Lecture 1.Introduction of Hematologic System and Disorders
and General Oncology
Clinical Oncology
DAY I Monday, Sept, 7
th
2015
SEPT,7th 2009
SEPT,7th 2009
Sub topic : Introduction of Hematologic System and Disorders
Prof.Dr. dr. Ketut Suega, SpPD KHOM
Abstract Hematologic System and Disorders is the discipline that studies the normal and abnormal
conditions of the blood and is components. Plasma component of the blood consists of several proteins which are instrumental in the process of coagulation, anti-coagulation, as
well as fibrinolytic reactions. One of the most particular characteristics of the hematopoietic system is the perpetual regeneration process of blood cells throughout the lifespan of the
organism. Pluripotent hematopoietic stem cell HSC is the precursor of blood cells. The components
of blood from HSC that actively circulate are erythrocytes, leukocytes, and thrombocytes. Lymphocytes are among the components produced by HSC, and thus the field of
hematology also includes in it the studies of reticuloendothelial system and lymph nodes. No individual organ can be specifically linked to hematology disorders; the problems could
manifest themselves at the bone marrows, lymphatic organs, intravascular compartments where the red blood cells circulate, or endothelial cells along the blood vessels and the
proteins in the plasma component.
Sub theme General Oncology is the discipline that studies the general aspect of tumor malignancy cancer describe epidemiology, cancer prevention, therapy of cancer
rehabilitation patient with cancer.
At the end of this program, medical students are expected to: 1. Understand medical 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.
Udayana University Faculty of Medicine, MEU
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11. CONTENT OUTLINE AND LEARNING TASKS
Lecture 2.Introduction of Hematologic System and Disorders and General
Oncology
Sub topic : Introduction of Clinical Oncology
Dr. Wayan Sudarsa, SpBOnk
Laboratory picture of patient with blood cells disorder
Clinical Oncology 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.
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 Tuesday, Sept 8
th
2015
Dr. dr. Sianny Herawati, Sp.PK
Udayana University Faculty of Medicine, MEU
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Lecture 1. Hematopoesis Sub topic : Leukopoesis
Clinical Oncology
The differential diagnosis of anemia is broad. The likely cause of anemia in an individual patient can be narrowed by systematic evaluation. Critical information includes
measurements of the erythropoietic response and measurement ofRBC size. These data provide a framework that guides the selection of more specific studies to establish
underlying diagnosis. The complete blood count CBC is a laboratory report of the cellular elements of the blood.
CBC is now routinely performed with an automated instrument. Seven values relating to RBC are reported in CBC, including Hb, RBC count, MCV, MCH,
MCHC and RDW.
Hb is direct measure ofthe concentration of Hb in grams per deciliter.
Hct is the volume RBCs expressed as a percentage of whole blood
volume. RBC count is direct measure of the 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 9
th
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.
Granulocytopoiesis
Udayana University Faculty of Medicine, MEU
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Lecture 2. Hematopoesis Sub topic:Thrombopoesis
Clinical Oncology
Eosinophil, Basophil and Neutrophil are derive from unipotential stem cell ,respectively, CFU-Eo, CFU-Ba, and CFU-G. Each of these stem cells is descendant of pluripotential
stem cell CFU-S. Thus, CFU-Eo, CFU-Ba and CFU-G undergo mitosis giving rise to myoblasts. Myoblast undergo mitosis giving rise to promyelocytes, which in turn divide to
form myelocytes. On this step the specific granules are present and three granulocyte lines may be recognized. The subsequent stage of maturation is metamylocyte then to the
granulocyte with a band-shaped nucleus, and finally to the mature granulocyte neutrophil, eosinophil, and basophil.
Monocytopoiesis Monocyte is derive from the bipotential stem cell, CFU-GM, whose undergoes mitosis and
gives rise to two unipotential stem cells, CFU-G and CFU-M monoblasts. The next stage of maturation is promonocytes and finally to the mature monocyte. Every day, the
average adult forms more than 10
10
monocytes, most of which enter the circulation. Within a day or two, the newly formed monocytes enter the connective tissue spaces of the body and
differentiate into macrophages.
Lymphopoiesis The multipotential stem cell CFU-Ly divides in the bone marrow to form the two unipotential
progenitor cells, CFU-Ly B and CFU-Ly T, neither of which is immunocompetent. CFU-LyB migrates to a bursa-equivalent location in the bone marrow, divides several times and
giving rise to immunocompetent B lymphocytes. CFU-lyT cells undergo mitosis, forming immunocompetent T cells, which travel to the cortex of thymus. On thymus CFU-lyT
proliferate, mature and begin to express cell surface markers. As these surface markers appear on T-cell plasmalemma, the cell become immunocompetent T lymphocytes.
Learning Tasks :
1. Explain the classification, structure and function of leucocyte 2. Explain the formation of the leucocytes
3. Explain the regulation of the leucocytes formation 4. Explain the maturation of lymphocyte
5. Discuss in your group the definition, sign and symptom, causes, diagnosis and
treatment of the agranulositosis
6. Discuss in your group the abnormality of leucocyte formation
Self Assessment :
1. Describe the structure of the leucocytes 2. Describe the Granulocytopoiesis, Monocytopoiesis, and Lymphopoiesis
Dr.dr. Sianny Herawati, Sp.PK
Learning Task:
1. Describe about trombopoiesis 2. Describe about the mechanism of platelet release.
3. Describe about thrombocyte maturation 4. Describe regulation of trombopoiesis
Udayana University Faculty of Medicine, MEU
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Lecture 1. Hematopoesis Sub topic : Erythropoesis
Clinical Oncology
Self assessment:
1. Explain the characteristics of the thrombocyte 2. Explain about thrombopoietin
3. Explain the ultrastructural of thrombocyte 4. Explain the characteristics of megakaryocyte
5. Explain role of the spleen in platelet production. 6. Explain platelet life span and turnover of platelet
DAY 4 Thursday, Sept 10
th
2015
dr. NI Kadek Mulyantari, Sp.PKK
ABSTRACT Under physiologic condition, the red-cell mass is maintained in equilibrium by appropriate
adjustments of red-cell production. The erythropoiesis results from the action of erythropoietin on colony-forming unit –erythroid CFUe. Erythropoietin is produce by the
action of renal erythropoietic factor REF, which is derived from the kidneys under the secondary influence of hypoxic condition.
In vivo, the mature erythrocyte is a biconcave disk with a surfact-to-volume ratio that enables optimal gaseous interchange. The cells also is deformed easily and, consequently,
can pass through small vessels and capillary without rupture. The re-cells membrane is composed of matrix formed from a double layer of phospholipids.
The main fuction of red-cells membrane are to maintain cell-shape deformability for osmotic balance between plasma and cell cytoplasm, to help in the tranfostation of essential cellular
ions and gases. Maturation entails changes in the nucleus and the cytoplasm of cells. As maturation
progress, the nuclei became smaller, and their structure becomes denser and more coarse. Normal red-cell maturation : Pronormoblast rubriblast- Basophilic normoblast –
Polychromatic normoblast – Orthochromatic normoblast –reticulocyte – mature erythrocyte. The average life of a red cell approximates 120 days, and fewer than 2 of the circulating
cells are newly produce and released from the bone marrowas reticulocytes.
Learning Tasks :
1. Explain the erythropoesis process and normal red-cell maturation 2. What is the erythrocyte function?
3. Mention the nutritional requirement of erythropoesis process 4. In normal condition, what kind of erythrocytes series can we find in peripheral blood
and in bone marrow? 5. Describe the structure of erythrocyte if lack of this nutrient : vitamin B12 and iron
during the erythrocytopoesis
Self Assesment :
1. Understand the erythropoesis process and normal red-cell maturation. 2. Understand the erythrocyte function
3. Understand about the factors that influence of erythropoesis process
Udayana University Faculty of Medicine, MEU
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Lecture 2. Hematopoesis Sub topic : Synthesis of hemoglobin, function of
blood and blood cells metabolism
Prof. dr. Nyoman Agus Bagiada,SpBiok
Clinical Oncology
Case 1. Women patient 35 years old, visiting her family physician complaining tired and feeling weak
after delivery one week ago. The baby weight 4 kg. She got 5 stitches on perineum. Physical examination showed that the heart rate 100 xmint, and face pale. The breathing
frequency 30 xmint. Blood examination found Hb 7 mg and haematocrite 35
Learning task
1. What happenedin this patient? 2. What is the cause?
3. Why she feel weak and tired? 4. What is the normal value of women Hb and haematocrite?
5. Why the heart rate and breathing rate increase? 6. What is 2,3 BPG. What is the function?
7. What happen when some one come to high altitude? 8. How many kind of Hb do you know and what are difference?
Self Assessment
1. Define the normal value of whole blood in man and women 2. Define the complete blood function
3. How Hb are synthesize an degradation 4. What are the iron function in Hb
5. What is the similar and the difference of Hb and Mb
DAY 5 Friday sept, 11
th
2015
Udayana University Faculty of Medicine, MEU
24
Lecture 1. Anemia Sub topic : Pathophysiologi and
Classification of anemia
Dr. Ketut Ariawati, SpA K
Lecture 1. Anemia Sub topic : Pathophysiologi and
Classification of anemia
Dr. Ketut Ariawati, SpA K
Clinical Oncology 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.
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 gdL, 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
Udayana University Faculty of Medicine, MEU
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Nutritional Anemia Sub topic General Information Nutritional Anemia
Sub topic Patofisiology of Iron Deficiency Anemia
Clinical Oncology
Learning task
1. What is definition of polisitemia? 2. Explain the pathophysiology of polisitemia?
3. Mention the sign and symptom of polisitemia 4. What are laboratory finding in polisitemia?
DAY 6 Monday, Sept 14
th
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 grdl, MCV 72 fl, MCH 25 pg ,
MCHC 28, SI 50 ngdl, 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
Udayana University Faculty of Medicine, MEU
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Lecture 2. POLISITEMIA
dr. Tjokorda Gde Dharmayuda, SpPD KHOM
Lecture 2. POLISITEMIA
dr. Tjokorda Gde Dharmayuda, SpPD KHOM
Nutritional Anemia The diagnostic of iron deficiency anemia
Dr.dr. Ketut Suega, SpPD-KHOM
Nutritional Anemia Sub topic Pathophysiology and management diagnostic of
folic acid and B12 deficiency anemia
Sub topic The diagnostic of folic acid and B12 deficiency anemia
Dr. Ni Made Renny Anggreni Rena, SpPD Study Guide Hematologic System Disorders
Clinical Oncology
DAY 7 Tuesday, Sept 15
th
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 grdl, MCV 72 fl, MCH 25 pg , MCHC 28, SI 50 ngdl, TIBC 525 ng Dl. Physical examination found with angular
cheilitis, liver and spleen without any abnormality.
1. What are the supporting examinations needed to confirm the dignosis above? 2. Explain the blood smear and bone marrow examinations finding will found at the
patient above 3. What is the other possibility diagnosis of the case? Explain your answer
4. What are the possible etiology caused the anemic condition of the case?
Self Asessment
1. Understand clinical manifestation of IDA 2. Understand the way to make diagnosis of IDA
3. Understand how to prevent the IDA
DAY 8 Wednesday, Sept 16
th
2015
ABSTRACT
Udayana University Faculty of Medicine, MEU
27
Acute Leukemia Subtopic AML, ALL
Clinical Oncology 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.
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 KHOM dr. AA Widnyana, SpA
Abstract Acute leukemia is defined as the malignant accumulation of transformed hematopoietic
progenitor cells. Leukemic blast cells retain the capability of self renewal, but unlike normal hematopoietic stem cells HSCs, they have limited or no potential for terminal
differentiation. Leukemic infiltration of the marrow space ultimately leads to bone marrow failure, so most patient present with consequences of cytopenias. The acute leukemias can
be classified by morphology, histochemical staining, and immunophenotype into two broad category : acute myelocytic leukemia AML and acute lymphocytic leukemia ALL. The
distinction between the two acute leukemias in clinically important because the treatments and prognoses are different.
Learning Task
Udayana University Faculty of Medicine, MEU
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Lecture 1. Nutritional Anemia Sub 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
Clinical Oncology 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 10
9
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 ?
Self Assessment
1. What are the symptoms and sign of acute leukemia ? 2. Do you know the general classification for leukemia ?
3. When would it be suitable to forward a leukemia patient?
Learning Task
1. How do you define malignant hematology?
2. Name the types of malignant hematology
3. What are the prognostic factors for acute myeloblastic leukemia?
4. Outline the classification for acute myeloblastic leukemia
5. Explain the principles for treating acute myeloblastic leukemia.
How would you educate an acute myeloblastic leukemia patient?
DAY 10 Friday, Sept 18
th
2015
Learning task: 1 Describe the normal mechanism of regulation of iron absorption in the body
2. Describe the normal mechanism of regulation of iron storage in the body 3. Describe the acute and chronic toxicity of iron
4. Sketch and explain the enzymatic reaction that use folates 5. Describe the clinical applications of vitamin B12 and folic acid
Self assessment
1. Explain role of iron in the body
Udayana University Faculty of Medicine, MEU
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Aplastic Anemia Anemia of Chronic Diseases
Clinical Oncology 2. Describe the clinical applications of iron
3. Whey iron should not given in hemolytic anemia? 4. Explain role of vitamin B12 and folic acid in the body
DAY 11 Monday, Sept 21
th
, 2015
dr. Losen Adnyana, SpPD KHOM
Aplastic Anemia Abstract
Aplastic anemia is one type of anemia with incidence worldwide is 2 to 5 casesmillion 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 gdL, WBC 1.1 x 10
9
l ANC 0.3 x 10
9
l, platelets 17 x 10
9
l. Her chest X ray shows pneumonia. a. What further investigations should be undertaken?
b. What are the possibility diagnostic for this patient? c. What seems to be the cause of this case?
Self Assessment :
1. Explain about the principles of pathogenesis of aplastic anemias. 2. Mention the type of aplastic anemias.
3. Mention the clinical manifestation and laboratory findings in Aplastic Anemia
Anemia of Chronic Disease Abstract
Anemia associated with chronic infection, inflammatory disease or neoplasma disease. One or two months of sustained disease is required for anemia develop.
Anemia is moderate, with a hemoglobin level between 7 and 11 gdl 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
Udayana University Faculty of Medicine, MEU
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Platelet function and disorder Sub topic trombositosis
Sub topic trombositopenia
DR Dr Ketut Suega,SpPD-KHOM Dr Ni Made Renny Anggreni Rena,SpPD
Clinical Oncology The cause of the anemia of chronic disease is multifactorial and includes a mildly decreased
life span of erythrocytes coupled with deregulation iron absorption and transport, a direct inhoibition of hematopoiesis and a relative deficiency of erythropoietin. Research over past
decade has delineated the important role of inflammatory cytokines in each of these causes and the emerging role of the iron regulator hepcidin in the patogenesis of ACD.
No treatment my be necessary. Iron by mouth or parenterally is contraindicated. Paced red cell transfusion my be given, if the anemia is symptomatic. Recambinant human
erythropoietin therapy is efeective if serum EPO is low.
Male, 40 years old come to clinic with complain: Cough since 1 years ago. There are phlegm and blood cough. Cough companied by fever and decrease of body weight 5 kg in
six months. Physical examination: Blood pressure 11080 mmHg, Pulse rate 98 xmint, T 37,5
C. Chest x-ray: support lung tuberculosis. Laboratory result WBC 12.10
3
mm
3
, Hb 8,5 gdl, MCV 75, MCH 26 dan PLT 440.10
3
mm
3
.
Learning task:
1. Explain the patient problema 2. What are diagnosis?
3. Explain the mechanism of anemia in this case 4. Explain the patient management
Self assessment: 1. Describe the sign and symptom of ACD
2. Explain the pathophysiology of ACD 3. Mention the kinds of test for ACD
4. Explain the patient management
DAY 12 Tuesday, Sep 22
th
2015
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 600,000μL. 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.
Udayana University Faculty of Medicine, MEU
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Hemostasis Sub topic Principle of hemostasis
Sub topic DIC, APS
DR Dr Ketut Suega,SpPD-KHOM Dr Ni Made Renny Anggreni Rena,SpPD
Clinical Oncology
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 13 Wednesday, Sep, 23
th
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 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
Udayana University Faculty of Medicine, MEU
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Lecture 1. Hemofilia
Dr AA Widnyana,SpA
Lecture 2. Von Willebrand’s disease
Dr Ni Made Renny Anggreni Rena,SpPD Study Guide Hematologic System Disorders
Clinical Oncology
DAY 14 Friday, Sep 25
th
2015
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 ?
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
Udayana University Faculty of Medicine, MEU
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Malignan Lymphoma and Diagnostic Pathology
Lecture 1. Hemolytic Anemia Sub topic Congenital hemolytic anemia, hemoglobinopati
Clinical Oncology 2. Describe the bleeding manifestation in von Willebrand diasease
3. Understand the laboratory examination support the VWD.
DAY 15 Monday, Sep 28
th
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 entity 3. Mention the clinical differences between HL and NHL
4. Mention the Ann Arbor staging system of Lymphoma 5. Mention the grouping lymphomas by clinical behavior
DAY 16 Wednesday, Sept 30
th
2015
Dr. Ketut Ariawati, SpAK
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.
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Lecture 2. Hemolytic Anemia Sub topic Acquired hemolytic anemia
dr. Tjokorda Gde Dharmayuda, SpPD KHOM Study Guide Hematologic System Disorders
Clinical Oncology 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 gdL, 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
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
Udayana University Faculty of Medicine, MEU
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Blood transfusion and Blood banking
Dr. Ni Kadek Mulyantari, Sp.PKK
Clinical Oncology anemia. When bone marrow erythropoesis cannoyt keep up with the shortened length of
RBC survival, hemolytic anemia result.
Learning Task :
1. Young female come with complain of yellowish eyes, feeling weak and dizzy since around 3 days before admitted to hospital. On physical examination found icteric on
eyes, and pale on hand and foot. Patient without history of bleeding before. Laboratory results HGB 8.3 mgdL, Leukosit 5900mm
3
, thrombocyte 410.000mm
3
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 1
st
2015
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
Udayana University Faculty of Medicine, MEU
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Lecture 1. Multiple myeloma
Dr. Losen Adnyana, SpPD KHOM
Clinical Oncology 3. Indications of transfusion
4. Complications of transfusion
CASE STUDY One patients foreigner was hospitalezed in sanglah. Hospitalized because of anemia, she
was bleeding while having a baby and need blood transfusion. 1. What kind of information you need before you ask some blood to the Blood Bank?
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 2
nd
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
Udayana University Faculty of Medicine, MEU
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Lecture 2. MDS, Langerhans cell tumor
dr. Losen Adnyana,SpPD Study Guide Hematologic System Disorders
Clinical Oncology 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 15090 mmHg, PR 108
xmenit, Tax 38
o
C. Palpebra: Paleness. Laboratory result: WBC 15.10
3
mm
3
, Hb 8,4 grdl, PLT 100.10
3
mm
3
, BUN 78 mgdl, creatinin 4 mgdl. Bone survey : lesi osteolitik multipel in vertebre
Learning task
1. Make the problem list for the patient 2. What is diagnose fo the patient?
3. What kind of test should we do? 4. Base on the data, Explain the stage of this disease?
5. Explain the patient management?
Self asessment
1. Understand the sign and symptom Multiple myeloma 2. Understand the pathogenesis of Multiple myeloma.
3. Understand about how to diagnose Multiple myeloma. 4. Understand about the management of Multiple myeloma.
Abstract Myelodysplasia is the term used to encompass a diverse group of neoplasms that have in
common their origin in somatic mutation in multipotential hematopoietic cell. Characterized by ineffective hematopoiesis, cytopenias, qualitative disorders of blood cells and their
precursors and variable predilection to evolve into acute myelogenous leukemia. Spectrum disease ranges from indolent mild to moderate anemia to more troublesome multycytopenia
with hypercelluler marrow.
The fundamental alteration is a somatic mutations in a multipotential hematopoietic cell resulting in trilineage blood cell abnormalities in most cases. Exposure to benzene,
chemotherapeutic agents especially alkylating agent or high dose radiation can cause myelodysplastic disoerder as well as acute myelogenous leukemia.
Onset is usually after age 50 years but it may be seen in children. In younger adults, it is often preceded by chemotherapy or irradiation. May be asymptomatic if mild
anemia and small changes in platelet and white cell counts. If moderate or severe anemia and or granulocytopenia and thrombocytopenia develop, pallor, dysneu on exertion, easy
bruising.
Anemia occur more than 85 and my be macrocytic with circulating nucleated blast. Netropenia occurs in about 50, coarse chromatin, nuclear hyposegmentation, and
Udayana University Faculty of Medicine, MEU
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Lecture 1. Chronic Leukemia Subtopic CLL, CML
Clinical Oncology decreased cytoplasmic granulation of neutrophils commonly occur. Morrow abnormalities
include hypercellularity, delayed nuclear maturation, pathologic sideroblast, megakaryocytes with uni- or bolobed nuclei, mycromegakaryocytes and increased number of myeloblast.
Chromosomal abnormalities occur in up to 80 patients. Commonly abnormalities very similar to those in AML.
Treatment of patient with MDS remains challenging fort several reason. First, patient with this disorder are likely to be enderly, so comorbid disease and performance status are
critical components in deciding specific therapy. Second, the disease is heterogenous, 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 11080 mmHg, PR 108 xmenut, T 38,5
C, mild hepatosplenomegali +. Laboratory result: WBC 2.10
3
mm
3
, Hb 8,5 gdl, MCV 75, MCH 26 dan PLT 40.10
3
mm
3
.
Learning task
1. Make the problem list for the patient 2. What is diagnose fo the patient?
3. What kind of test should we do? 4. Base on the data, Explain the stage of this disease?
5. Explain the patient management?
Self asessment
1. Understand the sign and symptom MDS 2. Understand the pathogenesis of MDS.
3. Understand about how to diagnose MDS 4. Understand about the management of MDS
.
DAY 19 Monday, Oct 5
th
2015
dr. Losen Adnyana, SpPD KHOM
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 :
Udayana University Faculty of Medicine, MEU
39
Clinical Oncology 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 gdL, WBC 39 x 10
9
, platelets 91 x 10
9
l. Biochemical analysis shows : Urea 13 mmoll, Na+ 142 mmoll, K+ 5.5 mmoll, Ca2+ 3.15 mmoll.
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