I.

OVERVIEW
What is Anemia?
Anemia is an abnormally low number of
circulation RBCs, low hemoglobin
concentration, or both.
Decrease number of circulating RBCs is the
usual cause of anemia. This may result from
blood loss,
inadequate RBC production or increase RBC
destruction. Insufficient or deficient
hemoglobin within RBCs
contributes to anemia. Depending on its
severity, anemia may affect all major organ
system. (Lemone,
p934)
II. DIFFERENT TYPES OF ANEMIA:
A. According to cause:
1. Decreased Erythrocyte Production
 IRON DEFICIENCY ANEMIA
Iron deficiency anemia is the most common
type of anemia. It develops when the supply of
iron is inadequate of optimal RBC formation.
The body cannot synthesize hemoglobin
without iron. Iron-deficiency anemia results in
fewer numbers of RBCs, microcytic and
hypochromic RBCs, as well as malformed
RBCs (poikilocytosis). Iron deficiency anemia
may
result from inadequate dietary iron intake. The
body can store about ¼ to 1/3 of its iron,
and it is not until those stores are depleted that
iron-deficiency anemia actually begins to
develop. IDA is particularly common in older
adults. Chronic, occult (hidden) blood loss may
occur from slowly bleeding ulcers,
gastrointestinal inflammation, hemorrhoids, an
cancer.
Inadequate dietary iron intake also contributes
to anemia in older adults. Access to
transportation may limit fresh food
consumption, a factor contribution to poor iron
intake
among all adults, especially people with limited
or fixed incomes.
ETIOLOGY:
•
Results in unavailability of iron hemoglobin
synthesis
•
Due to low iron intake
x
Diminished absorption
x
Physiologically requierement such as pregnancy
x
Excessive iron loss such as chronic hemorrhage
x
Inadequate utilization of iron such as anemia and
chronic disorder
MANIFESTATIONS:
Chronic iron deficiency may lead to:
x
Brittle spoon shaped nails
x
Cheilosis (cracks at the corner of the mouth)
x
A smooth soar tongue
x Pica (cravings for unusual substances such as
clay or starch)
 THALASSEMIA
Thalassemia is another disease caused by
decreased production of erythrocyte. It is an
autosomal recessive genetic disorder of
inadequate production of normal hgb. Though
hemolysis also occurs, the predominant
problem is the insufficient production of normal
hgb. Thalassemia involves the problem with
the globulin protein as compared to IDA where
hehe synthesis is the problem.
Members of ethnic group whose origin are
near the Mediterranean sea and equatorial or
near equatorial regions of Asia and Africa.
There are two form of disease: heterozygons
and homozygon. An individual who is
heterozygous has one thalassemic gene and
one normal gene and is said to have
thalassemia minor, is milder than a
homozygous person who has two thalassemic
genes causing thalassemia major.
ETIOLOGY:

The causes of thalassemia are directly linked

to genetics and how the genes that affect
hemoglobin production are inherited. People
with moderate to severe forms received variant
genes from both parents. People who are
carriers of the disease received variant genes
from one parent and normal genes from the
other parent. Regardless of the causes of
thalassemia, treatment options are available
for all forms of the disease.
CLINICAL MANIFESTATIONS:
Thalassemia minor
 Asymptomatic  Splenomegaly  Mild
jaundice
Thalassemia major
 Retarded physical and mental growth
 Pale
 Pronouncial hepatomegaly and splenomegaly
 Jaundice
 Thickening of the cranium and malillary cavity,
caused by bone marrow hyperplasia
leading to an appearance presembling doven
syndrome
 FOLIC ACID DEFICIENCY ANEMIA
o

VITAMIN B12 DEFICIENCY

Vitamin B12 is necessary for DNA synthesis
and is almost exclusively found in foods
derived
from animals. Vit.B12 deficiency occurs when
inadequate VitB12 is consumed, or more
commonly, when it is poorly absorbed from the
gastrointestinal tract. Deficiency of this
vitamin impairs cell division and maturation,
especially in rapidly proliferating red blood
cells. As a result, microlytic, misshapen (oval
rather than concave) RBCs with thin
membranes are produced. Great numbers of
these large, immature RBCs enter the
circulation. These cells are fragile, incapable of
carrying adequate amounts of oxygen and
have a shortened life span.
ETIOLOGY OF VITB12 DEICIENCY:
• Malabsorption disorders

• Resection of the stomach/ileum

• Loss of pancreatic secretions

• Chronic gastritis (affect vitB12 absorption)

• Dietary deficiency of vitB12 (occurs among strict

vegetarians)
MANIFESTATIONS:
• Manifestations develop gradually as bodily stores
of the vitamin are depleted

Pallor/slight jaundice and weakness develop

Paresthesias (altered sensations, such as numbness
or tingling) in
extremities

Problems with proprioception ( sense of one’s
position in place)
 MEGALOBLASTIC ANEMIA
Are a group of disorders caused by impaired
DNA synthesis resulting in defective RBCs.
These anemias share the morphology of
megablast (then large, abnormal, and
premature RBCs) in the blood and bone
marrow.
ETIOLOGY

They are caused by deficiencies of

vitB12(cobalamine) and folic acid.
MANIFESTATIONS:
Common feature include the following:
•
leukopenia, (a decrease number of white blood
cells)
•
thrombocytopenia (a decreased number of platelets)
•
oral, GI, and neurologic manifestations
•
a favorable response to injections of either vitB12
or folic acid
•
Loss of appetite
•
Diarrhea
•
Tingling and numbness of hands and feet
•
Pale skin color
•
Tiredness
•
Headaches
•
Sore mouth and tongue
•
Change in skin color
 PERNICIOUS ANEMIA
A type of Megalobastic anemia. Pernicious
anemia is a decrease in red blood cells that
occurs
when the body cannot properly absorb vitamin
B12 from the gastrointestinal tract. Vitamin
B12
is necessary for the formation of red blood
cells. Pernicious anemia, which results from
deficiency, occurs most frequently in older
than age 60 who have fair complexion and a
family
history of family history of the disease.
ETIOLOGY:
Vitamin B12 deficiency usually results from
malabsorption of the vitamin because of the
deficiency of the intrinsic factor that protects
the vitamin so that it can be absorbed in the
ileum.
Vitamin B12 normally binds chemically with the
intrinsic factor that promotes its absorption. In
certain conditions, such as atrophy of the
gastric mucosal cells, lack of secretion of the
intrinsic
factor leads to malabsorption of vitB12. Normal
erythrocyte maturation is dependent in
adequate amounts of vitB12 for the synthesis
of DNA molecules. Without vitB12, a
microcytic or
megaloblastic anemia results, with marked
anisocytosis (variation in RBC size) and
poikilocytosis (variation in RBC shape).
Ineffective eryhtropoiesis a nd increased
erythroblast
destruction result in hyperbilirubenemia.
Although the most pronounced changes arise
in RBCs,
mild neutropenia and thrombocytopenia may
occur.
The onset of symptoms usually is insidious but
maybe hastened by condition such as
infection. Persons with pernicious anemia do
not secrete hydrochloric acid (on gastric
analysis) even after parenteral stimulation with
histamine.
MANIFESTATIONS:
Signs and symptoms of pernicious anemia are
common to any of the anemic states.
•
Anorexia
•
Fatigue
•
Shortness of breath
•
Irritability
•
Soreness of the tongue characteristically occurs
early in the illness and progressively
worsens(soreness is quickly relieved after adequate
vitB12 treatment)
•
Symmetric numbness and tingling of the toes and
fingers occur on 10 percent of these
people (this may indicate early Neurologic disease)
•
Ataxia (loss of vibration sense) also maybe noted
(Neurologic symptoms may not entirely
remit after treatment)