Anemia

Anemia Due to Excessive Bleeding

Anemia from excessive bleeding results when loss of red blood cells through bleeding exceeds production of new red blood cells.

When blood loss is rapid, blood pressure falls, and people may be dizzy.
When blood loss occurs gradually, people may be tired, short of breath, and pale.
Stool, urine, and imaging tests may be needed to determine the source of bleeding.
The cause of bleeding is corrected, and transfusions and iron supplements are given if needed.

Excessive bleeding is the most common cause of anemia. When blood is lost, the body quickly pulls water from tissues outside the bloodstream in an attempt to keep the blood vessels filled. As a result, the blood is diluted, and the hematocrit (the percentage of red blood cells in the total blood volume) is reduced. Eventually, increased production of red blood cells by the bone marrow may correct the anemia. However, over time, bleeding reduces the amount of iron in the body, so that the bone marrow is not able to increase production of new red blood cells to replace those lost.

Rapid Blood Loss: The symptoms may be severe initially, especially if anemia develops rapidly from a sudden loss of blood, such as from an injury, surgery, childbirth, or a ruptured blood vessel. Losing large amounts of blood suddenly can create two problems:

Blood pressure falls because the amount of fluid left in the blood vessels is insufficient.
The body’s oxygen supply is drastically reduced because the number of oxygen-carrying red blood cells has decreased so quickly.

Either problem may lead to a heart attack, stroke, or death.

Chronic Blood Loss: Far more common than a sudden loss of blood is chronic (long-term) bleeding, which may occur from various parts of the body. Although large amounts of bleeding, such as from nosebleeds and hemorrhoids are obvious, small amounts of bleeding may not be noticed. For example, a small amount of blood may not be visible in the stool. This type of blood loss is described as occult. If a small amount of bleeding continues for a long time, a significant amount of blood may be lost. Such gradual bleeding may occur with common disorders, such as ulcers in the stomach or small intestine and diverticulosis, polyps, or cancers in the large intestine. Other sources of chronic bleeding include kidney or bladder tumors, which may cause blood to be lost in the urine, and heavy menstrual bleeding.

Symptoms and Diagnosis

Symptoms are similar to those of other types of anemia and vary from mild to severe, depending on how much blood is lost and how rapidly. When the blood loss is rapid—over several hours or less—loss of just one third of the blood volume can be fatal. Dizziness upon sitting or standing after a period of lying down (orthostatic hypotension) is common when blood loss is rapid. When the blood loss is slower—over several weeks or longer—loss of up to two thirds of the blood volume may cause only fatigue and weakness or no symptoms at all, if the person drinks enough fluids.

Other symptoms may occur from the bleeding or the disorder that causes the bleeding. People may notice black, tarry stools if they have bleeding from the stomach or small intestine. Bleeding from the kidney or bladder may cause red or brown urine. Women may notice long, heavy menstrual periods. Some disorders that cause chronic bleeding, such as stomach ulcers, produce discomfort. Other disorders, such as diverticulosis and intestinal cancers and polyps at an early stage, cause no symptoms.

Doctors do blood tests to detect anemia when people describe symptoms of anemia, have noticed bleeding, or both. Stool and urine are tested for blood in an effort to identify the source of bleeding. Imaging tests or endoscopy may be needed to identify the source of bleeding.

Treatment

For large or rapid blood loss, the source of bleeding must be found and the bleeding stopped. Transfusion of red blood cells may be needed.

With slow or small blood loss, the body may produce enough red blood cells to correct the anemia without the need for blood transfusions. Because iron, which is required to produce red blood cells, is lost during bleeding, most people who have anemia from bleeding need to take iron supplements, usually tablets, for several months.

Anemia of Chronic Disease

In anemia of chronic disease, some chronic disorder slows the production of red blood cells, the result of production of proteins called cytokines that interfere with the production of red blood cells.

Chronic disease often leads to anemia, especially in older adults. Conditions such as infections, inflammation, and cancer particularly suppress production of red blood cells in the bone marrow. Since the suppression is usually not severe, anemia develops slowly and is evident only after time. Problems with how the body uses iron contribute to anemia of chronic disease. Because the bone marrow is unable to use stored iron to create new red blood cells, this type of anemia is often called iron-reutilization anemia.

Because this type of anemia develops slowly and is generally mild, it usually produces few or no symptoms. When symptoms do occur, they usually result from the disease causing the anemia rather than from the anemia itself. There are no specific laboratory tests, so the diagnosis is typically made by excluding other causes.

Because no specific treatment exists for this type of anemia, doctors treat the disorder causing it. Taking additional iron or vitamins does not help. On the rare occasion that the anemia becomes severe, transfusions may help. Alternatively, erythropoietin Some Trade Names
EPOGEN/PROCRIT
or darbepoietin, drugs that stimulate the bone marrow to produce red blood cells, may be given.

Aplastic Anemia: When the Bone Marrow Shuts Down

When the bone marrow cells that develop into mature blood cells and platelets (stem cells) are damaged or suppressed, the bone marrow can shut down. This bone marrow failure is called aplastic anemia. A common cause of aplastic anemia is an autoimmune disorder, in which the immune system suppresses bone marrow stem cells. Other causes include infection with parvovirus, radiation exposure, toxins (such as benzene), chemotherapy drugs, and other drugs (such as chloramphenicol Some Trade Names
CHLORAMPHENICOL).

The bone marrow failure leads to too few red blood cells (anemia), too few white blood cells (leukopenia), and too few platelets (thrombocytopenia). The anemia causes fatigue, weakness, and paleness. The leukopenia causes increased susceptibility to infection. The thrombocytopenia causes easy bruising and bleeding. In some people, only red blood cell production is affected (resulting in a condition called pure red blood cell aphasia). When parvovirus infection is the cause, only red blood cell production is likely to be affected. Aplastic anemia is diagnosed when microscopic examination of a sample of bone marrow (bone marrow biopsy) reveals a sharp decrease in the number of stem cells and in the maturation of blood cells.

People with severe aplastic anemia quickly die unless immediately treated. Transfusions of red blood cells, platelets, and substances called growth factors may temporarily increase the numbers of red blood cells, white blood cells, and platelets. Stem cell or bone marrow transplantation can cure aplastic anemia in younger and middle-aged people. Older adults and people without a suitable bone marrow donor often respond to treatment with corticosteroids and drugs that suppress the immune system.

Autoimmune Hemolytic Anemia

Autoimmune hemolytic anemia is a group of disorders characterized by a malfunction of the immune system that produces autoantibodies, which attack red blood cells as if they were substances foreign to the body.

Some people have no symptoms, and other people are tired, short of breath, and pale.
Severe disease may cause jaundice or abdominal discomfort and fullness.
Blood tests are used to detect anemia and determine the cause of the autoimmune reaction.
Some people need corticosteroids or drugs that suppress the immune system.

Autoimmune Hemolytic Anemia

Autoimmune hemolytic anemia is an uncommon group of disorders that can occur at any age. These disorders affect women more often than men. About half of the time, the cause of autoimmune hemolytic anemia cannot be determined (idiopathic autoimmune hemolytic anemia). Autoimmune hemolytic anemia can also be caused by or occur with another disorder, such as systemic lupus erythematosus (lupus), and rarely it follows the use of certain drugs, such as penicillin.

Destruction of red blood cells by autoantibodies may occur suddenly, or it may develop gradually. In some people, the destruction may stop after a period of time. In other people, red blood cell destruction persists and becomes chronic. There are two main types of autoimmune hemolytic anemia: warm antibody hemolytic anemia and cold antibody hemolytic anemia. In the warm antibody type, the autoantibodies attach to and destroy red blood cells at temperatures equal to or in excess of normal body temperature. In the cold antibody type, the autoantibodies become most active and attack red blood cells only at temperatures well below normal body temperature.

Symptoms

Some people with autoimmune hemolytic anemia may have no symptoms, especially when the destruction of red blood cells is mild and develops gradually. Others have symptoms similar to those that occur with other types of anemia, especially when the destruction is more severe or rapid. When severe or rapid destruction of red blood cells occurs, mild jaundice may also develop. When destruction persists for a few months or longer, the spleen may enlarge, resulting in a sense of abdominal fullness and, occasionally, discomfort.

When the cause of autoimmune hemolytic anemia is another disease, symptoms of the underlying disorder, such as swollen and tender lymph nodes and fever, may dominate.

Diagnosis

Once doctors diagnose anemia, increased destruction of red blood cells is suspected when a blood test shows an increase in the number of red blood cells that are immature (reticulocytes). Alternatively, a blood test may show an increased amount of a substance called bilirubin and a decreased amount of a protein called haptoglobin.

Autoimmune hemolytic anemia as the cause is confirmed when blood tests detect increased amounts of certain antibodies, either attached to red blood cells (direct antiglobulin or Coombs’ test) or in the liquid portion of the blood (indirect antiglobulin or Coombs’ test). Other tests sometimes help determine the cause of the autoimmune reaction that is destroying red blood cells.

Treatment

If symptoms are mild or if destruction of red blood cells seems to be slowing on its own, no treatment is needed. If red blood cell destruction is increasing, a corticosteroid such as prednisone is usually the first choice for treatment. High doses are used at first, followed by a gradual reduction of the dose over many weeks or months. When people do not respond to corticosteroids or when the corticosteroid causes intolerable side effects, surgery to remove the spleen (splenectomy) is often the next treatment. The spleen is removed because it is one of the places where antibody-coated red blood cells are destroyed. When destruction of red blood cells persists after removal of the spleen or when surgery cannot be done, immunosuppressive drugs, such as cyclophosphamide Some Trade Names
LYOPHILIZED CYTOXAN or azathioprine Some Trade Names IMURAN
, are used.

When red blood cell destruction is severe, blood transfusions are sometimes needed, but they do not treat the cause of the anemia and provide only temporary relief.

Vitamin Deficiency Anemia

Vitamin deficiency anemia results from low or depleted levels of vitamin B₁₂ or folate (folic acid).

People may be weak, short of breath, and pale.
Nerves may also malfunction.
Blood tests can detect abnormal cells that indicate vitamin deficiency anemia.
The deficient vitamin is replaced.

Vitamin B₁₂ deficiency and folate (folic acid) deficiency cause megaloblastic anemia. In megaloblastic anemia, the bone marrow produces red cells that are large and abnormal (megaloblasts).

Deficiency of vitamin B₁₂ (see Vitamins: Vitamin B12 Deficiency) or folate (see Vitamins: Folate Deficiency) most often develops due to a lack of these vitamins in the diet or an inability to absorb these vitamins from the digestive tract. Deficiency of these vitamins is sometimes caused by drugs used to treat cancer, such as methotrexate Some Trade Names
TREXALL
, hydroxyurea Some Trade Names
HYDREA
, fluorouracil Some Trade Names
CARAC
, and cytarabine. A form of vitamin B₁₂ deficiency called pernicious anemia results from an inability to absorb vitamin B₁₂ from the diet.

Symptoms and Diagnosis

Symptoms of anemia due to vitamin B₁₂ or folate deficiency develop slowly and are similar to symptoms produced by other types of anemia. Vitamin B₁₂ deficiency can also cause nerves to malfunction, causing tingling, loss of sensation, and muscle weakness (see Vitamins: Vitamin B12 Deficiency).

Once anemia has been diagnosed, tests are done to determine if a deficiency of vitamin B₁₂ or folate is the cause. Anemia due to vitamin B₁₂ or folate deficiency is suspected when megaloblasts are seen in a blood sample that is examined under a microscope. Changes in white blood cells and platelets also can be detected, especially when people have had megaloblastic anemia for a long time.

The blood levels of vitamin B₁₂ and folate are measured, and other tests may be done to determine the cause of the vitamin deficiency.

Treatment

The treatment of anemia due to vitamin B₁₂ or folate deficiency consists of replacing the deficient vitamin.

Commonly, vitamin B₁₂ is administered by injection. At first, injections are given daily or weekly for several weeks until the blood levels of vitamin B₁₂ return to normal. Then injections are given once a month. Vitamin B₁₂ can also be taken daily as a nose spray, a tablet placed under the tongue, or a tablet that is swallowed. Generally, intramuscular injections of vitamin B₁₂ are necessary to correct pernicious anemia. People who have anemia due to vitamin B₁₂ deficiency usually must take vitamin B₁₂ supplements for life.

Folate can be taken as one tablet daily. People who have trouble absorbing folate take supplements for life.

Thalassemias

Thalassemias are a group of inherited disorders resulting from an imbalance in the production of one of the four chains of amino acids that make up hemoglobin (the oxygen-carrying protein found in red blood cells).

Symptoms depend on the type of thalassemia.
Some people have jaundice, skin ulcers, and abdominal fullness or discomfort.
Diagnosis usually requires special hemoglobin tests.
Mild thalassemia may not require treatment, but severe thalassemia may require bone marrow transplantation.

Hemoglobin is made up of two pairs of globin chains. Normally, adults have one pair of alpha chains and one pair of beta chains. Sometimes one or more of these chains is abnormal. Thalassemias are categorized according to the amino acid chain affected. The two main types are alpha-thalassemia (the alpha globin chain is affected) and beta-thalassemia (the beta globin chain is affected). Alpha-thalassemia is most common in blacks (25% carry at least one copy of the defective gene), and beta-thalassemia is most common in people from the Mediterranean area and Southeast Asia. Thalassemias are also categorized according to whether people have one copy of the defective gene (thalassemia minor) or two copies of the defective gene (thalassemia major).

All thalassemias have similar symptoms, but they vary in severity. In alpha-thalassemia minor and beta-thalassemia minor, people have mild anemia with no symptoms. In alpha-thalassemia major, people have moderate or severe symptoms of anemia, including fatigue, shortness of breath, paleness, and an enlarged spleen.

In beta-thalassemia major, people have severe symptoms of anemia, and they may also have jaundice, skin ulcers, and gallstones. People may also have an enlarged spleen, which leads to a feeling of fullness and abdominal discomfort. Overactive bone marrow may cause some bones, especially those in the head and face, to thicken and enlarge. The long bones in the arms and legs may weaken and fracture easily.

Children who have beta-thalassemia major may grow more slowly and reach puberty later than they normally would. Because iron absorption may be increased and frequent blood transfusions (providing even more iron) are needed, excessive iron may accumulate and be deposited in the heart muscle, eventually causing iron overload disease and heart failure and early death.

Thalassemias are more difficult to diagnose than other hemoglobin disorders. Testing a drop of blood by electrophoresis is helpful but may be inconclusive, especially for alpha-thalassemia. Therefore, the diagnosis is usually based on special hemoglobin tests and determination of hereditary patterns.

Most people who have a mild thalassemia do not need treatment, but people who have a severe form may need bone marrow transplantation. Gene therapy, in which normal genes are inserted in the person, is being studied but to date has been unsuccessful.

Sickle Cell Disease

Sickle cell disease is an inherited condition characterized by sickle (crescent)-shaped red blood cells and chronic anemia caused by excessive destruction of red blood cells.

People usually have anemia and jaundice.
Worsening anemia, fever, and shortness of breath with pain in the long bones, abdomen, and chest indicate sickle cell crisis.
A special blood test called electrophoresis can be used to determine whether people have sickle cell disease.
Avoiding activities that may cause crises and treating infections and other disorders quickly can help prevent crises.

Sickle cell disease affects blacks almost exclusively. About 10% of blacks in the United States have one copy of the gene for sickle cell disease (that is, they have sickle cell trait). People who have sickle cell trait do not develop sickle cell disease, although rarely they may notice blood in their urine. About 0.3% of blacks have two copies of the gene. These people develop the disease.

Red Blood Cell Shapes

Red Blood Cell Shapes

Normal red blood cells are flexible and disk-shaped, thicker at the edges than in the middle. In several hereditary disorders, red blood cells become spherical (in hereditary spherocytosis), oval (in hereditary elliptocytosis), or sickle-shaped (in sickle cell disease).

In sickle cell disease, the red blood cells contain an abnormal form of hemoglobin (the protein that carries oxygen). The abnormal form of hemoglobin is called hemoglobin S. When red blood cells contain a large amount of hemoglobin S, they can become deformed into a sickle-shape. Not every red blood cell is sickle-shaped. The sickle-shaped cells become more numerous when people have infections or low levels of oxygen in the blood.

The sickle cells are fragile and break apart easily. Because the sickle cells are stiff, they have difficulty traveling through the smallest blood vessels, causing blocked blood flow, and reduced oxygen supply. The blocked blood flow can cause pain and, over time, cause damage to the spleen, kidneys, brain, bones, and other organs. Kidney failure and heart failure may occur.

Symptoms and Complications

People who have sickle cell disease always have some degree of anemia and mild jaundice. Some people have few other symptoms. Others have severe, recurring symptoms that cause enormous disability and early death. Sickle cell trait usually does not cause any problems, but rarely, people die suddenly while undergoing very strenuous exercise that causes severe dehydration, such as during military or athletic training.

Sickle Cell Crisis: Anything that reduces the amount of oxygen in their blood, such as vigorous exercise, mountain climbing, flying at high altitudes without sufficient oxygen, or an illness, may bring on a sickle cell crisis. A sickle cell crisis may consist of a sudden worsening of anemia, pain (often in the abdomen or long bones of the arms and legs), fever, and sometimes shortness of breath. Abdominal pain may be severe, and vomiting may occur.

In children, sickle cell crisis may take the form of a chest syndrome, characterized by severe chest pain and difficulty breathing. The exact cause of the chest syndrome is unknown but may be related to or produced by an infection or a blocked blood vessel resulting from a blood clot or an embolus (a piece of a blood clot that has broken off and lodged in a blood vessel).

Complications: Most people who have sickle cell disease develop an enlarged spleen during childhood. By the time the person reaches adolescence, the spleen is often so badly injured that it shrinks and no longer functions. Because the spleen helps fight infection, people with sickle cell disease are more likely to develop pneumococcal pneumonia and other infections. Viral infections, in particular, can decrease blood cell production, so anemia becomes more severe.

The liver can become progressively larger throughout life, and gallstones often form from the pigment of broken-apart red blood cells.

The heart usually enlarges, and heart murmurs are common.

Children who have sickle cell disease often have a relatively short torso but long arms, legs, fingers, and toes. Changes in the bones and bone marrow may cause bone pain, especially in the hands and feet. Episodes of joint pain with fever may occur, and the hip joint may become so damaged that it eventually needs to be replaced.

Poor circulation to the skin may cause sores on the legs, especially at the ankles. Young men may develop persistent, often painful erections (priapism). Episodes of priapism may permanently damage the penis so that the man can no longer have erections. Blocked blood vessels may cause strokes that damage the nervous system. In older people, lung and kidney function may deteriorate.

Diagnosis

Doctors recognize anemia, stomach and bone pain, and nausea in a young black person as signs of a sickle cell crisis. When doctors suspect sickle cell disease, they do blood tests. Sickle-shaped red blood cells and fragments of destroyed red blood cells can be seen in a blood sample examined under a microscope. Another blood test called hemoglobin electrophoresis is also done. In electrophoresis, an electrical current is used to separate the different types of hemoglobin and thus detect abnormal hemoglobin.

Screening: Blood tests are done on relatives of people with the disorder because they also may have sickle cell disease or trait. Discovering the trait in people may be important for family planning, to determine their risk of having a child with sickle cell disease.

Newborns are routinely screened with a blood test. Newer tests can be done during early pregnancy to screen the fetus and allow prenatal counseling (see Genetic Disorders Detection: Carrier Screening) for couples who are at risk of having a child with sickle cell disease. Fetal cells obtained through amniocentesis or chorionic villus sampling are tested for the presence of the sickle cell gene.

Treatment

Because sickle cell disease is rarely cured, treatment is aimed at preventing crises, controlling the anemia, and relieving symptoms. People who have this disease should try to avoid activities that reduce the amount of oxygen in their blood and should seek prompt medical attention for even minor illnesses, such as viral infections. Because people are at increased risk of infection, they should receive pneumococcal and Haemophilus influenzae vaccines.

Sickle cell crisis may require hospitalization. People are given fluid intravenously and drugs to relieve pain. Blood transfusions and oxygen may be given if doctors suspect that anemia is severe enough to pose a risk of stroke, heart attack, or lung damage. Conditions that may have caused the crisis, such as an infection, are treated.

Drugs can help control sickle cell disease. Hydroxyurea Some Trade Names
HYDREA
increases the production of a form of hemoglobin found predominantly in fetuses, which decreases the number of red blood cells becoming sickle-shaped. Therefore, it reduces the frequency of sickle cell crises.

Bone marrow or stem cells from a family member or other donor who does not have the sickle cell gene may be transplanted in a person with the disease. Although such transplantation may be curative, it is risky, and recipients must take drugs that suppress the immune system for the rest of their lives.

Gene therapy, a technique in which normal genes are implanted in precursor cells (cells that produce blood cells), is being studied.

Iron Deficiency Anemia

Iron deficiency anemia results from low or depleted stores of iron, which is needed to produce red blood cells.

Excessive bleeding is the most common cause.
People may be weak, short of breath, and pale.
Blood tests can detect low levels of iron.
Iron supplements are used to restore iron levels.

Iron deficiency anemia usually develops slowly, because it may take several months for the body’s iron reserves to be used up. As the iron reserves are decreasing, the bone marrow gradually produces fewer red blood cells. When the reserves are depleted, the red blood cells are not only fewer in number but also abnormally small.

Iron deficiency is one of the most common causes of anemia, and blood loss is the most common cause of iron deficiency in adults. In men and postmenopausal women, iron deficiency usually indicates bleeding in the digestive tract. In premenopausal women, menstrual bleeding is the most common cause of iron deficiency in. Iron deficiency may also result from too little iron in the diet (see Minerals and Electrolytes: Iron Deficiency), especially in infants, young children, adolescent girls, and pregnant women.

Did You Know…

In the United States, anemia rarely results from consuming too little iron because supplemental iron is added to many foods.

Symptoms and Diagnosis

Symptoms of iron deficiency anemia tend to develop gradually and are similar to symptoms produced by other types of anemia. Many people with iron deficiency anemia have pica. People with pica have a craving to ingest something, most commonly ice but sometimes a substance that is not food, such as dirt, clay, or chalk.

Once doctors diagnose anemia, tests for iron deficiency are often done. With iron deficiency, the red blood cells tend to be small and pale. Blood levels of iron and transferrin (the protein that carries iron when it is not inside red blood cells) are measured and compared. The most accurate test for iron deficiency is a measurement of the blood level of ferritin (a protein that stores iron). A low level of ferritin indicates iron deficiency. However, sometimes ferritin levels are misleading because they can be falsely elevated (and thus appear normal) by liver damage, inflammation, infection, or cancer. In this case, doctors may measure the level of a protein on the surface of cells that binds to transferrin (transferrin receptor).

Treatment

Because excessive bleeding is the most common cause of iron deficiency, the first step is to locate its source.

Normal dietary iron intake usually cannot compensate for iron loss from chronic bleeding, and the body has a very small iron reserve. Consequently, lost iron must be replaced by taking iron supplements.

Correcting iron deficiency anemia with iron supplements usually takes 3 to 6 weeks, even after the bleeding has stopped. Iron supplements are usually taken by mouth. An iron supplement is absorbed best when taken 30 minutes before breakfast with a source of vitamin C (either orange juice or a vitamin C supplement). Iron supplements are typically continued for 6 months after the blood counts return to normal to fully replenish the body’s reserves. Blood tests are done periodically to ensure that the iron supply is sufficient. Treating the iron deficiency treats pica.

Hemoglobin C, S-C, and E Diseases

Hemoglobin C, S-C, and E diseases are inherited conditions characterized by abnormally shaped red blood cells and chronic anemia that is caused by excessive destruction of red blood cells.

Hemoglobin C, S, and E are abnormal forms of hemoglobin (the protein in red blood cells that carries oxygen). These abnormal forms of hemoglobin result from inheriting an abnormal gene.

Hemoglobin C disease occurs mostly in blacks. One copy of the gene that causes hemoglobin C disease is present in 2 to 3% of blacks in the United States. However, people must inherit two copies of the abnormal gene to develop the disease. In general, symptoms are few. Anemia varies in severity. People who have this disease, particularly children, may have episodes of abdominal and joint pain, an enlarged spleen, and mild jaundice, but they do not have severe crises, as occur in sickle cell disease.

Hemoglobin S-C disease occurs in people who have one copy of the gene for sickle cell disease and one copy of the gene for hemoglobin C disease. Hemoglobin S-C disease is more common than hemoglobin C disease, and its symptoms are similar to those of sickle cell disease but milder.

Hemoglobin E disease affects primarily people from Southeast Asia. This disease produces anemia but none of the other symptoms that occur in sickle cell disease and hemoglobin C disease. Diagnosis is by a blood test called hemoglobin electrophoresis. Treatment varies depending on the severity of symptoms but can include some of the same treatments that are used in people with sickle cell disease.

Category: Vascular system

studynursing

Anemia

Anemia Due to Excessive Bleeding

Anemia of Chronic Disease

Autoimmune Hemolytic Anemia

Autoimmune Hemolytic Anemia

Vitamin Deficiency Anemia

Thalassemias

Sickle Cell Disease

Iron Deficiency Anemia

Hemoglobin C, S-C, and E Diseases

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studynursing

Anemia

Anemia Due to Excessive Bleeding

Anemia of Chronic Disease

Autoimmune Hemolytic Anemia

Autoimmune Hemolytic Anemia

Vitamin Deficiency Anemia

Thalassemias

Sickle Cell Disease

Iron Deficiency Anemia

Hemoglobin C, S-C, and E Diseases

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