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Anaemia

2007 Schools Wikipedia Selection. Related subjects: Health and medicine

   CAPTION: Anaemia
   Classifications and external resources

     ICD- 10   D50-D64
     ICD- 9    280- 285
   DiseasesDB  663
   MedlinePlus 000560
    eMedicine  med/132  emerg/808 emerg/734

   Anaemia (AmE) or anaemia (BrE), from the Greek (Ἀναιμία) meaning
   "without blood", refers to a deficiency of red blood cells (RBCs)
   and/or hemoglobin. This results in a reduced ability of blood to
   transfer oxygen to the tissues, causing hypoxia; since all human cells
   depend on oxygen for survival, varying degrees of anaemia can have a
   wide range of clinical consequences. Hemoglobin (the oxygen-carrying
   protein in the red blood cells) has to be present to ensure adequate
   oxygenation of all body tissues and organs.

   The three main classes of anaemia include excessive blood loss (acutely
   such as a hemorrhage or chronically through low-volume loss), excessive
   blood cell destruction ( hemolysis) or deficient red blood cell
   production (ineffective hematopoiesis). In menstruating women, dietary
   iron deficiency is a common cause of deficient red blood cell
   production.

   Anemia is the most common disorder of the blood. There are several
   kinds of anemia, produced by a variety of underlying causes. Anaemia
   can be classified in a variety of ways, based on the morphology of
   RBCs, underlying etiologic mechanisms, and discernible clinical
   spectra, to mention a few.

   Different clinicians approach anemia in different ways; two major
   approaches of classifying anaemias include the "kinetic" approach which
   involves evaluating production, destruction and loss , and the
   "morphologic" approach which groups anaemia by red blood cell size. The
   morphologic approach uses a quickly available and cheap lab test as its
   starting point (the MCV). On the other hand, focusing early on the
   question of production (e.g., via the reticulocyte count) may allow the
   clinician more rapidly to expose cases where multiple causes of anemia
   coexist. Regardless of one's philosophy about the classification of
   anaemia, however, any methodical clinical evaluation should yield
   equally good results.

Signs and symptoms

   Anemia goes undetected in many people, and symptoms can be vague. Most
   commonly, people with anemia report a feeling of weakness or fatigue,
   general malaise and sometimes a poor concentration. People with more
   severe anaemia sometimes report shortness of breath. Very severe
   anaemia prompts the body to compensate by increasing cardiac output,
   leading to palpitations and sweatiness, and to heart failure.

   Pallor (pale skin, mucosal linings and nail beds) is often a useful
   diagnostic sign in moderate or severe anaemia, but it is not always
   apparent.

Diagnosis

   The only way to diagnose most cases of anaemia is with a blood test.
   Generally, clinicians order a full blood count. Apart from reporting
   the number of red blood cells and the hemoglobin level, the automatic
   counters also measure the size of the red blood cells by flow
   cytometry, which is an important tool in distinguishing between the
   causes of anaemia. A visual examination of a blood smear can also be
   helpful, and is sometimes a necessity in regions of the world where
   automated analysis is less accessible.

   In modern counters, four parameters (RBC Count, hemoglobin
   concentration, MCV and RDW) are measured, allowing others (hematocrit,
   MCH and MCHC) to be calculated, and compared to values adjusted for age
   and sex. For males, the hemoglobin level that is suggestive of anaemia
   is usually less than 13.0 g/dl, and for females, it is less than 12.0
   g/dl.

   Depending on the clinical philosophy, whether the hospital's automated
   counter can immediately add it to the initial tests, and the
   clinicians' attitudes towards ordering tests, a reticulocyte count may
   be ordered either as part of the initial workup or during followup
   tests. This is a nearly direct measure of the bone marrow's capacity to
   produce new red blood cells, and is thus the most used method of
   evaluating the problem of production. This can be especially important
   in cases where both loss and a production problem may co-exist. Many
   physicians use the reticulocyte production index – a calculation of the
   ratio between the level of anaemia and the extent to which the
   reticulocyte count has risen in response. Even in cases where an
   obvious source of loss exists, this helps evaluate whether the bone
   marrow will be able to compensate for the loss, and at what rate.

   When the cause is not obvious, clinicians use other tests to further
   distinguish the cause for anaemia. These are discussed with the
   differential diagnosis, below. A clinician may also decide to order
   other screening blood tests that might identify the cause of fatigue;
   serum glucose, ESR, ferritin, serum iron, RBC folate level, serum
   vitamin B12, renal function tests (e.g. serum creatinine) and
   electrolytes may be part of such a workup.

Classification

Production vs. destruction or loss

   The "kinetic" approach to anemia yields what many argue is the most
   clinically relevant classification of anaemia. This classification
   depends on evaluation of several hematological parameters, particularly
   the blood reticulocyte (precursor of mature RBCs) count. This then
   yields the classification of defects by decreased RBC production versus
   increased RBC destruction and/or loss. Clinical signs of loss or
   destruction include abnormal peripheral blood smear with signs of
   hemolysis; elevated LDH suggesting cell destruction; or clinical signs
   of bleeding, such as guiaic-positive stool, radiographic findings, or
   frank bleeding.

   Here is a simplified schematic of this approach:








   Anaemia







































   Reticulocyte production index shows inadequate production response to
   anaemia.



   Reticulocyte production index shows appropriate response to anaemia =
   ongoing hemolysis or blood loss without RBC production problem.


































   No clinical findings consistent with hemolysis or blood loss: pure
   disorder of production.

   Clinical findings and abnormal MCV: hemolysis or loss and chronic
   disorder of production*.

   Clinical findings and normal MCV= acute hemolysis or loss without
   adequate time for bone marrow production to compensate**.


































                        Macrocytic anaemia (MCV>100)

   Normocytic anaemia (80<MCV<100)


   Microcytic anaemia (MCV<80)




   * For instance, sickle cell anemia with superimposed iron deficiency;
   chronic gastric bleeding with B12 and folate deficiency; and other
   instances of anaemia with more than one cause. ** Confirm by repeating
   reticulocyte count: ongoing combination of low reticulocyte production
   index, normal MCV and hemolysis or loss may be seen in bone marrow
   failure or anaemia of chronic disease, with superimposed or related
   hemolysis or blood loss.

Red blood cell size

   In the morphological approach, anaemia is classified by the size of red
   blood cells; this is either done automatically or on microscopic
   examination of a peripheral blood smear. The size is reflected in the
   mean corpuscular volume (MCV). If the cells are smaller than normal
   (under 80 fl), the anaemia is said to be microcytic; if they are normal
   size (80-100 fl), normocytic; and if they are larger than normal (over
   100 fl), the anaemia is classified as macrocytic. This scheme quickly
   exposes some of the most common causes of anemia; for instance, a
   microcytic anaemia is often the result of iron deficiency. In clinical
   workup, the MCV will be one of the first pieces of information
   available; so even among clinicians who consider the "kinetic" approach
   more useful philosophically, morphology will remain an important
   element of classification and diagnosis.

   Here is a schematic representation of how to consider anaemia with MCV
   as the starting point:











   Anaemia























































   Macrocytic anaemia (MCV>100)





   Normocytic anaemia (80<MCV<100)





   Microcytic anaemia (MCV<80)










































   High reticulocyte count





   Low reticulocyte count




   Other characteristics visible on the peripheral smear may provide
   valuable clues about a more specific diagnosis; for example, abnormal
   white blood cells may point to a cause in the bone marrow.

Microcytic anaemia

     * Iron deficiency anaemia is the most common type of anemia overall,
       and it is often hypochromic microcytic. Iron deficiency anaemia is
       caused when the dietary intake or absorption of iron is
       insufficient. Iron is an essential part of hemoglobin, and low iron
       levels result in decreased incorporation of hemoglobin into red
       blood cells. In the United States, 20% of all women of childbearing
       age have iron deficiency anemia, compared with only 2% of adult
       men. The principal cause of iron deficiency anaemia in
       premenopausal women is blood lost during menses. Studies have shown
       that iron deficiency without anaemia causes poor school performance
       and lower IQ in teenage girls.

   In older patients, iron deficiency anaemia is often due to bleeding
   lesions of the gastrointestinal tract; fecal occult blood testing,
   upper endoscopy and lower endoscopy are often performed to identify
   bleeding lesions, which can be malignant. Iron deficiency is the most
   prevalent deficiency state on a worldwide basis. Iron deficiency
   affects women from different cultures and ethnicities. Iron found in
   animal meats are more easily absorbed by the body than iron found in
   non-meat sources. In countries where meat consumption is not as common,
   iron deficiency anaemia is six to eight times more prevalent than in
   North America and Europe. This is due to the importance of meat in the
   diets of North Americans and Europeans. Iron deficiency is sometimes
   the cause of abnormal fissuring of the angular (corner) sections of the
   lips ( angular cheilitis).
     * Hemoglobinopathies -- much rarer (apart from communities where
       these conditions are prevalent)
          + Sickle-cell disease
          + Thalassemia

   Microcytic anaemia is primarily a result of hemoglobin synthesis
   failure/insufficiency, which could be caused by several etiologies:
     * Heme synthesis defect
          + Iron deficiency
          + Anaemia of Chronic Disorders (which, sometimes, is grouped
            into normocytic anaemia)
     * Globin synthesis defect
          + alpha-, and beta-thalassemia
          + HbE syndrome
          + HbC syndrome
          + and various other unstable hemoglobin diseases
     * Sideroblastic defect
          + Hereditary Sideroblastic anaemia
          + Acquired Sideroblastic anaemia including lead toxicity
          + Reversible Sideroblastic anaemia

   A mnemonic commonly used to remember causes of microcytic anaemia is
   TAILS: T - Thalassemia, A - Anaemia of chronic disease, I - Iron
   deficiency anaemia, L - Lead toxicity associated anaemia, S -
   Sideroblastic anaemia.

Normocytic anaemia

   Normocytic anaemia is when the overal Hb levels are decreased, but the
   red blood cell size ( MCV) remains normal. Causes include:
     * Acute blood loss
     * Anaemia of chronic disease
     * Aplastic anaemia (bone marrow failure)

Macrocytic anaemia

     * Megaloblastic anaemia due to a deficiency of either vitamin B12 or
       folic acid (or both) due either to inadequate intake or
       insufficient absorption. Folate deficiency normally does not
       produce neurological symptoms, while B12 deficiency does.
       Megaloblastic anemia is the most common cause of macrocytic
       anaemia.
     * Pernicious anaemia is an autoimmune condition directed against the
       parietal cells of the stomach. Parietal cells produce intrinsic
       factor, required to absorb vitamin B12 from food. Therefore, the
       destruction of the parietal cells causes a lack of intrinsic
       factor, leading to poor absorption of vitamin B12.
     * Alcoholism
     * Methotrexate, zidovudine, and other drugs that inhibit DNA
       replication. This is the most common etiology in nonalcoholic
       patients.

   Macrocytic anemia can be further divided into "megaloblastic anemia" or
   "non-megaloblastic macrocytic anemia". The cause of megaloblastic
   anemia is primarily a failure of DNA synthesis with preserved RNA
   synthesis, which result in restricted cell division of the progenitor
   cells. The megaloblastic anemias often present with neutrophil
   hypersegmentation (6-10 lobes). The non-megaloblastic macrocytic
   anaemias have different etiologies (i.e. there is unimpaired DNA
   synthesis,) which occur, for example in alcoholism.

   The treatment for vitamin B12-deficient macrocytic and pernicious
   anaemias was first devised by William Murphy who bled dogs to make them
   anaemia and then fed them various substances to see what (if anything)
   would make them healthy again. He discovered that ingesting large
   amounts of liver seemed to cure the disease. George Minot and George
   Whipple then set about to chemically isolate the curative substance and
   ultimately were able to isolate the vitamin B12 from the liver. For
   this, all three shared the 1934 Nobel Prize in Medicine. Symptoms of
   vitamin B12 deficiency include having a smooth, red tongue.

Dimorphic anaemia

   Here there are two types of anaemia simultaneously, e.g., macrocytic
   hypochromic, due to hookworm infestation leading to deficiency of both
   iron and vitamin B12 or folic acid or following a blood transfusion.
   One hint that this kind of anaemia may exist is a wide RBC distribution
   width (RDW), which suggests a wider-than-normal range of sizes of red
   blood cells.

Specific anaemias

     * Fanconi anaemia is an hereditary disorder or defect featuring
       aplastic anaemia and various other abnormalities
     * Hemolytic anaemia causes a separate constellation of symptoms (also
       featuring jaundice and elevated LDH levels) with numerous potential
       causes. It can be autoimmune, immune, hereditary or mechanical
       (e.g. heart surgery). It can result (because of cell fragmentation)
       in a microcytic anemia, a normochromic anemia, or (because of
       premature release of immature red blood cells from the bone
       marrow), a macrocytic anaemia.
     * Hereditary spherocytosis is a hereditary defect that results in
       defects in the RBC cell membrane, causing the erythrocytes to be
       sequestered and destroyed by the spleen. This leads to a decrease
       in the number of circulating RBCs and, hence, anaemia.
     * Sickle-cell anaemia, a hereditary disorder, is due to the presence
       of the mutant hemoglobin S gene.
     * Warm autoimmune hemolytic anaemia is an anaemia caused by
       autoimmune attack against red blood cells, primarily by IgG
     * Cold Agglutinin hemolytic anaemia is primarily mediated by IgM

Possible complications

   Anaemia diminishes the capability of individuals who are affected to
   perform physical labor. This is a result of one's muscles being forced
   to depend on anaerobic metabolism. The lack of iron associated with
   anaemia can cause many complications, including hypoxemia, brittle or
   rigid fingernails, cold intolerance, impaired immune function, and
   possible behavioural disturbances in children.

   Hypoxemia resulting from anemia can worsen the cardio-pulmonary status
   of patients with pre-existing chronic pulmonary disease. Brittle or
   rigid fingernails may be a result of abnormal thinness of nails due to
   insufficient iron supply. Cold intolerance occurs in one in five
   patients with iron deficiency anaemia, and becomes visible through
   numbness and tingling. Impaired immune functioning leading to increased
   likelihood of sickness is another possible complication.

   Doctors attempt to avoid blood transfusion in general, but there are
   several instances where doctors are now more aggressive than in the
   past. For instance, the currently accepted Rivers protocol for early
   goal directed therapy for sepsis requires keeping the hematocrit above
   30; this is based on evidence that even moderate anaemia reduces
   survival . The presumed physiological principle is that the reduction
   in oxygen delivery associated with anaemia is especially dangerous to
   people who are already at risk for organ damage from lack of perfusion.
   There is controversy about what hematocrit or hemoglobin levels should
   be used as "triggers" for transfusion in other settings. Anaemia also
   may be especially risky for people with acute coronary syndromes, again
   because anaemia hampers already-impaired oxygen delivery to the heart.
   However, the point at which this danger emerges in other settings is
   controversial and awaits further study.

   Finally, chronic anemia may result in behavioral disturbances in
   children as a direct result of impaired neurological development in
   infants, and reduced scholastic performance in children of school age.
   Behavioural disturbances may even surface as an attention deficit
   disorder.

Anaemia during pregnancy

   Anaemia affects 20% of all females of childbearing age in the United
   States. Because of the subtlety of the symptoms, women are often
   unaware that they have this disorder, as they attribute the symptoms to
   the stresses of their daily lives. Possible problems for the fetus
   include increased risk of growth retardation, prematurity, intrauterine
   death, rupture of the amnion and infection.

   During pregnancy, women should be especially aware of the symptoms of
   anaemia, as an adult female loses an average of two milligrams of iron
   daily. Therefore, she must intake a similar quantity of iron in order
   to make up for this loss. Additionally, a woman loses approximately 500
   milligrams of iron with each pregnancy, compared to a loss of 4-100
   milligrams of iron with each period. Possible consequences for the
   mother include cardiovascular symptoms, reduced physical and mental
   performance, reduced immune function, tiredness, reduced peripartal
   blood reserves and increased need for blood transfusion in the
   postpartum period.

Diet and anaemia

   Consumption of food rich in iron is essential to prevention of iron
   deficiency anemia; however, the average adult has approximately nine
   years worth of B12 stored in the liver, and it would take four to five
   years of an iron-deficient diet to create iron-deficiency anaemia from
   diet alone.

   Iron-rich foods include red meat; green, leafy vegetables; dried beans;
   dried apricots, prunes, raisins, and other dried fruits; almonds;
   seaweeds; parsley; whole grains; and yams. In extreme cases of anaemia,
   researchers recommend consumption of beef liver, lean meat, oysters,
   lamb or chicken, or iron drops/tablets may be introduced. Certain foods
   have been found to interfere with iron absorption in the
   gastrointestinal tract, and these foods should be avoided. They include
   tea, coffee, wheat bran, rhubarb, chocolate, soft drinks, red wine, ice
   cream, and candy bars (Bauer, 2). With the exception of milk and eggs,
   animal sources of iron provide iron with better bioavailability than
   vegetable sources (Scrimshaw).

Treatments for anaemia

   There are many different treatments for anemia, including increasing
   dietary intake of readily available iron and iron supplementation; the
   treatment is determined by the type of anaemia that is diagnosed.

   If an increase in dietary intake is prescribed, then additionally
   increasing one's intake of Vitamin C may aid in the body's ability to
   absorb iron.

   In anemia of chronic disease, anemia associated with chemotherapy, or
   anaemia associated with renal disease, some clinicians prescribe a
   recombinant protein version of erythropoietin, epoetin alfa, to
   stimulate red blood cell production.

   In severe cases of anaemia, a blood transfusion may be necessary.
   Retrieved from " http://en.wikipedia.org/wiki/Anaemia"
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