Pernicious Anemia  Irritable

 Has chronic diarrhea

-
- The tongue appears to be smooth and
V
beefy red due to papillary atrophy.

itamin B12 is necessary for maturation

of RBCs. Pernicious anemia results
from deficiency or inability to use the
vitamin (Waterbury, 2007).
- Laboratory findings reveal low serum
- In children, the cause is more often lack
level of vitamin B12.
of ingestion of vitamin B12. The vitamin
is found primarily in foods of animal
Management:
origin, including both cow’s milk and
 If cause by a B12-deficient diet,
breast milk.
temporary injections of B12 will
- For absorption of vitamin B12 from the
reverse the symptoms.
intestine, an intrinsic factor must be
 If caused by lack of the intrinsic
present in the gastric mucosa. In adults,
factor, lifelong monthly
lack of the intrinsic factor is the most
intramuscular injections of B12 may
frequent cause of the disorder.
be necessary.
- If a child has an intrinsic factor
deficiency, symptoms can occur as early Folate Deficiency Anemia
as the first 2 years of life (once the - A deficiency of folic acid combined with
intrauterine stores of vitamin B12 have vitamin C deficiency produces an
been exhausted). anemia in which the erythrocytes are
- The child appears to be: abnormally large. There is often
 Pale accompanying neutropenia and
 Anorexic thrombocytopenia.
- Megaloblastic arrest, or inability of o With iron-deficiency anemia,
RBCs to mature past an early stage, may RBCs are both small in size
occur in the first year of life from the (hypocytic) and pale
continued use of infant food containing (hypochromic) due to the stunted
too little folic acid or from an infant hemoglobin.
drinking goat’s milk, which tends to be o Causes in Infants. Several causes
deficient in folic acid. lead to iron-deficiency anemia:
- Treatment is daily oral administration of  When an infant’s diet
folic acid. lacks sufficient iron, the
infant usually has enough
Microcytic-Hypochromic Anemia
in reserve to last for the
- When hemoglobin synthesis is
first 6 months. After that,
inadequate, the erythrocytes appear pale
if the infant’s diet
(hypochromia). Hypochromia is
continues to be iron
generally accompanied by a reduction in
deficient, there will be
the diameter of cells (RBCs are also
difficulty forming
microcytic).
adequate RBCs.
 Iron-Deficiency Anemia
 As a preventive measure,
they may be given an iron
supplement beginning at
about 2 months of age.
 Iron-deficiency anemia
can be prevented in
formula-fed infants by
giving them iron-fortified
formula. If an infant is
breastfed, iron-fortified
cereal should be
introduced when solid
foods are introduced in
the first year.
 o Causes in Older Children. In
children older than 2 years,
o result from depression of
chronic blood loss is the most
hematopoietic activity in the
frequent cause of iron-deficiency
bone marrow or reduced RBC
anemia. This is caused by
production.
gastrointestinal tract lesions such
o Drugs that may cause this
as:
 polyps include:

 ulcerative colitis  chloramphenicol

 Crohn’s disease  sulfonamides

 protein-induced  arsenic (contained in rat

enteropathies poison, sometimes eaten

 parasitic infestation by children)

 frequent epistaxis.  hydantoin

Normocytic-Normochromic Anemia  benzene

- marked by impaired production of  quinine

erythrocytes by the bone marrow, or by o Exposure to insecticides also

abnormal or uncompensated loss of may cause severe bone marrow

circulating RBCs, as with acute dysfunction.

hemorrhage. The RBCs are normal in o Chemotherapeutic drugs

both color and size, but there are simply temporarily reduce bone marrow

too few of them. production.

 Aplastic Anemia Management:

 The ultimate therapy for both
congenital and acquired
aplastic anemia is
hemopoietic stem cell
transplantation.
 Such infants become listless and
inactive.
Management:
 Should be placed in a supine
position to provide as much
circulation as possible to
brain
 Keep the child warm with
blankets or place in an
incubator or radiant heat

 Posthemorrhagic anemia/ Acute blood warmer

loss anemia  Blood transfusion may be

o Blood loss from the vascular necessary

space
Hemolytic Anemia
o Children are in shock from acute
- are those in which the number of
blood loss and appear pale. As
erythrocytes decreases due to increased
the heart attempts to push the
destruction of erythrocytes.
reduced amount of blood through
 Sickle-cell Anemia
the body more rapidly,
tachycardia will occur. Loss of
RBCs needed for oxygen
transport causes body cells to
register an oxygen deficit, and
children begin to breathe rapidly.
Newborns may have gasping
respirations, sternal retractions,
and cyanosis. They will not o the presence of abnormally
respond to oxygen therapy
shaped (elongated) RBCs.
because they lack RBCs to
o The erythrocytes become
transport and use the oxygen.
characteristically elongated and
crescent-shaped (sickled) when o When RBCs sickle, they can not
they are submitted to low oxygen move freely through vessels.
tension (less than 60% to 70%), a Stasis and further sickling occur
low blood pH (acidosis), or (a sickle-cell crisis - the term
increased blood viscosity, such as used to denote a sudden, severe
occurs with dehydration or onset of sickling.). Blood flow
hypoxia.

halts and tissue distal to the

blockage becomes ischemic,
resulting in acute pain and cell
destruction (Linker, 2009).

 Thalassemia
- are autosomal recessive anemias
associated with abnormalities of the beta
chain of adult hemoglobin (HgbA).
o Thalassemia Minor
o a mild form of this anemia,
 o produce both defective beta - G6PD deficiency may be diagnosed by a
hemoglobin and normal rapid enzyme screening test or
hemoglobin. Children may have electrophoretic analysis of RBCs.
no symptoms other than pallor.  Hereditary/ Congenital spherocytosis
They require no treatment, and - Congenital spherocytosis is a hemolytic
life expectancy is normal. anemia that is inherited as an autosomal
o Thalassemia Major dominant trait. RBCs are small and
o also called Cooley’s anemia defective, apparently due to

or Mediterranean anemia. abnormalities of the protein of the cell

o Unable to produce normal membrane that make them unusually

beta hemoglobin, the child permeable to sodium. The life span of

shows symptoms of anemia: erythrocytes is diminished.

pallor, irritability, and - The disease may be noticed shortly after

anorexia (Muncie, 2008). birth, although symptoms may appear at

any age. The hemolysis of RBCs:
o appears to occur in the spleen,
apparently from excessive
absorption of sodium into the
cell.
o The abnormal cell swells,
ruptures, and is destroyed.

  G6PD/ Glucose-6-Phosphate
Dehydrogenase Deficiency
- The enzyme glucose-6-phosphate
dehydrogenase (G6PD) is necessary for
maintenance of RBC life. Lack of the
enzyme results in premature destruction
of RBCs. The disease is transmitted as a
sex-linked recessive trait.
 o Chronic jaundice and
splenomegaly (enlarged spleen)
develop.
- The treatment is generally splenectomy
at approximately 5 to 6 years. This
measure will increase the number of
RBCs present but will not alter their
abnormal structure.