1.  National family health survey
(NFHS-III) in 2005-06 found that
the prevalence of anemia under 5
children approach about 70%.it is
highest in children between 6-35
months of age.

2. PRESENTED BY
DR. VIJAY KR. SINGH(DNB PED)
UNDRE GUIDENCE OF
DR. T. K. MONDAL MD(PED)
M R BANGUR HOSPITAL
TOLLYGUNJ
KOLKATA

3.  Decreased erythropoesis either due to deficiency
of nutrition or defect in erythipoesis
 Increased blood loss.
 Diminished red cell survival as a result of
immune disorder and chronic diseases.
 Inadequate iron supply at birth like- prenatal or
maternal nutrition deficiency, prematurity, low
birth weight, multiple birth.

4.  Inadequate absorption of iron-
Gluten induced entrepathy,
atrophic gastritis, post –
gasterectomy, presence of phytats
in diet and calcium, presence of
recurrent diarrhea.

5.  A. disorder of red cell production in which the
rate of red cell production is less than
expected.
 1. marrow faillure
 - Aplatic anemia( congenital and aquired)
 2. Pure red cell aplasia
 congenital
 Diamond- Blackfan Syndrome

6.  Aese Symdrome
 Transient erthroblastopenia of childhood
 C. Bone marrow replacement
 malignancy
 Ostipetrosis
 Myelofibrosis
 Chronic renal disesas
 Vitamin D

7.  Chronic renal disease
 Hypothyriodism
 Chronic infection
 Protein energy malnutrition
 Hemoglobin mutant with decreased affinity of
O2

8.  Abnormalities in cytoplasmic maturation
 Iron deficiency
 Thalassemia syndrome
 Lead poisoning
Abnormalities in nuclear maturation
Vitamin B12
folic acid
Thiamin respond megaloblastic anemia
hereditary abnormalities in folate
metabolism
Orotic aciduria

9.  Iron deficiency anemia is the most
wide spread micronutrient deficiency
and affect nearly 1.5 billion people
globally.
 Infant,pre school children,
adolescent, and growing children are
at greater risks.
 According to NFHS-III in 2005-06,
the prevalence of anemia under -5
yrs of children is about 70%.

10.  Normal infant have 75mg of iron
of per kg body weight.
 Two third present in RBC.
 The majority of body iron is in the
form of Hb with about 10% in iron
containing protien like myoglobin
ant cytochrome.

11.  Pulses
 green leafy vegetable
 Dal
 Bajra, dates, Nuts,
 Jaggery
 Meat and fish
 Administration of Vitamin- C
increased the absorption of iron

12.  A. Decreased iron store
Preterm
Small for date baby
Twins
B. Decreased intake assimilation
Delayed intake of complementary feeding
Malnutrition
Poor iron diet
Mal absorption
Chronic diarrhoea/ infection
Gastero- intestinal surgery

13.  C. Increased loss
Gastro intestinal bleeding
Malaria
Hook worm infestation, trichuris
trichuria.
H. pylori.
Peptic ulcer.
Diveticulutis, bleeding diathesis,
feto- femoral haemorrahagem, repeated
venous sampling.

14.  Prematurity
 LBW Baby
 Recovery from mal nutrition
 Adolescence

15.  Mostly are asymptomatic.
 Pallor is most important clinical sign but
usually not visible until Hb fall to 7-8gm/ dl.
 Initial manifestation irritability, anorexia,
pallor, hyper dynamic circulation leads to
palpitation.
 Shortness of breath, easy fatigability, exercise
intorelerance, heart failure.
 Sign- koilonychias, glossittis, angular chellitis,
these are more common in long standing
Anemia.

16.  Hb 6 month-5yrs < 11gm/dl
6- 11yrs <11.5gm/dl
non pregnant <12gm/dl
pregnant < 11gm/DL
MCV <82
Transferring saturation <16%
Serum ferritin < 5yrs<12
>5yrs 15
in infection < 30
erythrocytes Zinc protoporphyrin < 5yrs >70
> 5yrs >80

17. Serum ferritin
decreased
Serum iron
decreased
Iron binding
capacity increased

18.  RDW – Increased>19
 RBC- Decreased
 Peripheral smear shows-
Hypochoromic microcytic red cell
with sustacial variation in cell
size, elliptocytic or cigar shaped
red cell are seen.

20. Study Iron deficiency
anemia
thalassemia Anemia of
chronic diseases
Hemoglobin Decreased Decreased decreased
MCV Decreased Decreased Decreased-
Normal
RDW Increased Decreased Normal-
Decreased
RBC Decreased Normal-
Increased
Normal-
Decreased
Serum ferritin Decreased Normal Increased
Total iron
binding capacity
Increased Normal Dcreased
Reticulocyte Decreased Normal Normal -

21.  Daily doses of 3-6 mg of elemental iron per kg of
body weight in two or three divided doses
 Parental iron prepation is usually used only in
malabsorption,poor compliance.
 Parental iron sucrose and gluconoate complex have
a lower risk of serious reaction than dextran.
 Doses of parental iron-2.3x body weight( 15-
patient Hb in gm/dl) +500 to 1000 mg, given in
divided doses.
 Excessive intake of milk should be avoided

22.  Repeat blood count after 4weeks
 Hb begins to increased 0.1 to 0.4
gm/ dl per day.
 Iron medication should be
continue for 8weeks after blood
value normalized to re-
establishment a response to
therapy.

23. Time after
iron
administration
Response
12-24 hrs Replacement of intracellular iron enzyme , subjective
improvement, decreased irritability, increased appetite
36- 48 hrs Initial bone marrow response, erythroid hyperplasia
48-72hrs Reticulocytisis, peaking at 5-7 days
4- 30 days Increased in Hb level
1- 3 months Repletion of store

24.  Poor compliance.
 Incorrect dose or administration.
 Malabsorption of absorbed iron.
 On going blood loss.
 Concurrent vitamin B 12 deficiency or fIoate
deficiency.
 Diagnosis other than iron deficiency like
Thalassemias
Hb C and E disorder
Anemia of chronic diseases
lead poisoning, sickle cell anemia

25.  Sideroblastic anemia result from
disorder of heme synthesis.
Characterized by microcytic, mixed
with normal RBC a picture of
dimorphic anemia with high RDW,
serum iron elevated and trasferrin
saturation increased. Elevated iron
deposited in mitochondria.

26.  Megaloblastic anemia is characterized by
macrocytic red cells and erthroid precursor which
show nuclear dymaturity.
 The common causes are Vitamin B12 and Folic
acid.
Incidence
incidence of folate deficiency as 6.8% and vitamin
B12 32% and combined 20%.

27.  Megaloblastic anemia affect all hem
poetic cell line resulting anemia,
thrombocytopenia, and leucopenia.
 DNA synthesis impaired because of
lack of methytetrahydrofolate, vit B12
plays an important role as co factor
which is necessary for DNA synthesis.

28.  Folate deficiency caused by
Decreased ingestion
celiac disease
Malabsorption state
Drugs like
Methotrexate
6- mercaptopurine
Trimithprine, azathiprine, phynatoin and other
anticonvulsent and increased requirement infancy,
hyperthyroidism, chronic hemolytic disease.
Vitamin B 12 deficiency causesd by
Decreased ingestion
intestinal parasite

29. Intritrisic intestinal diseas
intrinsic factor deficiency
Oritic aciduria
HIV infection
H. pylori infection

30.  Pallor
 Anorexia
 Irritability
 Thrombocytopenia, neurtopenia,
 Glossitis, stomatitis, hyper pigmentation over skin
on knuckles
 Enlarged liver and spleen in 30- 40% cases.
 loss of position sense, vibration sensation,
memory loss, confusion, and neuron psychiatric
symptoms.

31.  MCV>110
 Hyper segmented neutrophil.
 Bone marrow shows one or more cell
line affected
 Bone marrow is cellular and nuclear –
cytoplasmic asynchrony.
 Elevated lactate and billirubin.

32.  Folate- 1-5 mg/day for 3-4 weeks
 Vitamin B 12 500-1000micro gram for 2-3
weeks then 100-250 micro gram once in a
month to prevent recurrence.
 Treatment with folic acid alone can produce
hematological response in vitamin B 12
deficiency but does not currect neurological
impairment caused by Vitamin B12

33.  Difinition- A term infant have higher
hemoglobin and hematocrit and larger RBC than
older child and adult, within the 1st week of life a
progressive decline of Hb level begins then
persist for 6-8wks of life called physiological
anemia of infancy.
 Causes – there is gradual , normal development
switch from Hb F to adult Hb after birth which is
capable of delivering of more oxygen to the
tissue.The increased in blood oxygen content
and delivery result in the down regulation of
erythropoietin production leading to suppression
of eryththropoesis.
 Tratment- No therapy required

34.  Hb may decreased to 8gm /dl at 4-8 weeks
of life in premature neonate with birth
weight less than 1.5 kg.
 Factors which contributes development of
anemia
Reduced hematopoietic activity as evident
by decreased reticulocytes counts
Reduced red cell survival.
Treatment – recombinant human
erythropoietin with or without transfusion.
with adequate protein vitamin E, iron to
achieve full benefit of medication.

35.  DEFINITION
 A plastic anemia is defined by as
presence of any two peripheral
blood criteria ANC(Absolute
neutrophil count) < 1500/mm
platelet count < 40,000/cumm.

36.  Congenital
Fanconi anemia
Dyskeratotic congenita
Reticular dysgenesis
Shwachman- Diamond syndrome
Acquired
Idiopathic
Radiation
Viruses- hepatitis, epstein – Bar virus, Parvo virus
pregnancy,Hypogamaglubenumia, thymoma,
Enophilic fascitis,pre- leukemic state
Chemical- benzene,sniffing insectiside

37.  Infection
 hepatitis, parvo virus,Epsttien bar
virus
 Drugs
 sulfa, anticancer drugs
chlotramphenical,gold,carbamazepi
n .indomethacin .
 Radiation.

38.  Thrombocytopenia, with bleeeding in
skin, mucasal, GI tract, hematuria,
menorrhagia.
 Neutropenia leads to fever, infection.
 Anemia appears last with
breathlessness, puffiness of face,
edema of feet, congestive cardiac
failure

39.  Peripheral smear- normocytic
normochromic RBC,leukopenia,
decreased ANC, Thrombocytopenia.
 Coagulation parametre will be normal.
Bone marrow biopsy
hypocellular marrow with empty
spicule, increased fat space,
hypoplasia.

40.  Curative-stem cell transplant
 Criteria for stem cell transplant
1. Patient who are young
2. Severe a plastic anemia
3. Matched related sibling donor
 Other treatment
 Antithymocyte globin(ATG)
 G-CSF
 CyclosporineA

41. condition Inheritan
cce
Associated features Risk of malignancy
Falconi
anemia
AR Absent thumb,absent radius,
microcephaly,renal
anomalies,short stature,skin
pigmentation
AML,
Myelodysplasia,o
ral and liver
cancer
Dyskerato
sis
congenita
X–
linked,
AD, AR
Nail dustrophy, leukoplakia, Squamous cell
calcinoma,
myelodysplasia
Diamond
Blackman
AD, AR Short stuture,congenital
anomalies , elevated Hb F,
Raised adenosine deaminase,
Leukemia,
myelodypkasia

42.  Diamond blackman syndrome is isolated
erythroid hypoplasia occurs in early child
hood and associated with congenital
anomalies like stabismus, webbed neck,
deformed thumb, bony abnormalities of
finger and thumb, double ureter,
hydronephrosis.
 Bone marrow shows profound erythroid
hypoplasia, macrocytosis. Inceased Hb F
 Treatment-transfusion therapy, and
steroid

43.  A rare disorder characterized by
diminised megakaryocytic tith
stem cell defect without
associated physical defect or
abnormal defect.

44.  A variety of cells are abnormally sensitive
by complement, due to defect in
glycosylphosphatidylinositol anchor, which
bind protein to the cell membrane.
 Chronic hemolytic is more common than
sleep- induced hemoglobinuria.
 Diagnosis – molecular testing of CD-56

45.  It is characterized by presence of
vacuoles in bone marrow precursor
cells along with sideroblastic anemia
with pancreatic exocrine
abnormalities.

46. 