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Medical Nutrition Therapy for Anemia

Medical Nutrition Therapy for Anemia. Anemia. Definition : deficiency in size or number of red blood cells or amount of hemoglobin they contain Defined as a hemoglobin concentration below the 95 th %ile for healthy reference populations

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Medical Nutrition Therapy for Anemia

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  1. Medical Nutrition Therapy for Anemia

  2. Anemia • Definition: deficiency in size or number of red blood cells or amount of hemoglobin they contain • Defined as a hemoglobin concentration below the 95th %ile for healthy reference populations • Not a disease but a symptom of conditions including extensive blood loss, excessive blood cell destruction, or decreased blood cell formation

  3. Classification of Anemia Based on cell size (MCV) • Macrocytic (large) MCV 100+ fl (femtoliters) • Normocytic (normal) MCV 80-99 fl • Microcytic (small) MCV<80 fl Based on hemoglobin content (MCH) • Hypochromic (pale color) • Normochromic (normal color)

  4. Iron Deficiency Anemia • Characterized by the production of small (microcytic) erythrocytes and a diminished level of circulating hemoglobin • Last stage of iron deficiency • Represents the end point of a long period of iron deprivation

  5. Causes of Iron Deficiency Anemia • Inadequate ingestion • Inadequate absorption • Defects in release from stores • Inadequate utilization • Increased blood loss or excretion • Increased requirement

  6. Stages of Iron Deficiency • Stage1: moderate depletion of iron stores; no dysfunction • Stage2: Severe depletion of iron stores; no dysfunction • Stage3: Iron deficiency • Stage4: Iron deficiency (dysfunction and anemia)

  7. Tests for Iron Deficiency • Serumiron: poor indicator, highly variable day to day and during the day • Ferritin - most sensitive—chief storage form of iron; directly proportional to iron stored in cells

  8. Tests for Iron Deficiency • Zincprotoporphyrin/hemeratio(ZPPH) protoporphyrin binds iron to form heme or zinc to form zinc protoporphyrin • In the presence of iron deficiency, ratio will rise (iron deficiency defined as ratio>1:12,000) • Not affected by hematocrit or other causes of anemia; specific to iron deficiency

  9. Tests for Iron Deficiency • Totalironbindingcapacity(TIBC)—capacity of transferrin to bind iron • Transferrin—globulin that binds/transports Fe from gut wall to tissues • Percentsaturationoftransferrin (calculate by dividing serum iron by the TIBC) • TIBC increases in iron deficiency • As stored iron falls, saturation of transferrin decreases

  10. Early Inadequate muscle function Growth abnormalities Epithelial disorders Reduced immunocompetence Late Defects in epithelial tissues Gastritis Cardiac failure Iron Deficiency: Clinical Findings

  11. Nutritional deficiency anaemiaclinical application Angular Cheilosis Glossitis Koilonychia Marrow iron stores Plummer-Vinson syndrome

  12. Koilonchia—A Sign of Iron Deficiency (From Callen JP, Greer KE, Hood AF, Paller AS, Swinyer LJ. Color Atlas of Dermatology. Philadelphia: W.B. Saunders, 1993.)

  13. Supplementation for Iron Deficiency Anemia • Oralironsalts • Ferrous forms better absorbed than ferric (ferrous sulfate, ferrous lactate, ferrous fumarate) • Best absorbed on an empty stomach but if irritation occurs, give with meals • Dosage 50-200 mg of elemental iron for adults; 6 mg/kg body weight for children • Generally supplement for 3 months (4-5 months if taken with meals)

  14. Nutritional Management of Iron-Deficiency Anemia • Increase absorbable iron in the diet • Include vitamin C at every meal • Include meat, fish or poultry at every meal • Decrease tea and coffee consumption

  15. Restoring Iron Levels Factors to consider: • Bioavailability of iron—the lower the Fe stores, the greater the rate of absorption • Vitamin C—binds iron to form a readily absorbed complex • Heme sources (meat, poultry, fish)— about 15% absorbable • Nonheme iron (grains, vegetables, eggs)—about 3% to 8% absorbable

  16. Supplementation for Iron Deficiency Anemia If patient fails to respond • May not be taking supplements • May not be absorbing iron (celiac disease, steatorrhea, hemodialysis) • May be bleeding • May need IV iron dextran (can cause allergic reactions)

  17. Rx of iron deficiency: Children Elemental iron 3-6mg/kg/day, contd.. 4-6 months Check Hb at 4 weeks Adults Ferrous sulphate/gluconate/fumarate Iron polymaltose complex Elemental iron 200mg/day Parental Iron Normal Hb/PatientHbXwt(kg)X2.2

  18. Diet for Iron Deficiency: In adults, limit milk intake - 500 mL/day Avoid excess caffeine Eat iron-rich foods Protein foodsVegetables  Meats  Greens  Fish & Shelfish Dried peas & beans  Eggs FruitsGrains  Dried fruit  Iron-fortified breads  Juices Dry cereals  Most fresh fruits  Oatmeal cereal

  19. Disorders Associated with Iron Toxicity • Thalassemias • Sideroblastic anemias • Chronic hemolytic anemia • Aplastic anemia • Ineffective erythropoiesis • Transfusional iron overload • Alcoholic cirrhosis

  20. Megaloblastic Anemias • A form of anemia characterized by the presence of large, immature, abnormal red blood cell progenitors in the bone marrow • 95% of cases are attributable to folic acid or vitamin B12 deficiency

  21. Static Test for Folate/B12 Status Folate • Measured in whole blood (plasma and cells) and then in the serum alone • Difference is used to calculate the red blood cell folate concentration (may better reflect the whole folate pool) • Can also test serum in fasting patient B12 • Measured in serum

  22. Functional Tests for Macrocytic Anemias • Homocysteine: Folate and B12 are needed to convert homocysteine to methionine; high homocysteine may mean deficiencies of folate, B12 or B6 • Methylmalonicacid measurements can be used along with homocysteine to distinguish between B12 and folate deficiencies • Schillingtest: radiolabeled cobalamin is used to test for B12 malabsorption

  23. Pernicious Anemia A macrocytic, megaloblastic anemia caused by a deficiency of vitamin B12. • Usually secondary to lack of intrinsic factor (IF) • May be caused by strict vegan diet • Also can be caused by ↓gastric acid secretion, gastric atrophy, H-pylori, gastrectomy, disorders of the small intestine (celiac disease, regional enteritis, resections), drugs that inhibit B12 absorption including neomycin, alcohol, colchicine, metformin, pancreatic disease

  24. Symptoms of Pernicious Anemia • Paresthesia (especially numbness and tingling in hands and feet) • Poor muscular coordination • Impaired memory and hallucinations • Damage can be permanent

  25. Vitamin B12 Depletion • Stage I—early negative vitamin B12 balance • Stage II—vitamin B12 depletion • Stage III—damaged metabolism: vitamin B12 deficient erythropoiesis • Stage IV—clinical damage including vitamin B12 anemia • Pernicious anemia—numbness in hands and feet; poor muscular coordination; poor memory; hallucinations

  26. Causes of Vitamin B12 Deficiency • Inadequate ingestion • Inadequate absorption • Inadequate utilization • Increased requirement • Increased excretion • Increased destruction by antioxidants

  27. Treatment of B12 Deficiency • Before 1926 was incurable; until 1948 was treated with liver extract • Now treatment consists of injection of 100 mcg of vitamin B12 once per week until resolved, then as often as necessary • Also can use very large oral doses or nasal gel • MNT: high protein diet (1.5 g/kg) with meat, liver, eggs, milk, milk products, green leafy vegetables

  28. Folic Acid Deficiency • Tropical sprue; pregnancy; infants born to deficient mothers • Alcoholics • People taking medications chronically that affect folic acid absorption • Malabsorption syndromes

  29. Causes of Folate Deficiency • Inadequate ingestion • Inadequate absorption • Inadequate utilization • Increased requirement • Increased excretion • Increased destruction • Vitamin B12 deficiency can cause folate deficiency due to the methylfolate trap

  30. Methylfolate Trap • In the absence of B12, folate in the body exists as 5-methyltetrahydro-folate (an inactive form) • B12 allows the removal of the 5-methyl group to form THFA

  31. Stages of Folate Depletion and Deficiency • Stage I—early negative folate balance (serum depletion) • Stage II—negative folate balance (cell depletion) • Stage III—damaged folate metabolism with folate-deficient erythropoiesis • Stage IV—clinical folate deficiency anemia

  32. Diagnosis of Folate Deficiency • Folate stores are depleted after 2-4 months on deficient diet • Megaloblastic anemia, low leukocytes and platelets • To differentiate from B12, measure serum folate, RBC folate (more reflective of body stores) serum B12 • High formiminoglutamic acid (FIGLU) in the urine also diagnostic

  33. Other Nutritional Anemias • Copper deficiency anemia • Anemia of protein-energy malnutrition • Sideroblastic (pyridoxine-responsive) anemia • Vitamin E–responsive (hemolytic) anemia

  34. Copper Deficiency • Copper is required for mobilization of iron from storage sites • In copper deficient state, result is low serum iron and hemoglobin, even when iron stores are normal • Copper is widespread in foods and needed in tiny amounts • Sometimes occurs in infants fed deficient formula or cow’s milk, adults and children with malabsorption or on TPN without copper • Diagnosis is important, since more iron won’t help and may interfere with copper absorption

  35. Sideroblastic Anemia • Microcytic, hypochromic form • Inherited defect of heme synthesis enzyme • High serum and tissue iron levels • Buildup of immature sideroblasts—hence the name • B6 is essential—must replace 25 to 100 times the RDA; may need lifelong replacement • Pyridoxine-responsive anemia, distinguished from anemia caused by pyridoxine deficiency

  36. Hemolytic Anemia • Oxidative damage to cells—lysis occurs • Vitamin E is an antioxidant that seems to be protective. • This anemia can occur in newborns, especially preemies.

  37. Non-nutritional Anemias • Sports anemia (hypochromic microcytic transient anemia) • Anemia of pregnancy: dilutional • Anemia of inflammation, infection, or malignancy (anemia of chronic disease) • Sickle cell anemia • Thalassemias

  38. Sports Anemia • Transient—usually in athletes who are runners; from compression of RBCs in feet until they burst, releasing hemoglobin • Check lab values • Counsel about a proper diet

  39. Sickle Cell Anemia • Protein-energy malnutrition common; may have poor intake and increased energy needs • Be careful not to overdo iron in diet or supplements; iron stores are often high due to frequent transfusions; avoid iron rich foods, alcohol, and ascorbic acid which enhance iron absorption • Promote foods high in copper, zinc and folate as needs are increased due to constant replacement of erythrocytes • Zinc supplements may be useful

  40. Thalassemia • Severe inherited anemia affecting mostly people of Mediterranean extraction • Defective globin formation in hemoglobin leads to increased blood volume, splenomegaly, bone marrow expansion, facial deformities, osteomalacia, bone changes • Iron buildup due to transfusions requires chelation therapy to remove excess iron

  41. Medical and Nutritional Management of Anemia • It is important to be familiar with the etiology and treatment of nutritional and non-nutritional anemias • Many non-nutritional anemias have nutritional implications • It is critical to DIAGNOSE before treating anemias with nutritional or non-nutritional therapies

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