Determinasi anemia gizi
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Determinasi anemia gizi
Ikeu EkayantiProgram studi IKM –S2
FKM UNAIRSem ganjil 2013/2014
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PERTEMUAN KE-1
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DARAH DAN ZAT BESII. Pendahuluan
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CAIR TUBUH TUBUH PADAT (40%) CAIR (60%)
CAIRAN CAIRAN
EKSTRASEL(20%) INTRASEL (40%)
CAIRAN CAIRAN
INTRAVASKULAR (5%) INTERSTITIAL (15%)
Total Volume Darah : 8 %
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DARAH• Darah merupakan unit fungsional
seluler pada manusia yang berperan untuk membantu proses fisiologis dalam tubuh
• Viskositas : 1,7 x air• pH : 7,38• darah : 8 % dari BB
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Fungsi DarahMengangkut zat makanan dan oksigen ke seluruh tubuhMengangkut sisa-sisa metabolosme ke organ yang berfungsi untuk pembuanganMempertahankan tubuh dari serangan bibit penyakitMengedarkan hormon-hormon untuk membantu proses fisiologisMenjaga stabilitas suhu tubuhMenjaga kesetimbangan asam basa jaringan tubuh untuk menghindari kerusakanMencegah pendarahan
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Komponen darah
Secara umum darah digolongkan dalam dua komponenPlasma darahSel-sel darah
Sel-sel darah
Plasma 55%
45%
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KOMPOSISI DARAH
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Perhatikan urutan komposisinya !
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Sel-sel Darah
Terdiri dariEritrosit (sel darah merah)Leukosit (sel darah putih)Trombosit (keping-keping darah)
Animasi
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GAMBARAN DARAH
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Erythros = merahKytos = ruang sel
Warna merah pada sel dikarenakan adanya unsur haem yang lebih dikenal dengan kata Haemoglobin (Hb)
Eritrosit
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Karakteristik ErythrocyteTerdapat Di pembuluh darahKomponen dasar Haemolobin yang
mengandung unsur besi (Fe)
Dihasilkan Bayi : hatiOrang dewasa: sumsum tulang belakang
bentuk bikonkaf, tidak mempunyai inti
umur 120 hariinti Tidak ada
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Fungsinya mengangkut zat makanan, oksigen dan zat sisa metabolime
Hb(aq)+O2(g)HbO2(aq)
Sel darah merah dianggap tua ketika berumur 120 hari,
Hati & limpa
Haem →Zat warna empedu
Fe(besi) → Membentuk sel darah merah baru
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PLASMABagian yang tidak mengandung sel darah.
Warna :
• tergantung species, jumlah, jenis makanan• warna kuning tergantung dari : pigmen
bilirubin, karotin dll.
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Plasma Darah91 % AIR8 % SUBSTANSI LAIN terdiri dari albumin, fibrinogen, globulin 0,9 % ENZIM diantaranya asam amino, lemak, glukosa, urea, garam, sodium bikarbonat0,1 % HORMON, ANTIBODI, GAS
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Komposisi Plasma Darah :Air 91-93%ProteinBahan organikBahan inorganik 7-9%Enzim, hormon, vitamin, pigmen
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Bahan organik : - NPN ( Non Protein Nitrogen ) : urea, asam urat, kreatin, kreatinin , asam amino, glutathion, xanthine, hypoxanthin - Glukosa, fosfolipid, kolesterol dll.
Bahan inorganik :- Ca, Mg, K, Na, Cl, Co, Fe, I , Cu, Zn, Mn,
PO4, SO4 dll.
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Protein plasma 7 gr/dl plasma terdiri dari :
1. Albumin ( 57% ) - menjaga tekanan osmotik koloid
2. Globulin ( 40% ) - terdiri dari α1, α 2, ß , γ globulin.
- berperan dlm kekebalan tubuh.3. Fibrinogen ( 3% )
- mengandung faktor-faktor koagulasi
Semua di sintesa di Hati, kecuali γ globulin di limfosit dan plasma sel.
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Serumcairan berwarna kuning supernatan yg terdpt pd darah yg mengalami koagulasi
Tidak mengandung :1. fibrinogen2. faktor koagulasi
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stem cell yg mampu membuat keseluruhan sel darah
belum dapat di identifikasi
merupakan cikal bakal keseluruhan darah.
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ERITROSIT = Sel Darah Merah
Fungsi : - membawa Hb u/ transport gas
pernafasan transport O2 HbO2 CO2 Hb CO2
- buffer/penyangga
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Morfologi Eritrosit : bentuk : cakram bikonkaf : 7,5 m tebal : 0,8- 1,9 m luas : 135 m2
pada mamalia : tidak berinti
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Volume Eritrosit• Pada spesies yang sama Vol. Eritrosit
tergantung dari:• umur• jenis kelamin • hormon
• Manusia : 5 - 6 juta/ mm3
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Komposisi Eritrosit : Air 62-72%
Bahan padat - Hemoglobin 95 % - protein, lemak, vit, glukosa, enzim, mineral 5 %
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Eritrogenesis
Dikontrol oleh :
Eritropoeitin ( EPO ) = haemopoeitinDiproduksi oleh : - ginjal 80-90 %
- hepar 10-20% Perangsang : -hipoksia, adrenalin,
prostaglandin
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Zat-zat yang diperlukan untuk eritrogenesis :
1. Zat Besi (Fe ) sintesa Hb
2. Asam Folat pembentukan RNA
3. Vitamin B12 pendewasaan & pembelahan inti
4. Faktor intrisik terdapat di lambung u/ penyerapan vit B12 dan asam folat.
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Masa hidup eritrosit :
manusia : 4 bulan ( 120 hari )anjing : 100- 130 harikucing : 70-80 harikuda : 140-150 hariayam : 20-30 hari
Σ eritrosit dalam sirkulasi terbatas
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Regulasi Eritrogenesis1. bukan o/ konsentrasi eritrosit dlm
darah, ttp o/ kemampuan fungsional eritrosit u/ mentransport O2 ke jaringan.
2. Setiap keadaan yg menyebabkan O2 yg ditransport ke jaringan berkurang me kecepatan pembentukan eritrosit.
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REGULASI ERITROSIT
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Hematokrit (HCt)
= PCV ( Packed Cell Volume )
Banyaknya sel darah merah dalam presentase
Domestic animal rata-rata : 45 %
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Hb terdiri dari : 4 rantai polipeptida yang masing-
masing mengikat heme,
tiap heme mengikat 1 atom Fe,
tiap Fe mengikat 1 molekul O2
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METABOLISME ZAT BESI
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Normal Peripheral Smear
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Zat Gizi yang berperan dalam proses
Erythropatroesis
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ZAT BESI (Iron Stores)
Humans contain ~2.5 g of iron, with 2.0 - 2.5 g circulating as part of heme in hemoglobinAnother ~0.3 g found in myoglobin, in heme in cytochromes, and in Fe-S complexesIron stored in body primarily as protein complexes (ferritin and hemosiderin)
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Distribusi besi pada tubuh manusia (70 kg)
g %Hemoglobin 2.5 68Myoglobin 0.15 4Transferrin 0.003 0.1Ferritin tissue 0.1 27Ferritin serum 0.0001 0.0004Enzymes 0.02 0.6Total 3.7 100
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Nutritional Iron Balance
Intake– Dietary iron intake– Medicinal iron – Red cell transfusions – Injection of iron complexes
Excretion– Gastrointestinal bleeding– Menses
Losses can be as much as 4 - 37mg/menstrual cycle
– Other forms of bleeding– Loss of epidermal cells from the skin and gut
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Iron AbsorptionDietary iron content is closely related to total caloric intake (approximately 6 mg of elemental iron per 1000 calories)Iron bioavailability is affected by the nature of the foodstuff, with heme iron (e.g., red meat) being most readily absorbed– Heme iron> Organic iron (Ferrous gluconate)
> Inorganic iron (ferrous sulfate)Average iron intake in an adult male is 15 mg/d with 6% absorption; average female, the daily intake is 11 mg/d with 12% absorption– intestinal mucosa
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– Acid pH and presence of reducing agents: ascorbic acid (vitamin C) reduces Fe+++ to Fe++ which promotes passage across
Vegetarians are at an additional disadvantage because certain foodstuffs that include phytates and phosphates reduce iron absorption by about 50% Takes place in the mucosa of the proximal small intestine–Absorption increase to 20% in iron-
deficient persons
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Pangan sumber zat besi• Daging merah > unggas
& ikan• Sayuran secara umum
bkn pangan sumber fe yg baik, karena mengandung : oxalate, phytate, tannins, etc. • Bayam
mengandung , ~780 mg oxalate/100 g
catatan :penyerapan Heme iron dari diet tdk dipengaruhi oleh ascorbate atau phytate
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Bahan pangan Kandungan besi (mg/100mg)
Kacang hijau 7,5Kacang kedele 10.0
Tempe kedelei murni 4.0Tahu 3.4
Takwa 8.5Kacang merah kering 10.3
Kacang tanah 5.7Bayam 3.5
Kangkung 2.5Pepaya 1.7
Kandungan Besi berbagai bahan pangan nabati (mg/100g)
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Bahan pangan Kandunhgan besi (mg/100mg)
Daging sapi 2.8Daging ayam 1.5
Ikan segar 2.0Telur bebek 5.5Telur ayam 3.0
Terasi 78.5Ugang segar 8.0
Hati sapi 6.6
Kandungan besi pada pangan hewani (mg/100 mg)
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Availability Konsumsi pangan Penyerapan (%)Rendah Pangan hewani
< 100 gram Atau
Vitamin C < 25 mg
3
Sedang Pangan hewani 100 – 300 gram
AtauVitamin C 25 – 75 mg
5
Tinggi Pangan hewani > 300 gram atauo
vitamin C > 75 gramAtau
Pangan hewani > 100 gram dan
vitamin C > 25 mg
8
Konsumsi pangan hewani dan vitamin C Terhadap (%) penyerapan
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Iron Exchange80% of iron passing through the plasma transferrin pool is recycled from broken-down red cellsAbsorption of about 1 mg/d is required from the diet in men, 1.4 mg/d in women to maintain homeostasis
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II. ANEMIA
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ANEMIA Suatu keadaan kekurangan eritrosit, yang disebabkan oleh hilangnya darah secara cepat atau lambatnya produksi eritrosit.
Kurang zat tertentu gizi : defisiensi besi, Vit B12, asam folat. Tembaga, Zn dll
Infeksi parasit : cacing
Kerusakan Ginjal eritropoietin tidak terproduksi
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Penurunan produksi sel darah merah (RBC)– Sumsum tulang tidak mampu memproduksi dalam
jumlah yang cukup– Gangguan kematangan sel
Meningkatnya kehilangan sel darah merah– Perdarahaan
Dektrusi sel darah merah– Intrinsik (sikle cell)– Ekstrinsik (mechanical cardiac valve)– Kombinasi keduanya
Klasifikasi anemia berdasarkan etiologi
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Classification of anemias by MCV
Microcytic (<80 fL) – Iron deficiency – Thalassemia – Anemia of chronic disease
Macrocytic (>100 fL)– Vitamin B12 deficiency– Folate deficiency – Myelodysplasia– Chemotherapy– Liver disease – Increased reticulocytosis– Myxedema
Normocytic– Anemia of chronic disease– Aplasia– Protein-energy malnutrition– Chronic renal failure– Post-hemorrhagic
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1. Berdasarkan ukuran (size)– Microcytic : penurunan MCV– Normocytic : normal MCV– Macrocytic : peningkatan MCV
2. Berdasarkan Warna– Normochromic : normal– Hypochromic : pucat
Klasifikasi anemia berdasarkan morfologi sel darah merah (RBC)
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Mekanisme terjadinya anemia
Marrow production defects/terganggunya produksi sel darah merah pada sumsum tulang belakang (hypoproliferation)– Low reticulocyte count– Little or no change in red cell morphology (a
normocytic, normochromic anemia Red cell maturation defects/terganggunya proses kematangan sel darah merah (ineffective erythropoiesis)
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– Slight to moderately elevated reticulocyte count
– Macrocytic or microcytic anemia
Decreased red cell survival (blood loss/ hemolysis).
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Proses terjadinya RBC yg tidak matang (Adolescent RBC)– Sekresi erythropoietin dari ginjal– Sumsum tulang merespon– Reticulocyte di produksi– Dilepas ke sirkulasi darah
Percepatan produksi RBC dapat menghasilkan reticulocyte yang lebih banyak
Reticulocytes ?
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Kadar normal : 1 – 2 % dari RBC adalah reticulocytePenurunan terjadi ketika sumsum tulang tidak membuat RBC–Defisiensi besi–Anemia aplastik– Infeksi kronis–Anemia pernicious yang tidak rawat
Kapan retyculocyte menurun ?
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PATHOLOGY, SYMPTOMS, AND SIGNS OF ANEMIA
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II.1. ANEMIA GIZIPERTEMUAN KE -2
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Anemia gizi : keadaan dimana kadar hemoglobin, hematokrit dan sel darah merah berada di bawah nilaI normal, sebagai akibat dari defisiensi salah satu atau lebih zat gizi esensial yang dapat mempengaruhi terjadinya defisiensi tersebut
Anemia Gizi
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ANEMIA DEFISIENSI BESI
II.1.A
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Defisiensi besi : terjadi karena interaksi dari berbagai faktor penyebab yang menimbulkan ketidakseimbangan antara kebutuhan besi dengan jumlah besi yang berhasil diserap tubuh
Penyebab Defisiensi Besi
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Diet (dietary)1. Rendahnya konsumsi pangan sumber besi2. Rendahnya bioavailabilitas besi dari
pangan yang di konsumsi3. Bentuk besi dalam pangan
(hewani/nabati=hem/nonheme)4. Tingginya faktor inhibitor5. Rendahnya faktor enhancerrs/pemicu
penyerapan
Faktor kunci penyebab defisiensi besi (Unicef/UNU/WHO/MI Technical
Workshop)
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Gaya hidup (life style)1. Kehamilan yg berulang2. Perdarahan yg ada hubungan sedangan
pemakaian alat kontrasepsi intrauterine (IUDs)3. Mestruasi yang berlebihan (perdarahan)4. Meningkatan kebutuhan karena faktor
fisiologis (kehamilan, anak yang sedang tumbuh, remaja)
5. Bayi defisiensi besi krn lahir dari ibu yg defisiensi besi juga saat hamil
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Status penyakit (disease states)Kehilangan darah kronis –Infestasi cacing–Schistosomiasis
Kehilangan darah patologis–Haemorrhoids–Petic ulcer–Penyakit GI lainnya
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–Adanya proses yang mengganggu penyerapan dan utilisasi/penggunaan besi dalam tubuh
Malabsorption syndromesDiare kronis atau berulangFaktor genetik
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Dampak dari status sosial ekonomi yang rendah1. Keamanan pangan2. Kurangnya perawatan kesehatan
dan akses terhadap pelayanan kesehatan
3. Sanitasi lingkungan yanhg buruk4. Higiene perorang yang jelek
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Faktor genetik penyebab anemia1. Penyakit sickle cell2. Thalassemia mayor3. haemoglobinopathies
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Causes of Iron DeficiencyIncreased demand for iron and/or hematopoiesis– Rapid growth in infancy or adolescence– Pregnancy– Erythropoietin therapy
Increased iron loss– Chronic blood loss– Menses– Acute blood loss– Blood donation– Phlebotomy as treatment for polycythemia vera
Decreased iron intake or absorption– Inadequate diet– Malabsorption from disease (sprue, Crohn's disease)– Malabsorption from surgery (post-gastrectomy)– Acute or chronic inflammation
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Iron Deficiency AnemiaFacts and Figures– Most common cause of anemia– 500 million cases worldwide– Prevalence is higher in less developed
countries
Unique Physical Exam findings– Cheilosis
fissures at the corners of the mouth– Koilonychia
spooning of the fingernails
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Iron Deficiency Anemia
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Iron Deficiency Anemia - koilonychia
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Tahap 1 : Iron depletion– Simpanan besi menurun (serum ferritin
menurun)– Besi serum dan hemoglobin normal
Tahap 2 : Iron deficient erythropoiesis (iron deficiency without anemia)– Serum ferrritin semakin menurun– Besi serum dan transferrin menurun– Hemoglobin menurun sedikit atau normal
Tahapan perkembangan defisiensi besi – anemia defisiensi besi (Gibson , 2005)
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Tahap 3 : Iron deficiency anemia–Serum ferritin semakin menurun atau
habis–Besi serum, kejenuhan transferin
(TS) menunurun–Hemoglobin dan hematokrit menurun
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Stages of Iron Deficiency
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Iron Deficiency Anemia – Lab Findings
Serum IronLOW (< 60 micrograms/dL)
Total Iron Binding Capacity (TIBC)HIGH ( > 360 micrograms/dL)
Serum FerritinLOW (< 20 nanograms/mL)Can be “falsely”normal in inflammatory states
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Nilai batas normal
IndikatorAnemia berdasarkan tahapannya
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Golongan Umur Hemogllobin (g/dl)
Hematokrit(%)
Anak (6 bln – 5 thn) 11.0 33Anak (5 – 11 thn) 11.5 34Anak (12 – 13 thn) 12.0 36Laki-laki dewasa 13.0 39Wanita dewasa tdk hamil
12.0 36
Wanita hamil 11.0 33
Tabel 1. Ambang batas Hemoglobin dan Hematokrit menurut golongan umur dan jenis kelamin
(INACG/WHO/UNICEF, 1998)
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Status besi Single Multipledefisiensi besi Salah satu:
Serum ferritin ≤ 12μg/lSerum ferritin < 16 μg/lTransferin saturation < 16 %
Serum ferritin ≤ 12 μg/lDanTransferrin saturation < 16%
Anemia defisiensi besi
hemoglobin < 12.0 g?dl
Hemoglobin < 12.0 g/dlSerum Ferritin ≤ 12 μg/lTransferrin saturation < 16 %
Tabel 2. Kriteria penentuan statu besi (Rangan, AM, 1997 dan Hallberg, 1993)
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Tingkat anemia Hemoglobin (g/dl)
Hematokrit (%)
Mild (ringan)
11.0 – 11.9 33 - 35
Moderate (sedang)
8.0 – 10.9 24 - 32
Severe (berat) < 8.0
Tabel 3. tingkat keparahan anemia pada wanita tdk hamil dan anak (6 – 14 thn) (WHO, 2000)
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Tingkat anemia Hemoglobin(g/dl)
Hematokrit(%)
Mild(ringan)
10.0 – 10.9 30 - 32
Moderate(sedang)
7.0 – 9.9 21 - 29
Severe(berat)
< 7.0 < 21
Tabel 4. Tingkat keparahan anemia pada wanita hamil dan anak < 6 tahun (WHO, 2000)
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Kategori masalah kesehatan masyarakat
Prevalensi anemia (%)
Tinggi ≥ 40Medium 20 - 40Rendah 5.0 - 20
Tabel 5. klasifikasi besaran prevalensi anemia dan defisiensi besi menjadi masalah kesehatan
masyarakat (WHO, 2000)
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Treatment of Iron Deficiency1. Red Blood Cell Transfusion2. Oral Iron Therapy
– Ferrous sulfate– Ferrous fumarate– Ferrous gluconate
3. Parenteral Iron
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Iron Supplementation in special populations
Pregnant Women– During the last two trimesters, daily iron
requirements increase to 5 to 6 mg Infancy– Normal-term infants are born with sufficient iron
stores to prevent iron deficiency for the first 4–5 months of life
– Thereafter, enough iron needs to be absorbed to keep pace with the needs of rapid growth
– Nutritional iron deficiency is most common between 6 and 24 months of life
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ANEMIA MEGALOBLASTIKKelainan berkurangnya ∑ eritrosit akibat adanya gangguan sintesis DNA yg ditandai adanya sel megaloblastiSel yang paling dipengaruhi adalah sel yang membelah cepat : termasuk sel darah dan epitel usus
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Kebanyakan disebabkan adanya defisiensi vitamin B-12 dan asam folatKekurangan keduanya dapat menyebabkan gangguan sintesa DNA sehingga proses pembelahan sel menjadi terganggu.
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Megaloblastic AnemiaMacrocytic RBCHypersegmented Neutrophil
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DEFISIENSI VITAMIN B-12II.1.B.
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Causes of Vitamin B 12 deficiency
– Inadequate intake: vegans (rare) – Malabsorption
Defective release of cobalamin from food Gastric achlorhydriaPartial gastrectomyDrugs that block acid secretion Inadequate production of intrinsic factor (IF) –Pernicious anemia–Total gastrectomy
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Disorders of terminal ileum–Sprue–Regional enteritis–Intestinal resection
Competition for cobalamin –Fish tapeworm (Diphyllobothrium
latum)–Bacteria: "blind loop" syndrome –Drugs: p-aminosalicylic acid,
colchicine, neomycin
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Clinical Manifestations of Vitamin B12 Deficiency
Hematologic– Macrocytic Anemia
Gastrointestinal– Glossitis– Anorexia– Diarrhea
Neurologic (found in 3/4th of individuals with pernicious anemia)– Numbness and paresthesia in the extremities, Weakness, Ataxia– Sphincter disturbances– Disturbances of mentation
Mild irritability and forgetfulness to severe dementia or frank psychosis. – Demyelination, Axonal degeneration, and then Neuronal death
Last stage is irreversible
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Vitamin B12 affects two Major Pathways
Homocysteine
Methionine
Methylmalonyl CoA
Succinyl CoA
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The effects of Vitamin B12 on the conversion of
homocysteine to methionine
Homocysteine
Methionine
Methylcobalamin
Methionine Synthase
5-methyltetrahydrofolate tetrahydrofolateTetrahydrofolate methyltransferase
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The effects of Vitamin B12 on the conversion of
Methylmalonyl CoA to Succinyl CoA
Methylmalonyl Co A
Succinyl CoA
Adenosylcobalamin
Methylmalonyl CoA mutase
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Vitamin B12 Deficiency homocysteine and methylmalonyl CoA
Increase in methylmalonyl CoA– Increased enzyme activity in fatty acid
synthesisBuild up of odd fatty acids around peripheral nerves
Increase in homocysteine– Vascular/nervous problems
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Vitamin B12 DeficiencyExcess homocysteine & MMA excreted in urine– Diagnosis for cobalamin deficiencyMethylmalonyl CoA mutase & Methionine synthase affect amino acid metabolism– Amino acid metabolism inhibited by
deficiency
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GEJALA KLINIS DEFISIENSI VITAMIN B12
AnemiaMuka pucat mata kekuninganKadar bilirubin meningkatNyeri lidah, lidah papilnya halus dan kemerahan.Anoreksia mungkin dengan diareMatirasa, kelemahan dan ataksia, mudah lupa, sampai psikosis, reflek lutut menurun
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Vitamin B12 Absorption – Oral Phase
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Vitamin B12 Absorption – Gastric Phase
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Vitamin B12 Absorption – Intestinal Phase
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Terapi defisiensi vitamin B12Kobalamin 1000 mikrogram tiap minggu sampai 6 mingguBila membaik diberikan 1 bulan sekaliBisa dilanjutkan oral 2 mg/hariBila perlu tranfusi PRC pelan pelanPengobatan penyakit penyebabAsam folat oral dosis tinggi
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Sources of Vitamin B12FishEggsMeat Dairy Products
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DEFISIENSI ASAM FOLATII.1.C.
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Causes of folat deficiency
– Inadequate intake: unbalanced diet (common in alcoholics, teenagers, some infants)
– Increased requirements PregnancyInfancyMalignancyIncreased hematopoiesis (chronic hemolytic anemias)Chronic exfoliative skin disordersHemodialysis
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– Malabsorption SprueDrugs: Phenytoin, barbiturates, (?) ethanol
– Impaired metabolismInhibitors of dihydrofolate reductase: methotrexate, pyrimethamine, triamterene, pentamidine, trimethoprim AlcoholRare enzyme deficiencies: dihydrofolate reductase, others
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Tahapan defisiensi asam folat
1. Negative folate balance (decreased serum folate)
2. Decreased RBC folate levels and hypersegmented neutrophils
3. Macroovalocytes, increased MCV, and decreased hemoglobin
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Diagnosis of folate deficiencyPeripheral blood and bone marrow biopsy look exactly like B12 deficiencyPlasma folate <3 ng/ml—fluctuates with recent dietary intakeRBC folate—more reliable of tissue stores <140 ng/mlOnly increased serum homocysteine levels but NOT serum methylmalonic acid levels
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GEJALA KLINIS DEF ASAM FOLAT
Mirip def B12 tetapi tidak tampak gangguan neurologis
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Vitamin B12 Deficiency Versus Folate Deficiency
Vitamin B 12 Deficiency
Folate Deficiency
MCV > 100 > 100Smear Macrocytosis
with hypersegmented neutrophils
Macrocytosis with hypersegmented neutrophils
Pernicious anemia
Yes NO
Homocystine Elevated Elevated
Methylmalonic Acid
Elevated NORMAL
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Aspek gizi vitamin B12 dan asam folatVitamin B 12 Asam folatasupan
makananAsupan normal dalam makanan
7 – 30 μg 600 – 1000 μg
Sumber pangan Pangan hewani Sebagian besar pangan hewani (hati), sayuran hijau dan ragi
Efek pengolahan Sediikit pengaruh Mudah rusakKebutuhan min sehari 1 – 2 μg 100 – 200 μgSimpanan tubuh 2 – 3 μg ( untuk 2 –
4 tahun)10 – 12 μg (untuk 4 bulan )
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Lanjutan …..Vitamin B 12 Asam folate
Tempat penyerapan Ileum Duodenum dan jejunum
Mekanisme penyerapan
Faktor intrinsik Dikonversi menjadi metiltetrahiklrofolat
Batas penyerapan 2 – 3 μg per hari 50 – 80 % kandungan asam folat dalam makanan
Bentuk fisiologis intrasel terutama
Metil dan adenosin cobalamin
Derivat poliglutamat tereduksi
Bentuk terapeutik hidroksicabalamin Asam folat ( peterolglutamat)
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TERIMA KASIHATAS PERHATIANNYA……….