immunity, And Tumor Immune
Surveillance?
5. Whats Immune Tolerance And Immune Evasion Of Cancer?
6. How Is The Role Of Regulatory T Cells In Immune Tolerance In Cancer?
7. Can The Immune System Be Manipulated To Overcome Tumor-Induced Tolerance
And Immune Evasion?
(Refer To: Abeloffs Clinical Oncology 2008, Chapter 6. Available on CD).
DAY 22 (Thursday, Oct 9th 2014)

Lecture 1. Management diagnostic, therapy and referal
cancer patient
dr. N Wiadnyana Steven Christian, SpB Onk
42

Clinical Oncology
Abstract
Cancer is often considered to be a difficult and complex field of medicine. Cancer
encompasses over one hundred different malignant diseases, each of which may present in
an early or late stage, and with different tumor characteristics. Most of the patient may come
at the first of his or her visit to the hospital with late stage of disease. Over 1.3 million
individuals in the United State are diagnosed with invasive cancer each year. Currently, 1 in
4 deaths in United State is due to cancer rank second only to heart disease as the leading
cause of mortality.
In generally, there are two important classification of tumors, first is solid tumor and
second is non-solid tumor. This simple classification according to the implementation of
treatment. Solid tumors mostly be treated by surgery and non solid tumors be treated by
medical. Clinical diagnosis of tumor whether malignant or benign is confirmed by various
ways. The procedure of diagnosis is started from anamneses, physical investigation and
followed by imaging and histopathology examination. Anamnesis based on seven sacred or
fundamental four procedures. The right anamnesis and physical examination may lead to
the right management on cancer patient. There are six basic cancer patient management
include (1) Clinical diagnosis completion, (2) Staging establishment, (3) Performance status
determination, (4) Planning therapy, (5) Therapy implementation (6) Follow up.
Cytology and or histo-pathology investigation is one important investigation to
confirm diagnosis of neoplasm. A tissue diagnosis is critical to the care of all cancer
patients. Depending on the type of tumor and its location, the method of biopsy will vary.
Common diagnostic techniques use included needle aspiration biopsy, core needle biopsy,
incisional biopsy and excisional biopsy. Clinical diagnosis of cancer patient is very
important be confirmed quickly. In oncology management no treatment may apply for any
individual patient with cancer before diagnosis confirmed. There are many crucial questions
in focused for diagnosis and treatment of cancer patients such as:
1.
2.
3.
4.
5.
6.
7.
8.
When do I have to be on the alert for a malignant disease?

What can I see?
How do I have to examine the patient?
Which relevant investigations are required?
What are the dos and donts?
What should be my pattern of referral?
What is going to happen to the patient and why?
How to take care of the patient at home?
Oncology is a multidisciplinary area of medicine, which means that several medical

disciplines are involved in the diagnosis, staging and treatment of individual patients with
cancer. This multidisciplinary approach is reflected in cancer education. An Oncology team
usually includes a Surgeon, a Pathologist, a Radiotherapist, and an internist
Chemotherapist, anesthesiologist as well. Surgery is still as the first modality therapy on
solid cancer. Others modalities therapy are chemotherapy, radiotherapy, hormonal therapy,
immunotherapy, targeting therapy. Treatment planning for the individual patient with cancer
depends on tumor factors, patient factors, and doctor factors. There are two goals in
treatment of patient with cancer, one for curative intent and other for non curative intent.
Learning task
Women, 55 year old, with a huge tumor on the left breast. She comes to the hospital, where
you are working. The photograft was shown as below.
43

Clinical Oncology
PLEASE ANSWER AND DISCUSS THESE QUESTIONS AS BELOW

1.
2.
3.
4.
What are the principles of cancer patient management ? Please mention it!
How should diagnosis be done in above patient?
Do you need imaging investigation? Please explain of each imaging if needed!
Explain all things that you observe in physical investigation? Is this breast tumor
malignant or benign? Please give the reason!
5. Do you need cytology or histopathology investigation? Please mention it!
6. How do you communicate to the patient, his family to explain what have you found
and what will you plan to do?
7. What treatment should you suggest to perform?
8. What is the goal of surgery to be expected?
9. What alternative treatment do you suggest, if patient reject surgery?
10. Do you need to refer this patient for further treatment? Where do you want her to
refer?
References
Michael S. Sabel, Oncology. Current Surgical Diagnosis and Treatment, 12
1329-1350
th
Ed. 2006: 46;
Haagedoorn EML, Oldhoff J, Bender W,Clarke W>D, Sleijfer D Th. Essential Oncology for
Health Professional. Van Gorsum, Assen, The Netherlands. 1994
Barry W Feig, Berger H David, Fuhrman George M. The MD Anderson Surgical Oncology.
Handbook. Lippincott Williams and Wilkins. 2006
DAY 23 (Friday, Oct 10th 2014)

Lecture 1. Diagnostic pathology, tumor markers and
staging of cancers
44

Clinical Oncology
Abstract:
Every year the approach to laboratory diagnosis of cancer becomes more complex,
more sophisticated and more specialized. Two conventional methods used are cytologic and
histopathologic examination. The cytologic method is divided into exfoliative cytology (pap
smear, urine, sputum, body fluid, etc.) and non exfoliative cytology (FNA). While
histopathologic method requires sample from excision or biopsy of the lesion. By both
cytologic and histopathologic methods, the pathologists determine malignancy
morphologically. Morphologic sign of malignancy is called anaplasia. Cytologic and
histopathologic diagnosis of cancer is, in most instances, not difficult. Hence they become
the most widely used methods until recently. However, new techniques are being constantly
added to the tools of the surgical pathologist, i.e. immunohistochemistry, flow cytometry and
molecular diagnosis.
Tumor markers are biochemical indicators of the presence of a tumor. They include
cell surface antigens, cytoplasmic proteins, enzymes and hormones. In clinical practice,
however, the term usually refers to a molecule that can be detected in plasma or other body
fluid. Some examples of tumor markers are CEA, AFP, PSA, etc.
Prognosis of cancer disease depends on grading and staging. Grading of a cancer is
based on the degree of differentiation of the tumor cells and the number of mitoses within
the tumor as presumes correlates of the neoplasm aggressiveness. The staging of cancer is
based on the size of the primary lesion, its extent of spread to regional lymph nodes and the
presence or absence of blood borne metastases. The higher the grading and the staging of
the tumor, the poorer is likely the prognosis.
Learning task:
1. Two most widely used methods in pathologic diagnosis of cancer are cytology and
histopathology. Differentiate their purposes and the way to collect and handle the
sample to the laboratory!
2. Differentiate the pathologic sign of benign and malignant tumor (macroscopy and
microscopy)!
3. Now day immunohistochemichal examination has been used in many cases of
cancer in clinical setting. Explain about their purposes!
4. Explain about tumor marker and its examples!
5. Differentiate between grading and staging of cancer! Explain it with examples!
Self assessment:
1. By both cytologic and histopathologic methods, the pathologists determine
malignancy morphologically. Morphologic sign of malignancy is called anaplasia.
Explain about anaplasia!
2. A 60 year old man complains about right upper abdominal mass since 1 month ago.
On palpation, the mass shows irregular surface and hard consistency. You
suspected it as a malignancy of the liver. What kind of tumor marker do you choose
to confirm?
3. A malignant tumor, histopathologically consists of small round cell that can not be
distinguish whether it is a carcinoma, sarcoma or lymphoma. What examination do
you suggest for confirmation?
4. Explain about TNM staging system!
5. A breast cancer shows marked nuclear pleomorphia, few tubular formation and large
amount of mitosis. As conclusion, the tumor is in advanced stage. Is the conclusion
correct? Explain it with reason!
Lecture 2. Diagnostic imaging and strategy therapy of

cancer
Dr. Elysanti Dwi Martadiani, SpRad
45

Clinical Oncology
Abstract
The role of imaging in oncology include screening of the primary tumor, radiological
diagnostic of the primary tumor, evaluate tumor extension and metastatic of the tumor
radiologically (radiological staging), treatment planning, and follow up (evaluation of the
treatment result and detection of the recurrence tumor). There are many kind of imaging
modality that can be use in oncology field. Those imaging modality including conventional
radiography (plain or contrast study), ultrasonography, computed tomography (CT) scan,
magnetic resonance imaging (MRI), also radioisotope scanning/ nuclear medicine. For
oncologic imaging manner, those imaging modality can be combine each other, depend on
the indication of each disease. While choosing imaging modality, we should be always
considered about indication, weakness and advantage of each imaging modality, so that the
radiological examination will give optimal benefit for the patient.
Learning task
1. A 23-years woman complained about having a mobile lump at her left breast since
one month ago.
Question :
a. What the diagnosis possibility ?
b. What kind of imaging examination that can be used for helping establish the
diagnosis ?
2. A 50-years woman, has complained about having a hard, non mobile lump at her left
breast and left axillar region since one month ago. She also complained about
retracted nippled at her left breast.
Question :
a. What the diagnosis possibility ?
b. What kind of imaging examination that can be used for helping establish the
diagnosis and staging for this patient?
c. If you have an asymptomatic patient (age > 50 year), what kind of breast
cancer radiological screening that should be performed by this patient?
3. A young health man has a family history of colon cancer. What kind of imaging
examination that can be use for screening ?
Self Assessment :
1. Explain about the role of imaging in oncology.
2. Mention about type of imaging modality for evaluating malignancy process of the
bone, liver, brain, spinal cord, lung, breast and large bowel (colo-rectal).
Learning resources :
DeVita. Cancer : Principles and Practice of Oncology (6 th edition). Lippincott Williams &
Wilkins. Chapter 24: Advanced imaging Methods. Page 589-611.
Sutton D. Radiology and Imaging for Medical Students (7th edition). Churchill
Livingstone. 1998.
DAY 24 (Monday, Oct 13th 2014)

Basic Clinical Skills (Clinical Pathology)
dr. Ni Kadek Mulyantari, Sp.PK
46

Clinical Oncology
DAY 25 (Tuesday, Oct 14th 2014)

Basic Clinical Skills (Pathology Anatomy)
Day 26 (Wednesday, Oct, 15th 2014)

Silent Day
Day 27 (Thursday, Oct, 16th 2014)
Evaluation
~ CURRICULUM MAP ~
Smstr
Program or curriculum blocks
10
Senior Clerkship
47

Clinical Oncology
Senior Clerkship
Senior clerkship
Medical
Emergency
(3 weeks)
Special Topic:
-Travel medicine
(2 weeks)
Elective Study III

(6 weeks)
Clinic Orientation
(Clerkship)
(6 weeks)
BCS (1 weeks)
The Respiratory
System and
Disorders
(4 weeks)
The
Cardiovascular
System and
Disorders
(4 weeks)
The Urinary
System and
Disorders
(3 weeks)
The Reproductive
System and
Disorders
(3 weeks)
BCS (1 weeks)
Alimentary
& hepatobiliary systems
& disorders
(4 Weeks)
BCS (1 weeks)
The Endocrine
System,
Metabolism and
Disorders
(4 weeks)
BCS (1 weeks)
Clinical Nutrition
and Disorders
(2 weeks)
BCS (1 weeks)
BCS (1 weeks)
Musculoskeletal
system &
connective
tissue disorders
(4 weeks)
Neuroscience
and
neurological
disorders
(4 weeks)
Behavior Change
and disorders
(4 weeks)
BCS (1 weeks)
Hematologic
system & disorders & clinical
oncology
(4 weeks)
BCS (1 weeks)
Immune
system &
disorders
(2 weeks)
BCS(1 weeks)
Infection
& infectious
diseases
(5 weeks)
BCS
(1 weeks)
The skin & hearing
system
& disorders
(3 weeks)
BCS (1 weeks)
Medical
Professionalism
(2 weeks)
BCS(1 weeks)
Evidence-based
Medical Practice
(2 weeks)
BCS (1 weeks)
Health Systembased Practice
(3 weeks)
BCS(1 weeks)
Community-based
practice
(4 weeks)
BCS (1 weeks)
Studium
Generale and
Humaniora
(3 weeks)
Medical
communication
(3 weeks)
BCS (1 weeks)
The cell
as biochemical machinery
(3 weeks)
Growth
&
development
(4 weeks)
BCS (1 weeks)
BCS(1 weeks)
BCS: (1 weeks)
BCS (1 weeks)
Elective Study
II
(1 weeks)
5
BCS (1 weeks)
Special Topic :
- Palliative
medicine
-Compleme
ntary &
Alternative
Medicine
- Forensic
(3 weeks)
Elective
Study II
(1 weeks)
Special Topic
- Ergonomi
- Geriatri
(2 weeks)
Elective
Study I
(2 weeks)
The Visual
system &
disorders
(2 weeks)
Pendidikan Pancasila & Kewarganegaraan (3 weeks)
11. REFFERENCES
Student Standard References:
WINTROBE S CLINICAL HEMATOLOGY
48

Clinical Oncology
Elevent edition. Vol 1. 2. 2004
Lippincott Williams & Wilkins
Philadelphia
ESSETIAL HEMATOLOGY
A.V.Hoffbrand, J.E. Pettit and P.A.H. Moss
Fourt Edition, 2001
Reprinted with corrections 2005
Blackwell Science Ltd
Massachusetts 02148-5020 USA
HEMATOLOGY FOR MEDICAL STUDENT
Alvin H.Schmaier, MD ; Lilli M. Petruzzelli, MD, PhD. Lippincott Williams & Wilkins. A
Wolters Kluwer Company. Tokyo. 2005
Additional Recommended Reading
BUKU RINGKAS HEMATOLOGI
Prof.DR.dr.I Made Bakta SpPD KHOM
Udayana 2004
Denpasar
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Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

3. Planners Team & Lecture

5. Seven General Core Competency

6. Curriculum Block: The Hematology System &Disorder & Clinical Oncology

8. Meeting of student representatives..

10. Student Project .

11. Content outline and learning task.....

12. Curriculum Mapping. 48

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Dr. dr. Ketut Suega, SpPD KHOM

dr. Ni Made Renny Anggreni Rena, Sp.PD

Udayana University Faculty of Medicine, MEU

Div HOM Lab. Interna

Study Guide Hematologic System & Disorders &

dr. Nyoman Suryawati , M.Kes,

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

5. THE SEVEN GENERAL CORE COMPETENCY

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Comprehend the erythropoiesis, granulopoiesis, thrombopoiesis, basic

Sub thema 1 : Hematologic system and disorders.

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Therapy Folic acid

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Basic Clinical Skill

Basic Clinical Skill

dr. Winarti, SpPA

8. MEETING OF STUDENT REPRESENTATIVES

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

10. STUDENT PROJECT

10-15 pages, 1.5 spasi, Times new romance 12

Patophisiology of Iron Deficiency Anemia

Udayana University Faculty of Medicine, MEU

Study Guide Hematologic System & Disorders &

Acute Lympoblatic Leukemia

B12 Deficiency Anemia

Chronic Myeloblatic Leukemia

Aquired Hemolytic Anemia

Interpretation of Complete Blood Count Result

Laboratory Screening for Hemostasis

Promotion and Prevention of Iron Deficiency Anemia

Management of Iron Deficiency Anemia

Acute Myeloblatic Leukemia

Chronic Lympoblatic Leukemia

Folic Acid Deficiency Anemia

Epidemiologi, Screening and diagnositic Of Cancer

Congenital Hemolytic Anemia