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hemolytic anemia

 
Medical Encyclopedia: Hemolytic Anemia

Definition

Red blood cells have a normal life span of approximately 90–120 days, at which time the old cells are destroyed and replaced by the body's natural processes. Hemolytic anemia is a disorder in which the red blood cells are destroyed prematurely. The cells are broken down at a faster rate than the bone marrow can produce new cells. Hemoglobin, the component of red blood cells that carries oxygen, is released when these cells are destroyed.

Description

As a group, anemias (conditions in which the number of red blood cells or the amount of hemoglobin in them is below normal) are the most common blood disorders. Hemolytic anemias, which result from the increased destruction of red blood cells, are less common than anemias caused by excessive blood loss or by decreased hemoglobin or red cell production.

Since a number of factors can increase red blood cell destruction, hemolytic anemias are generally identified by the disorder that brings about the premature destruction. Those disorders are classified as either inherited or acquired. Inherited hemolytic anemias are caused by inborn defects in components of the red blood cells—the cell membrane, the enzymes, or the hemoglobin. Acquired hemolytic anemias are those that result from various other causes. With this type, red cells are produced normally, but are prematurely destroyed because of damage that occurs to them in the circulation.

— Teresa Norris, RN



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Dictionary: hemolytic anemia
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n.
Anemia resulting from the lysis of red blood cells, as in response to certain toxic or infectious agents and in certain inherited blood disorders.


Oncology Encyclopedia: Hemolytic Anemia
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Key Terms: Erythrocytes, Erythropoietin, Hemolysis, Spherocytosis, Stem cells.

Description

Red blood cells (erythrocytes) transport oxygen and carbon dioxide in the bloodstream, maintain a normal acid-base balance, and determine how thick or thin the blood is. Hemolytic anemia refers to the premature, increased destruction of erythrocytes. Hemolysis is the rupture of these erythrocytes with the release of hemoglobin into the plasma, and anemia is a reduced delivery of oxygen to the tissues. Some of the symptoms of hemolytic anemia include nosebleeds, bleeding gums, shortness of breath, fatigue, rapid heartbeat, pale skin color or yellow skin color (jaundice), chills, and dark-colored urine.

Causes

Erythrocyte (red blood cell) formation takes place in the red bone marrow in an adult and in the liver, spleen, and bone marrow of the fetus. Their formation requires an adequate supply of iron, cobalt, copper, amino acids, and certain vitamins. When the bone marrow loses its ability to compensate for the destruction of the erythrocytes by increasing their production, hemolytic anemia occurs. There are many types of hemolytic anemia, which are classified according to the location of this inability to produce red blood cells. If the problem lies within the red blood cell itself, it is referred to as an intrinsic factor, and if the problem is outside the red blood cell, it is referred to as an extrinsic factor. The overall incidence of hemolytic anemia is approximately 4 per 100,000 people.

Rh factor incompatibility refers to genetically determined substances capable of producing an immune response (antigens). This can cause hemolytic anemia not only during pregnancy when the mother is Rh negative and the fetus is Rh positive, but in mismatched blood transfusions as well. There are a number of industrial poisons that produce hemolytic anemia. These include:

  • antimalarial agents
  • organic solvents (benzene)
  • certain chemotherapies
  • hypersensitivity to certain antibiotics
  • metals (chromium, platinum salts, nickel, lead, copper)
  • Pyridium
  • arsenic
  • intravenous (IV) water (an IV that is not normal or half-normal saline)
  • snake bites (if the venom contains hemolytic toxins) These are all factors external to the red blood cell and thus are extrinsic in nature.

One important extrinsic factor in the cause of hemolytic anemia is in the course of widespread cancer, leukemia, Hodgkin's disease, acute alcoholism and liver disease. Many of the chemotherapy agents (cisplatin, carboplatin and nonplatinum drugs) utilized in treating various cancers have side effects that cause a suppression of bone marrow activity, which results in severe hemolytic anemia. In essence, an individual is not only anemic as a result of cancer, but this anemia is worsened by the treatment. Since nausea, vomiting, and lack of appetite are also side effects of chemotherapy, it is extremely difficult for the patient to overcome this anemia with diet and supplements. Eventually, severe hemolytic anemia is the end result.

Intrinsic factors would include disorders in the immune response and genetically inherited disorders such as glucose-6-phosphate dehydrogenase deficiency, an essential enzyme. People with this disorder do not display any symptoms until exposed to certain medications or stress. Aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) can precipitate this reaction. This disorder is more common among African-American males, with approximately 10% to 14% of the population being affected. Other genetic disorders include sickle cell anemia, thalassemia, and spherocytosis. All of these produce structurally abnormal red blood cells to varying degrees.

Treatments

The treatment depends upon the cause and severity of the anemia. Medicines like folic acid and corticosteroids may be used to treat the anemia if it is not severe. Severe hemolytic anemia may be very quickly fatal and immediate hospitalization is required for transfusion of washed and packed red blood cells. Severe anemias can aggravate pre-existing heart disease, lung disease and cerebrovascular disease.

Frequently with cancer treatments, a patient may undergo numerous blood transfusions to accomodate for the severe anemia suffered as a result of chemotherapy. Researchers, investigating ways to enhance the quality of life for chemotherapy patients, have primarily looked at controlling pain and loss of appetite (anorexia). Recent studies, however, have examined the use of erythropoietin (a protein hormone that stimulates red blood cell production) in improving fatigue symptoms and enhancing overall quality of life. Once-weekly therapy with erythropoietin was found to increase hemoglobin levels, decrease transfusion requirements, and improve quality of life in patients with cancer and anemia undergoing chemotherapy.

Alternative and Complementary Therapies

Since there is no known prevention for hemolytic anemia, there is relatively little that can be done except to be aware of the risk factors and know the potential for genetic disorders within the family. Avoiding exposure to chemicals that precipitate the reaction, eating natural, whole grain foods, avoiding stress, and taking vitamin supplements can be helpful. With cancer patients, yoga and meditation provide a means of enhancing relaxation, reducing stress, and incorporating visualization for healing. Those patients who attend and participate in support groups have an increased quality of life with better outcomes from treatments.

Resources

Books

Jarvis, Carolyn. Physical Examination and Health Assessment. Philadelphia: W.B. Saunders Company, 2000.

Periodicals

Gabrilove, J.L., C.S. Cleeland, R.B. Livingston, et al. "Once-Weekly Dosing of Epoetin Alfa in Chemotherapy Patients." Journal of Clinical Oncology 19 (2001): 2875–82.

Mantovani, L., G. Lentini, B. Hentschel, et al. "Treatment of Anaemia in Myelodysplastic Syndromes." British Journal of Haematology 109 (2000): 367–75.

Osoba, D. "Health-Related Quality-of-Life Assessment in Clinical Trials." Support Care Cancer 8 (2000): 84–8.

Parsons, S.K. "Hematopoietic Growth Factors for Children With Cancer." Current Opinions in Pediatrics 12 (2000): 10–7.

—Linda K. Bennington, C.N.S., M.S.N.

Dental Dictionary: hemolytic anemia
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n

An anemia characterized by an increased rate of destruction of red blood cells, reticulocytosis, hyperbilirubinemia, and/or increased urinary and fecal urobilinogen, and, generally, splenic enlargement. Hereditary hemolytic anemias include congenital hemolytic jaundice, sickle cell anemia, oval cell anemia, and thalassemia. Acquired hemolytic anemias include paroxysmal nocturnal hemoglobinuria and those caused by immune mechanisms (erythroblastosis fetalis), transfusions of incompatible blood, infections, drugs, and poisons. Autoimmune hemolytic anemias are acquired hemolytic anemias associated with antibody-like substances that may not be true autoantibodies or even antibodies; they may be primary (idio-pathic), or they may be secondary to lymphoma, lymphatic leukemia, disseminated lupus erythematosus, or sensitization to drugs and pollens.

Wikipedia: Hemolytic anemia
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Hemolytic anemia
Classification and external resources
ICD-10 D55.-D59.
ICD-9 282, 283, 773
DiseasesDB 5534
MedlinePlus 000571
eMedicine med/979
MeSH [1]

Hemolytic anemia is anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs) either in the blood vessels (intravascular hemolysis) or elsewhere in the body (extravascular). It has numerous possible causes, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either acquired or inherited. Treatment depends on the cause and nature of the breakdown.

In a healthy person, a red blood cell survives 90 to 120 days in the circulation, so about 1% of human red blood cells break down each day. The spleen (part of the reticulo-endothelial system) is the main organ which removes old and damaged RBCs from the circulation. In healthy individuals, the breakdown and removal of RBCs from the circulation is matched by the production of new RBCs in the bone marrow.

In conditions where the rate of RBC breakdown is increased, the body initially compensates by producing more RBCs; however, breakdown of RBCs can exceed the rate that the body can make RBCs, and so anemia can develop. Bilirubin, a breakdown product of hemoglobin, can accumulate in the blood causing jaundice, and be excreted in the urine causing the urine to become a dark brown colour.

Contents

Symptoms

Signs of anemia (fatigue and, later, heart failure) are generally present. Jaundice may be present. Certain aspects of the medical history can suggest a cause for hemolysis, such as drugs, fava bean or other sensitivity, prosthetic heart valve, or another medical illness.

Tests

Clinical findings in hemolytic anaemias:

  • increased serum bilirubin levels in blood, therefore jaundice
  • pallor in mucous membrane and skin
  • increased urobilinogen in urine
  • Splenomegaly
  • Pigmented gallstones may be found.

Classification of hemolytic anemias

Causes of hemolytic anemia can be either genetic or acquired.

Genetic

Genetic causes can involve the RBC membrane, metabolism, or hemoglobin conditions.

Acquired

Acquired hemolytic anemia can be divided into immune and non-immune mediated.

Differential diagnosis

Therapy

Definitive therapy depends on the cause.

  • Symptomatic treatment can be given by blood transfusion, if there is marked anemia.
  • In severe immune-related hemolytic anemia, steroid therapy is sometimes necessary.
  • Sometimes splenectomy can be helpful where extravascular hemolysis is predominant (ie most of the red blood cells are being removed by the spleen).

 
 

 

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Dictionary. The American Heritage® Dictionary of the English Language, Fourth Edition Copyright © 2007, 2000 by Houghton Mifflin Company. Updated in 2009. Published by Houghton Mifflin Company. All rights reserved.  Read more
Oncology Encyclopedia. Gale Encyclopedia of Cancer. Copyright © 2006 by The Gale Group, Inc. All rights reserved.  Read more
Dental Dictionary. Mosby's Dental Dictionary. Copyright © 2004 by Elsevier, Inc. All rights reserved.  Read more
Wikipedia. This article is licensed under the Creative Commons Attribution/Share-Alike License. It uses material from the Wikipedia article "Hemolytic anemia" Read more