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Study Guide Hematologic System & Disorders & Clinical Oncology

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 20 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, DME, 2017

1. PREFACE

1


1. Preface ...……………………………………………………………………………………. 1

2. List of Contents ….…..……………………………………….…………………………... 2

3. Planners Team &Lecture …...…………………………………………………………… 3

4. Facilitators ……………………………………………………………………………. 4

5. Seven General Core Competency ……………………..………………………….. 5

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

7. Time Table

- Regular class…….……………………………………………………………………….. 7

- English class……..…………………………………………………………………….. 7

8. Meeting of student representatives……………………………………………………….. 14

9. Assessment method……………………………………………………………………….. 14

10. Student Project …………………………………………………………………………….14

11. Content outline and learning task……………………………………………….....……… 19

12. Curriculum Mapping…………………………………………………………………………. 50

13. References……….…………………………………………………………………………. 51


2. LIST OF CONTENT

2


No. NAME DEPARTEMENT PHONE1. dr. LosenAdnyana, Sp.PD KHOM(Head) Internal Medicine 08123995536

2.Dr. dr. KetutSuega, SpPD KHOM

Div HOM Lab. Interna

081338728421

3. Dr.dr. SiannyHerawati, SpPK Clinical pathology 0818566411

4. Dr.dr. WayanSudarsa, SpBOnk Surgery 0811398971

5. dr. KetutAriawati, SpA (K) Dept. of Child Health 08123600792

6. dr. TjokordaGdeDharmayuda, SpPD KHOM

Internal Medicine 081338728421

7. dr. Ni Made RennyAnggreni Rena, Sp.PD KHOM


081803651656

8. dr. Ni WayanWinarti,SpPA AnatomyPathology 087862457438

9. Dr. Ni KadekMulyantari, Sp.PK(K) Clinical Pathology 08123647413

10.dr. Cokorda A Wahyu P, M.Biomed, SpPD


081337189997

LECTURERS

NAME DEPARTEMENT PHONEProf.Dr. dr. I B TjakraManuaba, MPH Sp.BOnk Div Onkologi Lab Bedah 08113937779

dr. TjokordaGdeDharmayuda, Sp.PD KHOM Div HOM Lab. Interna 0811394108

Dr.dr. KetutSuega, Sp.PD KHOM Div HOM Lab. Interna 081338728421

Dr.dr. WayanSudarsaSp.BOnk Div Onkologi Lab Bedah 0811398971

dr. N. Wiadnyana Steven Christian, Sp.BOnk Div Onkologi Lab Bedah 08123801156

Dr.dr. SiannyHerawati, Sp.PK Lab. PatologiKlinik 0818566411

Dr. dr. ElysantiSp.Rad, Lab Radiologi 081805673099

dr. KetutAriawati, Sp.A(K) Div HOM Lab Pediatri 08123600792

dr. LosenAdnyana, Sp.PD KHOM Div HOM Lab. Interna 08123995536

dr. Ni WayanWinarti, Sp.PA Lab. PatologiAnatomi 087862457438

dr. Ni Made RennyAnggreni Rena, Sp.PD-KHOM Div HOM Lab. Interna 081803651656

dr. Ni KadekMulyantari, Sp.PK(K) Lab. Patologi Klinik 08123647413

dr. AA Widnyana, Sp.A Div HOM Lab Pediatri 081338550049

dr. Cokorda A Wahyu P, M.Biomed, Sp.PD Div HOM Lab. Interna 081337189997

Dr.dr. Bagus Komang Satriyasa, M.Repro Farmakologi 081237166686

Desak Ketut Ernawati, S.Si, PGPharm, M.Pharm, PhD Farmakologi 081236753646


3. PLANNERS TEAM

3


(REGULAR CLASS)

No Name Group Departement Phone Venue(3rd floor)

1 dr. Ni Nengah Dwi Fatmawati, Sp.MK, Ph.D A1 Microbiology 087862200814 3rd floor:

R.3.01

2 dr. Ida Bagus Ngurah, M.For A2 Pharmacology 08123687288 3rd floor: R.3.02

3 dr. A.A Gd Yuda Asmara, SpOT (K) A3 Orthopaedy 081337870347 3rd floor:

R.3.03

4 Prof. Dr.dr. I Putu Gede Adiatmika, M.Kes A4 Physiology 08123811019 3rd floor:

R.3.04

5 dr. I Kadek Swastika, M.Kes A5 Parasitology 08124649002 3rd floor: R.3.05

6 dr. I Wayan Surudarma, Msi A6 Biochemistry 081338486589 3rd floor: R.3.06

7 dr. Ketut Agus Somia, Sp.PD-KPTI A7 Internal Medicine 08123989353 3rd floor:

R.3.07

8 Dr. dr. Ni Made Linawati, M.Si A8 Histology 081337222567 3rd floor: R.3.08

9 dr. I Gusti Ayu Harry Sundariyati, S.Ked A9 DME 081805380277 3rd floor:

R.3.21

10 dr. Yukhi Kurniawan, Sp.And A10 Andrology 08123473593 3rd floor: R.3.22

(ENGLISH CLASS)


4. FACILITATORS

4

No Name Group Departement Phone Venue(3rd floor)

1 dr. Arif Winata, SpB(K)Onk B1 Surgery 081933067391 3rd floor: R.3.01

2 Dr. dr. Susy Purnawati, M.KK B2 Physiology 08123989891 3rd floor: R.3.02

3 Prof. dr. I G M. Aman, Sp.FK B3 Pharmacology 081338770650 3rd floor: R.3.03

4 dr. I Komang Arimbawa, Sp.S B4 Neurology 081338226892 3rd floor: R.3.04

5 dr. I Wayan Sugiritama, M.Kes B5 Histology 08164732743 3rd floor: R.3.05

6 Dr. dr. I Made Muliarta, M.Kes B6 Physiology 081338505350 3rd floor: R.3.06

7 dr. Muliani, M.Biomed B7 Anatomy 085103043575 3rd floor: R.3.07

8 dr. Wayan Citra Wulan Sucipta Putri, MPH B8 Public Health 087761838141 3rd floor:

R.3.08

9 dr I Gde Haryo Ganesha S.Ked B9 DME 081805391039 3rd floor: R.3.21

10 dr Putu Gede Sudira Sp.S B10 DME 081805633997 3rd floor: R.3.22


1. Patient careDemonstrate 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 baseMastery 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. CommunicationDemonstrate 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 managementDemonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to patient’s 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 system- based practiceDemonstrate awareness and responsiveness to larger context and system of health care, and ability to effectively use system resources for optimal patient care


5. THE SEVEN GENERAL CORE COMPETENCY

5


Aims:

1. Comprehend the erythropoiesis, granulopoiesis, thrombopoiesis, basic principles of haemostasis and transfusion medicine

2. Apply and interpret physical examination, laboratory, and imaging diagnosis of hematology system disorders.

3. Apply general principles of approach and management of patient with malignancy.

4. Diagnose and manage patient with common forms of anemias and to recognize or identify common forms of white blood cell disorders.

5. Diagnose and manage common forms of hemostatic or coagulation disorder.6. Diagnose and refer special patients with hematology system disorders7. Plan patient, family, and necessary community education about hematology

system disorders and clinical oncology.

Sub thema1 : Hematologic system and disorders.Sub thema2 : General and clinical oncology.

Sub thema 1

LEARNING OUTCOMES 1. Describe the biology of the hemopoetic system and its clinical implications2. Describe the general principles and mechanisms of hemostasis and coagulation3. Apply the general principles of transfusion medicine4. Recognize or identify common forms of thrombotic and thromboembolic disorders5. Recognize or identify common forms of splenic disorders (hypersplenism,

splenomegaly, and spleen rupture)6. Differentiate and diagnose common form anemia7. Differentiate acute and chronic leukemias, and myelodysplastic syndrome8. Differentiate Hodgkin’s and non Hodgkin’s lymphoma

Sub thema 2

LEARNING OUTCOMES 1. Describe the general principles of cancer genetic and cancer cell biology and

immunology of cancer2. Apply general principles of prevention and early detection of cancer3. Apply general principles Clinical and Pathological approach to patient with cancer4. Describe general principles of cancer therapy5. Apply general principles of follow up, rehabilitation, palliative care, ethic and

psychosocial to cancer patient.


6. CURRICULUM BLOCK: THE HEMATOLOGIC SYSTEM AND DISORDERS AND CLINICAL

ONCOLOGY

6


Day Date Topic Learning situation

EnglishClass

Regular Class

PIC

1 ThursdayDec, 7, 2017

General Information The Hematology system disorder

Intro. Lect 08.00-08.30 09.00-09.30 Dr.dr. KetutSuega, SpPD KHOM

General Information General Oncology

Intro.Lect 08.30-09.00 09.30-10.00 Dr.dr. WayanSudarsa, SpBOnk

Ind. Learning 09.00-10.30 12.00-13.30

FacilitatorSGD 10.30-12.00 13.30-15.00Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Dr.dr.

KetutSuega, SpPD KHOM&Dr.dr. WayanSudarsa, SpBOnk

2 FridayDec, 8 2017

Overview of anemia,Agranulositosis

Intro. Lect 08.00-09.00 09.00-10.00 dr. LosenAdnyana, SpPDKHOM

Ind. Learning 09.00-10.30 12.00-13.30

FacilitatorSGD 10.30-12.00 13.30-15.00Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr.

LosenAdnyana, SpPDKHOM

3 Monday,Dec,11,

2017

Iron Deficiency Anemia (IDA)(epidemiology, pathophysiology, and diagnosis)


Ind. Learning 09.00-10.30 12.00-13.30

FacilitatorSGD 10.30-12.00 13.30-15.00Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Dr.dr.

KetutSuega, SpPD KHOM

4 TuesdayDec, 12,

2017

IDA : Therapeutic aspect in adult


IDA : Therapeutic aspect in pediatric

08.30- 09.00 09.30-10.00 dr. AA Widnyana, Sp.A

Ind. Learning 09.00-10.30 12.00-13.30FacilitatorSGD 10.30-12.00 13.30-15.00


7. TIME TABLE

7



EnglishClass

Regular Class

PIC

Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Dr.dr.

KetutSuega, SpPD KHOMdr. AA Widnyana, Sp.A

5 Wednesday

Dec, 13, 2017

Overview of hemolytic anemia

Intro. Lect 08.00-09.00 09.00-10.00 dr. KetutAriawati, SpA(K)

Ind. Learning 09.00-10.30 12.00-13.30


KetutAriawati, SpA(K)

6 ThursdayDec, 14,

2017

Anemia Hemolytic Congenital

Intro. Lect 08.00-08.30 09.00-09.30 dr. KetutAriawati, SpA(K)

Anemia Hemolitic Acquired

Intro. Lect 08.30-09.00 09.30-10.00 Dr. Cokorda A Wahyu P, MBiomed., SpPD.

Ind. Learning 09.00-10.30 12.00-13.30


KetutAriawati, SpA(K)Dr. Cokorda A Wahyu P, MBiomed., SpPD

7 FridayDec, 15,

2017

Aplastic Anemia Intro. Lect 08.00-09.00 09.00-10.00 dr.LosenAdnyana, SpPD KHOM

Ind. Learning 09.00-10.30 12.00-13.30

FacilitatorSGD 10.30-12.00 13.30-15.00Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr.LosenAdnyan

a, SpPD KHOM8 Monday

Dec, 18, 2017

Macrocytic andMegaloblastic Anemia

Intro. Lect 08.30-09.00 09.30-10.00 dr. Renny A Rena, SpPDKHOM

Udayana University Faculty of Medicine, DME, 2017 8



EnglishClass

Regular Class

PIC

Ind. Learning 09.00-10.30 12.00-13.30

FacilitatorSGD 10.30-12.00 13.30-15.00Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr. Renny A

Rena, SpPDKHOM

9 TuesdayDec, 19,

2017Polisitemia Intro. Lect 08.00-09.00 09.00-10.00 Dr.

TjokGdeDharmayuda, SpPD. KHOM


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Dr.


10 Wednesday

Dec, 20, 2017

Bleeding disorders (Thrombositopeni, Hemofilia, von Willebrand)

Intro. Lect 08.00-09.00 09.00-10.00 Dr. AA Widnyana, Sp.A


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Dr. AA

Widnyana, Sp.A11 Thursday

Dec, 21, 2017

DIC Intro. Lect 08.00-08.30 09.00-09.30 dr. Renny A Rena, SpPDKHOM

Thrombosis Intro. Lect 08.30-09.00 09.30-10.00 dr. Renny A Rena, SpPD KHOM


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr. Renny A

Rena, SpPDKHOM

12 FridayDec, 22,

2017

Incompatibilities ABO

Intro. Lect 08.00-08.30 09.00-09.30 Dr. Ni KadekMulyantari, Sp.PK(K)


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30




EnglishClass

Regular Class

PIC

Pleno 14.00-15.00 15.00-16.00 Dr. Ni KadekMulyantari, Sp.PK(K)

13 Wednesday

Dec, 27, 2017

Acute and chronic Leukemia

Intro. Lect 08.00-09.00 09.00-10.00 Dr. TjokGdeDharmayuda, SpPD. KHOM




14 Thursday, Dec, 28,

2017

Multiple Myeloma andLymphoma

Intro. Lect 08.00-09.00 09.00-10.00 dr. LosenAdnyana, SpPD KHOM


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr.

LosenAdnyana, SpPD KHOM

15 Friday, Dec, 29,

2017

Overview Limphadenopaty

Intro. Lect 08.00-09.00 09.00-10.00 Dr. KetutAriawati,Sp.A(K)



KetutAriawati,Sp.A(K)

16 Tuesday,Jan,2,2018

Limphadenopaty (pathogenesis and Diagnosis)

Intro. Lect 08.00-09.00 09.00-10.00 Dr. BedahOnkologi



BedahOnkologi

17 Wednesday

Jan, 3,2018

Limphadenitis (surgery aspect)

Intro. Lect 08.00-08.30 09.00-09.30 Dr. BedahOnkologi

Limphadenitis (medical aspect)

Intro. Lect 08.30-09.00 09.30-10.00 Dr. TjokGdeDarmay




EnglishClass

Regular Class

PIC

udha, SpPD. KHOM



BedahOnkologiDr. TjokGdeDharmayuda, SpPD. KHOM

18 ThursdayJan, 4,2018

Medical therapeutic in Hematology

Intro. Lect 08.00-09.00 09.00-10.00 Desak Ketut Ernawati, Apt. PhDDr.dr. Bagus Komang Satriyasa, M.Repro


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 Desak Ketut

Ernawati, Apt. PhDDr.dr. Bagus Komang Satriyasa, M.Repro

19 FridayJan, 5,2018

Laboratory Picture Intro. Lect 08.00-09.00 09.00-10.00 DR.dr. SiannyHerawati, SpPK


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 DR. dr.

SiannyHerawati, SpPK

20 MondayJan, 8,2018

Diagnostic Pathology Tumor

Intro. Lect 08.00-08.30 09.00-09.30 dr. Ni WayanWinarti, SpPA

Diagnostic imaging of Cancer

Intro. Lect 08.30-09.00 09.30-10.00 Dr.dr. ElysantiSpRad


Break 12.00-12.30 11.30-12.00Student Project 12.30-14.00 10.00-11.30Pleno 14.00-15.00 15.00-16.00 dr. Ni

WayanWinarti, SpPA




EnglishClass

Regular Class

PIC

Dr.dr. ElysantiSpRad

Day 21 (Tuesday,January, 9th2018)Silent Day

Day 22 (Wednesday, January, 10th2018) Evaluation



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).

Assessment in this thema consists of:SGD :5%SP (review article) :15 %Final exam : 80%.

Format Paper (Article Review)TITLE

(subject/topic: choose from compentency list)

NameNIM

Faculty of Medicine Udayana University

2016

1. Introduction (Pendahuluan)2. Content (Isi, sesuai topik yang dibahas)3. Summary (Ringkasan)4. Refferences: (Daftar Pustaka, minimal 10, 5 tahunterakhir)VanCouver style,

Example:JournalPunnonen 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.

TextbookLibby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D, Hoster S, Longo D, Jamason S (eds). Harrison’s principles of internal medicine. 15thed. New York: McGraw Hill; 2001. p. 1977-82.InternetWHO. 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 12Subject/topic


9. ASSESSMENT METHOD

8. MEETING OF STUDENT REPRESENTATIVES

10. STUDENT PROJECT

13

http://www.who.int/blood/publications/facts/%20


REGULAR CLASS

NO TOPIC GROUP1 Patophisiology of Iron Deficiency Anemia 1

2 Acute Lympoblatic Leukemia 2

3 B12 Deficiency Anemia 3

4 Chronic Myeloblatic Leukemia 4

5 Aquired Hemolytic Anemia 5

6 Interpretation of Complete Blood Count Result 6

7 Polycytemia 7

8 Laboratory Screening for Hemostasis 8

9 Multiple Myeloma 9

10 Hemophilia B 10

ENGLISH CLASSNO TOPIC GROUP1 Management of Iron Deficiency Anemia 1

2 AcuteMyeloblatic Leukemia 2

3 Chronic Lympoblatic Leukemia 3

4 Folic Acid Deficiency Anemia 4

5 Epidemiologi, Screening and diagnositic Of Cancer 5

6 Congenital Hemolytic Anemia 6

7 Hemophilia A 7

8 Limphoma 8

9 Anemia on Chronic Disease 9

10 Immune Thrombocytopenia Purpura (ITP) 10



The Schedule for Student Project Presentation

NO Date Topic Learning Situation

English Class Regular Class Lecture

1. Tuesday,Jan,2,2018

Management of Iron Deficiency Anemia (English class)

Acute Myeloblatic Leukemia(English class)

Patophisiology of Iron Deficiency Anemia(regular class)

Acute Lympoblatic Leukemia (regular class)

Student Project

12.30 – 14.00 10.00 -11.30 DrTjokordaGdeDharmayuda, Sp.PD KHOM

2. Wednesday

Jan, 3,2018

B12 Deficiency Anemia

(regular class)

Chronic Myeloblatic Leukemia(regular class)

Chronic Lympoblatic Leukemia(English class)

Folic Acid Deficiency Anemia(English class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. Ni Made Renny

Anggreni Rena, Sp.PD

3. ThursdayJan, 4,2018

Epidemiologi, Screening and diagnositic Of Cancer(english class)

Congenital Hemolytic Anemia(English class)

Aquired Hemolytic Anemia (regular class)

Interpretation of Complete Blood Count Result(regular class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. AA Widnyana,

SpA



4. FridayJan, 5,2018

Hemophilia A(english class)

Limphoma(english class)

Polycytemia(regular class)

Laboratory Screening for Hemostasis(regular class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. LosenAdn

yana, Sp.PD KHOM

5. MondayJan, 8,2018

Multiple Myeloma(regular class)

Hemophilia B(regular class)

Anemia on Chronic Disease(english class)

Immune Thrombocytopenia Purpura (ITP)(english class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. LosenAdn

yana, Sp.PD KHOM

NOTE : Presenter will be choosen by moderator on site



Article Review Assessment FormFaculty of Medicine, Udayana University

___________________________________________________________________________

Block :Hematology systems & disorders and clinical oncologyName : ________________________________________Student No. (NIM) : ________________________________________Facilitator : ________________________________________Title : -__________________________________________________

__________________________________________________

__________________________________________________

Time table of consultationPoint of discussion Week Date Tutor sign

1. Title 12. Refferences 23. Outline of paper 34. Content 45. Final discussion 5

AssessmentA. Paper structure : 7 8 9 10B. Content : 7 8 9 10C. Discussion : 7 8 9 10

Total point : ( 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.


Lecture 1.Introduction of Hematologic System and Disorders and General

Oncology


DAY I (Thursday, December, 7th 2017)

Subtopic : Introduction of Hematologic System and Disorders

Dr. dr. KetutSuega, SpPD KHOM

AbstractHematologic 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 doctor’s 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. Learnhow to understandwhatishematology?2. How to evaluateBlood Celluler Function?


11. CONTENT OUTLINE AND LEARNING TASKS

19

Lecture 2.Introduction of Hematologic System and Disorders and General OncologySub topic : Introduction of Clinical Oncology

Dr.dr.WayanSudarsa, SpBOnk

Overview of anemiaAgranulositosis


3. What is the physical stage of blood?4. Explain what are the hematology disorders?

Self assessment1. Understand what is hematology consisting of.2. Understand the physical stage of blood as well as cellular element of the blood.3. Understand in general hematology disorders.

AbstractOncology 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

bodyaccording of Global Cancer Statistics ? (www.IARC.org).4. On your opinion, is cancer can be prevented?

DAY 2 (Friday, December8th 2017)

dr. LosenAdnyana, SpPDKHOM

AbstractAnemia 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 patient’s 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.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 aHb 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


Lecture 1Iron Deficiency Anemia: Therapeutic aspect in

adult


DAY 3 (Monday, December11st 2017)

Epidemiology, Patofisiology and Diagnosisof Iron Deficiency Anemia

Dr.dr. KetutSuega, SpPD KHOM

Abstract

Iron deficiency anemia (IDA) develops when body stores of iron drop too low to support normal red blood cell (RBC) production. Inadequate dietary iron, impaired iron absorption, bleeding, or loss of body iron in the urine may be the cause. [1] Iron equilibrium in the body normally is regulated carefully to ensure that sufficient iron is absorbed in order to compensate for body losses of iron

Learning Tasks :A 56 years old male, come with chief complain palpitationandfeelveryweak. 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 Assessment :1. Understand the iron metabolism in the body2. Understand the absorbtion of the iron in the body3. Understand the function and cycle of iron in the body

DAY 4 (Tuesday, December12nd 2017)

Dr.dr. KetutSuega, SpPD KHOM

AbstractTreatment of iron deficiency anemia consists of correcting the underlying etiology and replenishing iron stores. Iron therapy is as follows: Oral ferrous iron salts are the most economical and effective form Ferrous sulfate is the most commonly used iron salt Better absorption and lower morbidity have been claimed for other iron salts Toxicity is generally proportional to the amount of iron available for absorption Reserve parenteral iron for patients who are either unable to absorb oral iron or who

have increasing anemia despite adequate doses of oral iron


Lecture 2. Iron Deficiency Anemia: Therapeutic Aspect in Pediatric

dr. AA Widnyana, Sp.A


Reserve transfusion of packed RBCs for patients who are experiencing significant acute bleeding or are in danger of hypoxia and/or coronary insufficiency

Learning Tasks:A 56 years old male, come with chief complain palpitationandfeelveryweak. 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 bloodsmear andbonemarrowexaminations 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?5. What is the therapeutic choises for this patient?

Self Assesment :1. Understand clinical manifestation of IDA2. Understand the way to make diagnosis of IDA3. Understand how to prevent the IDA4. Understand how to treatment IDA

Abstract, Learning Task, Self Asessment& Case Study on Lecture

DAY 5(Wednesday,December13rd 2017)


DAY 6 (Thursday, December14th2017)


Overview of Hemolytic Anemia

Dr. KetutAriawati, SpA (K)

23

Lecture 1: Congenital Hemolytic Anemia

Lecture 2. Acquired hemolytic anemia

dr. Cokorda A Wahyu P., M.Biomed, SpPD


Dr. KetutAriawati, SpA (K)

AbstractCongenital hemolytic anemia result from mutations that quantitatively or qualitatively influence the function of red blood 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 hemolytic anemia: 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.

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, uncojugated 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 taskPatients 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 laboratory test you need to confirm this disease?3. What is differential diagnosis of patient above?

Self assessment1. Describe classification of congenital hemolytic anemia.2. Explain clinical presentation and laboratory evaluation of congenital hemolytic

anemia


Aplastic Anemia

dr. LosenAdnyana, SpPD KHOM


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. Laboratory results HGB 8.3 mg/dL, Leukosit 5900/mm3, thrombocyte 410.000/mm3Total bilirubin 4.5, Indirect Bilirubin 3.5, and Coomb’s test positive.

a. Mention the possibility diagnostic of the case above!b. Mention the examination supporting diagnostic!c. How to manage this patient?

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 7 (Friday, December15th 2017)

AbstractAplastic 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 consequences of cytopenias. Supporting examination recommended are complete blood count, and bone marrow aspiration.


Macrocytic and Megaloblastic Anemia

Dr. Ni Made RennyAnggreni Rena, SpPD KHOM


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 109/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

DAY 8 (Monday, December18th 2017)

AbstractThe 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 patient’s quality of life are dramatic and substantive.

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 Task1. 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 Assessment1. 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 (Tuesday, December19th 2017)


Lecture 1. Hemofilia

Dr AA Widnyana,SpA

Polycythemia

dr. TjokordaGdeDharmayuda, SpPD KHOM


AbstractPolycythemia is an increased number of red blood cells in the blood. In polycythemia,

the levels of hemoglobin (Hgb), hematocrit (Hct), or the red blood cell (RBC) count may be elevated when measured in the complete blood count (CBC), as compared to normal.

Hemoglobin levels greater than 16.5 g/dL (grams per deciliter) in women and greater than 18.5 g/dL in men suggest polycythemia. In terms of hematocrit, a value greater than 48 in women and 52 in men is indicative of polycythemia.

Production of red blood cells (erythropoiesis) occurs in the bone marrow and is regulated in a series of specific steps.One of the important enzymes regulating this process is called erythropoietin (Epo). The majority of Epo is produced and released by the kidneys, and a smaller portion is released by the liver.

Learning Task1. What is definition of Polycythemia?2. Explain the pathophysiology of Polycythemia?3. Mention the sign and symptom of Polycythemia!4. What are laboratory finding in Polycythemia?5. What is the treatment for Polycythemia?

Self Assessment1. Explain about the principles of pathogenesis of Polycythemia.2. Mention the type of Polycythemia.3. Mention the clinical manifestation and laboratory findings in Polycythemia

DAY 10 (Wednesday, December20th2017)

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 Assessment1. 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 ?


https://www.emedicinehealth.com/liver/article_em.htm

https://www.emedicinehealth.com/complete_blood_count_cbc/article_em.htm



https://www.emedicinehealth.com/hematocrit_blood_test/article_em.htm

https://www.emedicinehealth.com/hemoglobin_levels/article_em.htm

Lecture 1. DIC

Dr Ni Made Renny Anggreni Rena,SpPD KHOM

Lecture 2. Von Willebrand’s disease

Dr AA Widnyana,SpA


ABSTRACTVon Willebrand’s 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 Task1. 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. Describe the pathophysiology and classification of von Willebranddisease!2. Describe the bleeding manifestation in von Willebranddiasease!3. Understand the laboratory examination support the VWD.

DAY 11 (Thursday, December21st, 2017)

AbstractCellular 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 Task1. Learn how to make diagnosis and treat DIC patient

Case Study


Lecture 2. Plateletfunction and disorderSub topictrombositosis

Dr Ni Made Renny Anggreni Rena,SpPD KHOM


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. Explain what are clinical features supporting DIC on that case!2. What kinds of laboratory test are needed for the diagnosis?3. How to manage this patient? Explain your answer!4. What is Consumptive coagulopathy? Explain your answer!

Self Assessment1. Understand the principle of hemostasis2. Describe the possible etiology, clinical features, laboratory findings of DIC

AbstractPlatelets 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/μL. 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 Task1. 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 it’s cause?4. How to diagnose and to treat an ITP patient?

Self Assessment1. Understand the primary and secondary thrombocytosis.2. Understand the etiology of thrombocytopenia.3. Describe the clinical manifestation and how to confirm diagnosis and to treat ITP.

DAY 12 (Friday, December 22nd 2017)


Blood transfusion, Blood banking and Incompatibilities ABO

Dr. Ni Kadek Mulyantari, Sp.PK(K)


ABSTRACTCriteria for acceptability of blood donors are established to protect the health of

donor and recipient. Blood donations are processed into components. Stored blood components undergo changes that can influence the effectiveness of transfusion. Routine pre-transfusion testing should be done before the transfusion. In unexpected RBC ab are found, the antigen specificity is determined and antigen neg RBC are provide. Transfusion is generally be safe but can result in adverse out come. The reactions can be mild clinical effects. More serious reaction which are un common include, hemolysis, bacterial contamination, anaphylaxis and TRALI. Serious transfusion-transmitted diseases are now rare due to progress in donor screening and testing how ever hepatitis and HIVare still possible

Learning task1. 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?

CASE STUDYOne 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?2. If you work in the Blood Bank, what will you do?3. If you know that the patient’s blood type was AB Rh positive 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 already 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!

Self Assessment1. Characteristic of blood donations2. Components of blood3. Indications of transfusion4. Complications of transfusion

DAY 13 (Wednesday, December27th 2017)


Acute and Chronic Leukemia

dr. Tjokorda Gde Dharmayuda, SpPD KHOM


Acute LeukemiaAbstractAcute 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 TaskKadek, 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 questions1. What diagnosis is most likely for this case ?2. What additional test can be performed ?3. What is the prognosis of the case ?

Learning Task1. 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. 6. How would you educate an acute myeloblastic leukemia patient?

Self Assessment1. 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?



Chronic LeukemiaCLLAbstract

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 Balinese 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 109/, 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:1. Describe the clinical presentation of CLL2. Describe the hematology manifestation of CLL3. Mention how to diagnose CLL

CMLAbstract

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 pluripotenlymphohematopoietic 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/µl and often above 100,000/µl. 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.


Lecture 1. Multiple myeloma

Dr. LosenAdnyana, SpPDKHOM


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.

CaseMale, 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 procesusxipoideus. Laboratory result WBC 120.103/mm3 dominated by neutrophils, Hb 7,5 g/dl, and 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 CML2. Mention the CML Phase3. Mention the kind of test for diagnose CML4. Explain the general management of CML

DAY 14 (Thursday, December 28th 2017)

AbstractMultiple myeloma 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, dose-intensive 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.

CaseFemale 67 years old come with pain on vertebra since 2 years ago and she also complain about body weakness and dizziness. Pyshicalexamination BP 150/90 mmHg, PR 108 x/menit, Tax 38 oC. Palpebra: Paleness. Laboratoryresult: WBC 15.103/mm3, Hb 8,4 gr/dl, PLT 100.103/mm3, BUN 78 mg/dl, creatinin 4 mg/dl. Bonesurvey : lesi osteolitikmultipel in vertebre

Learning task1. Make the problem list for the patient!2. What is diagnosefo the patient?3. Whatkind of testshouldwedo?4. Base on the data, Explain the stage of thisdisease?!5. Explain the patient management!?

Self asessment1. Understand the sign and symptom Multiplemyeloma2. Understand the pathogenesisofMultiplemyeloma.3. UnderstandabouthowtodiagnoseMultiplemyeloma.

Understandabout the management ofMultiplemyeloma


Overview Lymphadenopathy

Lymphadenopaty: Patogenesis and DiagnosisDoctor from Oncology Surgery department

Lecture 2. Malignant Lymphoma and Diagnostic Pathology

Dr. LosenAdnyana, SpPDKHOM


Learning Task :Case An 18-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 x-ray 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 entity3. Mention the clinical differences between HL and NHL 4. Mention the Ann Arbor staging system of Lymphoma5. Mention the grouping lymphomas by clinical behavior

DAY 15 (Friday, December 29th 2017)

Dr.KetutAriawati, SpA(K)


DAY 16 (Tuesday, January 2nd 2018)



Lecture 1. Lymphadenitis : Surgery Aspect

Doctor from Oncology Surgery department

Lecture 2. Lymphadenitis: Medical Aspect


DAY 17 (Wednesday, January 3rd 2018)


dr. TjokordaGdeDharmayuda, SpPD KHOM

AbstractLymphadenitis is the inflammation or enlargement of a lymph node. Lymph nodes are

small, ovoid nodules normally ranging in size from a few millimeters to 2 cm. They are distributed in clusters along the course of lymphatic vessels located throughout the body. The primary function of lymph nodes is to filter out microorganisms and abnormal cells that have collected in lymph fluid.

Lymph node enlargement is a common feature in a variety of diseases and may serve as a focal point for subsequent clinical investigation of diseases of the reticuloendothelial system or regional infection. The majority of cases represent a benign response to localized or systemic infection. Most children with lymphadenitis exhibit small, palpable cervical, axillary, and inguinal lymph nodes. Less common is enlargement of the suboccipital or postauricular nodes. Palpable supraclavicular, epitrochlear, and popliteal lymph nodes are uncommon, as are enlarged mediastinal and abdominal nodes.

Lymphadenitis may affect a single node or a group of nodes (regional adenopathy) and may be unilateral or bilateral. The onset and course of lymphadenitis may be acute, subacute or chronic.

Learning task1. What is the definition of Lymphadenitis?2. What are the etiopatogenesis of Lymphadenitis?3. How to diagnose Lymphadenitis?4. What is the treatment of Lymphadenitis?

Self Assessment1. Understand pathophysiology of Lymphadenitis?2. Understand to manage patient with Lymphadenitis?


Medical Therapeutic in HematologyDr.dr. Bagus Komang Satriyasa, M.Repro

Desak KetutErnawati, Apt.,PhD


DAY 18 (Thursday, January 4th 2017)

Medical Therapeutic in Hematology

Anti-anemia

Bagus Komang Satriyasa

AbstractMicrocytic hypochromic anemia, caused by iron deficiency, is the most common type

of anemia. Megaloblastic anemias are caused by a deficiency of vitamin B12 or folic aci, cofactors required for the normal maturation of red blood cells. Pernicious anemia, the most common type of vitamin B12 deficiency anemia, is caused by a defect in the synthesis of intrinsic factor, a protein required for efficient absorption of dietary vitamin B12, or by surgical removal of that part of the stomach that secrets intrinsic factor.

Regulation of body iron content occurs through modulation of intestinal absorption. There is no mechanism for the efficient exretion of iron. As a result, increased gastrointestinal iron absorbtion can be a cause of diseases associated with excess iron stores (eg, hemochromatosis). Like vitamin B12, folic acid is required for normal DNA synthesis, and its deficiency usually presents as megaloblastic anemia. In addition, deficiency of folic acid during pregnancy increases the risk of neural tube defects in the fetus.

Learning task1. Lists efficacy (pharmacology/pharmacokinetics), safety (adverse drug reactions),

suitability (contraindication), and dose of Iron salts, Vitamin B12 and Folic Acid. 2. A 23-year old pregnant woman is referred by her obstetrician for evaluation of

anemia. She is in her fourth month of pregnancy and has no history of anemia; her grandfather had perniciouns anemia. Her hemoglobin is 10g/dL (normal,12-16g/dL).A) If this woman has macrocytic anemia, an increased serum concentration of

transferring, and a normal serum concentration of vitamin B12 , the most likely cause of her anemia is deficiency of

a. Cobalamin b. Erythoropoietinc. Folic acidd. Intrinsic factore. Iron

B) The laboratory data for your pregnant patient indicate that she does not have macrocytic anemia but instead has microcytic anemia. Optimal treatment of normocytic or mild microcytic anemia associated with pregnancy uses

a. A high-fiber dietb. Erythropoietin injectionsc. Ferrous sulfate tabletsd. Folic acid supplementse. Hydroxocobalamin injections



C) Write a prescription for this patient based on your answer in the above D) If this patient has a young child at home and is taking iron-containing prenatal

supplements, she should be warned that they are a common source of accidental poisoning in young children and advised to make a special effort to keep these pills out of her child’s reach. Toxicity is associated with acute iron poisoning usually includesa. Dizzines, hypertension, and cerebralhemorhageb. Hyperthermia, delirium, and comac. Hypotension, cardiac arrhythmias, and seizuresd. Necrotizing gastroenteritis, shock, and metabolic acidosise. Severe hepatic injury, encephalitis, and coma

Anticoagulants, anti-thrombocytes, thrombolytic, hemostatic systemic agentsDesak Ketut Ernawati

AbstractAnti-coagulants inhibit activities of factors in the coagulation cascades. These drugs prevent thrombus formation and emboli. These drugs also use in preventing coagulation during laboratory examination.There are three drug classes of anticoagulants: heparin, oral anticoagulant (warfarin), and anticoagulant calcium binder. Anti-thrombocytes are drugs which inhibit thrombocytes aggregation which then delaying thrombus formation mostly in artery. Aspirin, Clopidogrel, Sulfinpirazone, Ticlopidineand Dextran are in this class.Thrombolytic drugs have an opposite action to anticoagulants. These drugs mostly used in acute myocardium infarction, vena thrombosis, and pulmonary emboli. Streptokinase and alteplase are in this class. Hematologic disorders may be associated with lack of intrinsic factors in coagulation cascade. Vitamin K and Tranexamate acid belong to hemostatic systemic agents.

Learning Task1. Lists efficacy (pharmacology/pharmacokinetics), safety (adverse drug reactions),

suitability (contraindication), and dose of Warfarin, Aspirin, Clopidogrel.2. List efficacy (pharmacology/pharmacokinetics), safety (adverse drug reactions),

suitability (contraindication), and dose of Streptokinase, Vitamin K and Tranexamate acid

Self-assessment1. Discuss mechanism of action of anticoagulant drugs2. Discuss mechanism of action of thrombolytic drugs3. Explain the different mechanism of anticoagulant and thrombolytic drugs

Chemotherapy and immunosuppressive agentsDesak Ketut Ernawati

AbstractThe aim of chemotherapy is to cure it or if it is not possible, effective palliation. Chemotherapy agents can be classified based on how they work, their chemical structure and their relationship to other drugs. Chemotherapy inhibits mechanism of cell proliferation which may not specific to tumor cells thus they may not specific to treat particular cancer. Further, understanding on how drug works is important in predicting adverse drug reactions. This is because most chemotherapy agents have narrow therapeutic index. Thus, medical doctor needs to understand how the drugs works, doses of drug given and potential adverse drug reaction and drug interactions which may associate with chemotherapy treatment. Immunosuppressive agents may be used to treat autoimmune disease or diseases which


Laboratory picture of patient with blood cellsdisorder


are most likely autoimmune origin, to prevent rejection of transplant organs or tissues, and to threat some other autoimmune inflammatory diseases. Some immunosuppressive agents will be discussed in this topic.

Learning task:1. Discuss some considerations in selecting chemotherapy agents2. Discuss about potential drug interaction in a patient who is on chemotherapy agents

taking vitamins3. Discuss some considerations in selecting immunosuppressive agents.

Self-assessment1. Describe classification of chemotherapy agents2. Describe common adverse drug reactions of chemotherapy3. Describe route of administration of chemotherapy4. Describe classification of immunosuppressive agents

DAY 19 (Friday, January 5th 2018)

Dr.dr. SiannyHerawati, Sp.PK

Abstract: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. Hct is the volume RBCs expressed as a percentage of whole blood

volume. RBC count is direct measure of the numherofRBC 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


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


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 20 (Monday, January 8th 2018)

dr. Ni WayanWinarti, SpPA

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!


Lecture 2. Diagnostic imaging and strategy therapy of cancer

Dr. dr. ElysantiDwiMartadiani, SpRad


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!

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).


Day 21 (Tuesday,January, 9th2018) Silent Day

Day 22 (Wednesday, January, 10th2018) Evaluation

42


~ CURRICULUM MAP ~

Program or curriculum blocks10

Senior Clerkship

9 Senior Clerkship8 Senior Clerkship

7Health System-based Practice(3 weeks)

BCS (1 weeks)

Community-based practice

(4 weeks)

Evidence-based Medical Practice

(2 weeks)

Special topics :Health Ergonomy& Health Environment

(2 weeks)

Elective StudyIV (evaluation)

(2 weeks)

Compre Clinic Orientation (Clerkship)+ medical ethic(4 weeks)

18

6The Cardiovascular System and Disorders(3 weeks)BCS (1 weeks)

Medical Emergency(3 weeks)

BCS (1 weeks)

The Urinary System and Disorders(3 weeks)BCS (1 weeks)

The Reproductive System and Disorders (3 weeks)

BCS (1 weeks)

Elective StudyIII

(3 weeks)

19

5Neuroscience andneurologicaldisorders(3 weeks)

BCS (1 weeks)

The Respiratory System and Disorders(3 weeks)

BCS (1 weeks)

The skin & hearing system& disorders(3 weeks)

BCS (1 weeks)

Special Topic : - Palliative med- Complemnt& Alternative Med.

(2 weeks)

Forensic Medicine and Medicolegal(2 weeks)

Elective Study II(2 weeks)

18

4Musculoskeletal system &connective tissue disorders(3 weeks)BCS (1 weeks)

Alimentary & hepatobiliary systems & disorders(3 Weeks)BCS (1 weeks)

The Endocrine System, Metabolism and Disorders(3 weeks)BCS (1 weeks)

Clinical Nutrition and Disorders(2 weeks)

BCS (1 weeks)

The Visualsystem &disorders(2 weeks)

BCS (1weeks)

18

3Behavior Changeand disorders(3 weeks)

BCS (1 weeks)

Basic Infection & infectiousdiseases(3 weeks)BCS (1 weeks)

Immune system &disorders(2 weeks)BCS (1 weeks)

Hematologicsystem & disorder & clinical oncology(3 weeks)BCS (1 weeks)

Special Topic- Andro& aging- Geriatri-Travel medicine (4 weeks)

19

2BIOMEDIK III(4 weeks)

Growth&development(2 weeks)BCS: (1 weeks)

Medicalcommunication(2 weeks)

BCS (1 weeks)

Medical Professionalism(2 weeks)

BCS (1 weeks)

Basic Pharmaceutical medicine & drug etics(2 weeks)

Elective Study I(2 weeks)

17

1StudiumGenerale and Humaniora(2 weeks)

BIOMEDIK I(8 weeks)

The cellas biochemical machinery(2 weeks)BCS(1 weeks)

BIOMEDIK II(6 weeks)

19

Pendidikan Pancasila &Kewarganegaraan ( 3 weeks )

BIOMEDIK I : Anatomy, Histology, Physiology, Biochemistry.BIOMEDIK II : Microbiology, Parasitology, PharmacologyBIOMEDIK III : Pathology Anatomy, Clinical pathology


TOTAL :166 SKS

43


Student Standard References: WINTROBE ‘S CLINICAL HEMATOLOGY16th edition. Vol 1. 2. 2016Lippincott Williams & WilkinsPhiladelphia

ESSETIAL HEMATOLOGYA.V.Hoffbrand, J.E. Pettit and P.A.H. MossSixth Edition, 2017Blackwell Science LtdMassachusetts 02148-5020 USA

HEMATOLOGY FOR MEDICAL STUDENTAlvin H.Schmaier, MD ; Lilli M. Petruzzelli, MD, PhD. Lippincott Williams & Wilkins. A Wolters Kluwer Company. Tokyo. 2015

Abeloff’s Clinical Oncology 2008, Chapter 6. Available on CD

Michael S. Sabel, Oncology. Current Surgical Diagnosis and Treatment, 12 th Ed. 2006: 46; 1329-1350

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

DeVita. Cancer : Principles and Practice of Oncology (6th 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.

Additional Recommended Reading

BUKU RINGKAS HEMATOLOGIProf.DR.dr.I Made BaktaSpPD KHOMUdayana 2004Denpasar


11. REFFERENCES

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