+ All Categories
Home > Documents > 17. Anemia Makrositik & Megaloblastik (dr. Rahmawati Minhajat, Ph.D, Sp.PD).pdf

17. Anemia Makrositik & Megaloblastik (dr. Rahmawati Minhajat, Ph.D, Sp.PD).pdf

Date post: 30-Sep-2015
Category:
Upload: adjhy-aji-achmad
View: 39 times
Download: 9 times
Share this document with a friend
Popular Tags:
21
MACROCYTIC ANEMIA Rahmawati Minhajat Tutik Harjianti A. Fachruddin B Div. of Hematology & Medical Oncology Dept. of Internal Medicine, Medical Faculty Hasanuddin University
Transcript
  • MACROCYTIC ANEMIA

    Rahmawati Minhajat

    Tutik Harjianti

    A. Fachruddin B

    Div. of Hematology & Medical OncologyDept. of Internal Medicine, Medical Faculty

    Hasanuddin University

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    Deficiency of Cyanocobalamin

    B12 : all of it made from diet

    A food ingredients may from animal.

    Absorbtion : 5 ug / days

    Cofactor at 2 important reaction in a body

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    The role of Cyanocobalamin

    Methyl-Cobalamin is a cofactor for methionine-synthetase at rx change of homosystein metyonin.

    Adenosyl-Cobalamin is a cofactor at rx change of methyl-malonyl CoA succinyl-CoA

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    2. Peripheral blood smear:

    macro-ovalocyte & hypersegmented neutrophil

    3. Level of Vit B12

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    Macrocytic Normocytic

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    The Cause

    1. Deficiency vit B12 (diet)

    2. The decrease production of intrinsic factor

    (Anemia perniciosa, post-gastrectomy)

    2. The decrease absorbtion of vit B12 at the ileum

    (Post-op, Crohn ds)

    3. Helmynthyasis (tape-worm)

    4. Deficiency Transcobalamin II

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

    Physiology

    Vit B12 come in from IT binding with intrinsic factor (made from parietal mucosa gaster cell)

    abs in ileum terminal by spesific receptor come in to the plasma liver .

    There are 3 protein transporter in the plasma :

    Trans-cobalamin I, II & III (by leukocyte). Only

    Trans-cobalamin II that can transport vit B12

    into the cell.

  • Division of Hematology & Medical Oncology Dept. of Internal Medicine

  • Phatogenesis

    Hepar consist 2.000 5.000 ug vit B12

    Need : 3 5 ug / hari

    Defs vit B12 will be happen in 3 years after no more absorpsi.

    Defs caused by diet less vit B12 vary rare ( vegetarian )

  • Example :

    Gastrectomy the area produce factor intrinsik will decrease

    Over-growth bactery in intestinal

    Reseksi ileum the area of absorpsi vit B12 will decrease

    Helmenthyasis

    Crohns disease ileum destruction

    the area of absorpsi vit B12 will decrease

  • Anemia Perniciosa

    Often cause defs B12

    Abnormality Auto-Imun herediter

    Seldom show before 35 years old

    Scandinavia / Eropa Utara

    A black skin teenager, a hispanic woman

  • Anemia Perniciosa

    Clinic illustration :

    Likely anemia caused by defs vit B12,

    - Gastritis atrophic

    - Abnormal Auto-Imun ( rheumatoid arthritis

    Graves disease, defs IgA )

    - After several years some patient

    Gastritis Atrophic => Carcinoma Gaster

  • CLINIC MANIFESTATION OF

    DEFS. VIT B12

    Megaloblastic anemia

    May a hard anemia ( hematokrit < 10 % )

    A change mucosa cell : glossitis, anorexia, diare.

    Neurologic disturb:

    1. Perifer parestesi

    2. Cerebral difunction

  • Lab. Abnormal

    1. Megaloblastic Anemia

    2. MCV between 110 140 fl (increase)

    at some patients : MCV normal

    3. Blood Perifer : anisocytosis &

    poikilocytosis. Specif : macro-ovalocytes.

  • Blood Perifer

    4.Morfologi eritrosit is abnormal

    Likely Hemolytic Anemia

    5. Hypersegmentation of neutrophyls

    6. Decreased Reticulocyte amount

  • Bone Marrow Asp

    In-efective Erythropoesis ( abnormally RBC production)

    erythroid hyperplasia ( as respons )

    Abnormal megaloblastic Cell in BM and different shapes :

    * Large abnormal size,

    * nuclear maturation & cytoplasm are not

    synchronize.

    Maturasi cytoplasm is normal,

    DNA synthesis is bother

    Myeloid : Giant cell (meta-myelocyte)

  • Other Abnormal Lab :

    In-efective erytropoesis in BM may happen destruction of erythroid cell that in the

    development period increased level of LDH ( lactic-dehydrogenase ) and Bilirubin indirect

  • Diagnosis

    1. Level of vit B12 serum is low

    ( normal : 150-350 pg / mL )

    2. Schilling test ( for dx A Perniciosa /

    the decrease absorpsi vit B12 oral )

  • THERAPY

    * Anemia Pernisiosa (oral absorpsi disfunction)

    Intra-muscular Inj. Vit B12 ( IM )

    Dosis : 200 ug

    1st week : every day (replacement tx)

    2nd 4th week : every week

    Once a month

  • Respons Therapy

    Reticulocytosis 5 7 days.

    Abnormalitas hematologic disappear after 2 months.


Recommended