Anemia is a condition where there is deficiency of either hemoglobin or of red blood cells.
Thus, this leads to a condition where there is insufficient amount of oxygen circulating in the body. Anemia is said to be one of the most common condition affecting the blood. Anemia can occur in all age groups and populations, but it primarily affects women of childbearing age because of the loss of blood during menstruation. Common types of anemia 1. Iron Deficiency Anemia Iron deficiency anemia is one of the most common types of anemia seen in the world. It is one of the types of anemia in pregnancy, as it is one of the malnutrition diseases. This condition occurs due to deficiency of iron in the body, which is spurred on by a diet that is poor in iron and other nutrients. However, in some cases, this could also occur due to colon cancer, as there is loss of blood in stools. Causes, incidence, and risk factors Iron deficiency anemia is the most common form of anemia. Red blood cells bring oxygen to the body's tissues. Healthy red blood cells are made in your bone marrow. Red blood cells move through your body for 3 to 4 months. Parts of your body then remove old blood cells. Iron is a key part of red blood cells. Without iron, the blood cannot carry oxygen effectively. Your body normally gets iron through your diet and by re-using iron from old red blood cells. You get iron deficiency anemia when your body's iron stores run low. You can get iron deficiency if: You lose more blood cells and iron than your body can replace Your body does not do a good job of absorbing iron Your body is able to absorb iron, but you are not eating enough foods with iron in them Your body needs more iron than normal (such as if you are pregnant or breastfeeding) Iron loss can be due to bleeding. Common causes of bleeding are: Heavy, long, or frequent menstrual periods Cancer in the esophagus, stomach, or colon Esophageal varices The use of aspirin, ibuprofen, or arthritis medicines for a long time Peptic ulcer disease The body may not absorb enough iron in the diet due to: Celiac disease Crohn's disease Gastric bypass surgery Taking too many antacids that contain calcium You may not get enough iron in the diet if: You are a strict vegetarian You are an older adult and do not eat a full diet
Symptoms You may have no symptoms if the anemia is mild. Most of the time, symptoms are mild at first and develop slowly. Symptoms may include: Feeling grumpy Feeling weak or tired more often than usual, or with exercise Headaches Problems concentrating or thinking As the anemia gets worse, symptoms may include: Blue color to the whites of the eyes Brittle nails Light-headedness when you stand up
Pale skin color Shortness of breath Sore tongue Symptoms of the conditions that cause iron deficiency anemia include: Dark, tar-colored stools or blood Heavy menstrual bleeding (women) Pain in the upper belly (from ulcers) Weight loss (in people with cancer)
Signs and tests To diagnose anemia, your doctor may order these blood tests: Hematocrit and hemoglobin (red blood cell measures) RBC indices Tests to check iron levels in your blood include: Bone marrow exam (rare) Iron binding capacity (TIBC) in the blood Serum ferritin Serum iron level Tests that may be done to look for the cause of iron deficiency: Colonoscopy Fecal occult blood test Upper endoscopy
Treatment Taking supplements and eating iron-rich foods are important parts of treating iron deficiency anemia. However, you and your health care provider must first search for the cause of your anemia. Iron supplements (most often ferrous sulfate) are needed to build up the iron stores in your body. Patients who cannot take iron by mouth can take it through a vein (intravenous) or by an injection into the muscle. Pregnant and breastfeeding women will need to take extra iron because their normal diet usually will not provide the amount they need. The hematocrit should return to normal after 2 months of iron therapy. However, keep taking iron for another 6 - 12 months to replace the body's iron stores in the bone marrow. Iron-rich foods include: Chicken and turkey Dried lentils, peas, and beans Eggs (yolk) Fish Meats (liver is the highest source) Peanut butter Soybeans Whole-grain bread Other sources include: Oatmeal Raisins, prunes, and apricots Spinach, kale, and other greens
2. Sickle Cell Anemia Sickle cell anemia is a disease where the red blood cells assume an abnormal shape, which is sickle like, as they become flattened and pointed at ends. Thus, this leads to insufficient oxygen carrying capacity of the cells. This sickling occurs due to a point mutation in the hemoglobin gene. Thus, when the red blood cells circulate in the bloodstream, due to their sickled structure, they are very fragile. This leads to excessive breakage of the cells, which in turn leads to a state of hemolysis, which is the actual cause of anemia. Causes, incidence, and risk factors Sickle cell anemia is caused by an abnormal type of hemoglobin called hemoglobin S. Hemoglobin is a protein inside red blood cells that carries oxygen. Hemoglobin S changes the shape of red blood cells, especially when the cells are exposed to low oxygen levels. The red blood cells become shaped like crescents or sickles. The fragile, sickle-shaped cells deliver less oxygen to the body's tissues. They can also get stuck more easily in small blood vessels, and break into pieces that interupt healthy blood flow. Sickle cell anemia is inherited from both parents. If you inherit the hemoglobin S gene from one parent and normal hemoglobin (A) from your other parent, you will have sickle cell trait. People with sickle cell trait do not have the symptoms of sickle cell anemia. Sickle cell disease is much more common in people of African and Mediterranean descent. It is also seen in people from South and Central America, the Caribbean, and the Middle East. Symptoms Symptoms usually don't occur until after age 4 months. Almost all patients with sickle cell anemia have painful episodes (called crises), which can last from hours to days. These crises can affect the bones of the back, the long bones, and the chest. Some patients have one episode every few years. Others have many episodes per year. The crises can be severe enough to require a hospital stay. Common symptoms include: Attacks of abdominal pain Bone pain Breathlessness Delayed growth and puberty Fatigue Fever Paleness Rapid heart rate Ulcers on the lower legs (in adolescents and adults) Yellowing of the eyes and skin (jaundice) Other symptoms include: Chest pain Excessive thirst Frequent urination Painful and prolonged erection (priapism - occurs in 10 - 40% of men with the disease) Poor eyesight/blindness Strokes Skin ulcers
Signs and tests Tests commonly performed to diagnose and monitor patients with sickle cell anemia include:
Complete blood count (CBC) Hemoglobin electrophoresis Sickle cell test Other tests may include: Bilirubin Blood oxygen CT scan or MRI Peripheral smear Serum creatinine Serum hemoglobin Serum potassium Urinary casts or blood in the urine White blood cell count
Treatment The goal of treatment is to manage and control symptoms, and to limit the number of crises. Patients with sickle cell disease need ongoing treatment, even when they are not having a painful crisis. Folic acid supplements should be taken. Folic acid is needed to make red blood cells. Treatment for a sickle cell crisis includes: Blood transfusions (may also be given regularly to prevent stroke) Pain medicines Plenty of fluids Other treatments for sickle cell anemia may include: Hydroxyurea (Hydrea), a medicine that may help reduce the number of pain episodes (including chest pain and difficulty breathing) in some people Antibiotics to prevent bacterial infections, which are common in children with sickle cell disease Treatments for complications of sickle cell anemia may include: Kidney dialysis or kidney transplant for kidney disease Drug rehabilitation and counseling for psychological complications Gallbladder removal in those with gallstone disease Hip replacement for avascular necrosis of the hip Treatments, including surgery, for persistent, painful erections (priapism) Surgery for eye problems Wound care, zinc oxide, or surgery for leg ulcers
Bone marrow or stem cell transplants can cure sickle cell anemia. However, they are current not an option for most patients. Sickle cell anemia patients are often unable to find well-matched donors. In the past, sickle cell patients often died from organ failure between ages 20 and 40. Thanks to a better understanding and management of the disease, today, patients can live into their 50s or beyond. Causes of death include organ failure and infection. Some people with the disease experience minor, brief, infrequent episodes. Others experience severe, long-term, frequent episodes with many complications. Complications Acute chest syndrome Anemia Blindness/vision impairment Brain and nervous system (neurologic) symptoms and stroke Death
Disease of many body systems (kidney, liver, lung) Drug (narcotic) abuse Erectile dysfunction (as a result of priapism) Gallstones Hemolytic crisis Infection, including pneumonia, gallbladder inflammation (cholecystitis), bone infection (osteomyelitis), and urinary tract infection Joint destruction Leg sores (ulcers) Loss of function in the spleen Parvovirus B19 infection, leading to low red blood cell production (aplastic crisis) Splenic sequestration syndrome Tissue death in the kidney
Prevention Sickle cell anemia can only occur when two people who carry sickle cell trait have a child together. Genetic counseling is recommended for all carriers of sickle cell trait. About 1 in 12 African Americans has sickle cell trait. It is possible to diagnose sickle cell anemia during pregnancy. If you have sickle cell anermia, you can prevent the change in red blood cell shape by: Getting enough fluids Getting enough oxygen Quickly treating infections Have a physical exam every 3 - 6 months to make sure that you are getting enough nutrition and activity, and that you are receiving the proper vaccinations. Regular eye exams are recommended. PREVENTING CRISES It is important to maintain good oxygen levels and to prevent dehydration. The following steps can help prevent a sickle cell crisis: Avoid strenous activities, stress, smoking, high-altitudes, nonpressurized flights, and other events that reduce your oxygen level Always have plenty of fluids with you Avoid too much sun exposure Consider having the child with sickle cell anemia wear a Medic Alert bracelet. Share the above information with teachers and other caretakers, when necessary. PREVENTING INFECTIONS People with sickle cell anemia need to keep their immunizations up to date to prevent illness. Some patients may receive antibiotics to prevent infections.
3. Megaloblastic Anemia This anemia has a very different type of etiology behind it. In cases of people suffering from atrophic gastritis, there is destruction of the gastric parietal cells. These cells are responsible for absorption of vitamin B12, and hence, this condition is brought on by the inability of the body to absorb and utilize vitamin B12. Furthermore, even the folic acid that is ingested is not absorbed properly. Thus, the only treatment in such cases is to take vitamin B12 and folic acid intravenously. Symptoms Anemia
Painful tingling of the hands and feet Weakness Fatigue Loss of coordination Irritability and mental status changes Gastrointestinal problems (e.g., diarrhea) Decreased appetite Changes of taste perception Weight loss Risk Factors Vitamin B12 deficiency may result from: Deficiency of Intrinsic factor (IF): Intrinsic factor is a molecule produced in the stomach and required for absorption of vitamin B12. Deficiencies can occur due to stomach surgery, autoimmune disease, and as a result of aging. Malabsorption: Small bowel and pancreatic disease and alcohol abuse contribute to poor absorption of dietary vitamin B12. Elderly persons may also have reduced vitamin B 12absorption. Other gastric disease: Occasionally, individuals with gastritis, surgical removal of the stomach, or stomach stapling surgery may develop a vitamin B12 deficiency. Medications: Metformin, proton pump inhibitors (e.g., omeprazole), H2blockers (e.g., Zantac), antacids, and antibiotics may inhibit vitamin B12 absorption. HIV infection: Weight loss and diarrhea caused by HIV/AIDS are associated with vitamin B 12deficiency. Fish tapeworm infection Dietary deficiency: See Nutritional Considerations. Folic acid deficiency may result from: Alcohol abuse: Alcohol directly interferes with the absorption of folic acid. Malabsorption: Malabsorption diseases, such as inflammatory bowel disease and celiac sprue, decrease folic acid absorption. Pregnancy and breastfeeding: Because fetal and infant growth requires increased folic acid, pregnancy and breastfeeding may deplete a womans stores. In turn, an exclusively breastfed infant whose mother is deficient in folic acid will not receive adequate amounts. Medications: Intake of certain medications, such as methotrexate, phenytoin, and trimethoprim, may lead to folic acid deficiency. Vitamin B12 deficiency: Because Vitamin B12 is responsible for the conversion of folic acid to its metabolically active form, its deficiency can lead to folic acid deficiency. Dietary deficiency: See Nutritional Considerations. Megaloblastic Anemia: Diagnosis and Treatment Diagnosis A medical history and physical examination are the first steps. Blood testing diagnoses these disorders and distinguishes between the two. Note that the tests for vitamin B12 and folic acid levels may be rendered unreliable by pregnancy, alcohol intake, recent nutritional changes, or certain medications.
Bone marrow biopsy is usually not necessary for diagnosis, but may be recommended in some cases. Treatment The underlying cause of vitamin B12 or folate deficiency must be identified to ensure adequate longterm treatment. Vitamin B12 injections are usually given daily for one week, then weekly for four weeks, and then monthly until vitamin levels have stabilized. Patients with continued risk of deficiency should remain on monthly injections. Oral vitamin B12 pills may be used in some patients. Oral folic acid pills taken daily for several months usually correct the deficiency.
Alcohol use should be restricted. In individuals with alcoholic tendencies, psychiatric treatment along with substance abuse counseling and Alcoholics Anonymous meetings or other community support may be necessary.
Megaloblastic Anemia: Nutritional Considerations The following steps may reduce the risk of megaloblastic anemia: Vitamin B12 supplementation: Individuals following mixed diets generally have adequate vitamin B12 intake. However, many individuals, particularly elderly persons, have less than adequate B 12 absorption and may benefit from supplementation. Persons at risk for deficiency include those who have had stomach stapling surgery, alcoholics, and individuals who follow unsupplemented vegan diets for many years and their breastfed infants. In these groups, the risk for vitamin B 12 deficiency is easily eliminated with supplementation. Common multiple vitamins, B12 supplements, fortified breakfast cereals, fortified soymilk, and fortified meat analogues contain a reliable source of the vitamin. Increased intake of folic acid: Due to fortification of grain products with folic acid, anemia resulting from folic acid deficiency is becoming less common. However, alcoholism often leads to deficiency and may require supplementation. In addition, people with epilepsy who are taking anticonvulsant medications may benefit from folic acid supplementation. Increased intake of foods rich in folic acid is a wise choice for all. These include beans, legumes, citrus fruits and juices, wheat bran, whole grains, and dark green leafy vegetables 4. Aplastic Anemia Aplastic anemia is a condition where the bone marrow does not produce enough of red blood cells, due to which they are not replaced and replenished on a timely enough basis. Thus, the red blood cells, which have a lifespan of only 120 days, eventually die out, but they aren't replaced, due to which there is a deficiency of red blood cells in the body. In such cases, the only treatment option is bone marrow replacement. Aplastic Anemia Causes The mechanism of pathogenesis in aplastic anemia is represented by: Intrinsic stem cell defect. Failure of stromal microenvironment. Absence or deficiency of growth factors. Immune suppression of hemopoietic marrow. The main causes of aplastic anemia are: Chemicals (benzene and related compounds). Drugs ( chloramphenicol, gold salts, D-peniciline, phenylbutazone, carbamazepine, hydantoin and derived drugs, antineoplastic drugs and acetazolamide). Radiation. Viruses (hepatitic C virus, parvovirus B19, Epstein-Barr virus, cytomegalovirus). Fanconi anemia. Dyskeratosis congenita may evolve into aplastic anemia. Schwachmann Diamond syndrome (congenital granulocyte aplasia) may evolve into aplastic anemia. Idiopathic (in above 65% of cases). Other (connective tissue diseases, pregnancy).
Aplastic Anemia Symptoms Bleeding (epistaxis, gingival bleeding, metrorrhagia, purpura, ecchymoses after minor trauma) Infections
Fever Fatigue Headaches Los of apeyite Weight loss Dyspnea Palpitations recurrent infections which are secondary to cytopenias
Diagnosis Peripheral blood Pancytopenia. Low reticulocyte count and possible macrocytosis. Low absolute neutrophil count (if <200/ul, prognosis is extremely poor). Negative sucrose hemolysis test and HAM test (absence of hemolysis), to rule out paroxysmal nocturnal hemoglobinuria. Positive HAM test (hemolysis of patients erithrocytes by normal acidified serum) and sucrose hemolysis test associated with presence of hemosiderinuria are diagnostic findings for paroxysmal nocturnal hemoglobinuria in aplastic crisis.
Positive diagnosis of aplastic anemia is sustained by the following criteria: Bone marrow (one of the following criteria): Marrow cellularity less than 25% from normal or Marrow cellulatity less than 50% from normal with less than 30% hemopoietic cells. Peripheral blood (at least two of the following criteria): Absolute neutrophil count less than 500/ul. Platelet count less than 20,000/ul. Anemia with corrected reticulocyte index of less than 1. Evolution And Prognosis Median survival of untreated severe aplastic anemia is 3 to 6 months (20% survive longer than 1 year). Aplastic anemia is having a poor prognosis, death will occur due to complications: Acute Infectious: respiratory (Gramm negative microorganisms), cutaneous. Hemorrhagic: epistaxis, purpura, metrorrhagia, gastrointestinal bleeding, bleeding into the central nervous system. Malignant: acute leukemia and myelodysplastic syndrome. Chronic 1. Hemochromatosis due to repeated transfusion with its consequences: liver cirrhosis anddiabetes.
1. 2. 3.
Treatment Bone marrow transplantation represents the only curative option: Major indication in patients less than 40 years of age. Only one-third of patients have a HLA-identical or 1 antigen mismatched donor.
With an appropiate donor cure is achieved in 75% 85% of previously untransfused patients, whereas only 5560% of multiply transfused patients achive cure. Immunosuppressive therapy is not a curative option and is represented by: Antithymocyte globulin (ATG) Cyclosporine A (CSP-A) Androgen hormones in the treatment of moderate or severe aplastic ane is controversed because recent studies showed no efficacy as primray therapy. Hemopoietic growth factors have been used to treat neutropenia Granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte colony-stimulating factor (GCSF) resulted in temporary improvement in neutrophil counts in some patients treated with this cytokines. Interleukin-3 (IL-3) improved temporary the absolute neutrophil count in a few patients. Interleukin-1 (EL-l)was not effective in a study including a small group of patients. Other therapeutic measures: HLA typing of patient and siblings (ideal is the existence of a normal twin) in order to identify a HLA matched donor, marrow transplantation beeing the therapy of choice in patients less than 40 years of age. Transfusions should be administered only when imperious needed. In potential transplant recipients there will not be used family donors and under no circumstances the HLA matched donor. Platelet transfusions are used only on assessement of risk of life-threatening bleeding (not solely on platelet count). Platelet transfusions from a single donor should be used to minimize sensitization and subsequent refractoriness. When the patient has become refractory to platelet transfusions, only HLA matched donors canprovide efficient platelets. Red blood cells (RBCs) transfusions are indicated when hemoglobin level is less than 7-8 g/dl. In order to reduce subsequent sesitization packed RBCs (irradiated or washed) are to be transfused, or leukocyte-depleted blood products. In severe neutropenic, hospitalised patients, measures in order to reduce risk of infections shouldbe undertaken (isolation in aseptic room, no visits allowed, gloves and mask for the medical care personell). Prompt institution of broad spectrum antibiotics, intravenously for fever after the appropiate cultures have been obtained.
Rare types of anemia 1. 2. 3. 4. anemia of prematurity hereditary spherocytosis, myelophthisic anemia, etc.
