Drugs Used to

Treat
Anemias
 ANEMIA

- are disorders that involve too

few RBCs or ineffective RBCs
that can alter the blood’s ability
to carry oxygen.
 Anemia results from some alteration in
erythropoiesis, the process of RBC production, which
occurs in the myeloid tissue of the bone marrow. The
rate of RBC production is controlled by th
glycoprotein erythropoietin, which is released from
the kidneys in response to decreased blood flow or
decreased oxygen tension in the kidneys.
Under the influence of erythropoietin, an
undifferentiated cell in the bone marrow becomes a
hemocytoblast. This cell uses certain amino acids,
lipids, carbohydrates, vitamin B12, folic acid, and iron
to become an immature RBC. In the last phase of
RBC production, the cell loses its nucleus and enters
circulation. This cell, called a reticulocyte, finishes its
maturing process in circulation
 Types of Anemia
1. deficiency anemia- Fewer RBCs are produced,
and the ones that are produced are immature
and inefficient iron carriers.
2. megaloblastic anemia-which nvolves decreased
production of RBCs and ineffectiveness of those
RBCs that are produced (they do not usually
survive for the 120 days that is normal for the life
of an RBC).
3. hemolytic anemia-involves a lysing of RBCs
because of genetic factors or from exposure to
toxins.
• Iron-Deficiency Anemia- situations in which blood is
being lost, a negative iron balance might occur.
This can occur in certain rare GI diseases in which the
patient is unable to absorb iron from the GI tract, but
iron-deficiency anemia is also a relatively common
problem in certain groups, including the following:
a. Menstruating women, who lose RBCs monthly
b. Pregnant and lactating women, who have
increased demands for iron
c. Rapidly growing adolescents, especially those
who do not have a nutritious diet
d. Persons with GI bleeding, including individuals
with slow bleeding associated with use of
nonsteroidal antiinflammatory drugs (NSAIDs)
• Folic Acid Deficiency-Folic acid is essential for cell
division in all types of tissue. Deficiencies in folic
acid are noticed first in rapidly growing cells, such
as those in cancerous tissues, in the GI tract, and
in the bone marrow. Folic acid is very important
for the developing fetus, a site of very rapidly
growing cells. Pregnant women are urged to take
folic acid supplements to help prevent fetal
abnormalities, particularly neural tube defects.
.
• Vitamin B12 Deficiency-The most common cause of
this deficiency, however, is inability of the GI tract to
absorb the needed amounts of the vitamin. Gastric
mucosal cells produce a substance called intrinsic
factor, which is necessary for the absorption of vitamin
B12 by the upper intestine.
a. Pernicious anemia occurs when the gastric mucosa
cannotproduce intrinsic factor and vitamin B12 cannot be
absorbed
• Sickle Cell Anemia-is a chronic hemolytic anemia that
occurs almost exclusively in Blacks (“hemolytic” means
that the anemia involves a lysing or destruction of
RBCs).
 ERYTHROPOIESIS- STIMULATING
AGENTS
Drugs: drugs epoetin alfa (Epogen, Procrit),
darbepoetin alfa (Aranesp), and methoxy
polyethylene glycol-epoetin beta (Mircera).

Therapeutic Actions and Indications

a. Epoetin alfa acts like the natural glycoprotein
erythropoietin to stimulate the production of
RBCs in the bone marrow.
b. Darbepoetin alfa is an erythropoietin-like protein
produced in Chinese hamster ovary cells with the
use of recombinant DNA technology.
 Pharmacokinetics
All of these drugs can be given IV or by
subcutaneous injection. Epoetin alfa,
which is like endogenous erythropoietin,
is metabolized in the serum through the
normal process that the body uses to
clear erythropoietin. It has a slow onset
and peaks in 5 to 24 hours, and its
duration of effect is usually 24 hours. It
has a half-life of 4 to 13 hours and is
excreted in the urine.
 Contraindications and Cautions
All three of these drugs are contraindicated in
the presence of uncontrolled hypertension
because of the risk of even further
hypertension when RBC numbers increase and
the pressure within the vascular system
increases; with known hypersensitivity to any
component of the drug to avoid
hypersensitivity reactions; and with lactation
because of the potential for allergic-type
reactions with the neonate.
 Adverse Effects
The adverse effects most commonly associated with
these drugs include the CNS effects of headache,
fatigue, asthenia, and dizziness and the potential for
serious seizures. These effects may be the result of a
cellular response to the glycoprotein.
Nausea, vomiting, and diarrhea also are common
effects. Cardiovascular symptoms can include
hypertension, edema, and possible chest pain, all of
which may be related to the increase in RBC numbers
changing the balance within the cardiovascular system.
Patients receiving intravenous administration must
also be monitored for possible clotting of the access
line related to direct cellular effects of the drug.
AGENTS USED FOR IRONDEFICIENCY
ANEMIA

Agents: ferrous fumarate (Feostat),

ferrous gluconate (Fergon), ferrous
sulfate (Feosol), ferrous sulfate
exsiccated (Feratab, Slow FE), iron
dextran (InFeD), iron sucrose
(Venofer), and sodium ferric
gluconate complex (Ferrlecit).
Therapeutic Actions and Indications
Iron preparations elevate the serum iron
concentration. They are then either converted to
hemoglobin or trapped in reticuloendothelial cells
for storage and eventual release and conversion into
an usable form of iron for RBC production.

Pharmacokinetics
Ferrous fumarate, ferrous gluconate, ferrous
sulfate, and ferrous sulfate exsiccated are available
for oral administration. Iron dextran is a parenteral
form of iron given by the Z-track method, which
may be used if an oral form cannot be given or
cannot be tolerated.
Contraindications and Cautions
These drugs are contraindicated for patients with
known allergy to any of these preparations
because severe hypersensitivity reactions have
been associated with the parenteralnform of iron.
They also are contraindicated in the following
conditions: hemochromatosis (excessive iron);
hemolytic anemias, which may increase serum
iron levels and cause toxicity; normal iron balance
because the drug will not be absorbed and will
just pass through the body; and peptic ulcer,
colitis, or regional enteritis because the drug can
be directly irritating to these tissues and can
cause exacerbation of the diseases.
 Adverse Effects
The most common adverse effects
associated with oral iron are related to
direct GI irritation; these include GI
upset, anorexia, nausea, vomiting,
diarrhea, dark stools, and constipation.
With increasing serum levels, iron can be
directly toxic to the CNS, causing coma
and even death.