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)
  APLASTIC ANEMIA

A rare and serious blood disorder in which bone marrow stops making enough new blood cells.
aplastic anemia, normal production of all blood cells—red cells, white cells, and platelets—slows
or stops. This is because the stem cells have been damaged. The cause of this damage is often
unknown.

ETIOLOGY:
Aplastic anemia is caused by damage to stem cells in the bone marrow. Stem cells normally
develop into three types of blood cells: red blood cells, white blood cells, and platelets.
When stem cells are damaged, they do not grow into healthy blood cells.
In more than half of people with aplastic anemia, the cause of the damage to stem cells is
unknown. Some research suggests that stem cell damage may occur because the body’s
immune system attacks its own cells by mistake.

The cause of acquired aplastic anemia has been linked to outside agents, as well as to
diseases. Outside agents include toxins such as pesticides, arsenic, and benzene; radiation
and chemotherapy used to treat cancer; and medicines such as chloramphenicol, an
antibiotic now rarely used in the United States. Infectious diseases also can cause aplastic
anemia. Some of these diseases are hepatitis, Epstein-Barr virus, cytomegalovirus (si-to-
MEG-a-lo-VI-rus), parvovirus B19, and HIV. Autoimmune diseases, such as lupus and
rheumatoid arthritis (ROO-ma-toyd ar-THRI-tis), also can cause this condition.
Some inherited genetic disorders can lead to aplastic anemia. These include Fanconi
anemia, Shwachman-Diamond syndrome, and dyskeratosis congenita

MANIFESTATIONS:
Aplastic anemia is suspected when test results indicate that all three blood cell levels are
extremely low, but the cells themselves have a relatively normal appearance. It remains a
rare disease, striking only two to six of every 1 million people annually in the United States
and Europe.
In addition to low blood cell counts, aplastic anemia is characterized by other physical
symptoms of anemia such as pale skin and fingernails, rapid pulse, heart murmur and
fatigue. Children also may exhibit abnormal bleeding including multiple bruises, nosebleeds,
bleeding gums and small hemorrhages under the skin as well as infection, especially fever.
However, each child may experience symptoms differently. Other possible symptoms
include:

• Headache
• Dizziness
• Nausea
• Shortness of breath
• Blood in stool
• Sinus tenderness
• Enlarged liver or spleen
• Oral thrush, which produces white patches on a red, moist, swollen surface anywhere in
the mouth

2. Increased erythrocyte destruction

 SICKLE CELL ANEMIA

Severe hemolytic anemia that results from inheritance of the sickle hemoglobin gene which
causes the hemoglobin molecule to be defective. Sickle cell hemoglobin acquires a crystal-like
 formation when exposed to low oxygen tension (can be caused by low oxygen level in the
venous blood). RBC containing sickle hemoglobin loses its round, very pliable, biconcave disk
shape an becomes deformed, rigid, and sickle-cell shaped. Long rigid RBC can adhere to
endothelium of small vessels, and when they pile up to each other, blood flow to organ or
region maybe reduced (pain, swllig and fever if it results to ischemia and infarction). The
sickling process takes time. If RBC is again exposed to adequate amount of oxygen before the
membrane becomes too rigid it can revert to normal shape. Cold can aggravate sickling process
because vasoconstriction lows blood flow. Oxygen dwelling can be impaired by increased blood
viscosity. This type of anemia is the most severe form of sickle cell disease.

ETIOLOGY
Sickle cell disease is found in races of people from areas of the world where malaria is
endemic, including Africa, the Mediterranean, the middle east, and India. The
heterozygous from appears to be a selective advantage for the survival of malaria
because the parasite infected cells sickle and are removed.

MANIFESTATIONS:

• Sickle celled RBC have short ended life span

• Patients are always anemic (Hgb: 7-10gm/dl)
• Jaundice is characterized and usually obvious in sclera
• Enlargement of bones of the face and skull
• Tachycardia, cardiac murmurs, enlarged heart (chronic)
• Dysrythmias and heart failure ( in adults)

 HEMOLYTIC ANEMIA
An end result of many conditions that lead to hemolysis, te premature destruct
Ion of erythrocytes, can result from physical damage, intrinsic membrane defects, immune
destruction of RBCs by macrophages, or hypersplenism.

ETIOLOGIC
Result from hereditary disorders(due to intracorpuscular defects) or acquired hemolytic
coerythrocytic membrane and enzyme defects and Hb abnormalities include
spherocytosis and hereditary hemoglobinopathies (G-6-PD, thalassemia, and sickle cell
anemia).

Intrinsic
-RBC defects
-hemoglobinopathies
-inherited enzyme defects

Extrinsic
-drugs
-bacteria and other toxins
-antibodies mediated lysis
-physical trauma
-prosthetic heart valves
-vasculitis
-severe burns
-disseminated intravascular coagulation
Thrombocytonic purpur
-renal disease

MANIFESTATIONS
The clinical manifestations of hemolytic anemia are numerous and diverse and are due
primarily to anemia, the extent of compensation, previous treatment, and the
 underlying cause. The client with hemolytic anemia may suffer from all the general
manifestations of anemia discussed earlier

3. Anemia Caused by Blood Loss

Red blood cells can be lost through bleeding, which can occur slowly over a long period of time, and
can often go undetected. This kind of chronic bleeding commonly results from the following:

• Gastrointestinal conditions such as ulcers, hemorrhoids, gastritis (inflammation of the stomach)

and cancer
• Use of nonsteroidal anti-inflammatory drugs (NSAIDS) such as aspirin or Motrin
• Menstruation and childbirth in women, especially if menstrual bleeding is excessive and if there
are multiple pregnancies

III. PATHOPHYSIOLOGY
IV. GENERAL TREATMENT OR MANAGEMENT / NURSING MANAGEMENT

FOLIC ACID
TREATMENT:
• When anemia results from insufficient dietary intake of vitB12
 Increase intake of foods containing vitB12 (meats, eggs, dairy products)
• vitB12 supplements (for strict vegetarians and those with severe anemia)
• parenteral vit B12 replacement is required when malabsorption disorder / lack of intrinsic factor
is the cause

HEMOLYTIC ANEMIA
Management:
Minor - Requires no treatment because the body adapts to the reduction of normal hemoglobin
Symptoms of th blood thalassemia major are manage with blood transfusion in conjunct with IV
deferoxamine (DESFERAL) (a chelating agent that binds to iron) to reduce the iron over loading that
sometimes occurs with chronic transfusion therapy.
RBC’s are sequestered in enlarged spleen, thalassemia may be treated by splenectomy