Anemia megaloblástica en

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Megaloblastic anemia and Other lacking anemias.

Transcript of Anemia megaloblástica en

Megaloblastic anemiaand

Other lacking anemias.

Megaloblastic Anemia.

• Megaloblastic anemias are caused by a modification in the DNA synthesis, which makes cells bigger. The main megaloblastic anemias due to a lack of vitamin B12 and/or folic acid.

Anemia secondary to the lack of vitamin B12

• The lack of vitamin B12 usually produces anaemia, making important neurological changes.

• The massive use of HCl inhibitors, is one of the most frequently causes, becausedon’t allow the division of vitamin B12 from the food, making hard its absorption.

Diagnosis of the lack of vitamin B12

• There is a lack of vitamin B12, when its blood levels are under 200pg/mL.

• The main causes of a lack of vitamin B12:

• Bad digestion of the food.• Iron deficiency anaemia or Biermer disease• Inadequate diets• Malabsorption of colbalamine.• Enzymatic alterations of the colbalamine metabolism

Clinical manifestations of the deficit of vitamin B12

It’s linked to:• Haematological problems like pancytopenia,

hemolisys or megaloblastic anemia.• Neurological problems like: paresthesias, peripherial

neuropathies .• Digestive problems like: diarrhoeas, malabsorption,

mocucutaneus ulcers.• Psychiatric problems like: irritability, dementia,

depression, psychosis.• Cardiovascular problems: pulmonary embolism.

Causes of deficit of vitamin B12

• Maladigestion of the food.• Iron deficency anemia or Biermer disease..• Insufficient diet.

• The classical treatment is the administration of

vitamin B12 by intramuscular

via

Treatment of the deficit Of vitamina B12

Anemia secondary to the deficit of folic acid.

• The most important sources are fruits, vegetables, cereals, and lacteal products.

Clinical manifestations of the deficit of folic acid.

• The deficit of folic acid cause changes in the cells which divide.

• In pregnant women, the fetus demands a lot of folic acid, in the first trimester due to it’s essencial to the normal development of their CNS.

Causes of the folic acid deficiency.

• Insufficient supply.• Increase of the demands.• Malabsorption of folic acid.• Drugs, medicines.

Diagnostic of the secondary anemia to the deficiency of folic acid

• Folic acid blood levels under a 4ng/mL.

• The treatment of the folic acid deficiency is its reposition by oral via. The usual dose is 1mg/day.

Treatment of the folic acid deficiency

Other deficient anemias

• The majority of this cases aren’t isolate deficiencies and the patients show some vitamin deficiencies combined. Some of the patients are malnutritied, alcoholics or patients with special restrictive diets like vegetarians or other dangerous diets such as macrobiotic diet.

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• Vitamin A deficiency: usually seen in underdeveloped countries and in malnourished children. Those children have visual problems which turns into blindness. They treatment is having vitaminA.

• Vitamins B deficiency. Deficiency of vitamin B1 is Beriberi, it is seen in alcoholic people and it causes diseases in the nervous system.

Otras anemias carenciales.• Déficit de vitamina C. es el escorbuto, caracterizado por la

presencia de hemorragias cutáneas, encías inflamadas y fácilmente

sangrantes y otras hemorragias internas en articulaciones, peritoneo o pericardio. La anemia que presentan estos pacientes, suele deberse a un déficit de concomitante de ácido fólico o de hierro. Para corregir esta anemia, reciben concomitante fólico y hierro.

Other deficient anemias.

• Vitamin E deficiency. Vitamin E is a liposoluble vitamin that works as antioxidant . This disease is only associated to just born babies with an important malabsorption of fats. It has a haemolytic anemia associated to trombocytosis and oedema in the back of the feet and it is sorted aout giving vitamin E.

• Cooper deficiency. Is an anemia microcytic hipocromic, and it only appears in malnourished patients who have parenteral nutrition

Bibliographic

Bilbao Garay. Anemias Carenciales II: anemia

megaoloblástica y otras anemias carenciales.

Información terapéutica. 2006;30 (3):67-75

Ana Fernández Mata

Eva Fraile Jorge