A Wisdom Archive on Anemia

Spherocytosis - Treatment of acute symptoms. Acute symptoms of anemia and hyperbilirubinemia can indicate treatment with blood transfusions or exchanges. Transfusions treat anemia by adding healthy donor blood to the patient's own, providing needed red blood cells. As the transfused blood does not contain elliptocytes, it will not be hemolysed per se, but the overactive spleen may still break down a significant proportion of the transfused blood. Exchanges treat hyperbilirubinemia by replacing some portion of the patient's blood with healthy donor blood, thus re ...

Read more here: » Spherocytosis: Encyclopedia II - Spherocytosis - Treatment

In a peripheral blood smear, the abnormally small red blood cells lacking the central pallor as seen in non-heritary spherocytosis is typically more marked in hereditary spherocytosis. See the article on spherocytosis for details. Other protein deficiencies cause hereditary elliptocytosis, pyropoikilocytosis or stomatocytosis. In longstanding cases and in patients who have taken iron supplementation or received numerous blood transfusions, iron overload may be a significant problem, being a potential cause of cardiomyopathy and liver disease. Measuring iron stores is therefore considered part o ...

Read more here: » Hereditary spherocytosis: Encyclopedia II - Hereditary spherocytosis - Diagnosis

In peripheral blood smears, many of the red blood cells will appear abnormally small and will lack the central pallor--the lighter area in the middle of a RBC as seen under a microscope. The splenic cords are congested with red blood cells to be destroyed and macrophages of the spleen will show signs of actively destroying erythrocytes (erythrophagocytosis). This will result in elevated bilirubin counts. The bone marrow in its role of manufacturing red blood cells will display hyperplasia, the increased activity of replacing RBCs. As a result, immature red blood cell--or ...

Read more here: » Spherocytosis: Encyclopedia II - Spherocytosis - Diagnosis

The spleen's hemolysis results directly in varying degrees of anemia and hyperbilirubinemia, which in turn result in symptoms of fatigue, pallor, and jaundice. Acute cases can threaten hypoxemia through anemia and acute kernicterus through hyperbilirubinemia, particularly in newborns. Chronic symptoms include anemia and splenomegaly, or enlargement of the spleen due to its increased activity. Furthermore, the detritus of the broken-down blood cells--bilirubin--accumulates in the gallbladder, and can cause gallstones or "sludge" ...

Read more here: » Spherocytosis: Encyclopedia II - Spherocytosis - Symptoms

Hereditary spherocytosis is an autosomal dominant trait, most commonly (though not exclusively) found in Northern European and Japanese families, although an estimated 25% of cases are due to spontaneous mutations. A patient has a 50% chance of passing the disorder onto his/her offspring, presuming that his/her partner does not also carry the mutation. Hereditary spherocytosis is caused by a variety of molecular defects in the genes that code for spectrin, ankyrin, protein 4.1, and other erythrocyte membrane proteins. These proteins a ...

Read more here: » Hereditary spherocytosis: Encyclopedia II - Hereditary spherocytosis - Pathophysiology

As in non-heritary spherocytosis, acute symptoms of anemia and hyperbilirubinemia indicate treatment with blood transfusions or exchanges and chronic symptoms of anemia and splenomegaly indicate dietary supplementation of iron and splenectomy, the surgical removal of the spleen. See the article on spherocytosis for details. Experimental gene therapy exists to treat hereditary spherocytosis in lab mice; however, this treatment has not yet been tried on humans and because of the ...

Read more here: » Hereditary spherocytosis: Encyclopedia II - Hereditary spherocytosis - Treatment

Initial symptoms of ALL are quite aspecific, but worsen to the point that medical help is sought: Generalised weakness and fatigue Anemia Frequent or unexplained fever and infections Weight loss and/or loss of appetite Excessive bruising or bleeding from wounds, nosebleeds, petechiae (red pinpoints on the skin) Bone pain, joint pains (caused by the spread of "blast" cells to the surface of the bone or into the joint from the marrow cavity) Breathlessness< ...

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Although the exact cause of gout is not known, it is thought to be linked to defects in purine metabolism. Purine is an organic compound commonly found in the body and is metabolized by the body into uric acid. People with primary gout have either an increased production of uric acid or an impaired excretion of uric acid, or a combination of both. There are also different racial propensities to develop gout. The prevalence of gout is high among the peoples of the Pacific Islands, and the Maori of New Zealand, but paradoxically rare in the Australian aborigine despite the latter's higher mean concentration of se ...

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General information: Glucocorticoid. In pharmacologic (supraphysiologic) doses, glucocorticoids are used to suppress various allergic, inflammatory, and autoimmune disorders. They are also administered as posttransplantory immunosuppressants to prevent the acute transplant rejection and graft-versus-host disease. Nevertheless, they do not prevent an infection and also inhibit later reparative processes. Im ...

Read more here: » Immunosuppressive drug: Encyclopedia II - Immunosuppressive drug - Glucocorticoids

General information: Chemotherapy Cytostatics inhibit cell division. In immunotherapy, they are used in smaller doses than in the treatment of malign diseases. They affect the proliferation of both T cells and B cells. Due to their highest effectiveness, purine analogs are most frequently administered. The alkylating agents used in immunotherapy are nitrogen mustards (cyclophosphamide), nitrosoureas, platinum compounds and others. Cyclophosphamide is probably the most potent immunosuppressive compound. In small d ...

Read more here: » Immunosuppressive drug: Encyclopedia II - Immunosuppressive drug - Cytostatics