Anemia PDF

L1 Dr. Alaa AL- Sheek Mashhad Anemia Anemia is defined as a below-normal plasma hemoglobin concentration. It can be caused by: 1-Nutritional anemias are caused by dietary deficiencies ofsubstances such as iron, folic...

L1 Dr. Alaa AL- Sheek Mashhad Anemia Anemia is defined as a below-normal plasma hemoglobin concentration. It can be caused by: 1-Nutritional anemias are caused by dietary deficiencies ofsubstances such as iron, folic acid, and vitamin B12. 2-Chronic blood loss, bone marrow abnormalities,increased hemolysis. 3-Infections, malignancy. 4-Chronic diseases: Endocrine deficiencies, renal failure. 5-Drugs cause toxic effects on blood cells, hemoglobin production, or erythropoietic organs. 1  Iron deficiency anemia Iron deficiency is the most common cause of chronic anemia Iron forms the nucleus of the iron-porphyrin heme ring, which is together with globin chains forms hemoglobin. Normally, only a small amount of iron is lost from the body each day, so dietary requirements are small. 2  Iron deficiency results from: Hypochromic microcytic anemia will occur (due to low iron and small-sized red blood cells). Oral Iron Therapy: Oral iron correct the anemia just as rapidly and completely as parenteral iron Because ferrous iron is most efficiently absorbed, only ferrous salts should be used orally. Daily, we need 50-100 mg of iron. About 25% of oral iron given as can be absorbed, so, 200–400 mg of elemental iron should begiven daily to correct iron deficiency most rapidly. Treatment with oral iron should be continued for 3–6 months tocorrect the anemia and replenishes iron stores. 3 Ferrous sulphate hydrated Ferrous sulphate desiccated Ferrous gluconate Ferrous fumarate 4  Iron polymaltose complex Side effects: nausea, epigastric discomfort, black stools, abdominal cramps, constipation or diarrhea. Parenteral Iron Therapy: Parenteral therapy should be reserved for patients who are unable to tolerate or absorb oral iron and for patients with extensive chronic anemia who cannot be maintained with oral iron alone. The three available forms of parenteral iron are iron dextran, sodium ferric gluconate complex, and iron sucrose. 5  Iron dextran It is a stable complex of ferric oxy-hydroxide and dextranpolymers containing 50 mg of elemental iron per milliliter of solution. It can be given by deep intramuscular injection or byintravenous infusion. Intravenous administration eliminates the local pain and tissue staining that often occur with the intramuscular route Adverse effects: include headache, light-headedness, fever,arthralgia, nausea and vomiting, back pain, flushing, urticaria, bronchospasm, and, rarely, anaphylaxis and death. 6  Sodium ferric gluconate complex and iron-sucrose complex They are alternative parenteral iron preparations. These agents canbe given only by the intravenous route. They appear to be less likely to cause hypersensitivity reactions. The amount of iron needed by an individual patient is calculated by the following formula: Acute Iron Toxicity Acute iron toxicity is seen almost exclusively in young children as few as 10 tablets of any of oral iron preparations can be lethal in young children. 7  Stages of Iron Toxicity Stage Clinical effect Time 1 GIT Irritation 30 min - 6h 2 Recovery from GIT symptoms 6h - 24h 3 *Shock 6h - 72h *Metabolic acidosis *Dehydration *Lactic acidosis 4 *Hepatotoxicity & hepatic necrosis 12h – 96h *Fulminant hepatic failure 5 *Bowel obstruction 2wks – 8 wks *GIT mucosa healing leads to scaring Whole bowel irrigation to flush out unabsorbed pills. Supportive therapy for gastrointestinal bleeding, metabolic acidosis,and shock must also be provided. Hemodialysis is not effective because iron has large volume of distribution. Exchange transfusion is recommended for severely symptomatic patients with iron serum level more than 1mg/dl Deferoxamine, a potent iron-chelating compound, can be given systemically to bind iron that has already been absorbed and to promote its excretion in urine and feces. 8 Chronic iron toxicity (iron overload): It is known as hemochromatosis. Treatment is by intermittent phlebotomy. The oral iron chelator deferasirox is approved for treatment of iron overload. Folic acid (folate) deficiency anemia Folate deficiency leads to megaloblastic anemia and it may becaused by: 1-Increased demand (for example, pregnancy and lactation) 2-Poor absorption caused by pathology of the small intestine. 3-Alcoholism. 4-Treatment with drugs that are dihydrofolate reductase inhibitors(for example, methotrexate, pyrimethamine, and trimethoprim) 9 Folate is excreted in the urine and stool and destroyed by catabolism, so serum levels fall within a few days when intake is diminished. The usual dose of folic acid is 1 mg/d, by mouth, but higher doses (up to 5 mg/d) may be required S.E: usually mild GIT disturbances. Vitamin B12 (Cyanocobalamin) deficiency anemia Vitamin B12 (cobalamin) is a water-soluble vitamin obtained from fish, meat, and dairy products, also fortified cereals and supplements. It is co-absorbed with intrinsic factor of the parietal cells of the stomach, in the terminal ileum. Vitamin B12 is important for neurological function, red blood cell production, and DNA synthesis. Deficiency of vitamin B12 leads to megaloblastic anemia and neurologic abnormalities. It result from either low dietary levels or, more commonly, poorabsorption of the vitamin due to the failure of gastric parietal cells to produce intrinsic factor (as in pernicious anemia) or a loss of activity of the receptor needed for intestinal 10 uptake of the vitamin. Rare causes include bacterial overgrowth of the smallbowel, chronic pancreatitis, and thyroid disease or drugs like metformin. Because the normal daily requirements of vitamin B12 are only about 2 mcg, it would take about 5 years for all of the storedvitamin B12 to be exhausted. A deficiency of vitamin B12 causes the accumulation of homocysteine which is in turn increases the risk of atherosclerotic cardiovascular disease and causing neurologicproblems. It may be administered orally, nasally, intramuscularly, or deep subcutaneously Folic acid administration alone reverses the hematologic abnormality and, thus, masks the vitamin B12 deficiency, which can then proceed to severe neurologic dysfunction and disease. Vitamin B12 for parenteral injection is available as cyanocobalamin or hydroxocobalamin. Hydroxocobalamin is preferred because it is highly protein-bound and therefore remains longer in the circulation. 11 Initial therapy should consist of 100–1000 mcg of vitamin B12 intramuscularly daily or every other day for 1–2 weeks to replenish body stores. Maintenance therapy consists of 100–1000 mcg intramuscularly once a month for life. Side effects: rarely headache, nausea, vomiting, and rhinitis (for nasal spray) may occur. Agents used to treat sickle cell disease Hydroxyurea: The drug apparently increases fetal hemoglobin levels, thus diluting the abnormal hemoglobin S (HbS). 12 Side effects: bone marrow suppression and cutaneous vasculitis. Pentoxifylline: It improves erythrocyte flexibility and reduces theviscosity of blood. This decreases total systemic vascular resistance, improves blood flow, and enhances tissue oxygenation in patients with peripheral vascular disease. 13