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LaGuardia Community College

City University of New York


Practical Nursing Program
Class: SCL 103
Group Presentation
By
Anase Ikama
Rosemarie Mayne
Catherine Majorie

Joseph Charles
Lavern Simms
Juna Lucas

Zoya Poltilov
Kadian Green
Majorie Johnson

Disease: Anemia

TABLE of CONTENTS
I-

Introduction
. Definition of Anemia
. Types of Anemia

II-

Iron deficiency anemia


.What is iron deficiency anemia
. Etiology of iron deficiency anemia
.Signs and symptoms
.Treatment and prevention

III-

Pernicious anemia
.Definition of pernicious anemia
. Etiology
.Signs and symptoms
.Treatment and prevention

IV-

Folic acid deficiency


.Definition of folic acid deficiency
. Etiology
.Signs and symptoms
.Treatment and prevention

V-

Aplastic anemia
.Definition of aplastic anemia
. Etiology
.Signs and symptoms
.Treatment and prevention

VI-

Hemolytic anemia
.Definition of hemolytic anemia
. Etiology
.Signs and symptoms
.Treatment and prevention

VII-

Sickle cell anemia


.Definition of sickle cell anemia
. Etiology
.Signs and symptoms
.Treatment and prevention

VIII-

Thalassemia
.what is thalassemia
. Etiology
.Signs and symptoms
.Treatment and prevention

IX-

Anemia of chronic disease

X-

Sideroblastic anemia

Anemia occurs when the amount of hemoglobin in the red blood cells drops below normal
level. To understand red blood cells and their role in anemia, it is useful to know certain facts about the
blood. The Blood has two major components: Plasma: a clear yellow liquid that contains proteins,
nutrients, hormones, electrolytes, and other substances, constituting about 55% of blood; white and red
blood cells and platelets, which make up the rest of the blood. The white blood cells are the infection
fighters for the body, and platelets are necessary for blood clotting. The important factors in anemia,
however, are red blood cells. The red Blood Cells (RBCs), also known as erythrocytes, are the most
abundant cells in our bodies that carry oxygen throughout the body to nourish tissues and sustain life.
Each red blood cell contains between 200 and 300 hemoglobin molecules. Hemoglobin is a complex
molecule and the most important component of red blood cells. It is composed of protein and an ironcontaining molecule called heme, which binds to oxygen in exchange for carbon dioxide in the lungs.
Anemia is defined as a condition where the hemoglobin content of the blood is insufficient to satisfy
bodily needs. It is caused by decrease in circulating RBCs, but may also be caused by accelerated
hemolysis, side effects of medications, menstruation, and gastrointestinal bleeding (GI).
Red blood cells are extremely small and look something like tiny, flexible inner tubes. This unique
shape offers many advantages: It provides a large surface area to absorb oxygen and carbon dioxide. Its
flexibility allows it to squeeze through capillaries, the tiny blood vessels that join the arteries and veins.
The actual process of making red blood cells is called erythropoiesis. In Greek, erythro means "red" and
poiesis means "the making of things. The process of manufacturing, recycling, and regulating the number
of red blood cells is complex and involves many parts of the body. The body carefully regulates its
production of red blood cells so that enough is manufactured to carry oxygen but not so many that the
blood becomes thick or sticky (viscous). Most of the work of erythropoiesis occurs in the bone marrow. In
children younger than five years old, the marrow in all the bones of the body is enlisted for producing red
blood cells. As a person ages, red blood cells are eventually produced only in the marrow of the spine,
ribs, and pelvis. The life span of a red blood cell is between 90 and 120 days. Old red blood cells are
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removed from the blood by the liver and spleen. There they are broken down and iron is returned to the
bone marrow to make new cells. Anemia is caused by two major biological mechanisms: decreased red
cell production resulting from: Hematopoietic cell damage from infection, drugs, radiation, and other
similar agents; or an increased red blood cell loss due to destruction of red blood cells. What follows is a
description of the different types of anemia including: Iron-deficiency, vitamin B12 and folic deficiency,
aplastic, hemolytic, sickle cell, thalassemia anemia with chronic disease and sideroblastic anemia.
Iron deficiency anemia occurs when there is an inadequate production of red blood cells, and can
be caused by of conditions such as chronic blood loss, which is the major cause of iron deficiency anemia
in adults. This is most commonly occur from internal blood loss due to conditions that range in severity
from hemorrhoids, heavy menstruation, bleeding gastrointestinal lesions, carcinoma of the colon in the
United States, or hookworm disease in less developed countries. Dietary deficiency is another cause,
which is rare except in infants; because human milk is low in iron, therefore newborn storage iron is
depleted within the first 6 months, and so dietary supplement are given. Pica, a craving for non-food
substances such as ice, starch, or clay, is another possible cause of iron deficiency because it interferes
with iron absorption in the stomach.
Some people are born with iron deficiency; certain of these cases may be due to a mutation of the
Nramp2 gene, which regulates a protein responsible for delivering iron to the cells. Clinical
manifestations of iron deficiency anemia may include pallor, fatigue, or dyspnea on exertion. Laboratory
findings of iron deficiency anemia include decreased hemoglobin, hematocrit, and red blood cell count.
This makes iron deficiency anemia distinguished from other causes of anemia. Iron deficiency anemia
can be prevented by following the recommended diet for food high in iron such as beef liver, eggs, ironfortified food, kidney beans and whole grain.

Pernicious anemia is a type of megaloblastic anemia. M egaloblastic anemia is defined by


large, abnormal-appearing erythoird precursor cells in the bone marrow, which is caused by
deficiency of vitamin B12 or folate. Pernicious anemia is caused by a lack of intrinsic factor, which is

a substance, needed to absorb vitamin B-12 from the gastrointestinal tract, which is necessary for the
formation of red blood cells. When stomach secretions do not have enough intrinsic factor, vitamin B-12
is not completely absorbed. This result in pernicious anemia and other problems related to low levels of
vitamin B-12. Nerve and blood cells in the body need vitamin B-12 to function properly. Deficiency can
cause a wide variety of symptoms, including fatigue, shortness of breath, tingling sensations, difficulty
walking, and diarrhea. Very rarely, infants and children are born lacking the ability to produce effective
intrinsic factor. This form of congenital (born with) pernicious anemia is inherited as an autosomal
recessive disorder (obtain from each parent)However, pernicious anemia and other forms of
megaloblastic anemia in children results from other causes of vitamin B-12 deficiency or other vitamin
deficiencies.
Although this form of the disease can occur in children, pernicious anemia usually does not appear
before age 30. The average age at diagnosis is age 60. Pernicious anemia is diagnosed in about 1- 2% of
people over 60, with women having a higher risk than men. This disease occurs in all racial groups, but
occurs most often in people of Scandinavian or Northern European descent. Risk factors include family
history of pernicious anemia, Scandinavian or Northern European descent, and autoimmune endocrine
disorders. In addition to pernicious anemia, other causes of vitamin B-12 deficiency include: poor diet in
infant or poor maternal nutrition during pregnancy, infection of intestinal parasites and bacterial
overgrowth, gastrointestinal disease such as stomach removal surgery, celiac disease, Crohn's disease, and
drugs that are used for neomycin, tuberculosis treatment and metabolic disorders. Pernicious anemia is not
preventable, but with early detection and treatment of vitamin B12 deficiency, complications are readily
controlled. It should be noted that Vitamin B12 deficiency from diet is very rare, since the liver stores
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over a three-year supply. It usually does not occur in alcoholism, vegetarianism, or in malnourished
people with kidney failure or cancer. Since animal products are the chief source, however, true vegan
vegetarians may need a supplement, fortified food, or appropriate food selection known to contain
adequate amounts of this vitamin. Pernicious treatment include high dose supplements of vitamin B12,
however when a patients intestine cannot absorb vitamin B12 the individual will have to supplements for
the rest of their lives to prevent the disease from returning.
Folic acid deficiency is also a type of megaloblastic anemia. Folic acid or folate is one of the most
important vitamins critical for the development of the fetal nervous system. As stated by Kids Health web
site, [pregnant women who have inadequate intake of folic acid are at risk of having baby with a] serious
neural tube defect (a birth defect involving incomplete development of the brain and spinal cord.
Folic acid is a vitamin (B9) found mostly in leafy green vegetables, orange juice beans and
enriched grains. It involves in the maturation of red blood cells and the synthesis of DNA and its
deficiency results from inadequate intake of folic acid, as can happen during pregnancy. Signs and
symptoms of folic acid deficiency, according to Women Fitness, include extreme fatigue, weakness, pail
skin, dizziness, [shortness of breath], heart palpitation, and trouble concentrating The folic acid
deficiency can be prevented and treated, but for the physician to medically diagnose folic acid deficiency,
the amount of folic acid stored in the body has to be determined by performing a complete blood count
(CBC) and a low level of folic in a blood sample will then indicates deficiency.
During pregnancy, an increased intake of folic acid is needed to supply both the mother and the
fetus. Regardless of the socioeconomic and culture aspect of the diet, treatment of folic acid deficiency
should not interfere with most peoples religious or culture diets because citizens from different
socioeconomic should be able to boost their folic acid intake by consuming more leafy green, beans,
orange juice and enriched grain. However depending on how strict ones culture is, there is still the option
of taking folic acid pills. Kids Health web site concludes, Repeated studies have shown that women who
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get 400 micrograms (0.4milligrams) daily prior to conception and during early pregnancy reduces risks
[of having a baby with serious defect]. During the folic acid therapy, excess intake of folic acid can
cause deficiency in vitamin B12. As confirmed by Joyce Kee and Evelyn Hayes in the book titled
Pharmacology: A Nursing Process Approach, Vitamin B12 is essential for DNA synthesis, aids in the
conversion of folic acid to its active form, promotes cellular division and is needed for normal
hematopoiesis (development of red blood cell in bone marrow). Thus, a mother to be who is a strict
vegetarian will have a likelihood of developing a vitamin B12 deficiency during her pregnancy because,
according to Merck web site, very high doses [of folic acid intake] may worsen nerve damage in people
who have vitamin B12 deficiency
According to Davis Drug Guide, patient teaching should emphasize encouraging the patient to
comply with the diet recommendation of health care professional Explain that the best source of
vitamin is a well-balanced diet with foods from the four basic food groups [and that] food in high folic
acid includes vegetables, fruits, and organ meat. [Vegetables should not be overcooked as] Heat destroys
folic acid in foods [During folic therapy,] folic acid may cause urine more intensively yellow [in
addition, the client should] Notify health care professional if rash occurs, which may indicate
hypersensitivity(reference?) Some drugs, including Dilantin, methotrexate, trimethoprim, and
triamterene, may also hinder folate absorption. No neurological abnormalities (in contrast to vitamin B 12
deficiency.
Aplastic anemia is characterized by a hypocellular bone marrow which is almost a total loss of
hematopoietic cells, including erythroid, myeloid precursor cells, megakaryocytes by peripheral
pancytopenia. It is most often secondary to toxic exposure. Often, aplastic anemia can be caused by
suyoimmune dysfunction of cytotoxic T cells and can be induced by other etiologic agents such as
radiation exposure. Traveling through your bloodstream are red blood cells, white blood cells and
platelets, which all are important to your health. These blood components are produced in your bone
marrow. In aplastic anemia, the bone marrow stops producing enough new blood cells, which not only
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means that you have a deficit of red blood cells but also of white blood cells and platelets. Aplastic
anemia is rare, affect fewer than 1,000 people each year in the United States. Idiopathic aplastic anemia is
a condition known to cause aplastic anemia, which is been linked to exposure to chemicals such as
benzene and radiation. It is also believed that some cases of aplastic anemia are inherited and that some
cases are due to a viral infection.
In aplastic anemia, the bone marrow is described in medical terms as aplastic or hypoplastic meaning that it's empty, or containing very few blood cells... Factors that can temporarily or permanently
injure bone marrow include: high-dose radiation and chemotherapy treatments, which damage healthy
cells, including stem cells in bone marrow and Secondary aplastic anemia can be a temporary side effect
of these treatments; a viral infection in some people and the use of certain drugssuch as antibiotics can
cause secondary aplastic anemia. Aplastic anemia can develop at any age, but it's more commonly
diagnosed in children and young adults. Signs and symptoms of aplastic anemia and secondary aplastic
anemia are: fatigue, weakness, shortness of breath with exertion, rapid heart rate, pale skin, frequent
infections, unexplained bruising, easy bruising, nosebleeds and bleeding gums, prolonged bleeding from
cuts, skin rash and fever. The reduction in the level of each of the three blood cell types, which can lead to
unexplained infections, is related to fewer white blood cells and unexpected bleeding (due to fewer
platelets) and fatigue. To confirm a diagnosis of aplastic anemia, a physician examines a blood sample
and determines the number of each type of blood cell circulating in the blood. To confirm a diagnosis of
aplastic anemia, the doctor will need a bone marrow biopsy. In this procedure, a doctor uses a needle to
remove a small sample of bone marrow from a large bone in the body, such as the hipbone, which is
examined under a microscope to rule out other blood-related diseases.
To treat aplastic anemia for young individuals with, a bone marrow (stem cell) transplant can be used to
replace the defective bone marrow with healthy cells. Bone marrow transplant carries many risks, so it is
not used as a treatment for middle-aged or elderly individuals. For older individuals, treatment of aplastic
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anemia focuses on suppressing the immune system with anti-thymocyte globulin (ATG, Atgam),
cyclosporine (CSA, Sandimmune), or methylprednisolone (Solu-Medrol), alone or in combination. The
response to the drug treatment is slow, and about one-third of individuals have a relapse, which may
respond to a second round of medication. Since individuals with aplastic anemia have low numbers of
white blood cells, they are at high risk for infection. Therefore, preventing infections, and treating them
quickly once they occur, is important.
Bleeding due to low level of platelets is an acute medial emergency that should be treated with
platelets transfusion to prevent fatal hemorrhage. Platelet transfusions are the first course of treatment for
any aplastic anemia for a patient who is severely deficient in these blood cells, but it is very rare for a
patient to achieve a long-term recovery using this form of treatment alone. Platelet transfusions reduce the
high risk of having a fatal hemorrhage. Transfusions of red blood cells can help combat fatigue and
shortness of breath experienced by aplastic anemia patients. Patients with aplastic anemia are closely
monitored for signs of infections and are given antibiotics when appropriate. Bone marrow transplantation
- replacing diseased bone marrow with a healthy bone marrow from a donor can be the only successful
treatment option for people with severe aplastic anemia. Extracted through a surgical technique, the
healthy marrow is injected intravenously into the bloodstream of the person with aplastic anemia, where it
migrates to the bone marrow and may begin generating new blood cells in about two to four weeks.
Besides transfusion of platelets and transplantation of the bone marrow, drug therapy is also used to treat
aplastic anemia, and the two most common types of drugs used are immunosuppressive drugs (such as
antiglobulin (ALG), although the connection is not well-understood) and growth factors (such as
granulocyte-macrophage colony-stimulating factor (GM-CSF) which help stimulate the bone marrow to
produce new blood cells - especially white blood cells). Having aplastic anemia weakens your immune
system, therefore, control of infection depends on prompt, appropriate intravenous antibiotic therapy as
soon as fever or other signs of infection appear.
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Hemolytic anemia is a type of anemia in which the red blood cell has a shortened life span
(normal life span is 90-120 days). Abnormalities in the red blood cells may originate in the body
(intrinsic) or may be caused by extrinsic environmental factors such as autoantibodies to red blood cells or
damage from chemotherapy. People with an inherited hemolytic anemia received a defective red blood
cell gene from one (or both) of their parents. Different types of defective genes account for the different
types of inherited hemolytic anemia. In each of the types of inherited hemolytic anemia, the body
produces abnormal red blood cells. The red blood cell abnormality can involve the cell membrane (the
outer covering of the cell), the chemistry inside the cell, or the production of abnormal hemoglobin.
Intrinsic is the destruction of the red blood cells due to a defect within the red blood cells and intrinsic
hemolytic anemia is often inherited. These conditions produce red blood cells that do not live as long as
normal red blood cells whereas the autoimmune hemolytic anemia is a disorder where red blood cells are
produced healthy but are later destroyed by becoming trapped in a spleen destroyed by infection, or other
diseases such as hepatitis. Hemolytic anemia affects twice as many women as men, especially women in
the childbearing years.

Symptoms of hemolytic anemia include: nosebleeds, bleeding gums, chills,

fatigue, pallor (paleness), and shortness of breath, rapid heart rate, yellow sclera (whites of eyes) and skin.
Cold antibody hemolytic anemia most commonly affects elderly persons, and warm antibody hemolytic
anemia can affect anyone at any age.
Specific treatment for hemolytic anemia will be determined by a physician based on age, overall
health, medical history, extent of the disease, cause of the disease, tolerance for specific medications,
procedures, or therapies and expectations for the course of the disease. Conventional treatment involves
the use of Prednisone and other corticosteroids. The alternative nutritional medicine approach is to
identify hidden allergies by blood test and avoid those allergens (primarily foods). For best results this
should be done under the supervision of a doctor experienced in nutritional medicine. The approach used
in homeopathy is to attempt to restore the balance of the system using dilute solutions of natural
substances specific to the disorder. Hemolytic anemia is usually diagnosed during a medical examination
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through a routine blood test. The symptoms of hemolytic anemia may resemble other blood conditions or
medical problems. Nursing management medications include folic acid supplements (to meet the
increased metabol demands of the bone marrow), Hydration therapy as well as to improve blood flow,
reduce pain, and prevent renal damage during transfusion.
Sickle cell Anemia is an inherited, lifelong problem that is located within the red blood cells of the body.
A single chemical substitution in the protein hemoglobin inside the red blood cells causes that cell to take
on a hard sickle shape instead of the normal shape that allows red cells to move through blood vessels. To
develop sickle cell anemia, a person must receive sickle cell genes from both parents. People who inherit
a sickle cell gene from one parent and a normal gene from the other will have sickle cell traits. The sickle
cell shape causes blockages and red blood cell to break apart and die, often within 10-20 days compared
to 120 days for normal red blood cells. Sickle cell disease is most common among those of African
descent, but also occurs in other ethnic groups, including people from Mediterranean countries, Middle
East and India. According to Doctor Allan Sacerdote in A Patients Guide to Sickle Cell Disease and
Sickle Cell Trait, over 70000 people have sickle cell disease in the United States which is the most
common genetic disease in the country and about 2 million have sickle cell trait. His study also estimated
that about 1,000 babies are born with the trait each year. Sickle cell anemia can cause many symptoms
and life-threatening complications, including blood vessels which can worse anemia and serious
infections as well as jaundice accompanied by nausea, vomiting and abdominal pain. Clogging of the
small vessels in the eye can deprive the part of the eye that receives and processes light of needed
nutrients and can lead to blindness. Children with sickle cell anemia are prone to strokes, which can cause
permanent disabilities. To control the symptoms, nurses need to teach parents teach parents routine
childhood vaccines, give daily antibiotics from of 2 to 5 years of age and give to their infant multivitamin
supplements with iron.

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Thalassemia is also known as Thalassemia Major, Thalassemia Minor, and Cooleys anemia.
Anemia is an inherited condition that causes a problem in the production of hemoglobin, which leads to
anemia a condition in which red blood cells or the hemoglobin a protein in red blood cells is abnormally
low. As a result, the cells get insufficient oxygen. Thalassemia is more common in people of Africa,
Mediterranean, and Asian heritage. The symptoms of thalassemia depend on the genetic severity and may
include: paleness, jaundice, enlarged spleen and liver, and bony abnormalities, especially of the facial
bones. There is no cure for thalassemia. Treatments of thalassemia include regular blood transfusion and
the removal of the accumulated iron in the body, however, transfusion by the ongoing accumulation of
iron in organs such as heart and liver, which can severely be damaged or become fatal. Patient teaching
should encourage the client to follow a diet low in iron, avoiding or eliminationg iron-rich foods such as
oyster, pork, beans, beef, peanut butter and leafy vegetables.

Anemia of chronic disease is also known as myelophthistic anemia, is a type of anemia that
occurs when the normal marrow space is infiltrated and replaced by abnormal cells. The most common
causes of ACD is when bone marrow is replaced by metastic tumors, most often breast and prostate. It is
less commonly due to bone marrow destruction from non-neoplastic causes such as marrow fibrosis.
Other causes of ACD include myleloproliferative disorders and lipid storage. Any long-term disease can
lead to anemia, especially chronic disorders that cause inflammation. Some causes of ACD include:
cancer and inflammatory bowel disease, which is associated with iron deficiencies from both intestinal
malabsorption and GI bleeding. Chronic renal failure is also linked to mylelophthisic anemia with
deficiencies in erythropoietin. Poor diet coupled with alcoholism is another common cause of
Myelophthisic. The classification of drug that is used in the treatment of ACD is erythropoietin and
corticosteroids; an example is prednisone and hydroxyurea.

These drugs decrease spleen size and

normalize RBC values in many patients. Treatment is required for 6-8 months for response to be seen.

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Sideroblastic anemia is a term used to describe a group of rare blood disorders characterized by
the bone marrow's inability to manufacture normal red blood cells. Named for the Greek words for iron
and germ, sideroblastic anemia is one of the principal types of iron-utilization anemia. Abnormal, ironsaturated red cells are present in the blood of people who have this disease. Although the iron circulates
normally from the plasma to the bone marrow where new red blood cells are created, it is not properly
incorporated into new red blood cells. Sideroblastic anemia can be inherited, but the disease is usually
acquired as a result of illness or exposure to toxic substances and it often encountered in adults. The cause
of sideroblastic anemia cannot always be identified. Drug toxicity, alcohol abuse, and lead poisoning are
common causes of this condition. Sideroblastic anemia is also associated with: leukemia, lymphoma
(cancer of the lymph glands), myeloma (cancer of the bone marrow), rheumatoid arthritis, and other
inflammatory diseases. Symptoms of sideroblastic anemia are jaundice, enlarged liver and spleen, fever,
headache, loss of appetite, vomiting, and leg sores. Symptoms can be mild and often appear in childhood.
Infections, trauma, and pregnancy may trigger symptoms. Inherited or acquired after excessive alcohol
use, Alcoholism: Poor nutrition and lack of vitamins and minerals are associated with alcoholism drugs or
medications, such as alcohol, the antibiotic penicillin, or the high blood pressure drug methyldopa certain
medications, including chloramphenicol, or other disorders, including some cancers and rheumatoid
arthritis. More common in the elderly Deferoxamine (Desferal) is used to remove iron. Effectiveness is
increased when ascorbate is added to the regimen. Folate and pyridoxine are used, but their effectiveness
is under question.
In conclusion a popular misconception is that people who have anemia should simply take iron
supplements. As shown above, iron supplements should be avoided unless prescribed by a physician,
because an excess level of iron could damage the heart or other vital organs. Most forms of anemia can be
successfully treated with supplements, injections of specific vitamins and/or increased intake of nutrientrich foods.
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WORKED CITED

Aplastic Anemia Resources and Information. Aplastic Anemia Information. Retrieved April 25,
2007, from http://www.aplastic-anemia.org/aplastic-anemia-resources.htm
Deglin, H. Judith and April Hazard Vallerand. (8th Ed.). (2003). Daviss Drug Guide for Nurses.
Philadelphia: PA. (430-431).
Iron Disorders Institute. Preventic disease caused by Iron-Out of Balance. (2006, March 11).
Retrieved April 11, 2007, from http://www.irondisorders.org

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National Heart Lung and Blood Institute Diseases and conditions index. Pernicious Anemia.
(2006, May). Retrieved April 18, 2007 from
http://www.nhlbi.nih.gov/health/dci/Diseases/prnanmia/prnanmia_what.html
Platt Jr., F., Allan and Alan Sacerdote. A Patients and Parent's Guide to Pickle Cell Disease and
Sickle Cell Trait.
Women Fitness Fertility and Pregnancy. Anemia during Pregnancy. (1999-2006). Retrieved April
3, 2007 from http://www.womenfitness.net/anemia_and_preg.htm

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