RBC Indices and Anemia Classification
The values for MCV, MCHC, and MCH are derived from the hemoglobin (Hgb), hematocrit (Hct) and red blood cell count (RBC) by mathematical calculations:
|
Mean Corpuscular Volume (MCV) = Hct(%)x10/RBC(million/cmm) fL
Mean Corpuscular Hemoglobin Concentration (MCHC) = Hgb(g/dL)/Hct(%) g/dL
Mean Corpuscular Hemoglobin (MCH) = Hgb(g/dL)/RBC(million/cmm) pg
MCV values reflect the size, and MCH and MCHC reflect the amount and concentration of hemoglobin (color), of individual cells. These RBC indices are useful in the differential diagnosis of types of anemia.
Anemias are classified on the basis of cell size (MCV) and cell color (MCHC) and (MCH).
|
MCV less than lower limit of normal : microcytic
MCV within normal range : normocytic
MCV greater than upper limit of normal : macrocytic
MCHC less than lower limit of normal : hypochromic
MCHC within normal range : normochromic
Normocytic, normochromic anemia
Iron deficiency (detected early)
Chronic illness (sepsis, tumor)
Acute blood loss
Aplastic anemia (chloramphenicol toxicosis)
Acquired hemolytic anemias (prosthetic cardiac valve)
Micrositic, hypochromic anemia
Iron Deficiency (detected late)
Thalassemia
Lead poisioning
Micrositic, normochromic anemia
Renal disease (erythropoietin loss)
Macrocytic, normochromic anemia
Vitamin B12 or folic acid deficiency
Hydantoin ingestion
Chemotherapy
Decreased ability of the red blood cells to provide adequate oxygen supplies to body
tissues may be due to decreased number of red blood cells, decreased amount of substance in red blood cells which transports oxygen (hemoglobin), or decreased volume of red blood cells.
Anemia Causes
vitamin B12 deficiency
chronic disease
folate deficiency
drug-induced immune hemolytic anemia
hemolytic anemia
hemolytic anemia due to g6pd deficiency
idiopathic aplastic anemia
idiopathic autoimmune hemolytic anemia
immune hemolytic anemia
iron deficiency anemia
megaloblastic anemia
pernicious anemia
secondary aplastic anemia
sickle cell anemia
Vitamin B12 Deficiency
Vitamin B12 is essential for normal nervous system function and normal red cell, white cell and platelet production. All sources of vitamin B12 come from the diet in animal products,
including dairy and eggs. For vitamin B12 to be absorbed by the body, it must become bound to an intrinsic factor, a protein secreted by cells in the stomach. Causes of vitamin B12
deficiency include dietary (a strict vegetarian diet excluding all meat, fish, dairy products, and eggs); chronic alcoholism; abdominal or intestinal surgery that eliminates the site of intrinsic factor production or absorption; Crohn's disease; intestinal malabsorption disorders; fish tape worm; and pernicious anemia, which is caused by an inherited intrinsic factor deficiency. Risk factors are related to the causes. The incidence is 2 out of 1000 people.
Chronic Disease
Certain chronic infections and diseases cause several changes in the blood production (hematopoetic) system. These include a slightly shortened red blood cell life span,
decreases in the amount of iron that is available in the fluid portions of blood, and
decreases in the activity of the bone marrow. In the presence of these three effects a low to moderate grade anemia develops. The symptoms of the anemia often go unnoticed in the face of the primary disease.
Conditions associated with the anemia of infection and chronic diseases include such diverse diseases as chronic bacterial endocarditis, osteomyelitis, juvenile rheumatoid
arthritis, rheumatic fever, Crohn's disease, and ulcerative colitis. Chronic renal failure
may produce a similar anemia because it causes reduced levels of erythropoietin, the hormone which stimulates the production of red blood cells in the bone marrow.
Folate Deficiency
Folate or folic acid is necessary for red blood cell formation and growth. Dietary sources
of folate are found in green leafy vegetables and liver. Some medications such as Dilantin interfere with the absorption of this vitamin. Because folate is not stored in the body in large amounts, a continual dietary supply of this vitamin is needed.
In folate deficiency anemia, the red cells are abnormally large and are referred to as
megalocytes, and in the bone marrow as megaloblasts. Subsequently, this anemia may be referred to as megaloblastic anemia.
Causes of the anemia are poor dietary intake of folic acid as in chronic alcoholism,
malabsorption diseases such as celiac disease and sprue, and certain medications. A relative deficiency due to increased need for folic acid may occur in the third trimester of pregnancy. Risk factors are a poor diet (seen frequently in the poor, the elderly, and in people who do not buy fresh fruits or vegetables), overcooking food, alcoholism, having
a history of malabsorption diseases, and pregnancy. The incidence is 4 out of 100,000
people.
Drug-induced Immune Hemolytic Anemia
Drug-induced immune hemolytic anemia is an acquired form of hemolytic anemia caused by interaction of certain drugs with the red blood cell membrane, resulting in antibody production against the red blood cells and premature red blood cell destruction.
Drug-induced immune hemolytic anemia occurs when certain drugs interact with the red blood cell membrane, causing the cell to become antigenic (the body identifies the cell as tissue not belonging to the body). Antibodies form against the red blood cells. The antibodies combine with the affected red blood cells and result in their premature destruction. The incidence is rare in children.
Drugs that can cause secondary immune hemolytic anemia are penicillins, cephalosporins, levodopa, methyldopa, mefenamic acid, quinidine, salicylic acid, sulfonamides, Thiazide diuretics, antazoline, chlorpromazine, isoniazid, streptomycin, and Motrin. Drug-induced hemolytic anemia is most often associated with G6PD deficiency.
Hemolytic Anemia
Hemolytic anemia is a condition of inadequate number of circulating red blood cells (anemia), caused by premature destruction of red blood cells. There are a number of specific types of hemolytic anemia which are described individually.
Hemolytic anemia occurs when the bone marrow is unable to compensate for premature
destruction of red blood cells by increasing their production. When the marrow is able to
compensate, anemia does not occur.
There are many types of hemolytic anemia, which are classified by the location of the defect. The defect may be in the red blood cell itself (intrinsic factor) or outside the red blood cell (extrinsic factor).
Causes of hemolytic anemia include infection, certain medications, autoimmune disorders, and inherited disorders. Types of hemolytic anemia include:
aplastic anemia
secondary aplastic anemia
hemoglobin SC disease
hemolytic anemia due to G6PD deficiency
hereditary elliptocytosis
hereditary spherocytosis
hereditary ovalocytosis
idiopathic autoimmune hemolytic anemia
non-immune hemolytic anemia caused by chemical or physical agents
secondary immune hemolytic anemia
sickle thalassemia
The over all incidence of "hemolytic anemia" is 4 out of 100,000 people.
Hemolytic Anemia Due to G6PD Deficiency
G6PD deficiency is a hereditary, sex-linked, enzyme defect that results in the breakdown of red blood cells when the person is exposed to the stress of infection or certain drugs.
G-6-PD deficiency is an inheritable x-linked recessive disorder whose primary effect is
the reduction of G-6-PD in the red blood cell, with resultant hemolysis of the cell. The ultimate effect of the disease is to produce anemia, either acute hemolytic or a chronic
spherocytic type.
In the United States, the incidence of G-6-PD is much higher among the black American population with a heterozygote frequency (carrier state with one normal gene and one abnormal gene) of 24%. Approximately 10 to 14% of the black American male population is affected. The disorder may occasionally affect a few black females to a mild degree (depending on their genetic inheritance). People with the disorder are not normally anemic and display no evidence of the disease until the red cells are exposed to an oxidant or stress.
Drugs that can precipitate this reaction include:
antimalarial agents
sulfonamides (antibiotic)
aspirin
nonsteroidal antiinflammatory drugs (NSAIDs)
nitrofurantoin
quinidine
quinine
others
Also, exposure to certain chemicals such as those in mothballs. The chronic spherocytic anemia is unaffected by exposure to these drugs.
The risk of acute hemolytic crisis can be decreased by reviewing the family history for any evidence of hemolytic anemias or spherocytosis or testing before giving any medications belonging to the above class of chemicals. The episodes are usually brief, because newly produced (young) red cells have normal G6PD activity.
Risk factors are being of the black race, being male, or having a family history of G6PD
deficiency. Another type of this disorder can occur in whites who originated in the
Mediterranean basin. It, too, is associated with acute episodes of hemolysis. Episodes are longer and more severe than the other type of disorders.
Idiopathic Aplastic Anemia
Idiopathic aplastic anemia is a failure of the bone marrow to properly form all types of blood cells.
Idiopathic aplastic anemia is a condition that results from injury to the stem cell, a cell
that gives rise to other cell types when it divides. Consequently, there is a reduction in
all cell types--red blood cells, white blood cells and platelets--with this type of anemia,
which is called pancytopenia. The cause of idiopathic aplastic anemia is unknown, but is thought to be an autoimmune process (when the body reacts against its own cells). Causes of other types of aplastic anemia may be chemotherapy, radiation therapy, toxins, drugs, pregnancy, congenital disorder, or systemic lupus erythematosus.
Symptoms arise as the consequence of bone marrow failure. Anemia (low red blood cell count) leads to fatigue and weakness. Low white blood cell counts, or neutropenia, causes an increased risk of infection. Low platelet counts, or thrombocytopenia, results in bleeding of mucus membranes and skin. The disease may be acute or chronic, and is always progressive. Risk factors are unknown. The incidence is 2 out of 1 million people.
Idiopathic Autoimmune Hemolytic Anemia
Idiopathic autoimmune hemolytic anemia is a disorder resulting from an abnormality of the immune system that destroys red blood cells prematurely. The cause is unknown.
Idiopathic autoimmune hemolytic anemia is an acquired disease that occurs when antibodies form against the person's own red blood cells. In the idiopathic form of this disease, the cause is unknown. There are other types of immune hemolytic anemias where the cause may result from an underlying disease or medication. Idiopathic autoimmune hemolytic anemia accounts for one-half of all immune hemolytic anemias. The onset of the disease may be quite rapid and very serious. Risk factors are not known.
Immune Hemolytic Anemia
Immune Hemolytic Anemia is a disorder of premature destruction of red blood cells that is a result of an abnormality of the immune system.
Immune hemolytic anemia occurs when antibodies form against the body's own blood cells. The antibodies may be acquired by blood transfusion, pregnancy (if the baby's blood type is different from the mother's), as a complication of another disease, or from the blood cells' reaction to medications. If the cause of antibody formation is disease or medication, it is referred to as secondary immune hemolytic anemia. The antibodies will destroy the blood cells because they are recognized as foreign substances within the body. The cause may also be unknown, as in idiopathic autoimmune hemolytic anemia, which accounts for one-half of all immune hemolytic anemias. The onset of the disease may be quite rapid and very serious, or it may remain mild and not require specific therapy. Risk factors are related to the causes. The incidence is 1 out of 1,000 people.
Iron Deficiency Anemia
Iron deficiency anemia is a decrease in the red cells of the blood caused by too little iron. Iron deficiency anemia is the most common form of anemia. Approximately 20% of women, 50% of pregnant women, and 3% of men are iron deficient. Iron is an essential component of hemoglobin, the oxygen carrying pigment in the blood. Iron is normally obtained through the food in the diet and by the recycling of iron from old red blood cells.
The causes of iron deficiency are too little iron in the diet, poor absorption of iron by the body, and loss of blood (including from heavy menstrual bleeding). It is also caused by
lead poisoning in children. Anemia develops slowly after the normal stores of iron have been depleted in the body and in the bone marrow. Women, in general, have smaller stores of iron than men and have increased loss through menstruation, placing them at higher risk for anemia than men. In men and postmenopausal women, anemia is usually due to gastrointestinal blood loss associated with ulcers or the use of aspirin or nonsteroidal anti-inflammatory medications (NSAIDS).
High-risk groups include: women of child-bearing age who have blood loss through menstruation; pregnant or lactating women who have an increased requirement for iron;
infants, children, and adolescents in rapid growth phases; and people with a poor dietary intake of iron through a diet of little or no meat or eggs for several years. Risk factors related to blood loss are peptic ulcer disease, long term aspirin use, colon cancer, uterine cancer, and repeated blood donation. The incidence is 2 out of 1000 people.
Megaloblastic Anemia
Megaloblastic anemia is a blood disorder characterized by red blood cells that are larger than normal, low white blood count, and low platelet count resulting from a deficiency of folic acid or vitamin B-12.
Deficiencies of vitamin B-12 and folic acid are the most common causes of megaloblastic anemia. Other causes are leukemia, myelofibrosis, multiple myeloma, certain hereditary disorders, drugs that affect nucleic acid metabolism such as chemotherapy agents (methotrexate), and other causes. Risk factors relate to the causes. (See pernicious anemia below).
Pernicious Anemia
Pernicious anemia is a form of anemia caused by a lack of intrinsic factor, a substance needed to absorb vitamin B12 from the gastrointestinal tract.
People with pernicious anemia loose their ability to make intrinsic factor, a substance
that enables vitamin B12 to be absorbed from the intestine. Vitamin B12 deficiency results.
This condition may result from hereditary factors. Congenital pernicious anemia is inherited as an autosomal recessive disorder.
Pernicious anemia is also seen in association with some autoimmune endocrine diseases such as type 1 diabetes, hypoparathyroidism, Addison's disease, hypopituitarism, testicular dysfunction, Graves disease, chronic thyroiditis, myasthenia gravis, secondary amenorrhea, vitiligo, and candidiasis. Gradually the deficiency of vitamin B12 affects sensory and motor nerves, causing neurological effects. The anemia also affects the gastrointestinal system and the cardiovascular system.
The disease can affect all racial groups, but the incidence is higher among people of
Scandinavian or Northern European descent. Pernicious anemia usually does not appear before the age of 30, although a juvenile form of the disease can occur in children. Juvenile or congenital pernicious anemia is evident before the child is 3 years old.
Risk factors are a history of autoimmune endocrine disorders, a family history of pernicious anemia, and Scandinavian or Northern European descent. The incidence is 1 out of 1,000 people. (See megaloblastic anemia)
In the infant or young child, pernicious anemia may be secondary to poor absorption of
vitamin B12 caused by some of the following conditions:
defect in absorption
celiac disease (sprue)
methylmalonic aciduria
homocystinuria
tuberculosis treatment with para amino salicylic acid
poor diet in the infant
maternal dietary deficiency while pregnant can cause pernicious
anemia in an infant less than 4 months old
Pernicious Anemia Diagnostic Flow Chart
Secondary Aplastic Anemia
Secondary aplastic anemia is a failure of the blood-cell forming capacity of the bone marrow that affects all blood-cell types.
Secondary aplastic anemia is a condition that is a result of injury to the stem cell, a
cell that gives rise to other blood cell types when it differentiates. Consequently, there
is a reduction in all types of blood cells with this anemia: red blood cells, white blood
cells, and platelets (which is called pancytopenia).
Causes of secondary aplastic anemia include chemotherapy, drug therapy to suppress the immune system, radiation therapy, toxins such as benzene or arsenic, drugs, pregnancy, congenital disorders, infectious hepatitis, and systemic lupus erythematosus. The cause may be unknown, and is then referred to as idiopathic aplastic anemia.
Symptoms arise as a consequence of bone-marrow failure. Anemia (a low red blood cell count) leads to fatigue and weakness. A low white blood cell count (neutropenia) causes an increased risk of infection. A low platelet count (thrombocytopenia) results in bleeding of the mucus membranes, internal organs, and skin. The disease may be acute or chronic and is always progressive. The risk factors are unknown. The incidence is 4 out of 100,000 people.
Sickle Cell Anemia
Sickle cell anemia is an inherited, chronic blood disease in which the red blood cells become crescent shaped and function abnormally.
Sickle cell anemia, which is caused by an abnormal type of hemoglobin (oxygen carrying pigment) called hemoglobin S, is inherited as an autosomal recessive trait. It occurs in people who have inherited hemoglobin S from both parents. If hemoglobin S is inherited from one parent, the offspring will have sickle cell trait and is usually without symptoms.
The disease occurs primarily in people of African Heritage, with 1 out of 400 African-Americans affected. The disease produces a chronic anemia which may become life-threatening when hemolytic crises (the breakdown of red blood cells) or aplastic crises (bone marrow fails to produce blood cells) occur. Repeated crises can lead to damage of the kidneys, lungs, bone, liver, and central nervous system. Acute painful episodes caused by blocked blood vessels and damaged organs may occur and last hours to days affecting the bones of the back, the long bones, and the chest.
The overall incidence is 8 out of 100,000 people. The manifestations of this disease are a result of the fragility and inflexibility of the sickle red blood cells. When exposed to
dehydration, infection, and low oxygen supply, these fragile red blood cells assume a
crescent shape causing red blood cell destruction and thickening of the blood. Sickle cell anemia can affect many other body systems. Symptoms of this disease are most severe during periods called "sickle cell crisis." Although this disease is inherited and present at birth, symptoms usually don't occur until after 4 months of age.
Reference Source: Adam.com Encyclopedia
 |
|
|
|
Search THIS ENTIRE WEB SITE for CLS technical, financial or other data >>>
|
|
 E-mail
Irving |
This page is made
entirely from recycled electrons. Any similarity between this and
any other page may be completely intentional. Not tested on animals.
Void where prohibited. Return to Irving's Home Page
|