K15. Obat Anti-Anemia

FARMAKOLOGI
OBAT HEMATINIK
FKIK UNIB 2018

Diagnosis
 Anamnesis
- gejala anemia: pusing, kunang2, lesu, cepat lelah,
sukar konsentrasi, prestasi menurun
- komplikasi : gagal jantung
- faktor resiko
 anemia defisiensi besi: prematuritas, BBLR, ibu anemia,
vegetarian, diare kronik,
kecacingan, sering infeksi
 anemia hemolitik: perkawinan antar keluarga, obat,
racun makanan/serangga/kimia
 anemia aplastik: obat, irradiasi, hepatitis, malignansi
- gejala khas
● perdarahan kronis pasca perdarahan, defisiensi Fe
● ikterik, urin coklat, perut buncit  hemolitik
● mudah infeksi  aplastik, anemia krn keganasan
 Pemeriksaan Fisik
Umum: pucat, takikardi, pulsus seler, bising jantung &cardiomegali
Komplikasi: gagal jantung, hambatan pertumbuhan
Khusus:
Defisiensi besi: spoon nail, glositis (semua jarang tjd)

Defisiensi B12: paresis, ulkus tungkai
Hemolitik: ikterus, splenomegali
Aplastik: anemia berat, perdarahan, infeksi
Penyakit
primer
Keganasan: limfadenopati general, hepatosplenomegali, tumor
Tanda gagal ginjal  defisiensi eritropoetin
Tanda hipotiroidisme
 Laboratorium
Bukti pasti: Hb atau Ht < normal
Kelainan laboratorium:
Defisiensi besi: mikrositosis, hipokromia, anulosit, pencil cell
Defisensi B12: makrositosis, granulosit besar, hipersegmentasi
Anemia hemolitik: retikulosit , Bil indirek , urobilirubinuria
Anemia aplastik: pansitopenia,
Khusus
Defisiensi besi: SI, TIBC, saturasi transferin, feritin, deposit besi
Thalasemia B mayor: anisositosis, poikilositosis, sel target,

HbF >3g%, sumsung tulang
hiperaktif, elektroforesis Hb, fragilitas
eritrosit
Anemia hemolitik akuisita non imun:
Normositik normokromik
Coomb test (+)
Ham test utk PNH
Kadar G6PD
Anemia hemolitik imun (IHA, AIHA)

Pallor - nail bed in a patient with
anemia
Anemia Menurut morfologi SDM
1. Mikrositik hipokromik (MCH/MCV/MCHC
rendah):anemia def. Besi, thalasemi, keracunan
timah, sideroblastik, peny kronis
2. Normositik normokromik (MCV/MCHC N):
anemia aplastik, anemia hemolitik, anemia
hemorragik)
3. Makrositik normokromik (MCV tinggi, MCHC
N):
a. Anemia Megaloblastik
- Def vit B12 / as folat
- Efek Kemotherapi
- Synd Mielodisplastik
b. Non Megaloblastik
- Alkoholisme
- Peny.hepar
- Hemolisis, perdarahan
- Hipotiroidisme
Nutrient Roles in Erythropoesis
Anemia defisiensi Fe
 Anemia o.k cadangan besi berkurang
 Mikrositik hipokromik
 MCV,MCH,MCHC menurun
 Saturasi transferin menurun
 Kadar feritin serum menurun
 Hemosiderin ssm tulang menurun

Etiologi anemia defisiensi Fe
 Kehilangan besi:
uterus : haid banyak
Sal. Cerna:varises oesophagus, ulkus peptikum,
carsinoma lambung/colon, hemorrhoid, Cacingan,
Ulcerative colitis,Hiatus hernia
 Kebutuhan meningkat:
kehamilan, menyusui, pertumbuhan
 Intake kurang:
diit buruk, malabsorbsi: gasterektomi,
coeliac disease
Iron Cycle
 5 - 10% of ingested iron is
absorbed
 Once ingested the acid in

the stomach:
 1. Aids in ionization of
iron
 2. Splits chelated food
iron from chelator
 3. Maintains iron in
soluble form
 4. Allows iron to
remain in the
absorbable form Fe3+
Mechanism of Iron Absorption
Anemia megaloblastik
Anemia dimana terjadi kelaianan pada sel dan fungsi
di sumsum tulang dan darah tepi yang
disebabkan sintesis DNA yang tidak sempurna
Penyebab:
1. Defisiensi B12 dan asam folat : yg penting utk
sintesa DNA, Defisiensi menimbulkan
pematangan inti terlambat(megaloblastik)
2. Abnormalitas metabolisme B12/as folat
3. Cacad sintesa DNA :
a. defisiensi enzim kongenital
b. Akuisita : terapi hidroksiurea,
sitosin arabinosa
Vitamin B-12 Deficiency
acanthtosis (hypopigmentation)
 Sebab Defisiensi as Folat:
1. Nutrisional : Tua, Skorbut,Gastrektomi parsial
2. Malabsorbsi : Peny. Crohn, Gastrektomi parsial
3. Pemakaian berlebih :
- Fisiologis : kehamilan, laktasi
- Patologis : Hemolitik, Keganasan,Radang
(TBC, RA, Peny. Crohn, Psoriasis )
4. Pembuangan As. Folat >> : Peny. Hati, Jtg
5. Terapi obat antikonvulsan
6. Alkoholisme
Anemia Hemolitik
 Anemia karena peningkatan destruksi
eritrosit
 Terjadi hiperplasi eritropoetik &
perluasan anatomis tulang
 SS tl : 6 – 8 xN
 Retikulosit meninggi
Pembagian Anemia Hemolitik
1. Anemia hemolitik herediter/intrinsik:
a. Defek membran: sperositosis,eliptosit
b. Defek enzim/metabolik : G6PD, PK
c. Defek Hb : sickle sel, HbC, HbD, HbE,HbSC,HbM,
Hb Koln&Zurich, Thalasemia
2. Anemia hemolitik akuisita/ekstrinsik:

a. Autoimun : AIHA
b. Isoimun : Rx Tranfusi
c. Imun : Obat
d. Lain2 : zat kimia, mekanik, obat2an, infeksi defek
membran ekstrinsik/PNH
Sites of action for EPO
Therapeutic Uses of EPO
 Anemia of end stage renal disease
 To treat AIDS anemia caused by AZT’s

suppression of bone marrow
 Anemia related to cancer chemotherapy
 Others
 To increase RBC levels for autologous blood
donation
 Anemia associated with rheumatoid arthritis
 1. Granulocyte/Macrophage Colony Stimulating Factor
(GM-CSF)- Sargramostim
 Acts synergistically with IL-3 to stimulate the
formation and proliferation of colony forming cells:
CFU-GEMM, BFU-E, CFU-Meg, CFU-GM, CFU-M,
CFU-E
 Increases cytotoxic phagocytic activity of mature
granulocytes
 2. Interleukin 3 (IL-3)
 Acts synergistically with GM-CSF to stimulate the
formation of granulocytes, macrophages,
eosinophils and megakaryocytes.
 Acts synergistically with EPO to stimulate
formation of BFU-E colonies
 Induces CFU-S and leukemic blast cells into cell
cycle
 3. Colony stimulating Factor-1 (CSF-1 or M-
CSF)
 Acts synergistically with GM-CSF and
IL-3 to stimulate monocyte/macrophage
colony formation and function
 4. Granulocyte Colony Stimulating Factor

(G-CSF) - filgrastim
 Acts synergistically with IL-3, GM-CSF
and CSF-1 to stimulate formation of
megakaryocytes, granulocyte-
macrophage and high proliferative
potential (HPP) colonies
 Induces release of granulocytes from
marrow
 5. Thrombopoietin (TSF)
 Increases the size and number of
megakaryocytes.
(IL-11 also useful in stimulating production)
 Increases
the concentration of early
megakaryocytes cells (SACHE+cells) in bone
marrow.
 Produces an increase in megakaryocytes

endomitosis.
 Increases platelet size and number in plasma.

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FARMAKOLOGI

FKIK UNIB 2018

Komplikasi: gagal jantung, hambatan pertumbuhan

Defisiensi besi: spoon nail, glositis (semua jarang tjd)

Hemolitik: ikterus, splenomegali

Aplastik: anemia berat, perdarahan, infeksi

Tanda gagal ginjal  defisiensi eritropoetin

Defisiensi besi: mikrositosis, hipokromia, anulosit, pencil cell

Defisensi B12: makrositosis, granulosit besar, hipersegmentasi

Anemia hemolitik: retikulosit , Bil indirek , urobilirubinuria

Anemia aplastik: pansitopenia,

Defisiensi besi: SI, TIBC, saturasi transferin, feritin, deposit besi

Thalasemia B mayor: anisositosis, poikilositosis, sel target,

Coomb test (+)

Ham test utk PNH

Anemia hemolitik imun (IHA, AIHA)

 Saturasi transferin menurun

 Kadar feritin serum menurun

 Hemosiderin ssm tulang menurun

 Once ingested the acid in

2. Anemia hemolitik akuisita/ekstrinsik:

 To treat AIDS anemia caused by AZT’s

 Anemia related to cancer chemotherapy

 4. Granulocyte Colony Stimulating Factor

 Produces an increase in megakaryocytes

 Increases platelet size and number in plasma.

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