Study Guide Hematologic System & Disorders & Clinical Oncology CONTENTS
Table of contents ………..………..………. 2
Introduction …………..………. 3
Seven General Competition ………4
Curriculum………..……… 5
Block Team………...………... 6
Facilitators………..……… 7
Time Table ……….………...……… 8
Meeting of Students representatives ………13
Meeting of The Facilitators………..13
Assessment method………...13
Student Project ………...………...14
Learning Program……….17
Assessment Form ………40
Reference ……….41
Curriculum Mapping………...42
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,
Planners
Study Guide Hematologic System & Disorders & Clinical Oncology
1. . Patient care
Demonstrate capability to provide comprehensive patient care that is compassionate, appropriate, and effective for the management of health problems, promotion of health and prevention of disease in the primary health care settings.
2. Medical knowledge base
Mastery of a core medical knowledge which includes the biomedical sciences, behavioral sciences, epidemiology and statistics, clinical sciences, the social aspect of medicine and the principles of medical ethics, and apply them
3. Clinical skill
Demonstrate capability to effectively apply clinical skills and interpret the findings in the investigation of patient.
4. Communication
Demonstrate capability to communicate effectively and interpersonally to establish rapport with the patient, family, community at large, and professional associates, that results in effective information exchange, the creation of a therapeutically and ethically sound relationship.
5. Information management
Demonstrate capability to manager information which includes information access, retrieval, interpretation, appraisal, and application to 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 practice
Demonstrate awareness and responsiveness to larger context and system of health care, and ability to effectively use system resources for optimal patient care
Study Guide Hematologic System & Disorders & Clinical Oncology
Aims:
1. Comprehend the 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 disorders
7. Plan patient, family, and necessary community education about hematology system disorders and clinical oncology.
Sub theme 1 : Hematologic system and disorders. Sub theme 2 : General and clinical oncology. Sub theme 1
LEARNING OUTCOMES
1. Describe The Hematology System Disorder and General Oncology 2. Differentiate and diagnose common form anemia
3. Describe Diagnostic and Therapy of Iron Deficiency Anemia 4. Recognize of Polycythemia, DIC and thrombosis
5. Apply the general principles of transfusion medicine 6. Recognize or identify bleeding disorders
7. Differentiate acute and chronic leukemia
8. Differentiate Hodgkin’s and non-Hodgkin’s lymphoma, Multiple Myeloma 9. Recognize medicaments therapy in hematology
Sub theme 2
LEARNING OUTCOMES
1. Apply general principles of diagnostic and therapy of limphadenopathy
2. Apply general principles Clinical and Pathological approach to patient with cancer 3. Describe general principles of cancer therapy
4. Recognize diagnostic (laboratory, pathology and imaging) of tumor/cancer
Study Guide Hematologic System & Disorders & Clinical Oncology
PLANNERS
No. NAME DEPARTEMENT PHONE
1. dr. Losen Adnyana, SpPD KHOM (Head) Internal Medicine 08123995536 2. Dr. dr. Ketut Suega, SpPD KHOM Internal Medicine 081338728421 3. Dr. dr. Sianny Herawati, SpPK Clinical Pathology 0818566411 4. Dr. dr. Wayan Sudarsa, SpB Onk Surgery 0811398971 5. dr. Ketut Ariawati, SpA (K) Pediatric 08123600792 6. dr. Tjokorda Gde Dharmayuda,SpPD KHOM Internal Medicine 081338728421 7. Dr. dr. Bagus Komang Satriyasa, M.Repro Pharmacology 081805368922 8. dr. Ni Wayan Winarti, SpPA Anatomy Pathology 087862457438 9. dr. Ni Kadek Mulyantari, Sp.PK(K) Clinical Pathology 08123647413
LECTURERS
No
. NAME DEPARTEMENT PHONE
1 Prof. Dr. dr. I Made Bakta, SpPD-KHOM Internal Medicine 0811399625 2 Prof. Dr. dr. I B Tjakra Manuaba, MPH
SpB(K)Onk
Surgery 08113937779
3 dr. Tjokorda Gde Dharmayuda, SpPD-KHOM Internal Medicine 0811394108 4 Dr.dr. Ketut Suega, SpPD-KHOM Internal Medicine 08133872842
1
5 Dr.dr. Wayan Sudarsa SpB(K)Onk Surgery 0811398971
6 Dr. Ni G.A.A. Manik Y.W, SpB(K)Onk Surgery 08123214075 7
Desak Ketut Ernawati, Apt. PhD Pharmacology 081236753646 8 Dr. dr. Bagus Komang Satriyasa, M.Repro Pharmacology 08180536892
2
9 dr. Tjokorda Gde Oka, MS, SpPK Clinical Pathology 08133845424 5
10 dr. N Wiadnyana Steven Christian, SpB(K)Onk
Surgery 08123801156
11 Dr.dr. Sianny Herawati, SpPK Clinical Pathology 0818566411
12 Dr. dr. Elysanti SpRad, Radiology 08180567309
9
13 dr. Ketut Ariawati, SpA (K) Pediatric 08123600792
14 dr. Losen Adnyana, SpPD KHOM Internal Medicine 08123995536 15 dr. Ni Wayan Winarti, SpPA Anatomy Pathology 08786245743
8
16 dr. Ni Putu Ekawati,M.Repro, Sp.PA Anatomy Pathology 08113803933 17 dr. Ni Kadek Mulyantari, SpPK (K) Clinical Pathology 08123647413
18 dr. AA Widnyana, SpA Pediatric 08133855004
9
Study Guide Hematologic System & Disorders & Clinical Oncology
CLASS A (REGULAR CLASS)
NO NAME GROUP DEPT PHONE VENUE
1 dr. Ni Putu Wardani, M. Biomed, SpAn
A1 DME 08113992784 2nd floor: R.2.01 2 dr. I Dewa Ayu Inten Dwi
Primayanti, M. Biomed
A2 Physiology 08133776129 9
2nd floor: R.2.02 3 dr. Agung Nova Mahendra, M. Sc A3 Pharmacology 087861030195 2nd floor:R.2.03 4 dr. Muliani, M. Biomed A4 Anatomy 08510304357
5
2nd floor: R.2.04 5 Dr.rer.Nat. dr. Ni Nyoman Ayu
Dewi, M.Si
A5 Biochemistry 08133714150 6
2nd floor: R.2.05 6 dr. I G A Artini, M. Sc A6 Pharmacology 0812650481 2nd floor:R.2.06 7 Dr. dr. Ni Made Linawati, M. Si A7 Histology 081337222567 2nd floor:R.2.07 8 dr. Yuliana, M. Biomed A8 Anatomy 08579265236
3
2nd floor: R.2.08 9 dr. I Wayan Sugiritama, M. Kes A9 Histology 08164732743 2nd floor:
R.2.21 10 dr. I A Sri Indrayani, Sp. S A10 Neurology 081246751536 2nd floor:R.2.22
CLASS B (ENGLISH CLASS)
NO NAME GROUP DEPT PHONE VENUE
1 Dr. dr. Susy Purnawati, M.KK B1 Physiology 08123989891 2nd floor: R.2.01 2 dr. Putu Yuliandari, S. Ked B2 Microbiology 089685415625 2nd floor:R.2.02 3 dr. I Nyoman Gede Wardana, M. Biomed B3 Anatomy 087860405625 2nd floor:R.2.03 4 Dr. dr. Ni Nyoman Sri
Budayanti, Sp.MK (K)
B4 Microbiology 08553711398 2nd floor: R.2.04 5 dr. Putu Gede Sudira, Sp.S B5 DME 08180563399
7
2nd floor: R.2.05 6 dr. I Putu Bayu Mayura, S.Ked B6 Microbiology 082236165801 2nd floor:R.2.06 7 dr. Ayu Setyorini MM, M. Sc, Sp.A(K) B7 Pediatric 081353286780 2nd floor:R.2.07 8 Dr. dr. Elysanti Dwi
Martadiani, SpRad
B8 Radiology 08180567309 9
2nd floor: R.2.08 9 Prof. Dr. dr. I Putu Adiatmika,M.Kes B9 Physiology 08123811019 2nd floor:R.2.21 10 dr. I A Dewi Wiryanthini, M. Biomed B10 Biochemistry 081239990399 2nd floor:R.2.22
Study Guide Hematologic System & Disorders & Clinical Oncology
Day Date Topic Learning
Situation
Regular Class
English
Class PIC
1
Thursday Nov, 24, 2016
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(K)Onk Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dr. dr. Ketut Suega, SpPD KHOM Dr. dr. Wayan Sudarsa, SpB(K)Onk
2
Friday Nov, 25 2016
Overview of Anemia, Agranulocytosis
Intro. Lect 08.00-09.00 09.00-10.00 dr. Losen Adnyana, SpPD KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Losen Adnyana, SpPD KHOM
3
Monday, Nov,28, 2016
Iron Deficiency Anemia (IDA) (Epidemiology, Pathophysiology, Diagnosis)
Intro. Lect 08.00-09.00 09.00-10.00 Dr. dr. Ketut Suega, SpPD KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dr. dr. Ketut Suega, SpPD KHOM 4 Tuesday
Nov, 29, 2016
IDA, Aspect of Therapy in Adults
Intro. Lect
08.00-08.30 09.00-09.30 Dr. dr. Ketut Suega, SpPD KHOM IDA, Aspect of Therapy in
Children 08.30- 09.00 09.30-10.00 dr. AA Widnyana, Sp.A
Ind. Learning 09.00-10.30 12.00-13.30
Study Guide Hematologic System & Disorders & Clinical Oncology
Day Date Topic LearningSituation RegularClass EnglishClass PIC
Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dr. dr. Ketut Suega, SpPD KHOMdr. Ketut Ariawati, SpA(K)
5 WednesdayNov, 30, 2016
Overview of Hemolytic Anemias
Intro. Lect 08.00-09.00 09.00-10.00 dr. Ketut Ariawati, SpA(K) Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Ketut Ariawati, SpA(K)
6
Thursday Des, 1st, 2016
Congenital Hemolytic Anemias Intro. Lect 08.00-08.30 09.00-09.30 dr. Ketut Ariawati, SpA(K)
Acquired Hemolytic Anemias Intro. Lect 08.30-09.00 09.30-10.00 dr. Tjok Gde Darmayudha, SpPD. KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30 Pleno 14.00-15.00 15.00-16.00
dr. Ketut Ariawati, SpA(K)
dr. Tjok Gde Darmayudha, SpPD. KHOM
7
Friday Des, 2, 2016
Aplastic Anemia
Intro. Lect 08.00-09.00 09.00-10.00 dr. Losen Adnyana, SpPD KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Losen Adnyana, SpPD KHOM
8
Monday Des, 5, 2016
Macrocytic and Megaloblastic Anemias
Intro. Lect 08.30-09.00 09.30-10.00 dr. Losen Adnyana, SpPD KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Losen Adnyana, SpPD KHOM 9 Tuesday
Des, 6,
Study Guide Hematologic System & Disorders & Clinical Oncology
Day Date Topic LearningSituation RegularClass EnglishClass PIC
2016
Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Tjok Gde Darmayudha, SpPD. KHOM
10 Wednesday Des, 7, 2016
Bleeding Disorders: Hemophilia,
Von Willebrand Intro. Lect 08.00-08.30 09.00-09.30 dr. AA Widnyana, Sp.A Thrombocyte Disorders:
Thrombocytopenia /ITP, Thrombocytosis
Intro. Lect 08.30-09.00 09.30-10.00 dr. Ketut Ariawati, SpA(K) Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. AA Widnyana, Sp.A dr. Ketut Ariawati, SpA(K)
11
Thursday Des, 8, 2016
DIC Intro. Lect 08.00-08.30 09.00-09.30 Dr. dr. Ketut Suega, SpPD KHOM Thrombosis Intro. Lect 08.30-09.00 09.30-10.00 dr. Losen Adnyana, SpPD KHOM
Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dr. dr. Ketut Suega, SpPD KHOM dr. Losen Adnyana, SpPD KHOM
12
Friday Des, 9, 2016
ABO Incompatibilities
Intro. Lect 08.00-08.30 09.00-09.30
dr. Ni Kadek Mulyantari, Sp.PK(K) Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Study Guide Hematologic System & Disorders & Clinical Oncology
Day Date Topic LearningSituation RegularClass EnglishClass PIC
Des, 13, 2016
KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Tjok Gde Darmayudha, SpPD. KHOM
14
Wednesday , Des, 14, 2016
Multiple Myeloma and Lymphoma
Intro. Lect 08.00-09.00 09.00-10.00 dr. Losen Adnyana, SpPD KHOM Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Losen Adnyana, SpPD KHOM
15
Thursday, Des, 15, 2016
Overview of Lymphadenopathy
Intro. Lect 08.00-09.00 09.00-10.00 dr. Ketut Ariawati,Sp.A(K) Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 dr. Ketut Ariawati,Sp.A(K)
16
Friday, Des,16, 2016
Lymphadenopathy (Pathogenesis and Diagnosis)
Intro. Lect 08.00-09.00 09.00-10.00 Dokter Bedah Onkologi Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dokter Bedah Onkologi 17 Monday
Des, 19, 2016
Lymphadenitis (Surgical aspects) Intro. Lect 08.00-08.30 09.00-09.30 Dokter Bedah Onkologi
Lymphadenitis (Medical Aspects) Intro. Lect 08.30-09.00 09.30-10.00 dr. Tjok Gde Darmayudha, SpPD. KHOM
Ind. Learning 09.00-10.30 12.00-13.30 Facilitator SGD 10.30-12.00 13.30-15.00
Study Guide Hematologic System & Disorders & Clinical Oncology
Day Date Topic LearningSituation RegularClass EnglishClass PIC
Pleno 14.00-15.00 15.00-16.00
Dokter Bedah Onkologi
dr. Tjok Gde Darmayudha, SpPD. KHOM
18
Tuesday Des, 20, 2016
Medicaments Therapy in Hematology: Agent Used in Anemia
Intro. Lect 08.00-08.30 09.00-10.00 Dr.dr. Bagus Komang Satriyasa, M.Repro
Chemotherapy and
Immunosuppressive Agents Intro. Lect 08.30-09.00 09.00-10.00 Desak Ketut Ernawati, Ph.D., Apt Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30 Pleno 14.00-15.00 15.00-16.00
Dr.dr. Bagus Komang Satriyasa, M.Repro
Desak Ketut Ernawati, Apt. PhD
19
Wednesday Des, 21, 2016
Laboratory Picture
Intro. Lect 08.00-09.00 09.00-10.00 Dr.dr. Sianny Herawati, SpPK Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Pleno 14.00-15.00 15.00-16.00 Dr. dr. Sianny Herawati, SpPK
20
Thursday Des, 22, 2016
Pathology Diagnostic of Tumor Intro. Lect 08.00-08.30 09.00-09.30 dr. Ni Wayan Winarti, SpPA Imaging Diagnostic of Cancer Intro. Lect 08.30-09.00 09.30-10.00 Dr.dr. Elysanti SpRad
Ind. Learning 09.00-10.30 12.00-13.30
Facilitator SGD 10.30-12.00 13.30-15.00
Break 12.00-12.30 11.30-12.00 Student Project 12.30-14.00 10.00-11.30
Study Guide Hematologic System & Disorders & Clinical Oncology
In the middle of each block curriculum, a meeting is held among the student representatives, facilitators, and resource person of the block. The meeting is to discuss about the effectiveness of on going teaching and learning processes, facilitators and lectures as a feedback to improve process. This meeting is held on… ( schedule to be advise).
Assessment in this thema consists of:
SGD : 5 %
SP (review article) : 15 % Final exam : 80 %.
MEETING OF STUDENT REPRESENTATIVES
Study Guide Hematologic System & Disorders & Clinical Oncology
Format Paper (Article Review)
TITLE
(subject/topic: choose from compentency list)
Name NIM
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 tahun terakhir) VanCouver style, Example:
Journal
Punnonen K, Irjala K, Rajamaki A. Serum transferrin receptor and its ratio to serum ferritin in the diagnosis of iron deficiency. Blood. 1997;89(3):1052-7.
Textbook
Libby P. The Pathogenesis of atherosclerosis. In: Braunwald E, Fauci A, Kasper D, Hoster S, Longo D, Jamason S (eds). Harrison’s principles of internal medicine. 15th ed. New York: McGraw Hill; 2001. p. 1977-82.
Internet
WHO. Clinical Use of Blood. Geneva: WHO 1998. [cited 2005 July]. Available from: http://www.who.int/blood/publications/facts/ .
10-15 pages, 1.5 spasi, Times new romance 12
Study Guide Hematologic System & Disorders & Clinical Oncology
Subject/topic
REGULAR CLASS
N
O TOPIC
GROU P
DATE
1 Patophysiology of Iron Deficiency Anemia I Dec. 15th 2 Acute Lympoblastic Leukemia II Dec. 15th
3 B12 Deficiency Anemia III Dec. 16th
4 Chronic Myeloblastic Leukemia IV Dec. 16th
5 Acquired Hemolytic Anemia V Dec. 19th
6 Interpretation of Complete Blood Count Result VI Dec. 19th 7 Laboratory Screening for Hemostasis VII Dec. 20th
8 Multiple Myeloma VIII Dec. 20th
9 Hemophilia B IX Dec. 21st
10 Promotion and Prevention of Iron Deficiency Anemia X Dec. 21st
ENGLISH CLASS
N O
TOPIC GROU
P
DATE
1 Management of Iron Deficiency Anemia I Dec. 15th 2 Acute Myeloblastic Leukemia II Dec. 15th 3 Chronic Lympoblastic Leukemia III Dec. 16th 4 Folic Acid Deficiency Anemia IV Dec. 16th 5 Epidemiologi, Screening and Diagnositic of
Cancer
V Dec. 19th
6 Congenital Hemolytic Anemia VI Dec. 19th
7 Limphoma VII Dec. 20th
8 Idiopatic Thrombocytopenia Purpura (ITP) VIII Dec. 20th 9 Aplastic / Hypoplastic Anemia IX Dec. 21st
Study Guide Hematologic System & Disorders & Clinical Oncology The Schedule for Student Project Presentation
NO Date Topic Learning
Situation
Regular Class
English
Class Lecture
1. Dec. 13Thursday,th ,
2016
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 Dharmayud a, Sp.PD KHOM 2. Wednesd ay Dec, 14th, 2016
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. Losen Adnyana, Sp.PD KHOM 3. Thursday, Dec, 15th,
2016
Congenital Hemolytic Anemia (english class) Hemophilia (English class)
Acute Lympoblatic Leukemia (regular class)
Student
Project 12.30 – 14.00 10.00 -11.30
Dr. AA Widnyana,
SpA
4. Dec, 16Friday,th,
2015
Chronic Lympoblastic Leukemia (english class)
Chronic Myeloblatic Leukemia (regular class)
Student
Project 12.30 – 14.00 10.00 -11.30
Dr Tjokorda Gde Dharmayud
a, Sp.PD KHOM
5. Dec, 19Mondayth,
2016
Anemia on Chronic Disease (english class) Idiopatic Thrombocytopenia Purpura (ITP) (english class)
Aplastic /Hypoplastic Anemia (english class)
Student
Project 12.30 – 14.00 10.00 -11.30
Dr. Losen Adnyana, Sp.PD KHOM
6. ThursdayDec, 20th,
2016
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. Wednesd ay Dec, 21st,
2016
Epidemiologi, Screening and Diagnostic Of
Cancer (English class) StudentProject 12.30 – 14.00 10.00 -11.30
Dr. Winarti, SpA/dr. Elysanti,
Sp.Rad
Study Guide Hematologic System & Disorders & Clinical Oncology
DAY I (Thursday, November, 24th 2016)
Abstract
Hematologic System and Disorders is the discipline that studies the normal and abnormal conditions of the blood and is components. Plasma component of the blood consists of several proteins which are instrumental in the process of coagulation, anti-coagulation, as well as fibrinolytic reactions. One of the most particular characteristics of the hematopoietic system is the perpetual regeneration process of blood cells throughout the lifespan of the organism.
Pluripotent hematopoietic stem cell (HSC) is the precursor of blood cells. The components of blood from HSC that actively circulate are erythrocytes, leukocytes, and thrombocytes. Lymphocytes are among the components produced by HSC, and thus the field of hematology also includes in it the studies of reticuloendothelial system and lymph nodes. No individual organ can be specifically linked to hematology disorders; the problems could manifest themselves at the bone marrows, lymphatic organs, intravascular compartments where the red blood cells circulate, or endothelial cells along the blood vessels and the proteins in the plasma component.
Sub theme General Oncology is the discipline that studies the general aspect of tumor / malignancy / cancer describe epidemiology, cancer prevention, therapy of cancer rehabilitation patient with cancer.
At the end of this program, medical students are expected to:
1. Understand medical 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?
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.
CONTENT OUTLINE AND LEARNING TASKS
Lecture - 1
INTRODUCTION OF HEMATOLOGIC SYSTEM AND
DISORDERS AND GENERAL ONCOLOGY
Sub topic : Introduction of Hematologic
System and Disorders
Study Guide Hematologic System & Disorders & Clinical Oncology 3. Understand in general hematology disorders.
Abstract
Oncology is a study of Cancer. Cancer arises from a series of genetic alterations that promote self sufficiency in growth, escape from cell cycle exit, resistance to apoptosis, cellular immortalization, and ultimately the acquisition of properties that facilitate angiogenesis, invasion, and metastasis.
The scope of Oncology are basic sciences of oncology and clinical oncology. Basic science of oncology are mainly consist of molecular biology and immunology. Clinical Oncology is a multidisciplinary area of medicine, which means that several medical disciplines are involved in the prevention, screening and early detection of people with risk of cancer, and diagnosis, staging and treatment of individual patients with cancer as well
Learning Task:
1. At the level of molecular biology point of view, what is the definition of Cancer? 2. Would you elaborate what are the causes of Cancer?
3. Can you define the ten most common cancer that affected of the human body according of Global Cancer Statistics ? (www.IARC.org).
4. On your opinion, is cancer can be prevented?
DAY 2 (Friday, November 25th 2016)
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
1. Males and females have equivalent Hb values until puberty.
Lecture - 2
Introduction of Hematologic System and
Disorders and General Oncology
Sub topic : Introduction of Clinical Oncology
DR. Dr. Wayan Sudarsa, SpBOnk
ANEMIA
Sub topic: Overview of Anemia
Study Guide Hematologic System & Disorders & Clinical Oncology 2. The increase in Hb that occurs in men is largely attributed to the effect of androgens on the release of erythropoietin (EPO) and the responsiveness of red blood cell (RBC) precursors to EPO.
3. The gender disparity in the normal range for Hb concentration is less significant in elderly individuals.
B. Anemia is defined as Hb concentration more than to standard deviations below the normal range for age and gender. Using this definition, there is less than a 5% chance that a Hb concentration below the normal range is a “normal” value for the individual. Worldwide, almost one-third of the population is anemic.
The first step in diagnosis of anemia is to establish whether the abnormality is isolated to a single cell line (red blood cells only) or whether it is part of a multiple cell line abnormality (red cells, white cells and platelets). Abnormalities of to or three cell lines usually indicate one of the following :
bone marrow involvement, (e.g., aplastic anemia, leukemia), or
an immunologic disorder (e.g., connective tissue disease or immunoneutropenia, idiopathic thrombocytopenic purpura [ITP] or immune hemolytic anemia singly or in combination) or
sequestration of cells (e.g., hypersplenism).
The blood smear is very helpful in the diagnosis of anemia. It establishes whether the anemia is hypochromic, microcytic, normocytic, macrocytic or show spezcific morphologic abnormalities suggestive of red cell membrane disorders (e.g., spherocytes, stomatocytosis or elliptocytosis) or hemoglobinopathies (e.g., sickle cell disease, thalassemia).
The mean corpuscular volume (MCV) confirms the findings on the smear with reference to the red cell size, e.g., microcytic (<70 fl), macrocytic (>85 fl) or normocytic (72-79 fl). The mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) are calculated values and generally of less diagnostic.
Learning task
Patient of 2 years, girl with pale since 2 month ago, without fever and bleeding. Hemoglobin level is 6 g/dL, MCV is 68 fl.
Answer the following question :
1. Discuss what are steps you can perform on this patient (anamnesis, physical examination, other laboratorium).
2. What the differential diagnosis of this patient ?
Self Assessment
a. Defined of anemia !
b. Describe the classification of anemia based on etiologi !
c. What is the differential diagnosis of patients microcytic anemia ? d. What is the differential diagnosis of patients normocytic anemia ? e. Give the differential diagnosis of macrocytic anemia !
f. Describe of historical factors of importance in evaluating patients with anemia
Study Guide Hematologic System & Disorders & Clinical Oncology
Learning task
A 56 years old male, come with chief complain palpitation and feel very weak. Several days ago, he frequently had his stool with black color. He also suffered from nausea, vomiting, and pain on epigastrial. Laboratory findings are : Hb 7,6 gr/dl, MCV 72 fl, MCH 25 pg , MCHC 28%, SI< 50 ng/dl, TIBC 525 ng/ Dl. Physical examination found with angular cheilitis, liver and spleen without any abnormality.
1. What is the type of anemia the patient suffered from? 2. Explain how is the patomechanism of the case above! Self Asessment
1. Understand the iron metabolism in the body 2. Understand the absorbtion of the iron in the body 3. Understand the function and cycle of iron in the body
DAY 3 (Monday, November 28th 2016)
Learning Task
A 56 years old male, come with chief complain palpitation and feel very weak. Several days ago, he frequently had his stool with black color. He also suffered from nausea, vomiting, and pain on epigastrial. Laboratory findings are : Hb 7,6 gr/dl, MCV 72 fl, MCH 25 pg , MCHC 28%, SI < 50 ng/dl, TIBC 525 ng/ Dl. Physical examination found with angular cheilitis, liver and spleen without any abnormality.
1. What are the supporting examinations needed to confirm the dignosis above?
2. Explain the blood smear and bone marrow examinations finding will found at the patient above!
3. What is the other possibility diagnosis of the case? Explain your answer! 4. What are the possible etiology caused the anemic condition of the case? Self Asessment
1. Understand clinical manifestation of IDA
IRON DEFICIENCY ANEMIA
(The Epidemiology & Pathophysiology)
Dr. dr. Ketut Suega, SpPD KHOM
IRON DEFICIENCY ANEMIA
(The Diagnostic of Iron Deficiency Anemia)
Study Guide Hematologic System & Disorders & Clinical Oncology
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 4 (Tuesday, November 29th 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 5 ( Wednesday, November 30th 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 6 (Thursday, December 1st 2016)
IRON DEFICIENCY ANEMIA
(Aspect of Therapy in Adults)
Dr. dr. Ketut Suega, SpPD KHOM
Iron Deficiency Anemia
(Aspect of Therapy in Children)
dr. A.A. Widnyana, Sp.A
HEMOLYTIC ANEMIA
Sub Topic: Overview of Hemolytic Anemia
Study Guide Hematologic System & Disorders & Clinical Oncology
Dr. Ketut Ariawati, SpA(K)
Abstract
Congenital hemolytic anemias result from mutations that quantitatively or qualitatively influence the function of red vlood cell proteins. These mutations can be broadly grouped into three categories : membrane defects, enzymatic defects, and hemoglobin defects. While many mutations have been described in each category, only a small number are commonly encountered in clinical practice.
Clinical findings and specialized laboratory studies are often required to precisely define the underlying disease process. This general approach is true especially in the case of congenital hemolyitic anemias :
In all patients with hemolytic anemia, a careful history and physical examination are important.
1. The history should explore the chronicity of the problem, ethnic and racial background, family history, underlying or associated medical conditions, and new medications.
2. Jaundice is a common finding. Splenomegaly may also be associated with a wide variety of hemolytic disorders.
Various laboratory abnormalities are associated with hemolysis.
1. An elevated reticulocyte index is typical , consistent with a compensatory bone marrow response to anemia. Bone marrow examination is not necessary for most patients.
2. Increased lactate dehydrogenase, uncojugted bilirubin, and depressed or absent haptoglobin are also observed with hemolysis.
3. The red blood cell (RBC) morphology is frequently abnormal and provides an important clue to the underlying disease process.
4. The peripheral blood smear is rarely pathognomic.
Learning task
Patients of 2 years, male with pale since 2 month ago, not history of bleeding, and fever. The abdominal became more bigger since 1 months. History of transfusion ± six month ago because pale. Hemoglobin level is 3 g/dL, MCV is 68 fl, reticulocyte is 3%.
Answer the following questions :
1. Would you like to explain what kind the abnormalities in patient above. 2. What the laboratorium test you need to confirm this disease ?
3. What the differential diagnosis in patient above ?
Self assessment
1. Describe classification of congenital hemolytic anemia.
2. Explain clinical presentation and laboratory evaluation of congenital hemolytic anemias 3. Explain the principle management of congenital hemolytic anemias
Lecture - 1
HEMOLYTIC ANEMIA
Study Guide Hematologic System & Disorders & Clinical Oncology
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 :
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 7 (Friday, December 2nd 2016)
Abstract
Aplastic anemia is one type of anemia with incidence worldwide is 2 to 5 cases/million population per year in industrial countries. Characterized by pancytopenia and markedly hypocelluler marrow. The pathogenesis underlying anemia aplastic could be an immune suppression of marrow, toxic injury to stem and / or progenitor cells, and inherited instrinsic stem cell defect. Clinical features of aplastic anemia shown anemic syndrome, bleeding or infection as
Lecture - 2
HEMOLYTIC ANEMIA
Sub Topic: Acquired Hemolytic Anemia
dr. Tjokorda Gde Dharmayuda, SpPD KHOM
APLASTIC ANEMIA
Study Guide Hematologic System & Disorders & Clinical Oncology a consequences of cytopenias. Supporting examination recommended are complete blood count, and bone marrow aspiration.
Learning Task :
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, December 5th 2016)
ABSTRACT
The macrocytic anemias are a morphological classification of anemias that have an MCV of greater than 100 fL. Broadly defined, the macrocytic anemias are divided into two categories megaloblastic and nonmegaloblastic processes. If the source of the anemia is a vitamin B12 or folic acid deficiency, the anemia is termed megaloblastic. If the source of the anemia is unrelated to a nutritional deficiency, the anemia is macrocytic but not megaloblastic.
Vitamin B12 or folic acid deficiency leads to impaired DNA synthesis, a serious condition, and will affect all readily dividing cells, skin cells, hematopoietic cells, and epithelial cells. The effects on the bone marrow, peripheral smear, and the 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 Task
1. How is the metabolism of B12 and folic acid in the body?
2. Explain the possible etiology of B12 and folic acid deficiency anemia! 3. Explain the way of diagnostic B12 and folic acid deficiency anemia! Self Assessment
1. Understand the metabolism of B12 and folic acid in the body. 2. Mention the etiology of B12 and folic acid deficiency anemia.
3. Mention the clinical presentation of B12 and folic acid deficiency anemia.
MACROCYTIC & MEGALOBLASTIC ANEMIAS
Study Guide Hematologic System & Disorders & Clinical Oncology
DAY 9 (Tuesday, December 6th 2016)
Learning task
1. What is definition of polisitemia?
2. Explain the pathophysiology of polisitemia? 3. Mention the sign and symptom of polisitemia! 4. What are laboratory finding in polisitemia? Abstract, Self Asessment & Case Study on Lecture
DAY 10 (Wednesday, December 7th 2016)
Learning Task
Bayu, A seven years old man came to the pediatric emergrncy at Sanglah Hospital with hematoma at hand and femur with diameter 7 cm x 5 cm , 4 cm x 4 cm. Hematoma disappear after trauma four days ago. What do you do to diagnosis the patiens ? ( anamnesis, physical examination, laboratory evaluation )
Self Assessment
1. How the patterns of clinical bleeding in disorders of hemostasis ( primary hemostasis and secondary hemostasis ) ?
2. What the bleeding manifestation in hemophilia ?
3. Classify hemophilia A and B according to the degree of severity ?
POLYCITEMIA
dr. Tjokorda Gde Dharmayuda, SpPD KHOM
Lecture - 1
BLEEDING DISORDERS
Sub Topic: Hemophilia
Study Guide Hematologic System & Disorders & Clinical Oncology
ABSTRACT
Von 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 Task
1. Learn how the pathophysiology of VWD.
2. How is the clinical manifestation and type of VWD?
3. What are the laboratory evaluation needed as a diagnostic tools for VWD? Self Assessment
1. 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.
DAY 10 (Wednesday, December 7th 2016)
ABSTRACT
Platelets are produced in the bone marrow by fragmentation of the cytoplasm of megakaryocytes, one of the largest cells in the body. The main function of platelets is the formation of mechanical plugs during the normal haemostatic response to vascular injury. In the absence of platelets, spontaneous leakage of blood through small vessels may occur.
Thrombocythemia or thrombocytosis is present if the platelets are constantly elevated to more than 600,000/μL. Thrombocytosis can occur as primary which is the rarest part of
Lecture - 1
BLEEDING DISORDERS
Sub Topic: Von Willebrand
dr. A. A. Widnyana Sp.A
Lecture - 2
BLEEDING DISORDERS
Sub Topic: Thrombocyte Disorders:
Thrombocytopenia/ITP, Thrombocytosis
Study Guide Hematologic System & Disorders & Clinical Oncology Thrombocytopenia, by definition, exists when the platelet count drops below normal limit. It is possibly due either to decreased bone marrow production of platelets or increased destruction and sequestration of the platelets from the circulation, or both.
Learning Task
1. Learn how to differentiate the primary and secondary thrombocytosis?
2. What are the possible etiology caused the primary and secondary thrombocytosis? 3. How to classify the thrombocytopenia due to it’s cause?
4. How to diagnose and to treat an ITP patient? Self Assessment
1. 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 11 (Thursday, December 8th 2016)
ABSTRACT
Cellular systems and biochemical processes related to the bleeding prevention or blood coagulation mechanism of humans are very complex. The syntheses of the influential components (proteins, cells and blood vessels) constantly interact in balance so as to make sure that neither bleeding nor coagulation happen within the blood vessels throughout life. In this opportunity we will discuss approaches to patients with bleeding and those with abnormal blood coagulation as well as several situations that may happen to the patient as the result of the process disorders. Learning Task
1. Learn how to make diagnosis and treat DIC patient Case Study
A patient with decrease of consciousness after had snake bite. He got hematome in the bitten area and abdomen. He also had red color of urine.
1. 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 Assessment
1. Understand the principle of hemostasis
2. Describe the possible etiology, clinical features, laboratory findings of DIC 3. Mention the clinical features, laboratory findings of APS
Lecture - 1
DISSEMINATED INTRAVASCULAR
COAGULOPATHY
Study Guide Hematologic System & Disorders & Clinical Oncology
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 12 (Friday, December 9th 2016)
Abstract
1. Criteria for acceptability of blood donors are established to protect the health of donor and recipient
2. Blood donations are processed into components
3. Stored blood components undergo changes that can influence the efectiveness of transfusion
4. Routine pretransfusion testing should be done before the transfusion
5. In unexpected RBC ab are found, the antigen specifisity is determined and antigen neg RBC are provide
6. Transfusion is generally be safe but can result in adverse out come 7. The reactions can be mild clinical effects
8. More serious reaction wich are un common include, hemolysis, bacterial contamination, anaphylaxis and TRALI
9. Serious transusion-transmitted diseases are now rare due to progress in donor screening and testing how ever hepatitis and HIVare still possible
Learning task
1. Why the FDA establish the criteria for acceptability of the blood donor?
2. What are we doing to reduce the incidence of transfusion-transmitted diseases?
3. Although we are already make a good laboratory screening to the blood for transfusion, but the blood is still not 100% safe, why?
4. What is the benefit of using blood component?
5. Is using whole blood really not good? Please give your explanations?
Self Assessment
1. Characteristic of blood donations 2. Components of blood
Lecture - 2
THROMBOSIS
dr. Losen Adnyana, Sp.PD KHOM
ABO INCOMPATIBILITIES
Study Guide Hematologic System & Disorders & Clinical Oncology CASE STUDY
One patients foreigner was hospitalezed in sanglah. Hospitalized because of anemia, she was bleeding while having a baby and need blood transfusion.
1. What kind of information you need before you ask some blood to the Blood Bank? 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 13 (Tuesday, December 13th 2016)
Abstract
Acute leukemia is defined as the malignant accumulation of transformed hematopoietic progenitor cells. Leukemic blast cells retain the capability of self renewal, but unlike normal hematopoietic stem cells (HSCs), they have limited or no potential for terminal differentiation. Leukemic infiltration of the marrow space ultimately leads to bone marrow failure, so most patient present with consequences of cytopenias. The acute leukemias can be classified by morphology, histochemical staining, and immunophenotype into two broad category : acute myelocytic leukemia (AML) and acute lymphocytic leukemia (ALL). The distinction between the two acute leukemias in clinically important because the treatments and prognoses are different.
Learning Task
Kadek, six years old girl came to pediatric emergency at Sanglah Hospital with cheap complaint pale, hematoma at femur, gum bleeding, limfadenopati and hepatosplenomegali. Doctors at hospital do examination CBC.
Lab data : Erythrocyte and hemoglobin count are below normal Leucocyte total count 85 x 109 /L
Leucocyte distribution on differential count is as follows Blast form 86 %
Prolymphocyte 5 % Lymphocyte 9 % Platelet count is very low
Answer the following questions
1. What diagnosis is most likely for this case ? 2. What additional test can be performed ? 3. What is the prognosis of the case ?
LEUKEMIA
(Acute Leukemia)
Study Guide Hematologic System & Disorders & Clinical Oncology Self Assessment
1. What are the symptoms and sign of acute leukemia ? 2. Do you know the general classification for leukemia ? 3. When would it be suitable to forward a leukemia patient? Learning Task
1. How do you define malignant hematology? 2. Name the types of malignant hematology
3. What are the prognostic factors for acute myeloblastic leukemia? 4. Outline the classification for acute myeloblastic leukemia
5. Explain the principles for treating acute myeloblastic leukemia. 6. How would you educate an acute myeloblastic leukemia patient?
DAY 13 (Tuesday, December 13th 2016)
CLL Abstract:
Chronic Lymphocytic Leukemia is a neoplastic disease characterized by accumulation of small, mature lymphocytes in blood, marrow and lymphoid tissues. The incidence of about 3 per 100.000 population in the United States and become most commonly adult leukemia in Western societies. Hereditary factors, genetic and immunoglobulin abnormalities play a role in CLL. Ninety percent of patients are over age 50 years. Twenty five percent are asymptomatic, and others with lymph node enlargement. Examination supported the diagnosis are blood examination, marrow biopsy and lymph node biopsy.
Learning Task :
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 CLL 2. Describe the hematology manifestation of CLL 3. Mention how to diagnose CLL
CML Abstract
CML is a hematopoietic malignancy originating from transformation of primitive hematopoietic cell. CML progresses from an initial chronic phase characterized by marrow hyperplasia and increased numbers of circulating differentiated myeloid cells followed by
LEUKEMIA
(Chronic Leukemia)
Study Guide Hematologic System & Disorders & Clinical Oncology 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 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? Self assessment:
1. Describe the sign and symptom af CML 2. Mention the CML Phase
Study Guide Hematologic System & Disorders & Clinical Oncology DAY 14 (Wednesday, December 14th 2016)
Abstract
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 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.
Case
Female 67 years old come with pain on vertebra since 2 years ago and she also complain about body weakness and dizziness. Pyshical examination BP 150/90 mmHg, PR 108 x/menit, Tax 38 oC. Palpebra: Paleness. Laboratory result: WBC 15.103/mm3, Hb 8,4 gr/dl, PLT 100.103/mm3, BUN
Study Guide Hematologic System & Disorders & Clinical Oncology Learning task
1. Make the problem list for the patient! 2. What is diagnose fo the patient? 3. What kind of test should we do?
4. Base on the data, Explain the stage of this disease?! 5. Explain the patient management!?
Self asessment
1. Understand the sign and symptom Multiple myeloma 2. Understand the pathogenesis of Multiple myeloma. 3. Understand about how to diagnose Multiple myeloma. 4. Understand about the management of Multiple myeloma.
DAY 14 (Wednesday, December 14th 2016)
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 entity
3. Mention the clinical differences between HL and NHL 4. Mention the Ann Arbor staging system of Lymphoma 5. Mention the grouping lymphomas by clinical behavior
LYMPHOMA
Study Guide Hematologic System & Disorders & Clinical Oncology DAY 15 (Thursday, December 15th 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 16 (Friday, December 16th 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
DAY 17 (Thursday, December 19th 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
Overview of Lymphadenopathy
Doctors from Oncology Department
LYMPHADENOPATHY
(Pathogenesis & Diagnosis)
Doctors from Oncology Department
LYMPHADENOPATHY
(Surgical Aspects)
Doctors from Oncology Department
LYMPHADENOPATHY
(Medical Aspects)
Study Guide Hematologic System & Disorders & Clinical Oncology DAY 18 (Tuesday, December 20th 2016)
Abstract:
Microcytic 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 Task
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).
1. 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. Erythoropoietin c. Folic acid d. Intrinsic factor e. Iron
2. 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 diet
b. Erythropoietin injections c. Ferrous sulfate tablets d. Folic acid supplements e. Hydroxocobalamin injections
3. 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 associated with acute iron poisoning usually includes
a. Dizzines, hypertension, and cerebralhemorhage b. Hyperthermia, delirium, and coma
c. Hypotension, cardiac arrhythmias, and seizures
d. Necrotizing gastroenteritis, shock, and metabolic acidosis
Medicaments Therapy in Hematology
Agent used in anemias
Study Guide Hematologic System & Disorders & Clinical Oncology e. Severe hepatic injury, encephalitis, and coma
Abstract
The 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 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 agents
2. Discuss about potential drug interaction in a patient who is on chemotherapy agents taking vitamins
3. Discuss some considerations in selecting immunosuppressive agents. Self-assessment
1. Describe classification of chemotherapy agents
2. Describe common adverse drug reactions of chemotherapy 3. Describe route of administration of chemotherapy
4. Describe classification of immunosuppressive agents
DAY 19 (Wednesday, December 21st 2016)
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.
Medicaments Therapy in Hematology
Chemotherapy and immunosuppressive agents
Desak Ketut Ernawati., Ph.D., Apt
Laboratory Picture of Patient with Blood Cells
Disorder
Study Guide Hematologic System & Disorders & Clinical Oncology 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 of the 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 20 (Thursday, December 22nd 2016)
Abstract, Learning Task, Self Asessment & Case Study on Lecture
Lecture - 1
Pathology Diagnostic of Tumor
Study Guide Hematologic System & Disorders & Clinical Oncology
Abstract :
The role of imaging in oncology include screening of the primary tumor, radiological diagnostic of the primary tumor, evaluate tumor extension and metastatic of the tumor radiologically (radiological staging), treatment planning, and follow up (evaluation of the treatment result and detection of the recurrence tumor). There are many kind of imaging modality that can be use in oncology field. Those imaging modality including conventional radiography (plain or contrast study), ultrasonography, computed tomography (CT) scan, magnetic resonance imaging (MRI), also radioisotope scanning/ nuclear medicine. For oncologic imaging manner, those imaging modality can be combine each other, depend on the indication of each disease. While choosing imaging modality, we should be always considered about indication, weakness and advantage of each imaging modality, so that the radiological examination will give optimal benefit for the patient.
Learning task
1. A 23-years woman complained about having a mobile lump at her left breast since one month ago.
Question :
a. What the diagnosis possibility ?
b. What kind of imaging examination that can be used for helping establish the diagnosis ?
2. A 50-years woman, has complained about having a hard, non mobile lump at her left breast and left axillar region since one month ago. She also complained about retracted nippled at her left breast.
Question :
a. What the diagnosis possibility ?
b. What kind of imaging examination that can be used for helping establish the diagnosis and staging for this patient?
c. If you have an asymptomatic patient (age > 50 year), what kind of breast cancer radiological screening that should be performed by this patient?
3. A young health man has a family history of colon cancer. What kind of imaging examination that can be use for screening ?
Self Assessment :
1. Explain about the role of imaging in oncology.
2. Mention about type of imaging modality for evaluating malignancy process of the bone, liver, brain, spinal cord, lung, breas
