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  1. 1. ANEMIA
  2. 2. Medical Nutrition Therapy for Anemia
  3. 3. 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
  4. 4. Classification of Anemia Based on cell size (MCV) • Macrocytic (large) MCV 100+ fl (femtoliters) • Normocytic (normal) MCV 8-99 fl • Microcytic (small) MCV<80 fl Based on hemoglobin content (MCH) • Hypochromic (pale color) • Normochromic (normal color)
  5. 5. 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
  6. 6. Causes of Iron Deficiency Anemia • • • • • • Inadequate ingestion Inadequate absorption Defects in release from stores Inadequate utilization Increased blood loss or excretion Increased requirement
  7. 7. Stages of Iron Deficiency • Stage 1: moderate depletion of iron stores; no dysfunction • Stage 2: Severe depletion of iron stores; no dysfunction • Stage 3: Iron deficiency • Stage 4: Iron deficiency (dysfunction and anemia)
  8. 8. Tests for Iron Deficiency • • Serum iron: 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
  9. 9. Tests for Iron Deficiency • • • Zinc protoporphyrin/heme ratio (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
  10. 10. Tests for Iron Deficiency • • • Total iron binding capacity (TIBC)—capacity of transferrin to bind iron Transferrin—globulin that binds/transports Fe from gut wall to tissues Percent saturation of transferrin (calculate by dividing serum iron by the TIBC) • TIBC increases in iron deficiency • As stored iron falls, saturation of transferrin decreases
  11. 11. Iron Deficiency: Clinical Findings Early • Inadequate muscle function • Growth abnormalities • Epithelial disorders • Reduced immunocompetence Late • Defects in epithelial tissues • Gastritis • Cardiac failure
  12. 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. 13. Supplementation for Iron Deficiency Anemia • Oral iron salts • 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. 14. Nutritional Management of IronDeficiency 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. 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. 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. 17. Hemochromatosis A genetically determined form of iron overload that results in progressive hepatic, pancreatic, cardiac, and other organ damage
  18. 18. Hemochromatosis • It is one of the most common genetic disorders in the U.S. • Present in heterozygous (one gene) form in 12% of nonblacks and 30% of blacks • Present in homozygous form (2 gene) in 1 in 200 nonblacks and 1 in 100 blacks • Homozygotes will die of iron overload unless they give blood frequently • Homozygotes absorb three times more iron from food than other people • Even heterozygotes may be at risk for iron overload, increasing risk of heart disease
  19. 19. Hemochromatosis: Risk Factors • Higher risk in people of northern European descent • Men tend to manifest symptoms earlier because they have no way to dispose of excess iron (menstruation, pregnancy, lactation) • Men may develop symptoms in their 30s but may not be diagnosed until their 50s • Women often develop symptoms after menopause
  20. 20. Hemochromatosis: Symptoms • • • • • • • Joint pain Fatigue Lack of energy Abdominal pain Loss of sex drive Heart problems Abnormal pigmentation of the skin, making it look gray or bronze
  21. 21. Hemochromatosis: if untreated, may result in • Arthritis • Liver disease: cirrhosis, cancer, liver failure • Damage to the pancreas, leading to diabetes • Heart abnormalities, including arrhythmias and heart failure • Impotence or early menopause • Thyroid or adrenal problems
  22. 22. Hemochromatosis: Diagnosis and Treatment • Testing: serum ferritin and transferrin saturation can reveal excess stores of iron; followed by HFE (genetic) test and possible liver biopsy • Treatment: regular phlebotomy to remove excess iron • Avoidance of iron supplements and sources of iron in the diet, especially heme iron • Awareness of iron cooking vessels
  23. 23. Disorders Associated with Iron Toxicity • • • • • • • Thalassemias Sideroblastic anemias Chronic hemolytic anemia Aplastic anemia Ineffective erythropoiesis Transfusional iron overload Alcoholic cirrhosis
  24. 24. 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
  25. 25. 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
  26. 26. 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 • Methylmalonic acid measurements can be used along with homocysteine to distinguish between B12 and folate deficiencies (↑ in B12 deficiency) • Schilling test: radiolabeled cobalamin is used to test for B12 malabsorption
  27. 27. 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
  28. 28. Symptoms of Pernicious Anemia • Paresthesia (especially numbness and tingling in hands and feet) • Poor muscular coordination • Impaired memory and hallucinations • Damage can be permanent
  29. 29. 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
  30. 30. Causes of Vitamin B12 Deficiency • • • • • • Inadequate ingestion Inadequate absorption Inadequate utilization Increased requirement Increased excretion Increased destruction by antioxidants
  31. 31. 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
  32. 32. Folic Acid Deficiency • Tropical sprue; pregnancy; infants born to deficient mothers • Alcoholics • People taking medications chronically that affect folic acid absorption • Malabsorption syndromes
  33. 33. 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
  34. 34. Methylfolate Trap • In the absence of B12, folate in the body exists as 5methyltetrahydrofolate (an inactive form) • B12 allows the removal of the 5methyl group to form THFA
  35. 35. 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
  36. 36. 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
  37. 37. Other Nutritional Anemias • • • • Copper deficiency anemia Anemia of protein-energy malnutrition Sideroblastic (pyridoxine-responsive) anemia Vitamin E–responsive (hemolytic) anemia
  38. 38. 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
  39. 39. 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
  40. 40. 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.
  41. 41. Nonnutritional 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
  42. 42. 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
  43. 43. 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
  44. 44. 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
  45. 45. 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