anemia-defisiensife,b12danfolat(kbk) uisu.ppt

8/10/2019 Anemia-DefisiensiFE,B12danFolat(KBK) uisu.ppt

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HAEMATOLOGY

Anemia Defisiensi

Savita handayaniHematologi-Onkologi Medik

Departemen Ilmu Penyakit Dalam


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Normal Blood Cells:


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Proerythroblast

(Pronormoblast)Basophilic

Normoblast

Polychromatophilic

NormoblastOrthochromatophilic

Normoblast

Reticulocyte

Erythrocyte

Early Intermediate Late

Steps in Erythropoesis


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RBC disorders (Anemias) :

Anemia is decreased red

cell mass affect ing t issue

oxygenation

Pract ical - Low Hb* or Low Hematoc r i t*


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Mikrositikhipokrom

Normositiknormokrom Makrositik

MCV < 80 fL 80100 fL > 100 fL

MCH 27 pg >27 pg > 27 pg

MCHC < 30 g/dL 30 g/dL 30 g/dL

Penggolongan menurut Morfologi

volumetrik

MCV= (Ht/Eritosit)x10 fL

MCH=(Hb/Eritrosit)x10 pg

MCHC=(Hb/Ht)x100 g/dL


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Mechanism of Anemia :

Decreased Production: Nutrient Deficiency.

Iron, B12/Folate

Hemopoietic cell damage:

Aplastic, HypoplasticNeoplasms,radiation, drugs


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Iron Deficiency Anemia:

Most abundant metal but most commondeficiency..!

Common in developing world,

Parasitic Worm infestation + Malnutrition

Chronic blood loss GI & genitourinarytract


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Iron Metabolism

Recycling of iron

dead cells to new cells 10% of the 10 to 20 mg of dietary iron.

Iron is absorbed in Jejunum.

Stored as Ferritin & Hemosiderin.


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Minimum daily iron requirement 12-15mg/day.Absorbed 1-2.5 mg/day.

The normal iron content is 3-4 gr. It exists in thefollowing forms:

Hemoglobin = 2.5 grams

Iron containing proteins (myoglobin,cytochromes and catalase) = 400 mg

Iron bound to transferrin = 3-7 mg

Storage iron (ferritin or hemosiderin).

Iron Mathematics


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IDA - Etiology

Blood loss

BleedingParasites, Gynecologic, ulcers

Increased need

Pregnancy, children

Poor diet / poor absorption

Malnutrition (greens & meat), malabsorption,

intestinal surgery, gastric atrophy.


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IDAPathogenesis: Steps of IDA

Decreased Iron stores.Storage iron in adult men 10 mg/kg, mostly in liver,spleen, and bone marrow. Adult women have lessstorage iron.

Decreased Hb Synthesis Delayed maturation of erythroblasts

(cytoplasmic)

Decreased cytoplasm, more division(microcytes)

Decreased Hb content (hypochromia)

Anemia.


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PATHOGENESIS

Lack of iron interferes with heme synthesishemoglobin synthesisand defective erythropoiesis

There is decreased activity of iron-containing proteins

such as the cytochromes and succinic dehydrogenaseNeurologic dysfunction may occur, with impaired

intellectual performance, paresthesias

Gastric acid secretion is reduced, often irreversibly

Atrophy of oral and gastrointestinal mucosa may

occur


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Clinical Features:

General features of Anemia Pallor, Weakness, Lethargy,

Breathlessness on exertion

Palpitationsheart failurepedal edema Special features in IDA:

Angular cheilitis, atrophic glossitis,

Oesophageal atrophy/webdysphagia, Koilonychia, brittle nails, gastric atrophy.

Pica


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Angular cheilitis


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Koilonychia in Iron deficiency


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Koilonychia in Iron def.


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LABORATORY CHANGES

Red Blood Cells- Earlist change is anisocytosis and increased red cell

distribution width (RDW)

- Mild ovalocytosis, target cells

- Elongated hypochromic elliptocytes

- Progressive hypochromia (low MCH),microcytosis

(low MCV), MCHC variable

- Reticulocytes normal or reduced- The erythrocyte count, hemoglobin level and

hematocrit are all proportionately reduced


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LABORATORY CHANGES

LeucocytesLeukopenia (3000 to 4400/l) in some. Differential

count is normal

Platelets- Thrombocytopenia develops in 28 percent of

children and may occur in adult

- Thrombocytosis found in

- 35 % of children

- 50 to 70 % of adults-usually secondary to

chronic active blood loss


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LABORATORY CHANGES

Marrow- Marrow cellularity and M/E ratio variable

- Decreased to absent sideroblast

- Decreased to absent hemosiderin by Prussian blue

staining

- Erythroblasts may be small, with narrow rim of

ragged cytoplasm and poor hemoglobin formation


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LABORATORY CHANGES

Serum Iron Concentration- Usually low but may be normal

- May be reduced with concomitant acute or chronic

inflammation malignancy, acute myocardial

infarction in the absence or iron deficiency.- May be elevated 3 to 7 days after therapy

Total Iron Binding Capacity (TIBC)

- Usually increased in iron deficiency- Saturation (Iron/TIBC) is often 15 % or less but this

is not specific for iron deficiency


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LABORATORY CHANGES

Serum Ferritin- Level of less than 10 g/liter

- Level of 10 to 20 g/liter are presumptive, but not

diagnostic

- May be elevated with concomitant inflammatorydisease

Free Erythrocyte Protoporphyrin (FEP)

- Concentration is usually increased

- Very sensitive for diagnosis of iron deficiency and

suitable for large scale screening of children, detecting

both iron deficiency and lead poisoning


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Anemia Defisiensi Besi

Serum feritin 400 ng/mL

%100*TIBC

SIIST


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DIAGNOSIS

Evaluation of clinical information from areview of the history & physicalexamination

Evaluation of the basic bloodexamination & specialized laboratoryexamination

Micrositer, Hipochrom

Decreased SI and Elevated TIBC

SI/TIBC


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Iron values in the development of iron deficiency anaemia

131613-16

13-1612-14


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Rasio retikulosit=

Indeks/koreksi retikulosit(Normal: 5-15 .);

Pria :

Wanita :

Retikulosit

Hitung RetikulositHitung Eritrosit

x 1000

Rasio retikulositx42

Ht

Rasio Retikulosit ()HtHb

Rasio retikulositx39Ht

Pria Wanita

17 51 4.212.5 3.911.716 48 4.413.2 4.112.415 45 4.714.1 4.413.114 42 5.015.0 4.714.013 39 5.416.1 5.015.012 36 5.817.3 5.416.211 33 6.318.8 5.817.510 30 6.820.5 6.419.1

18 54 4.011.8 3.611.0


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TREATMENT

Therapeutic Trial

* Should be via oral route

* Expect

- peak reticulocytosis at 1 to 2 week

- significant increase in Hb concentration at 3-4 weeks

- one-half of Hb deficit corrected at 4-5 weeks

- Hb level normal at 2 to 4 months


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TREATMENT

Oral Iron Therapy* Dietary sources may not be sufficient for treatment

* Safest, cheapest are oral ferrous salt

* Nonenteric coated forms are preferred

* Avoid multiple hematinics

* Do not give with meals or antacids or inhibitor acid productions

* Continue for 12 months after Hb is normal to replenish iron stores

* Daily total 150-200 mg elemental iron in 3 to 4 doses, each 1 h ac


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Koreksi defisiensi besi serum

Untuk menaikkan Hb sebesar 1 gr/dL dibutuhkan Fe endogen 2,5mg/kgBB

Kebutuhan initial Fe:

Fe = (D Kadar Fe serum x 0,2 x BB) mg, atau

Fe = (D Hb x 2,5 x BB) mg

Iron Dextran max. 1,5 mg/kgBB/day

Jectofer 75 mg/2mL amp.

Cara 75 mg/deep im

Iron Sucrose Venofer 100 mg/amp

Cara infusi 100 mg in 100cc NS 1jam


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TREATMENT

Parenteral Iron Therapy* Routine use rarely justified

* Indications are:

- malabsorption

- intolerance to oral iron preparations (colitis, enteritis)

- needs in excess of amount that can be given orally- patient uncooperative or unavailable for follow-up

* Iron dextran:

- 50 mg elemental iron/ml

- Approximately 70 % readily available for Hb synthesis- May be given IM or IV

- Be aware of anaphylaxis or other systemic side effects


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TREATMENT

Parenteral Iron Therapy

* Continue therapy for 12 months after Hb is normal, in order toreplenish iron stores.

* Therapy may be needed indefinitely if bleeding continues

Failure to respond to therapy

* Wrong oral preparation

* Bleeding not controlled

* Therapy not long enough to show response

* Patient not taking medication

* Concomitant deficiencies (Vit. B12, folate, thyroid)* Concomitant illness (infection, malignancy, hepatic

disease, renal disease, inflammation)


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Hypochromic Microcytic RBC


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Megaloblastic anemia:

Vitamin B12/Folic acid deficiency

Multi System diseaseAll organs with

increased cell division.

Macrocytic anemia, pancytopenia.

Pernicious anaemia

autoimmune, Gastric atrophy, VitB12def.


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Megaloblastic anemia - Etiology

Malnutrition, vegetarian

Intrinsic factor Ab - Pernicious anemia

Gastrectomy, Ileal resection

Inflammatory bowel disease

Malabsorption syndromes - Sprue

Blind loop syndrome


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Megaloblastic anemia - Pathogenesis:

Decreased Vit B12/ Folate Decreased DNA Synthesis

Delayed maturation of erythroblasts

Increased cell size (macrocytes) Normal Hb content (Normochromia)

Decreased RBC number

Decreased WBC number (pancytopenia) Anemia & Pancytopenia.


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Diagnosis

Hb level, leukocyte, platelet, reticulocytes count, ESR

Red cells indices (MCV, MCH, MCHC) MCV >100 fl

Examination of peripheral blood film

Hypersegmented Neutrophil (Five Lobes)

BM examination

-B12defisiensi < 200 pg/ml (300-900 pg/ml)

-Folate defisiensi < 4 ng/ml (6-20 ng/ml)


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Deficiency Folic acid Serum

vit. B12

Serum RBC

Folic acid

Vit B12

Folic acid & B12

N /

N


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THERAPEUTIC TRIALS

Usual diet

0,2 mg folic acid oral

1 week

reticulocyte response

+ -

+ 1-2 g vit B12

reticulocyte response

M t


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Management

B12Defisiensi :B121000 ug IM weekly until 8 weeks,

and B121000 ug IM monthly

Folat Defisiensi :1 mg oral daily ( 5 mg daily maximal dose), treatmanefor 1 until 2 month or defisiensi corected.

Reticulosit Evaluation on day 4 and 5, than peak levelreticulosit on day 7.


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Macrocytic Anemia (Meg.):


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Macroovalocytes & Macropoly

b A


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Megaloblastic Anemia :


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anemia-defisiensife,b12danfolat(kbk) uisu.ppt

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