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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 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 1

1. PREFACE


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…………………………………………………………………………. 48

13. References……….…………………………………………………………………………. 49


2. LIST OF CONTENT


No. NAME DEPARTEMENT PHONE1. Dr. dr. Ketut Suega, SpPD KHOM

(Head)Internal Medicine 0811394108

2. dr. Ni Kadek Mulyantari, SpPK(K) (secretary)

Clinical Pathology 08123647413

3. Dr.dr. Sianny Herawati, SpPK Clinical pathology 08185664114. dr. Wayan Sudarsa, SpB Onk Surgery 08113989715. dr. Ketut Ariawati, SpA (K) Dept. of Child Health 081236007926. dr. Tjokorda Gde Dharmayuda, SpPD

KHOM Internal Medicine 081338728421

7. Dr. dr. Bagus Komang Satriyasa, M.Repro Pharmacology 0818053689228. dr. Ni Wayan Winarti, SpPA Anatomy Pathology 0878624574389. dr. Losen Adnyana, SpPD KHOM Div HOM Lab.

Interna08123995536

10. dr. Ni Made Renny Anggreni Rena, Sp.PD Div HOM Lab. Interna

081803651656

LECTURERS

NAME DEPARTEMENT PHONE

Prof. Dr. dr. I Made Bakta, SpPD KHOM Div HOM Lab. Interna 0811399625Prof.Dr. dr. I B Tjakra Manuaba, MPH SpBOnk Div Onkologi Lab Bedah 08113937779dr. Tjokorda Gde Dharmayuda, SpPD KHOM Div HOM Lab. Interna 0811394108Dr.dr. Ketut Suega, SpPD KHOM Div HOM Lab. Interna 081338728421Dr.dr. Wayan Sudarsa SpBOnk Div Onkologi Lab Bedah 0811398971dr. I Wayan Sugiritama, M.Kes Lab. Histologi 08164732743Prof. dr. N Agus Bagiada, SpBiok Lab. Biokimia 081338338611Dr. dr. Bagus Komang Satriyasa, M.Repro Lab. Farmakologi 081805368922dr. Tjokorda Gde Oka, MS., SpPK Lab Patologi Klinik 081338454245dr. N Wiadnyana Steven Christian, SpBOnk Div Onkologi Lab Bedah 08123801156Dr.dr. Sianny Herawati, SpPK Lab. Patologi Klinik 0818566411Dr. dr. Elysanti SpRad, Lab Radiologi 081805673099dr. Ketut Ariawati, SpA (K) Div HOM Lab Pediatri 08123600792dr. Losen Adnyana, SpPD KHOM Div HOM Lab. Interna 08123995536dr. Ni Wayan Winarti, SpPA Lab. Patologi Anatomi 087862457438dr. Ni Made Renny Anggreni Rena, Sp.PD Div HOM Lab. Interna 081803651656Drs. I Made Adioka , Apt, M.Si Lab.Farmasi 081999418471dr. Ni Putu Ekawati,M.Repro, Sp.PA Lab. Patologi Anatomi 08113803933dr. Ni Kadek Mulyantari, SpPK (K) Lab. Patologi Klinik 08123647413dr. AA Widnyana, SpA Div HOM Lab Pediatri 081338550049


3. PLANNERS TEAM


(REGULAR CLASS)

NO NAME GROUP DEPT PHONE VENUE1 dr. Ni Nyoman Margiani, Sp.Rad 1 Radiology 081337401240 3nd floor:

R.3.092 Dr. dr. Anak Agung Wiradewi

Lestari , Sp PK2 Clinical

Pathology 08155237937 3nd floor: R.3.10

3 Dr.dr. I B G Fajar Manuaba, Sp.OG, MARS

3 Obgyn 081558101719 3nd floor: R.3.11

4 dr. Ni Ketut Sri Diniari, Sp.KJ 4 Psychiatry 081338748051 3nd floor: R.3.12

5 dr. Made Agus Hendrayana , M.Ked

5 Mikrobiology 08123921590 3nd floor: R.3.13

6 dr. Komang Ayu Kartika Sari, MPH

6 Public Health 082147092348 3nd floor: R.3.14

7 dr. Kadek Agus Heryana, Sp.An 7 Anasthesi 081338568883 3nd floor: R.3.15

8 dr. Ketut Rai Purnami, Sp.PD 8 Interna 0818350703 3nd floor: R.3.16

9 dr. Ni Putu Ekawati, M.Repro, Sp.PA

9 Anatomy Pathology 08113803933 3nd floor:

R.3.1710 dr. I Gusti Lanang Ngurah Agung

Artha Wiguna, Sp.OT (K)10 Orthopaedi 0811388859 3nd floor:

R.3.19

(ENGLISH CLASS)

NO NAME GROUP DEPT PHONE VENUE1 dr. I Gusti Ayu Widianti ,

M.Biomed1 Anatomy 08123921765 3nd floor:

R.3.092 dr. I Gst.Ngr.Ketut Budiarsa ,

Sp.S2 Neurology 0811399673 3nd floor:

R.3.103 dr. Kadek Fajar Martha,

M.Biomed, Sp.OG3 Obgyn 081236297575 3nd floor:

R.3.114 Dr. dr. Bagus Komang

Satriyasa, M.Repro4 Pharmacology 081805368922 3nd floor:

R.3.125 Dr.dr. I Made Muliarta, M.Kes 5 Fisiology 081338505350 3nd floor:

R.3.136 dr. Ni Made Renny Anggreni

Rena , Sp.PD6 Interna 081803651656 3nd floor:

R.3.147 Dr.dr. Elysanti Dwi Martadiani,

Sp.Rad7 Radiology 081805673099 3nd floor:

R.3.158 dr. Ida Ayu Putri Wirawati,

Sp.PK8 Clinical

Pathology081933090039 3nd floor:

R.3.169 dr.Kumara Tini, Sp.S 9 Neurology 081238701081 3nd floor:

R.3.1710 Dr.rer.Nat. dr. Ni Nyoman Ayu

Dewi, M.Kes10 Biochemistry 081337141506 3nd floor:

R.3.19


4. FACILITATORS


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 management

Demonstrate 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


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 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 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


Day Date Topic Learning situation

Regular Class

EnglishClass

PIC

1 Monday Sept, 7, 2015

General Information The Hematology system disorder

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

General Information General Oncology

Intro.Lect 08.30-09.00 09.30-10.00 Dr.dr. Wayan Sudarsa, SpB Onk

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Ketut

Suega, SpPD KHOM &Dr.dr. Wayan Sudarsa, SpBOnk

2 TuesdaySept, 8 2015

Laboratory picture of patient with blood cells disorder (BSC)

Intro. Lect 08.00-09.00 09.00-10.00 Dr.dr. Sianny Herawati, Sp.PK

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Sianny

Herawati, Sp.PK3 Wednesd

ay,Sept 9, 2015

Leukopoesis, Intro. Lect 08.00-08.30 09.00-09.30 dr. I Wayan Sugiritama, M.Kes

Thrombopoesis Intro. Lect 08.30-09.00 09.30-10.00 Dr.dr. Sianny Herawati, Sp.PK

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. I Wayan

Sugiritama, M.Kes & Dr.dr. Sianny Herawati, Sp.PK

4 ThursdaySept, 10, 2014

Erythropoesis

Synthesis of Hb, function of blood and blood cells metabolism

Intro. Lect 08.00-08.30

08.30- 09.00

09.00-09.30

09.30-10.00

Dr. Ni Kadek Mulyantari, Sp.PK(K)Prof. dr. N Agus Bagiada, SpBiok


7. TIME TABLE


Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Kadek

Mulyantari, Sp.PK(K)Prof. dr. N Agus Bagiada, SpBiok

5 FridaySept, 11, 2015

Anemia

Polycythemia

Intro. Lect 08.00-08.30

09.00-09.30 dr. Ketut Ariawati, SpA(K)

Intro. Lect 08.30-09.00 09.30-10.00 dr. Tjokorda Gde Dharmayuda, SpPD KHOM

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Ketut

Ariawati, SpA (K) & dr. Tjokorda Gde Dharmayuda, SpPD KHOM

6 MondaySept, 14, 2015

Information Nutritional Anemia


Pathophysiology of Iron Deficiency Anemia



Suega, SpPD KHOM

7 TuesdaySep, 15, 2015

The diagnostic of iron deficiency anemia



Suega, SpPD KHOM

8 WednesdaySep, 16,

Pathophysiology folic acid and B12 deficiency anemia

Intro. Lect 08.30-09.00 09.30-10.00 dr. Ni Made Renny Anggreni Rena, Sp.PD



2015The diagnostic of folic acid and B12 deficiency anemia

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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 Made

Renny Anggreni Rena, Sp.PD

9 ThursdaySep, 17, 2015

AML Intro. Lect 08.00-08.30 09.00-09.30 dr. Losen Adnyana, SpPD KHOM

ALL Intro. Lect 08.30-09.00 09.30-10.00 Dr. AA Widnyana, Sp.A

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Losen

Adnyana, SpPD KHOMDr. AA Widnyana, Sp.A

10 FridaySep, 18, 2015

Management therapy of iron deficiency

Intro. Lect 08.00-08.30 09.00-09.30 Dr. dr. Bagus Komang Satriyasa, M.Repro

Therapy Folic acid and B12 anemia

Intro. Lect 08.30-09.00 09.30-10.00 Drs. I Made Adioka , Apt, M.Si

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Bagus

Komang Satriyasa, M.ReproDrs. I Made Adioka , Apt, M.Si

11 MondaySep, 21, 2015

-Anemia on chronic disease

Intro. Lect 08.00-08.30 09.00-09.30 dr. Losen Adnyana, SpPD KHOM

-Aplastic anemia Intro. Lect 08.30-09.00 09.30-10.00 dr. Losen Adnyana, SpPD KHOM




Adnyana, SpPD KHOM

12 TuesdaySep, 22, 2015

Thrombositosis Intro. Lect 08.00-08.30 09.00-09.30 Dr.dr. Ketut Suega, SpPD KHOM

Thrombocytopenia Intro. Lect 08.30-09.00 09.30-10.00 dr. Ni Made Renny Anggreni Rena, Sp.PD


Suega, SpPD KHOM &dr. Ni Made Renny Anggreni Rena, Sp.PD

13 WednesdaySep, 23, 2015

Principle of Hemostasis


DIC, APS, Intro. Lect 08.30-09.00 09.30-10.00 dr. Ni Made Renny Anggreni Rena, Sp.PD


Suega, SpPD KHOM &dr. Ni Made Renny Anggreni Rena, Sp.PD

14 Friday, Sep, 25, 2015

Hemophilia Intro. Lect 08.00-08.30 09.00-09.30 Dr. AA Widnyana, Sp.A

Von Willebrand’s disease

Intro. Lect 08.30-09.00 09.30-10.00 dr. Ni Made Renny Anggreni Rena, Sp.PD

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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.A & dr. Ni Made Renny Anggreni Rena, Sp.PD



15 Monday,Sep, 28,2015

Malignan lymphoma Intro. Lect 08.00-08.30 09.00-09.30 dr. Tjokorda Gde Dharmayuda, SpPD KHOM

Malignan lymphoma (diagnostic pathology)


Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Tjokorda Gde

Dharmayuda, SpPD KHOM& dr. Tjokorda Gde Dharmayuda, SpPD KHOM

16 Wednesday,Sep,30,2015

Congenital hemolytic anemia, hemoglobinopati

Intro. Lect 08.00-08.30 09.00-09.30 Dr. Ketut Ariawati, Sp.A(K)

Acquired hemolytic anemia Management


Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. Ketut

Ariawati, Sp.A(K)dr. Tjokorda Gde Dharmayuda, SpPD KHOM

17 ThursdayOct, 1,2015

Blood transfusion Intro. Lect 08.00-08.30 09.00-09.30 Dr. Ni Kadek Mulyantari, Sp.PK(K)

Blood banking(BCS)

Intro. Lect 08.30-09.00 09.30-10.00 Dr. Ni Kadek Mulyantari, Sp.PK(K)

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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 Kadek

Mulyantari, Sp.PK(K)

18 FridayOct, 2, 2015

Multiple Myeloma, Intro. Lect 08.00-08.30 09.00-09.30 dr. Losen Adnyana, SpPD KHOM

MDS Langerhans cell tumor

Intro. Lect 08.30-09.00 09.30-10.00 dr. Losen Adnyana, SpPD KHOM

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 12.00-12.30 11.30-12.00



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

Adnyana, SpPD KHOM

19 MondayOct, 5, 2015

CLL Intro. Lect 08.00-08.30 09.00-09.30 dr. Losen Adnyana, SpPD KHOM

CML Intro. Lect 08.30-09.00 09.30-10.00 dr. Losen Adnyana, SpPD KHOM


Adnyana, SpPD KHOM

20 TuesdayOct, 6,2015

Epidemiology of cancer

Intro. Lect 08.00-08.30 09.00-09.30 Dr.dr. W Sudarsa SpBOnk

Screening of cancer Intro. Lect 08.30-09.00 09.30-10.00 Dr.dr. W Sudarsa SpBOnk

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. W

Sudarsa SpBOnk

21 WednesdayOct, 7, 2015

Molecular biology of cancer

Intro. Lect 08.00-08.30 09.00-09.30 Prof.Dr. dr. I B Tjakra Manuaba, MPH SpBOnk

Immunology of cancer

Intro. Lect 08.30-09.00 09.30-10.00 Prof.Dr. dr. I B Tjakra Manuaba, MPH SpBOnk

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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 Prof.Dr. dr. I B

Tjakra Manuaba, MPH SpBOnk

22 ThursdayOct, 8, 2015

Management diagnostic of cancer

Intro. Lect 08.00-08.30 09.00-09.30 dr. N Wiadnyana Steven Christian, SpBOnk



Management therapy and referral of cancer

Intro. Lect 08.30-09.00 09.30-10.00 dr. N Wiadnyana Steven Christian, SpBOnk

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 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. N Wiadnyana

Steven Christian, SpBOnk

23 FridayOct, 9, 2015

Diagnostic pathology, tumor marker

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

Diagnostic Imaging of cancer

Intro. Lect 08.30-09.00 09.30-10.00 Dr.dr. Elysanti SpRad,

Ind. Learning 09.00-10.30 12.00-13.30SGD 10.30-12.00 13.30-15.00 FacilitatorBreak 12.00-12.30 11.30-12.00

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

Winarti, SpPA& Dr. dr. Elysanti SpRad

24 MondayOct, 12, 2015

Basic Clinical Skill(Clinical Pathology)

dr. Sianny Herawati, SpPK& dr. Ni Kadek Mulyantari, Sp.PK(K)

25. TuesdayOct, 13, 2015

Basic Clinical Skill (Pathology Anatomy)

dr. Ni Wayan Winarti, SpPA&dr. Ni Putu Ekawati, M.Repro, SpPA

26 WednesdayOct, 14 2015

Silent Day

27 ThursdayOct, 15, 2015

Evaluation Team


8. MEETING OF STUDENT REPRESENTATIVES


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

2014

1. Introduction (Pendahuluan)2. Content (Isi, sesuai topik yang dibahas)3. Summary (Ringkasan)4. Refferences: (Daftar Pustaka, minimal 10, 5 tahun terakhir) 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. 15th ed. 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

10. STUDENT PROJECT

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


REGULAR CLASSNO 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

11 Promotion and Prevention of Iron Deficiency Anemia 11

12 Transfusion Reaction 12

ENGLISH CLASSNO TOPIC GROUP1 Management of Iron Deficiency Anemia 1

2 Acute Myeloblatic 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 Idiopatic Thrombocytopenia Purpura (ITP) 10

11 Aplastic /Hypoplastic Anemia 11

12 Von Wilebrands Disease 12The Schedule for Student Project Presentation



NO Date Topic Learning Situation

Regular Class

English Class

Lecture

1. Thursday Oct, 1, 2015

Limfoma (English class)

Acute Myeloblatic Leukemia (English class)

Aquired Hemolytic Anemia (regular class)

Polycytemia (regular class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr Tjokorda Gde

Dharmayuda, Sp.PD KHOM

2. Friday Oct, 2, 2015

Patophisiology of Iron Deficiency Anemia (regular class)

B12 Deficiency Anemia (regular class)

Management of Iron Deficiency Anemia (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. Monday, Oct, 5, 2015

Congenital Hemolytic Anemia (english class)

Hemophilia A (English class)

Hemophilia B (regular class)

Acute Lympoblatic Leukemia (regular class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. AA Widnyana,

SpA

4. Tuesday, Oct, 6, 2015

Chronic Lympoblastic Leukemia (english class)

Chronic Myeloblatic Leukemia (regular class)Multiple Myeloma (regular class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. Losen Adnyana,

Sp.PD KHOM

5. Wednesd Anemia on Chronic Student 12.30 – 14.00 10.00 -11.30 Dr. Losen



ay Oct, 7, 2015

Disease (english class)

Idiopatic Thrombocytopenia Purpura (ITP) (english class)

Aplastic /Hypoplastic Anemia (english class)

Von Wilebrands Disease (english class)

Project Adnyana, Sp.PD KHOM

6. Thursday Oct, 8, 2015

Interpretation of complete blood count result (reguler class)

Laboratory screening for hemostasis(reguler class)

Promotion and prevention of iron deficiency anemia(reguler class)

Transfusion reaction (reguler class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. Ni Kadek

Mulyantari, Sp.PK(K)

7. FridayOct, 9, 2015

Epidemiologi, Screening and Diagnostic Of Cancer (English class)

Student Project

12.30 – 14.00 10.00 -11.30 Dr. Winarti, SpA/dr. Elysanti, Sp.Rad

NOTE : Presenter will be choosen by moderator on site

Article Review Assessment Form



Faculty 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 (Monday, Sept, 7th 2015)

Sub topic : Introduction of Hematologic System and Disorders

Prof.Dr. dr. Ketut Suega, 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. Learn how to understand what is hematology?2. How to evaluate Blood Celluler Function?3. What is the physical stage of blood?


11. CONTENT OUTLINE AND LEARNING TASKS

Lecture 2.Introduction of Hematologic System and Disorders and General

OncologySub topic : Introduction of Clinical

OncologyDr. Wayan Sudarsa, SpBOnk

Laboratory picture of patient with blood cells disorder


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

DAY 2 (Tuesday, Sept 8th 2015)

Dr. 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.


Lecture 1. HematopoesisSub topic : Leukopoesis


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 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 (Wednesday, Sept 9th 2015)

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.

GranulocytopoiesisEosinophil, 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).


Lecture 2. HematopoesisSub topic:Thrombopoesis


MonocytopoiesisMonocyte 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.

LymphopoiesisThe 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 !

Dr.dr. Sianny Herawati, Sp.PK

Learning Task:1. Describe about trombopoiesis2. Describe about the mechanism of platelet release.3. Describe about thrombocyte maturation4. Describe regulation of trombopoiesis

Self assessment:1. Explain the characteristics of the thrombocyte2. Explain about thrombopoietin3. Explain the ultrastructural of thrombocyte4. Explain the characteristics of megakaryocyte5. Explain role of the spleen in platelet production.


Lecture 1. HematopoesisSub topic : Erythropoesis


6. Explain platelet life span and turnover of platelet

DAY 4 (Thursday, Sept 10th 2015

dr. NI Kadek Mulyantari, Sp.PK(K)

ABSTRACTUnder 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 function3. Understand about the factors that influence of erythropoesis process


Lecture 2. HematopoesisSub topic : Synthesis of hemoglobin, function of

blood and blood cells metabolismProf. dr. Nyoman Agus Bagiada,SpBiok


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 task1. 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 Assessment1. Define the normal value of whole blood in man and women2. Define the complete blood function3. How Hb are synthesize an degradation4. What are the iron function in Hb5. What is the similar and the difference of Hb and Mb

DAY 5 (Friday sept, 11th 2015)

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 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


Lecture 1. AnemiaSub topic : Pathophysiologi and

Classification of anemiaDr. Ketut Ariawati, SpA (K)


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 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 taskPatient 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 Assessmenta. 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


Nutritional AnemiaSub topic General Information Nutritional AnemiaSub topic Patofisiology of Iron Deficiency Anemia


Learning task1. 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 (Monday, Sept 14th 2015)

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 body2. Understand the absorbtion of the iron in the body3. Understand the function and cycle of iron in the body


Lecture 2. POLISITEMIAdr. Tjokorda Gde Dharmayuda, SpPD KHOM

Nutritional Anemia The diagnostic of iron deficiency anemia

Dr.dr. Ketut Suega, SpPD-KHOM

Nutritional AnemiaSub 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


DAY 7 (Tuesday, Sept 15th 2015)

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 IDA2. Understand the way to make diagnosis of IDA3. Understand how to prevent the IDA

DAY 8 (Wednesday, Sept 16th 2015)

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


Acute LeukemiaSubtopic AML, ALL


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 (Thursday, Sept 17 th 2015)

dr. Losen Adnyana, SpPD KHOMdr. AA Widnyana, SpA

AbstractAcute 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.


Lecture 1. Nutritional AnemiaSub topic :Management therapy of iron deficiency,

Sub topic : Management therapy of Folic acid and Vit B12 Deficiency Dr. dr. Bagus Komang Satriyasa, M.Repro

Drs. I Made Adioka , Apt, M.Si


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 ?

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 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.

How would you educate an acute myeloblastic leukemia patient?

DAY 10 (Friday, Sept 18 th 2015)

Learning task:1 Describe the normal mechanism of regulation of iron absorption in the body2. Describe the normal mechanism of regulation of iron storage in the body3. Describe the acute and chronic toxicity of iron4. Sketch and explain the enzymatic reaction that use folates5. Describe the clinical applications of vitamin B12 and folic acid

Self assessment1. Explain role of iron in the body2. Describe the clinical applications of iron3. Whey iron should not given in hemolytic anemia?4. Explain role of vitamin B12 and folic acid in the body


Aplastic Anemia & Anemia of Chronic Diseases


DAY 11 (Monday, Sept 21th, 2015)

dr. Losen Adnyana, SpPD KHOM

Aplastic AnemiaAbstract

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 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

Anemia of Chronic DiseaseAbstract

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.


Platelet function and disorderSub topic trombositosis

Sub topic trombositopenia

DR Dr Ketut Suega,SpPD-KHOMDr Ni Made Renny Anggreni Rena,SpPD


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 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 12.103/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 ACD2. Explain the pathophysiology of ACD3. Mention the kinds of test for ACD4. Explain the patient management

DAY 12 (Tuesday, Sep 22th 2015)

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?


HemostasisSub topic Principle of hemostasis

Sub topic DIC, APS

DR Dr Ketut Suega,SpPD-KHOMDr Ni Made Renny Anggreni Rena,SpPD


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 13 (Wednesday, Sep, 23th 2015)

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 Task1. 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. 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 3. Mention the clinical features, laboratory findings of APS


Lecture 1. Hemofilia

Dr AA Widnyana,SpA

Lecture 2. Von Willebrand’s disease

Dr Ni Made Renny Anggreni Rena,SpPD


DAY 14 (Friday, Sep 25th 2015)

Learning TaskBayu, 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 ?

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 Willebrand disease!2. Describe the bleeding manifestation in von Willebrand diasease!3. Understand the laboratory examination support the VWD.


Malignan Lymphoma and Diagnostic Pathology

Lecture 1. Hemolytic AnemiaSub topic Congenital hemolytic anemia, hemoglobinopati


DAY 15 (Monday, Sep 28th 2015)

dr. Tjokorda Gde Dharmayuda, SpPD KHOM

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 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 16 ( Wednesday, Sept 30th 2015)

Dr. Ketut Ariawati, SpA(K)

AbstractCongenital 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 :


Lecture 2. Hemolytic AnemiaSub topic Acquired hemolytic anemiadr. Tjokorda Gde Dharmayuda, SpPD KHOM


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, 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 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 laboratorium test you need to confirm this disease ?3. What the differential diagnosis in patient above ?

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

anemias3. Explain the principle management of congenital hemolytic anemias

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.


Blood transfusion andBlood banking

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


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/mm3

Total 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.

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 (Thursday, Oct 1st 2015)

Abstract1. Criteria for acceptability of blood donors are established to protect the health of

donor and recipient2. Blood donations are processed into components3. Stored blood components undergo changes that can influence the efectiveness of

transfusion4. Routine pretransfusion testing should be done before the transfusion5. In unexpected RBC ab are found, the antigen specifisity is determined and antigen

neg RBC are provide6. Transfusion is generally be safe but can result in adverse out come7. The reactions can be mild clinical effects8. More serious reaction wich are un common include, hemolysis, bacterial

contamination, anaphylaxis and TRALI9. Serious transusion-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?

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


Lecture 1. Multiple myelomaDr. Losen Adnyana, SpPD KHOM


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 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 (Friday, Oct 2nd 2015)

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, 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


Lecture 2. MDS, Langerhans cell tumor

dr. Losen Adnyana,SpPD


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. Pyshical examination BP 150/90 mmHg, PR 108 x/menit, Tax 38 oC. Palpebra: Paleness. Laboratory result: WBC 15.103/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 task1. 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 asessment1. Understand the sign and symptom Multiple myeloma2. Understand the pathogenesis of Multiple myeloma.3. Understand about how to diagnose Multiple myeloma.4. Understand about the management of Multiple myeloma.

AbstractMyelodysplasia 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


Lecture 1. Chronic LeukemiaSubtopic CLL, CML


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, 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 38,50C, mild hepatosplenomegali +. Laboratory result: WBC 2.103/mm3, Hb 8,5 g/dl, MCV 75, MCH 26 dan PLT 40.103/mm3.

Learning task1. 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 asessment1. Understand the sign and symptom MDS2. Understand the pathogenesis of MDS.3. Understand about how to diagnose MDS4. Understand about the management of MDS

.DAY 19 (Monday, Oct 5th 2015)

dr. Losen Adnyana, SpPD KHOM

CLLAbstract:

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 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

CMLAbstractCML 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/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.

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?


Epidemiology and screening of cancer


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 20 (Tuesday, Oct 6th 2015)

dr. Wayan Sudarsa, SpB Onk

AbstractCancer 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 CancerLearning 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 DetectionLearning taskExplain 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?


Lecture 1. Molecular Biology and immunology of cancer


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 n. What is meant by Chemoprevention on Cancer, and name some examples.

Self Assessment

a. Screening for the cancers below have very strong evidence based, except:b. Mammography to screen for breast cancer on women above 50. c. Thorax: photo to screen for lung cancer d. Pap smear to screen for uteri cervix cancer e. FOBT to screen for Colorectal Cancer. f. Sigmoidoscopy to screen for Colorectal Cancer.

DAY 21 (Wednesday, Oct 7th 2015)

Prof.Dr.dr. I B Tjakra Manuaba, MPH SpB Onk

Molecular Biology of Cancer:Learning TaskExplain The Following Processes In Relation To Carcinogenesis And Cancer Progression:

1. Cell Signaling2. Cell Cycle3. Program Cell Death4. Angiogenesis5. Invasion And Metastasis

(Refer To: De Vita: Cancer. Principles And Practice Of Oncology 2008. Part I. Chapter 5-9. available on CD)

Immunology of CancerLearning Task

1. How Do Tumors Differ From Self Tissues?2. What’s The Tumor Associated Antigen And Tumor Specific Antigen? 3. How Important Is Immune Surveillance Of Cancer?4. What’s The Role Of Innate Immunity, Epithelial Immunity, And Tumor Immune

Surveillance?5. What’s 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: Abeloff’s Clinical Oncology 2008, Chapter 6. Available on CD).


Lecture 1. Management diagnostic, therapy and referal cancer patient


DAY 22 (Thursday, Oct 8th 2015)

dr. N Wiadnyana Steven Christian, SpB Onk

AbstractCancer 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. When do I have to be on the alert for a malignant disease?2. What can I see?3. How do I have to examine the patient?4. Which relevant investigations are required?5. What are the do’s and don’ts?6. What should be my pattern of referral?7. What is going to happen to the patient and why?8. 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 taskWomen, 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.

PLEASE ANSWER AND DISCUSS THESE QUESTIONS AS BELOW

1. What are the principles of cancer patient management ? Please mention it!2. How should diagnosis be done in above patient?3. Do you need imaging investigation? Please explain of each imaging if needed!4. 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 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


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


Barry W Feig, Berger H David, Fuhrman George M. The MD Anderson Surgical Oncology. Handbook. Lippincott Williams and Wilkins. 2006

DAY 23 (Friday, Oct 9th 2015)

dr. Ni Wayan Winarti, 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!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


Lecture 2. Diagnostic imaging and strategy therapy of cancer

Dr. Elysanti Dwi Martadiani, SpRad


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 ?


Basic Clinical Skills (Clinical Pathology)

Basic Clinical Skills (Pathology Anatomy)


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 (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.

DAY 24 (Monday, Oct 12th 2015)

Dr.dr. Sianny Herawati, SpPKdr. Ni Kadek Mulyantari, Sp.PK

DAY 25 (Tuesday, Oct 13th 2015)

dr. Ni Wayan Winarti, SpPAdr. Ni Putu Ekawati, Sp.PA


Day 26 (Wednesday, Oct, 14th 2015) Silent Day

Day 27 (Thursday, Oct, 15th 2015) Evaluation


~ CURRICULUM MAP ~Smstr Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerksh ip

7

Medical Emergency(3 weeks)

BCS (1 weeks)

Special Topic:-Travel medicine(2 weeks)

Elective Study III(6 weeks)

Clinic Orientation (Clerkship)(6 weeks)

6

The Respiratory System and Disorders(4 weeks)

BCS (1 weeks)

The Cardiovascular System and Disorders(4 weeks)

BCS (1 weeks)

The Urinary System and Disorders(3 weeks)

BCS (1 weeks)

The Reproductive System and Disorders (3 weeks)

BCS (1 weeks)

5

Elective Study II(1 weeks)

Alimentary & hepato-biliary 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)

Special Topic : - Palliative medicine-Complementary & Alternative Medicine - Forensic(3 weeks)

Elective Study II(1 weeks)

4

Musculoskeletal system &connectivetissue disorders(4 weeks)

BCS (1 weeks)

Neuroscienceandneurologicaldisorders(4 weeks)

BCS (1 weeks)

Behavior Changeand disorders(4 weeks)

BCS(1 weeks)

The Visualsystem &disorders(2 weeks)

BCS(1 weeks)

3

Hematologicsystem & disor-ders & clinical oncology(4 weeks)

BCS (1 weeks)

Immune system &disorders(2 weeks)

BCS(1 weeks)

Infection & infectiousdiseases(5 weeks)

BCS (1 weeks)

The skin & hearing system& disorders(3 weeks)

BCS(1 weeks)

2

Medical Professionalism(2 weeks)

BCS (1 weeks)

Evidence-based Medical Practice(2 weeks)

Health System-based Practice(3 weeks)

BCS (1 weeks)

Community-based practice(4 weeks)

Special Topic- Ergonomi- Geriatri(2 weeks)

Elective Study I(2 weeks)

1

StudiumGenerale and Humaniora(3 weeks)

Medicalcommunication(3 weeks)

BCS (1 weeks)

The cellas bioche-mical machinery(3 weeks)

BCS(1 weeks)

Growth&development(4 weeks)

BCS: (1 weeks)

Pendidikan Pancasila & Kewarganegaraan (3 weeks)



Student Standard References: WINTROBE ‘S CLINICAL HEMATOLOGYElevent edition. Vol 1. 2. 2004Lippincott Williams & WilkinsPhiladelphia

ESSETIAL HEMATOLOGYA.V.Hoffbrand, J.E. Pettit and P.A.H. MossFourt Edition, 2001Reprinted with corrections 2005Blackwell 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. 2005

Additional Recommended Reading

BUKU RINGKAS HEMATOLOGIProf.DR.dr.I Made Bakta SpPD KHOMUdayana 2004Denpasar


11. REFFERENCES

Documents

Content€¦ · Web view · 2017-05-31Point of discussion Week Date Tutor sign Title 1 Refferences 2 Outline of paper 3 Content 4 Final ... Patient without history of bleeding