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The red blood cells circulate in the bloodstream for about 120 days before they are broken down in the spleen. If the haemoglobin or number of red blood cells is low, the oxygen-carrying capacity of the blood is reduced and anaemia develops. Anaemia is a general name given to a variety of disorders affecting the red blood cells. Haemoglobin is measured in grams per 100 millilitres (1 decilitre or dl). The normal level in females is between 11.5 and 15.5gm per dl. A woman is considered to be anaemic if the haemoglobin is below 11.5gm per dl.

 IRON DEFICIENCY ANAEMIA  MEGALOBLASTIC ANAEMIA I. Folic acid anaemia II. Pernicious anaemia ( B12 deficiency) APLASTIC ANAEMIA  HAEMOLYTIC ANAEMIA I. Thalasemia II. Sickle cell anaemia III. G6PD deficiency  BLOOD LOSS 


Iron deficiency is a common problem, especially for women, so common, in fact, that 5% of women between the ages of 20 and 49 have iron deficiency with anemia and 11% have iron deficiency without anemia. What many people don't know, however, is that iron plays a key role not only in the body's oxygen transport and delivery system, but also in the regulation of metabolism. Iron is needed to synthesize vital substances such as the brain chemical, dopamine, DNA and white blood cells. Thus iron deficiency can do much more harm than merely causing anemia; it can have widespread effects from damaging a person's ability to think to weakening their resistance to infection.

Women in their childbearing years have greater iron needs than men as a result of menstrual blood loss, the increased iron demands of pregnancy and blood loss during childbirth. anything that causes heavier than normal menstrual periods, for example uterine fibroids, may lead to iron deficiency. Iron deficiency can also be caused by other types of chronic blood loss including internal bleeding from gastritis and ulcers, inflammatory bowel disease, parasitic infections (this is more common in Third World populations than developed countries) and hemorrhoids.


Fatigue decreased energy weakness shortness of breath lightheadedness palpitations (feeling of the heart racing or beating irregularly) looking pale

Iron level: An iron level may tell the doctor whether anemia may be related to iron deficiency or not. This test is usually accompanied by other tests that measure the body's iron storage capacity, such as transferrin level and ferritin level. Transferrin level: Evaluates a protein that carries iron around the body. Ferritin: Evaluates at the total iron available in the body. Ferritin concentration indicates how much iron is stored in the body. Chronic infection, inflammation or certain diseases causing tissue and organ damage can produce a false reading.

The Federal Centers for Disease Control and Prevention (CDC) recommends a three-month course of therapy for the treatment of iron deficiency. Some authorities, however, advise patients to continue iron supplementation for six to twelve months. An important note about iron supplements is that they can often produce black-colored stools. Whichever approach your doctor chooses, it is important that you add more iron in the form of iron-rich foods to your diet and that your doctor treats any correctable cause of blood loss. Patients with ongoing blood loss that cannot be corrected may need, in addition to eating a more iron-rich diet, to continue taking lowdose iron supplements indefinitely.

MEGALOBLASTIC ANAEMIA (folic acid anaemia)

Folate is a vitamin. You need folate for many important processes inside your body, including making red blood cells. If you have a short supply of folate, your body won't make as many red blood cells, they will be abnormally large in size and won't last as long as they should. If you don't have enough red blood cells, the tissues and organs of your body may not be getting enough oxygen. This leads to the symptoms of anaemia. Folic acid is needed to make new cells in the body, including red blood cells. The body does not store very much folic acid. You need a regular fresh supply to keep healthy. Many foods contain folic acid, including spinach, sprouts, broccoli, green beans, peas, chickpeas, brown rice, kidney, liver and potatoes. A normal balanced diet contains enough folic acid. However, a lack of folic acid will cause anaemia, and sometimes other symptoms.

Symptoms due to anaemia are caused by the reduced amount of oxygen in the body. Common symptoms include: tiredness, lethargy, feeling faint, becoming easily breathless. Less common symptoms include: headaches, palpitations, altered taste and ringing in the ears (tinnitus). You may look pale. depression, or other emotional changes

Not eating enough foods containing folic acid is the most common cause. This occurs most often in elderly people who do not eat well. Another group who often don't eat properly are people who are alcohol-dependent. Pregnancy causes reserves of folic acid in your body to be used by the growing baby. You are at risk of becoming low in folic acid during the later stages of pregnancy, particularly if you do not eat well during pregnancy. Some uncommon conditions of the gut may cause poor absorption of folic acid. For example, coeliac disease. Some blood disorders can lead to a very high turnover of red blood cells. For example, sickle cell disease and thalassaemia. Normal amounts of folic acid in the diet may then not be enough, and supplements may need to be taken. Some inflammatory conditions can lead to low folic acid levels - for example, severe Crohn's disease. This is less common though. Some medicines interfere with folic acid. Therefore, you may need to take extra folic acid whilst taking certain medicines. For example, colestyramine, sulfasalazine, methotrexate and some anticonvulsant medicines used to treat epilepsy. Drinking too much alcohol can reduce your body's ability to use folate.

Your GP will ask about your symptoms and examine you. He or she may also ask you about your medical history. This will include a full blood count (FBC) that shows the level of haemoglobin in your blood and how many of each of the different type of blood cell you have. A FBC test will also show the size of your red cells and the amount of haemoglobin each one contains. The normal amount - or concentration - of haemoglobin is: at least 13g/dl (13 grams of haemoglobin per decilitre (100ml) of blood) for men at least 11.5g/dl for women at least 11g/dl for pregnant women If your haemoglobin level is lower than the levels above, you may have folate-deficiency anaemia. Your doctor will also look at the size of your red blood cells. Folate deficiency causes enlarged red blood cells. If you have enlarged red blood cells, the condition is called macrocytic anaemia. The level of folate in your blood can also be measured with the blood test. Your level of vitamin B12 will be checked too, because it's possible to have deficiencies of both vitamins at the same time. Your GP may refer you to a haematologist - a doctor who specialises in treating blood disorders - to have further tests. This may include a bone marrow biopsy to examine your bone marrow.

Your doctor will try to identify why you're deficient in folate so that the cause of your deficiency can be treated. If you don't get enough folate in your diet, your doctor may give you advice on how to change your diet, or refer you to a dietitian. You may be advised to take folate tablets. Folate comes in a synthetic (artificial) form called folic acid. This is a water-soluble vitamin that your body can use instead of folate. You will usually need to take 5mg per day, for four months. Always read the patient information leaflet that comes with your medicine and ask your pharmacist or GP for advice if you have any questions. Before starting treatment, your doctor will check your vitamin B12 levels. This is because taking folate tablets can hide a vitamin B12 deficiency. If you're taking folate tablets, your GP will need to monitor your blood to check that they are working. You will be asked to have a blood test shortly after you start treatment, and again about eight weeks later to confirm that your treatment has been successful. Most people need to take folic acid for only four months and they see an improvement in their symptoms within this time. However, some people need to take folic acid for longer periods of time, and sometimes for life, if the cause of the deficiency isn't resolved.

MEGALOBLASTIC ANAEMIA (pernicious anaemia B12 deficiency)

Pernicious anemia is a condition in which the body produces insufficient numbers of red blood cells because the intestines cannot absorb vitamin B12 properly. Vitamin B12 is essential for the production of red blood cells in the bone marrow. This disorder occurs due to low levels of a protein called intrinsic factor, which is released by stomach cells and is necessary for the absorption of vitamin B12 in the intestines. The inability to produce intrinsic factor may be inherited or may arise from an autoimmune process, in which the bodys immune system attacks its own tissues, in this case, the lining of the stomach. Pernicious anemia can also develop from other conditions affecting the stomach lining, such as atrophic gastritis (inflammation and thinning of the stomach lining). Pernicious anemia is more common in people with Northern European or Scandinavian ancestry, and the average age of onset of symptoms is 60 years

Pernicious anemia is caused by the lack of a protein called intrinsic factor. This protein, which is produced by cells in the stomach lining, is essential for proper absorption of dietary vitamin B12 in the intestines. Low levels of intrinsic factor are often the result of an autoimmune condition, in which the body produces antibodies that attack its own stomach cells. Rarely, infants are born lacking ability to make intrinsic factor, a condition known as congenital pernicious anemia. Pernicious anemia can also develop as a result of atrophic gastritis, a condition that damages the lining tissues of the stomach, impairing their ability to produce intrinsic factor.

General symptoms of pernicious anemia Bleeding gums Dizziness Fatigue Headache Pale skin or pallor Poor concentration Shortness of breath Weakness (loss of strength) Digestive system symptoms of pernicious anemia Constipation Diarrhea Loss of appetite Nausea with or without vomiting Swollen tongue

A number of factors increase the risk of developing pernicious anemia. Not all people with risk factors will get pernicious anemia. Risk factors for pernicious anemia include: Family history of autoimmune disorders Family history of pernicious anemia Northern European or Scandinavian ancestry

A complete blood cell count (CBC) Examination of a blood smear (peripheral smear) under a microscope, often performed in association with a CBC Blood vitamin B-12 level measurements Tests for the presence of autoantibodies to intrinsic factor or stomach lining cells Blood levels of iron and iron-binding capacity Folate levels (which are often reduced when vitamin B-12 levels are low) Blood levels of methylmalonic acid or homocysteine, both of which may be sensitive indicators of vitamin B-12 deficiency The Schilling test, a measure of how well the body can absorb vitamin B12, is less commonly used today than in the past. Finally, bone marrow aspiration or bone marrow biopsy may be recommended in some cases if bone marrow disorders are suspected

Vitamin B-12 is typically given as an intramuscular injection (shot). An injection of 1000 micrograms (1 mg) of vitamin B-12 is generally given every day for one week, followed by 1 mg every week for four weeks and then 1 mg every month thereafter. In some cases, taking very high doses of vitamin B12 supplements by mouth may be effective, although in general, low levels of intrinsic factor limit the absorption of oral vitamin B12. Blood transfusions are rarely needed, but they may be used in severe cases.

Dementia Depression Increased risk of stomach cancer Nerve problems that cause pain, numbness or tingling Problems with balance or coordination Stomach polyps (benign growth of tissue)

Aplastic anemia is a condition where bone marrow does not produce sufficient new cells to replenish blood cells. The condition, per its name, involves both aplasia and anemia. Typically, anemia refers to low red blood cell counts, but aplastic anemia patients have lower counts of all three blood cell types:red blood cells, white blood cells, and platelets, termed pancytopenia. Idiopathic means the cause is unknown. However, idiopathic aplastic anemia is thought to occur when the body's immune system mistakenly destroys healthy cells. This is called an autoimmune disorder. Aplastic anemia may also be caused by certain medical conditions (such as pregnancy or lupus) or exposure to some toxins or drugs (including chemotherapy). See: Secondary (acquired) aplastic anemia In some cases, aplastic anemia is associated with another blood disorder called paroxysmal nocturnal hemoglobinuria (PNH).


Low red cell count (anemia) can cause: Fatigue Pallor (paleness) Rapid heart rate Shortness of breath with exercise Weakness Low white cell count (leukopenia) causes an increased risk of infection. Low platelet count (thrombocytopenia) results in bleeding, especially of the mucous membranes and skin. Symptoms include: Bleeding gums Easy bruising Frequent or severe infections Nose bleeds Rash--small pinpoint red marks on the skin (petechiae)

Bone marrow aspirate and biopsy: to rule out other causes of pancytopenia (i.e. neoplastic infiltration or significant myelofibrosis). History of iatrogenic exposure to cytotoxic chemotherapy: can cause transient bone marrow suppression X-rays, computed tomography (CT) scans, or ultrasound imaging tests: enlarged lymph nodes (sign of lymphoma), kidneys and bones in arms and hands (abnormal in Fanconi anemia) Chest X-ray: infections Liver tests: liver diseases Viral studies: viral infections Vitamin B12 and folate levels: vitamin deficiency Blood tests for paroxysmal nocturnal hemoglobinuria Test for antibodies: immune competency

Medical therapy of aplastic anemia often includes a short course of anti-thymocyte globulin (ATG) or anti-lymphocyte globulin (ALG) and several months of treatment with ciclosporin to modulate theimmune system. Mild chemotherapy with agents such as cyclophosphamide and vincristine may also be effective. Antibody therapy, such as ATG, targets T-cells, which are believed to attack the bone marrow. Steroids are generally ineffective, though are often used to combat serum sickness caused by ATG use. In moderate cases, blood transfusions and platelet transfusions will help correct the anemia and the risk of bleeding. However, over time, blood transfusions may stop working. Too much iron may build-up in the body tissues may occur because of the many transfusions. Severe aplastic anemia occurs when blood-cell counts are very low, and is a lifethreatening condition. Bone marrow transplant or stem cell transplant is recommended for severe disease in patients under age 40. However, their donor must be a brother or sister who is a good match. This is called a matched sibling donor.

Severe infections or bleeding Complications of bone marrow transplant (graft failure or graft-versus-host disease) Reactions to medications (patients can have reactions to anti-thymocyte globulin)




This is another group of hemoglobin-related causes of anemia. There are many types of thalassemia, which vary in severity from mild (thalassemia minor) to severe (thalassemia major). Thalassemia is more common in people from African, Mediterranean, and Southeast Asian ancestries. Thalassemia is a blood disorder passed down through families (inherited) in which the body makes an abnormal form of hemoglobin, the protein in red blood cells that carries oxygen. The disorder results in excessive destruction of red blood cells, which leads to anemia.

Normal hemoglobin is composed of four protein chains, two and two globin chains arranged into a heterotetramer. Thalassemia patients produce a deficiency of either or globin, unlike sicklecell disease which produces a specific mutant form of globin. The thalassemias are classified according to which chain of the hemoglobin molecule is affected. In thalassemias, production of the globin chain is affected, while in thalassemia production of the globin chain is affected. globin chains are encoded by a single gene on chromosome 11; globin chains are encoded by two closely linked genes on chromosome 16. Thus in a normal person with two copies of each chromosome, there are two loci encoding the chain, and four loci encoding the chain. Deletion of one of the loci has a high prevalence in people of African or Asian descent, making them more likely to develop thalassemias. thalassemias are common in Africans, but also in Greeks and Italians.

Alpha ( ) thalassemias The thalassemias involve the genes HBA1 and HBA2, inherited in a Mendelian recessive fashion. There are two gene loci and so four alleles. It is also connected to the deletion of the 16p chromosome. thalassemias result in decreased alpha-globin production, therefore fewer alpha-globin chains are produced, resulting in an excess of chains in adults and excess chains in newborns. The excess chains form unstable tetramers (called Hemoglobin H or HbH of 4 beta chains) which have abnormal oxygen dissociation curves. Beta ( ) thalassemias Beta thalassemias are due to mutations in the HBB gene on chromosome 11 , also inherited in an autosomal-recessive fashion. The severity of the disease depends on the nature of the mutation. Mutations are characterized as either o or thalassemia major if they prevent any formation of chains, the most severe form of thalassemia. Alternatively they are characterized as + or thalassemia intermedia if they allow some chain formation to occur. In either case there is a relative excess of chains, but these do not form tetramers: rather, they bind to the red blood cellmembranes, producing membrane damage, and at high concentrations they form toxic aggregates. Delta ( ) thalassemia As well as alpha and beta chains being present in hemoglobin about 3% of adult hemoglobin is made of alpha and delta chains. Just as with beta thalassemia, mutations can occur which affect the ability of this gene to produce delta chains[citation needed].

The most severe form of alpha thalassemia major causes stillbirth (death of the unborn baby during birth or the late stages of pregnancy). Children born with thalessemia major (Cooley's anemia) are normal at birth, but develop severe anemia during the first year of life. Other symptoms can include: Bone deformities in the face Fatigue Growth failure Shortness of breath Yellow skin (jaundice) Persons with the minor form of alpha and beta thalassemia have small red blood cells (which are identified by looking at their red blood cells under a microscope), but no symptoms.


A physical exam may reveal a swollen (enlarged) spleen. A blood sample will be taken and sent to a laboratory for examination. Red blood cells will appear small and abnormally shaped when looked at under a microscope. A complete blood count (CBC) reveals anemia. A test called hemoglobin electrophoresis shows the presence of an abnormal form of hemoglobin. A test called mutational analysis can help detect alpha thalassemia that cannot be seen with hemoglobin electrophoresis.

Treatment for thalassemia major often involves regular blood transfusions and folate supplements. If you receive blood transfusions, you should not take iron supplements. Doing so can cause a high amount of iron to build up in the body, which can be harmful. Persons who receive significant numbers of blood transfusions need a treatment called chelation therapy to remove excess iron from the body. Bone marrow transplant may help treat the disease in some patients, especially children.

Medical therapy for beta thalassemia primarily involves iron chelation. Deferoxamine is the intravenously or subcutaneously administered chelation agent currently approved for use in the United States. Deferasirox (Exjade) is an oral iron chelation drug also approved in the US in 2005. Deferiprone is an oral iron chelator that has been approved in Europe since 1999 and many other countries. It is available under compassionate use guidelines in the United States. The antioxidant indicaxanthin, found in beets, in a spectrophotometric study showed that indicaxanthin can reduce perferrylHb generated in solution from met-Hb and hydrogen peroxide, more effectively than either Trolox or Vitamin C. Collectively, results demonstrate that indicaxanthin can be incorporated into the redox machinery of -thalassemic RBC and defend the cell from oxidation, possibly interfering with perferryl-Hb, a reactive intermediate in the hydroperoxide-dependent Hb degradation

Untreated, thalassemia major leads to heart failure and liver problems, and makes a person more likely to develop infections. Blood transfusions can help control some symptoms, but may result in too much iron which can damage the heart, liver, and endocrine system.

HAEMOLYTIC ANAEMIA (sickle cell disease)

In some individuals, the problem may be related to production of abnormal hemoglobin molecules. In this condition the hemoglobin problem is qualitative, or functional. Abnormal hemoglobin molecules may cause problems in the integrity of the red blood cell structure and they may become crescent-shaped (sickle cells). There are different types of sickle call anemia with different severity levels. This is typically hereditary and is more common in those of African, Middle Eastern, and Mediterranean ancestry. Sickle cell anemia is a disease passed down through families in which red blood cells form an abnormal crescent shape. (Red blood cells are normally shaped like a disc.)

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.

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


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 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.

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

(Glucose-6-phosphate dehydrogenase deficiency)
G6PD deficiency is an inherited condition in which the body doesn't have enough of the enzyme glucose-6phosphate dehydrogenase, or G6PD, which helps red blood cells (RBCs) function normally. This deficiency can cause hemolytic anemia, usually after exposure to certain medications, foods, or even infections. Most people with G6PD deficiency don't have any symptoms, while others develop symptoms of anemia only after RBCs have been destroyed, a condition called hemolysis. In these cases, the symptoms disappear once the cause, or trigger, is removed. In rare cases, G6PD deficiency leads to chronic anemia.

Environmental triggers Many substances are potentially harmful to people with G6PD deficiency, variation in response to these substance makes individual predictions difficult. Antimalarial drugs that can cause acute haemolysis in people with G6PD deficiency include primaquine, pamaquine and chloroquine. There is evidence that other antimalarials may also exacerbate G6PD deficiency, but only at higher doses.Sulfonamides (such as sulfanilamide, sulfamethoxazole and mafenide), thiazolesulfone, methylene blue and naphthalene should also be avoided by people with G6PD deficiency, as should certainanalgesics (such as aspirin, phenazopyridine and acetanilide) and a few non-sulfa antibiotics (nalidixic acid, nitrofurantoin, isoniazid, dapsone, and furazolidone).[1][4][5] Henna has been known to cause haemolytic crisis in G6PD-deficient infants. Genetics All mutations that cause G6PD deficiency are found on the long arm of the X chromosome, on band Xq28. The G6PD gene spans some 18.5 kilobases.The following variants and mutations are well-known and described:


Paleness (in darker-skinned children paleness is sometimes best seen in the mouth, especially on the lips or tongue) Extreme tiredness Rapid heartbeat Rapid breathing or shortness of breath Jaundice, or yellowing of the skin and eyes, particularly in newborns An enlarged spleen Dark, tea-colored urine

Complete blood count and reticulocyte count; in active G6PD, Heinz bodies can be seen in red blood cells on a blood film; Liver enzymes (to exclude other causes of jaundice); Lactate dehydrogenase (elevated in hemolysis and a marker of hemolytic severity) Haptoglobin (decreased in hemolysis); A "direct antiglobulin test" (Coombs' test) - this should be negative, as hemolysis in G6PD is not immune-mediated; When there are sufficient grounds to suspect G6PD, a direct test for G6PD is the "Beutler fluorescent spot test", which has largely replaced an older test (the Motulsky dye-decolouration test). Other possibilities are direct DNA testing and/or sequencing of the G6PD gene. The Beutler fluorescent spot test is a rapid and inexpensive test that visually identifies NADPH produced by G6PD under ultraviolet light. When the blood spot does not fluoresce, the test is positive; it can be falsely negative in patients who are actively hemolysing. It can therefore only be done 23 weeks after a hemolytic episode. When a macrophage in the spleen identifies a RBC with a Heinz body, it removes the precipitate and a small piece of the membrane, leading to characteristic "bite cells". However, if a large number of Heinz bodies are produced, as in the case of G6PD deficiency, some Heinz bodies will nonetheless be visible when viewing RBCs that have been stained with crystal violet. This easy and inexpensive test can lead to an initial presumption of G6PD deficiency, which can be confirmed with the other tests.

The most important measure is prevention - avoidance of the drugs and foods that cause hemolysis. Vaccination against some common pathogens (e.g. hepatitis A and hepatitis B) may prevent infectioninduced attacks. In the acute phase of hemolysis, blood transfusions might be necessary, or even dialysis in acute renal failure. Blood transfusion is an important symptomatic measure, as the transfused red cells are generally not G6PD deficient and will live a normal lifespan in the recipient's circulation. Some patients may benefit from removal of the spleen (splenectomy), as this is an important site of red cell destruction. Folic acid should be used in any disorder featuring a high red cell turnover. Although vitamin E and selenium have antioxidant properties, their use does not decrease the severity of G6PD deficiency.

Blood loss can be as a result of very heavy menstrual periods. Most women lose about 44 ml of blood per cycle, but some may lose considerably more. Blood loss also occurs during childbirth or during major surgical procedures. Certain health issues may also contribute to iron loss, including chronic bleeding of the gums, hemorrhoids, or cancer of the stomach. In addition, prolonged treatment with certain drugs can cause gastrointestinal bleeding. Parasites can also cause anemia as they take blood and nutrients for themselves that are meant for the human host.

Bleeding can be caused by injuries or can occur spontaneously. Spontaneous bleeding is most commonly caused by problems with the joints or the gastrointestinal or urogenital tracts.

Blood coming from an open wound Bruising Shock, which may cause any of the following symptoms: Confusion or decreasing alertness Clammy skin Dizziness or light-headedness after an injury Low blood pressure Paleness (pallor) Rapid pulse, increased heart rate Shortness of breath Weakness Symptoms of internal bleeding may also include: Abdominal pain and swelling Chest pain External bleeding through a natural opening Blood in the stool (appears black, maroon, or bright red) Blood in the urine (appears red, pink, or tea-colored) Blood in the vomit (looks bright red, or brown like coffee-grounds) Vaginal bleeding (heavier than usual or after menopause) Skin color changes that occur several days after an injury (skin may black, blue, purple, yellowish green)

1. 2. 3. First aid is appropriate for external bleeding. If bleeding is severe, or if shock or internal bleeding is suspected, get emergency help immediately. Calm and reassure the person. The sight of blood can be very frightening. If the wound is superficial, wash it with soap and warm water and pat dry. Superficial wounds or scrapes are injuries that affect the top layers of skin and bleeding from such wounds is often described as "oozing," because it is slow. Lay the person down. This reduces the chances of fainting by increasing blood flow to the brain. When possible, raise up the part of the body that is bleeding. Remove any obvious loose debris or dirt from a wound. If an object such as a knife, stick, or arrow becomes stuck in the body, DO NOT remove it. Doing so may cause more damage and may increase bleeding. Place pads and bandages around the object and tape the object in place. Put pressure directly on an outer wound with a sterile bandage, clean cloth, or even a piece of clothing. If nothing else is available, use your hand. Direct pressure is best for external bleeding, except for an eye injury. Maintain pressure until the bleeding stops. When it has stopped, tightly wrap the wound dressing with adhesive tape or a piece of clean clothing. Place a cold pack over the dressing. Do not peek to see if the bleeding has stopped. If bleeding continues and seeps through the material being held on the wound, do not remove it. Simply place another cloth over the first one. Be sure to seek medical attention. If the bleeding is severe, get medical help and take steps to prevent shock. Keep the injured body part completely still. Lay the person flat, raise the feet about 12 inches, and cover the person with a coat or blanket. DO NOT move the person if there has been a head, neck, back, or leg injury, as doing so may make the injury worse. Get medical help as soon as possible.

4. 5.



8. 9.

1. 2. DO NOT apply a tourniquet to control bleeding, except as a last resort. Doing so may cause more harm than good. A tourniquet should be used only in a life-threatening situation and should be applied by an experienced person If continuous pressure hasn't stopped the bleeding and bleeding is extremely severe, a tourniquet may be used until medical help arrives or bleeding is controllable. It should be applied to the limb between the bleeding site and the heart and tightened so bleeding can be controlled by applying direct pressure over the wound. To make a tourniquet, use bandages 2 to 4 inches wide and wrap them around the limb several times. Tie a half or square knot, leaving loose ends long enough to tie another knot. A stick or a stiff rod should be placed between the two knots. Twist the stick until the bandage is tight enough to stop the bleeding and then secure it in place. Check the tourniquet every 10 to 15 minutes. If the bleeding becomes controllable, (manageable by applying direct pressure), release the tourniquet. DO NOT peek at a wound to see if the bleeding is stopping. The less a wound is disturbed, the more likely it is that you'll be able to control the bleeding DO NOT probe a wound or pull out any embedded object from a wound. This will usually cause more bleeding and harm DO NOT remove a dressing if it becomes soaked with blood. Instead, add a new one on top DO NOT try to clean a large wound. This can cause heavier bleeding DO NOT try to clean a wound after you get the bleeding under control. Get medical help

3. 4. 5. 6. 7.

Treatment entails restoring blood volume through intravenous (IV) administration of saline, dextran, albumin, or plasma. For large blood losses, transfusion of fresh whole blood is the treatment of choice. The anemia itself does not require specific therapy unless it is associated with iron, folate, or cobalamin (B12) deficiency. A normal erythrocyte count is usually evident within four to six weeks, but hemoglobin restoration can take up to eight weeks.