1. Skmarina Hanna Larose S.
P. Vesper J. N. Zamili
Adolf Finsensius Sarumaha
Agnes Meinulo Duha
Alhoi Lesley Davidson
Annisa Maichie Kurniasih
Evie Clarensia Lase
Louis Mapolo Sutian
Maruli Freddy Simamora
Nikko Fernando Venesia
Nita Fatmasari Bangun
Rosnilam Moho
Siti Ramadhani
Sri Wahyu Ratnasari
Nasution
Tiorasi Pakpahan

2. Adi, a six-year-old-boy, can’t take school activities in his school for
six days because of having severe fever, myalgia and anorexia,
but lately, Adi’s face comes paler, his heart beats faster, malaise,
lose appetite, bleeding around his gums and petechiae,
ecchymosis in superficial. Adi has history of eating Chlorampenicol
often and antipiretic which are bought by his mother. Hence Adi’s
condition is worse, Adi is taken to pediatrician. Doctor suggests to
do a complete blood examination and Bone Marrow Punction.
What has happened to Adi and how is the management?

3. • Myalgia : pain on muscle
• Ecchymosis : patch of bleeding under skin with diameter > 2
mm
• Petechiae : patch of bleeding under skin with diameter < 2 mm
• Anorexia : appetite disruption
• Bone Marrow Punction : an examination by doing aspiration of
bone marrow liquid

4. 1. Adi, a six-year-old-boy, can’t take school activities in his
school for six days because of having severe fever, myalgia
and anorexia, but lately, Adi’s face comes paler, his heart
beats faster, malaise, lose appetite, bleeding around his gums
and petechiae, ecchymosis in superficial.
2. Adi has history of eating Chlorampenicol often and antipiretic
which are bought by his mother.
3. Doctor suggests to do a complete blood examination and
Bone Marrow Punction.

5. 1. - Probably caused by infection
- Probably caused by aplastic anemia
- Patient has hemostatic disfunction
- Probably having thrombosis disfunction
- Probably having pancytopenia
2. - Probably caused by toxin of medicines
- Lack of knowledge of patient’s mom
3. To uphold the final diagnose

6. Adi, a-six-year-old-boy, probably is having
anemia aplastic

7. 1. Classification of anemia
2. Definition of aplastic anemia
3. Etiology of aplastic anemia
4. Epidemiology of aplastic anemia
5. Classification of aplastic anemia
6. Pathophysiology of aplastic anemia
7. Clinical symptoms of aplastic anemia
8. Anamnesis of aplastic anemia
9. Physical examination of aplastic anemia
10. Supporting examination of aplastic anemia
11. Management of aplastic anemia
12. Prevention of aplastic anemia
13. Complication of aplastic anemia
14. Prognosis of aplastic anemia

8. A. Based on etiopathogenesis
I. Disturbance in erythrocytes formation and marrow bone
a. Deficiency of essential
a. Iron Deficiency
b. Folic acid deficiency
c. Vitamin B12 deficiency
b. Disturbance in Iron utilization
a. Chronic disease
b. Sideroblastic anemia

9. c. Marrow bone destruction
a. Aplastic anemia
b. Mieloptisica anemia
c. Hematologic anemia
d. Dyserythropoiesis anemia
e. Myelodisplastic syndrome
d. Deficiency of erithropoiesis
II. Hemorrhagic cause
III. Hemolitic cause
IV. Unknown and complex pathogenesis

10. B. Based on morphology
I. Hypochromic microcytic
II. Normochromic normocytic
III. Macrocytic
a. Megaloblastic
b. Non-megaloblastic

11. Aplastic anemia is a condition caused by decreasing of
peripheral blood hematopoietic cells such as erythrocytes,
leukocytes and platelets as a result of the cessation of cell
production in bone marrow hemopoetic.

12. a. Congenital Factor : Fanconi syndrome
b. Acquired factors :
• Chemicals : Benzene, insecticides, compound As, Au, Pb.
• Drugs : Chloramphenicol, mesantoin (anticonvulsants),
piribenzamin (antihistamines ), santonin - calomel, a drug
sitostatica (myleran, methrotrexate, TEM, vincristine,
rubidomycine etc. ), anti- tumor drugs (nitrogen mustard),
anti- microbial.
• Radiation : Roentgen rays, radioactive.
• Infection : Miliary tuberculosis, hepatitis and others - others.
• Malignancy : Kidney disease, endocrine disorders, and
idiopathic.

13. The incidence of acquired aplastic anemia varies around the
world and range from 2 to 6 cases per 1 million population per
year with geographic variation. Acquired aplastic anemia
generally appears at the age of 15 to 25 years; peak incidence
appears after the age of 60 years.

14. I. Primary
1 . Congenital abnormalities
2 . Idiopathic
II . Secondary :
1 . Due to radiation, chemicals, or drugs
2 . Due to other causes :
a. Virus Infection : Hepatitis Viruses / other viruses
b . Due to pregnancy
c . Radiation

16. 1. Tachycardia
2. Increasing of breathing frequency
3. Pale
4. Weakness
5. Dizzy
6. Nausea
7. Decreasing quality of skin and hair

17. a. Complaints eritroblastopenia
b. Complaints thrombocytopenia
c. Complaints eukopenia
d. History of treatment :
• Consume drugs in a long period of time
• Chemotherapy
• Often exposed to radiation like x-rays and radioactive
rontgen
e. previous Illness History
d. Family history of sitopenia

18. a. Inspection :
1. Pale
2. There are bruises, petechiae, or ecchymosis
3. bleeding gums
b. Palpation :
1. body temperature increase
2. cold extremities
3. tachicardy
4. Hepatomegaly (found in a several patients)
c. Percussion :
Hepatomegaly (found in a fraction of patients)
d. Auscultation :
gallop rhytm and wheezing

19. 1. Laboratory Examination
a. Peripheral Blood
According to The International Agranulocytosis and Aplastic
Anaemia Study (IAAS) is called anemia aplastik when:
i. the levels of hemoglobin ≤ 10 g/dl or Hematokrit ≤ 30%
ii. Count of platelets ≤ 50,000/mm3
iii. Leukocyte Count ≤ 3500/mm3 or Granulocytes ≤ 1.5 ×
109/l

20. 2. bone marrow Biopsy
3. Radiological Examination
1. Nuclear Magnetic Resonance Imaging
2. Radionuclide Bone Marrow Imaging (Scanning Bone
Marrow)

21. Diagnosis differential
1. Idiopathic Thrombocytopenic Purpura (ITP) and
Thrombocytopenic Purpura Amegakaryocytic (ATP)
2. Type of aleukemik acute Leukemia, especially ALL
(Acute Lymphocytic Leukemia)
3. Preleukemik Stage of acute leukemia

22. Management
1. Supportive therapy
1. Leukocyte-poor red cells Transfusion (overcome anemia)
2. Platelet suspension transfusion (Overcome bleeding)
3. Antibiotics ( for infections, recommended antibiotics are b-lactam and
aminoglycosides)
4. Blood, urine, faeces, sputum, CSF culture
5. Avoiding the chemical and physical toxic and drugs.

23. 2. Medication Therapy
1. Androgen
Oksimetolon is better instead of testosteron, with dose 1-2
mg/kg/day
2. Imunosuppressive
a. Methylprednisolon ( 5 mg/kg IV 8 days then tappering)
b. Antilymphocyte-Globulin (40mg/kg IV for 12hours
+methylprednisolon 1mg/kg/hours IV for 4 days)
c. Antithymocyte-Globulin (100-2000mg/kg IV)
d. Cyclosporin A (8mg/kg/day PO for 14 day continue with
15mg/kg/day)
e. Cyclophosphamide (50mg/kg/day for 4 days, still
controversy)
3. Growth factor ( G-CSF with dose 5 ig/kg/day)

24. 4. Combination therapy
combination of ALG/ATG, methylprednisolon and CsA.
3. Blood Transfusion
4. Chelation Therapy
given when there is accumulation of iron due to blood transfusion
5. bone marrow transplant
6. Food
7. Rest
Relaps
in case of relaps then can be given CsA and if unsuccessful then can
be given repeat ATG

25. Prevention
1. Avoiding toxic materials
2. Avoiding drugs consumption which can trigger aplastic anemia
3. Avoiding radiation
4. Good hygiene
5. Management of bleeding and infection

26. 1. Infection
2. Bleeding
3. GVHD after transplantation
4. Death

27. Based on :
1. Bone Marrow representation
2. HbF > 200 mg% give a better prognosis
3. Granulocyte > 2000/mm3 give better prognosis
4. Secondary infection prevention

28. Diagnose : Adi, 6-year-old-boy, suffers Aplastic anemia
Supporting examination :
• Peripheral blood count to see pancytopenia, morfology of
erythrocyte, leucocyte and thrombocyte and count the sums.
• Bone Marrow Punction to see bone marrow representation.
Management :
• Stop using Chlorampenicol
• Give supporting therapy, such as :
• Make sure the etiology of Adi’s fever, if it is caused by bactery infection,
give antibiotic, such as B-Lactam and Aminoglicoside
• Take care of self-hygiene

29. • Result of supporting examination :
• If Hb , 7 gr% then do transfusion of red-packed cell
• If thrombocyte < 20.000/uL then do thrombocyte transfusion
• Observation patient, wether Adi’s condition comes better. If not
do combination therapy, consist of :
• Methylprednisolon 5 mg/KgBW IV for 8 days, then tappering until 1
mg/KgBB/day for 9-14 days.
• ALG is given 40 mg/KgBW for 12 hours, continued with infuse that
combinated with Methylprednisolon.
• Siklosporin A is given 8 mg/KgBB
• Last option is Transplation of Bone Marrow