Iron deficiency anemia is the most common type of anemia globally. It is caused by lack of sufficient iron intake and absorption to meet physiological needs, especially during periods of growth. Symptoms include fatigue, weakness, and pallor. Diagnosis involves blood tests showing microcytic hypochromic anemia. Treatment focuses on iron supplementation either orally or via injection, along with addressing any underlying causes of blood loss or impaired absorption. Preventive measures include antenatal iron/folic acid supplements, exclusive breastfeeding, and iron fortification of complementary foods.

1. ANEMIA

2. INTRODUCTION
 Anemia is a condition that develops when
your blood lacks enough healthy red blood
cells or hemo globin. Hemoglobin is the
main part of red blood cells which binds
oxygen. Anemia is the most common
condition in India. Women of reproductive
age, children under five years of age and
people with chronic diseases are at
increased risk of anemia.

3. TYPES OF ANEMIA
Iron deficiency anemia:Iron deficiency
anemia is caused by the lack of sufficient iron
for the syn thesis of hemoglobin. It is the most
prevalent nutritional and hematological
disorders among in fants and children. This is
the greatest single cause of anemia in children
which results in macro cytic (erythrocytes
larger than their normal volume) and
hypochromic (erythrocytes are paler than
normal) anemia.

4. 2. Megaloblastic anemia:
Maturation of erythrocytes is
impaired when deficiency of vitamin
B12 and/or folic acid occurs and
abnormally large erythrocytes
(megaloblasts) are found in the
blood. During normal erythropoiesis
several cell division occurs and the
daughter cells at each stage are
smaller than the parent cell because

5.  there is no much time for cell
enlargement between divisions.
When deficiency of vitamin B12
and/or folic acid occurs, the rate
of DNA and RNA synthesis is
reduced, delaying cell division.
The cells can therefore grow
larger than normal between
divisions.

6.  a. Pernicious anemia: Pernicious anemia is a
type of megaloblastic anemia associated with
vitamin B12 deficiency.
b.Folic acid deficiency anemia: Chronic
megaloblastic anemia is caused by folic acid
deficiency.
 Signs and symptoms: Fatigue, weakness, pallor,
dizziness, headache, tachycardia,

7.  Aplastic anemia: Aplastic anemia is a
disorder characterized by bone marrow
hypoplasia oraplasia, resulting in
pancytopenia (insufficient numbers of
RBCs, WBCs and platelets).
 Signs and symptoms: Pallor, weakness, fatigue, exertion,
dyspnea, palpitations, infection associ ated with
neutropenia, fever, headache, malaise, adventitious
breath sounds, abdominal pain, diarrhea or erythema.

9. IRON DEFICIENCY ANEMIA
Nutritional or iron deficiency
anemia is most common in
children. It refers to reduced red
blood cell count due to poor diet,
which is deficient in iron, folates
and/or vitamin B12.

10. ETIOLOGY
 Several factors may contribute to iron
deficiency anemia:
 1. Insufficient iron supply at birth (from
mother)
 2. Insufficient iron intake during periods of
rapid growth.
 3. Impaired iron absorption.
 4. Blood loss
 5. Improper diet
 6. Late start of weaning

11. 1. Insufficient iron supply at birth:
The infant might not have received
adequate supply of iron from the mother
during intrauterine life, because the
mother herself may have had severe iron
deficiency or the fetus may have been
born prematurely. The infant may also
have lost blood either before or during or
after birth.

12.  2. Insufficient iron intake during
period of growth: The full term
newborn have 0.5 g of iron which is present
in the hemoglobin of the circulatory RBCs
and the rest is stored in the liver, spleen
and bone marrow. The maternal supply of
iron is sufficient for the first 4 to 5 months
of the infant's life but after that 0.8 to
1.5mg

13. of iron per day is necessary for
optimum nutrition in infant life. The
mature infant who does not receive
maternal supply of iron can develop
anemia as early as 2 months after
birth, if supplemental dietary iron can
develop anemia as early as 2 month
after birth, if supplemental dietary
iron is not given.

14.  3.Breast fed infants may require less
additional iron from other infant
foods. Artificially fed infants, should
have formulae that have been fortified
with iron. Their iron intake in the
other diets should be increased.

15. 4.During the periods of rapid growth,
adolescents may also develop this type of
anemia because oftheir imbalance diet and
poor feeding habits.
5.Impaired absorption: The intake of iron is
proper but the absorption of iron inadequate,
e.g. in malabsorption syndrome, celiac
disease, chronic diarrhea, worm infestation,
etc.

16. PATHOPHYSIOLOGY
 During the last trimester of pregnancy, iron
is transferred from the mother to the fetus.
Most of the iron is stored in the circulating
erythrocytes of the fetus, with the
remainder stored in the fetal liver, spleen,
and bone marrow. These iron stores are
usually for the first 5-6 months in a full-
term infant for only 2-3 months in preterm
infants and multiple birth.

17. If dietary iron is not supplied to meet
the infant's growth demands after the
fetal iron stores are depleted, iron-
deficiency anemia results. Physiologic
anemia should not be confused with
iron-deficiency anemia resulting from
nutritional causes.

18. CLINICAL MANIFESTATION
 .Extreme fatigue
 • Weakness
 • Pale skin
 • Chest pain, fast heartbeat or shortness of
breath
 • Headache, dizziness or lightheadedness
 • Cold hands and feetInflammation or
soreness of your tongue

19. • Brittle nails
• Unusual cravings for non-nutritive
substances, such as ice, dirt or starch
• Poor appetite, especially in infants and
children with iron deficiency anemia

21. DIAGNOSTIC EVALUATION
 Blood examination reveals that:
 1. Peripheral blood smear shows microcytic
hypochromic RBCs with anisocytosis
(abnormal size) and poikilocytosis
(abnormal shape).
 2. Reticulocytes count may be normal or
reduced

22.  3. HB% is usually low.
 4. RBC count is reduced.
 5.PCV, MCH, MCHC and MCV values are low.
 6.WBC and platelets counts are normal.
 7. In case of secondary infections the
leukocytosis are also increased.
 8. Serum iron level is low and iron binding
capacity is high. Serum ferritin level is
decreased.

23.  9. Stool tests are performed to determine
the presence of occult blood and ova of
worms.
 10. In severe cases, tests may be
performed according to underlying disease
condition.

24. MANAGEMENT
Management of iron deficiency anemia
consists of detection and treatment of
underlying cause.
 1. Improvement of dietary intake,
specially iron and protein containing
food should be given.
 2. Chronic blood loss (rectal, polyp,
ulcerative colitis) should be diagnosed
and treated.

25. 3. Supplementary iron may be given by
oral route. A therapeutic dose of 6
mg/kg/24 hours/approxi mately 10 to 15
mg supplementary iron in three divided
dose. During mild anemia, therapeutic
dose can be given for 3 to 4 months. In
severe anemia the treatment is
prolonged.

26. 4. Iron medication should be given between
meals (because free hydrochloric acid
facilitates ironabsorption). It is better to give
iron with a form of ascorbic acid (vitamin C)
a citrus fruit or juice.
5. Liquid medication containing iron, may
temporarily stain the teeth. To prevent
dental staining medication can be given
infants with a medicine dropper or a syringe.
Older children can take a diluted solutions
through a drinking tube or straw and then
rinse the mouth.

27.  6.In severe cases, blood transfusion is
indicated only in severe cases of
anemia where Hb% need tobe
increased.
7. Children who show gastric
intolerance to iron preparations and
Hb level is very low, in such cases
imferon (an iron dextran complex
containing 50 mg elemental iron per
milliliter) a parenteral iron
preparation is used.

28. Increasing awareness about prevention of
iron deficiency anemia is essential among
parents, regarding proper administration of
oral supplements, the side-effects of iron
therapy and the imporetance of dietary
intake of iron.Prevention of Nutritional
Anemia in Children

29. PREVENTION OF NUTRITIONAL ANEMIA
IN CHILDREN
 Antenatal care: Provide adequate antenatal
care for prevention of anemia in pregnant
mother bysupplementing iron and folic acid
to all antenatal mothers.
 2 Prevention of LBW and preterm birth:
Prevention of pre-term and low birth
weight deliveries by pro viding antenatal
and intranatal care.
 3 Exclusive breastfeeding till six months of
age to all infants to prevent malnutrition.

30.  4.Supplementary feeding and weaning
should be started alongwith breast milk at
six months of age to all infants.
 5. Universal immunization to all children
to prevent communicable diseases.
 6. Iron and folic acid supplementation to all
children and adolescent girls.
 7. De-worm against parasitic infestation to
all children especially who are diagnosed as
mild anemia.

31. SICKLE CELL ANEMIA

33. Definition
Sickle Cell disease: is a genetic
disorder that affects erythrocytes
(RBC) causing them to become sickle
or crescent shaped.
> The effects of this condition due to
an abnormality of the hemoglobin
molecules found in erythrocytes.

34. Red blood cells are usually round and
flexible, so they move easily through
blood vessels. In sickle cell anemia,
some red blood cells are shaped like
sickles or crescent moons. These sickle
cells also become rigid and sticky,
which can slow or block blood flow.

35. CAUSES
 People who have sickle cell disease inherit
two faulty hemoglobin genes, called
hemoglobin S — one from each parent.
 A person has sickle cell trait when the
hemoglobin S gene is inherited from only
one parent and
 A normal hemoglobin gene — hemoglobin A
— is inherited from the other.

36. CLINICAL MANIFESTATION

37.  Anemia,
 mild jaundice,
 fever, headache,
 lethargy, progressive weakness.
 Growth retardation,
 bacterial infections
 enlarged heart,
 respiratory difficulties andnon healing
ulcers.
 Sickle cell anemia may be complicated
with multisystem disease and leads to
organ failure or Death.

38. PATHOPHYSIOLOGY
Sickle cell disease is an inherited
genetic condition that involves defects
in the shape and function of hemoglobin
in the blood. This increases the
likelihood of blockages in the blood
vessels and disrupted blood flow, which
can result in serious complications.

40. DIAGNOSIS
Diagnosis is confirmed by hemoglobin
levels in the range of 6-8 g/dl with a
high reticulocyte count.
In other forms of sickle cell anemia Hb
level tends to be higher but blood film
shows sickle shaped RBCs in the
peripheral blood smear.

41. MANAGEMENT
Management of SCD is done blood
transfusion, parenteral fluid therapy,
treatment of infection, correc tion of
acidosis, analgesic and supportive care.
1. Folic acid daily for life is
recommended. From birth to five years
of age, pencillin daily due to immature-
immune system that makes them more
prone to early childhood illnesses is
recommended.

42. 2.Malaria prevention: In fact, children
with SCD are more prone to malaria.
People with sickle cell disease living
in malarial countries should receive
anti malarial chemoprophylaxis for
life.
3. New drug hydroxyurea is useful drug
but it causes harmful effect and may
not be used for long time.

43. BLOOD TRANSFUSION
Blood transfusions are often used in
the management of sickle cell disease
in acute cases and to prevent
complications by decreasing the
number of red blood cells (RBCs) that
can sickle by adding normal red blood
cells.

44. In children, preventive RBC transfusion
therapy has been shown to reduce the
risk of first stroke or silent stroke when
transcranial Doppler ultrasonography
shows abnormal cerebral blood flow. In
those who have sustained a prior stroke
event, it also reduces the risk of
recurrent stroke and additional silent
strokes.

45. BONE MARROW TRASPLANTATION
 Bone marrow transplants have proven
effective in children; they are the only
known cure for SCD.However, bone marrow
transplants are difficult to obtain because
of the specific HLA typing necessary.
Ideally, a close relative (allogeneic) would
donate the bone marrow necessary for
transplantation.

46. PREVENTION

48. COMPLICATION
 Stroke
 Acute chest syndrome
 Pulmonary Hypertension
 Organ damage
 Blindness
 Leg ulcer
 Gall stones
 Deep vein thrombosis