anemia mnt - Medical Nutrition Therapy for Anemia Anemia...

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Unformatted text preview: Medical Nutrition Therapy for Anemia Anemia • • • Definition: deficiency in size or number Definition: of red blood cells or amount of hemoglobin they contain hemoglobin Defined as a hemoglobin concentration Defined below the 95th %ile for healthy reference below populations populations Not a disease but a symptom of Not conditions including extensive blood loss, excessive blood cell destruction, or decreased blood cell formation decreased Classification of Anemia Based on cell size (MCV) • Macrocytic (large) MCV 100+ fl Macrocytic (femtoliters) (femtoliters) • Normocytic (normal) MCV 8-99 fl • Microcytic (small) MCV<80 fl Based on hemoglobin content (MCH) • Hypochromic (pale color) • Normochromic (normal color) Iron Deficiency Anemia • • • Characterized by the production of small Characterized (microcytic) erythrocytes and a diminished level of circulating hemoglobin Last stage of iron deficiency Represents the end point of a long period Represents of iron deprivation of Causes of Iron Deficiency Anemia • • • • • • Inadequate ingestion Inadequate absorption Defects in release from stores Inadequate utilization Increased blood loss or excretion Increased requirement Stages of Iron Deficiency • • • • Stage 1: moderate depletion of iron stores; Stage no dysfunction no Stage 2: Severe depletion of iron stores; no Stage dysfunction dysfunction Stage 3: Iron deficiency Stage 4: Iron deficiency (dysfunction and Stage anemia) anemia) Tests for Iron Deficiency • • Serum iron: poor indicator, highly variable Serum day to day and during the day day Ferritin - most sensitive—chief storage form Ferritin of iron; directly proportional to iron stored in cells in Tests for Iron Deficiency • • • Zinc protoporphyrin/heme ratio (ZPPH) Zinc protoporphyrin binds iron to form heme or zinc to form zinc protoporphyrin or In the presence of iron deficiency, ratio In will rise (iron deficiency defined as ratio>1:12,000) Not affected by hematocrit or other Not causes of anemia; specific to iron deficiency deficiency Tests for Iron Deficiency • • • Total iron binding capacity (TIBC)—capacity of Total transferrin to bind iron transferrin Transferrin—globulin that binds/transports Fe Transferrin—globulin from gut wall to tissues from Percent saturation of transferrin (calculate by Percent dividing serum iron by the TIBC) dividing • TIBC increases in iron deficiency • As stored iron falls, saturation of transferrin As decreases decreases Iron Deficiency: Clinical Findings Early • Inadequate muscle Inadequate function function • Growth abnormalities • Epithelial disorders • Reduced Reduced immunocompetence immunocompetence Late • Defects in epithelial Defects tissues tissues • Gastritis • Cardiac failure 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.) Supplementation for Iron Deficiency Anemia • • • • Oral iron salts • Ferrous forms better absorbed than ferric Ferrous (ferrous sulfate, ferrous lactate, ferrous fumarate) fumarate) Best absorbed on an empty stomach but if Best irritation occurs, give with meals irritation Dosage 50-200 mg of elemental iron for adults; Dosage 6 mg/kg body weight for children mg/kg Generally supplement for 3 months (4-5 months Generally if taken with meals) if 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 Restoring Iron Levels Factors to consider: • • • • Bioavailability of iron—the lower the Fe Bioavailability stores, the greater the rate of absorption stores, Vitamin C—binds iron to form a readily Vitamin absorbed complex absorbed Heme sources (meat, poultry, fish)— about 15% absorbable Nonheme iron (grains, vegetables, eggs) —about 3% to 8% absorbable Supplementation for Iron Deficiency Anemia If patient fails to respond • May not be taking supplements • May not be absorbing iron (celiac disease, May steatorrhea, hemodialysis) steatorrhea, • May be bleeding • May need IV iron dextran (can cause May allergic reactions) allergic Hemochromatosis A genetically determined form of iron genetically overload that results in progressive hepatic, pancreatic, cardiac, and other organ damage organ Hemochromatosis • • • • • • It is one of the most common genetic disorders It in the U.S. in Present in heterozygous (one gene) form in Present 12% of nonblacks and 30% of blacks 12% Present in homozygous form (2 gene) in 1 in Present 200 nonblacks and 1 in 100 blacks 200 Homozygotes will die of iron overload unless Homozygotes they give blood frequently they Homozygotes absorb three times more iron Homozygotes from food than other people from Even heterozygotes may be at risk for iron Even overload, increasing risk of heart disease overload, Hemochromatosis: Risk Factors • • • • Higher risk in people of northern European Higher descent descent Men tend to manifest symptoms earlier because Men they have no way to dispose of excess iron (menstruation, pregnancy, lactation) (menstruation, Men may develop symptoms in their 30s but Men may not be diagnosed until their 50s may Women often develop symptoms after Women menopause menopause Hemochromatosis: Symptoms • • • • • • • Joint pain Fatigue Lack of energy Abdominal pain Loss of sex drive Heart problems Abnormal pigmentation of the skin, Abnormal making it look gray or bronze making Hemochromatosis: if untreated, may result in • • • • • • Arthritis Liver disease: cirrhosis, cancer, Liver liver failure liver Damage to the pancreas, leading Damage to diabetes to Heart abnormalities, including Heart arrhythmias and heart failure arrhythmias Impotence or early menopause Thyroid or adrenal problems Hemochromatosis: Diagnosis and Treatment • • • • Testing: serum ferritin and transferrin saturation Testing: can reveal excess stores of iron; followed by HFE (genetic) test and possible liver biopsy (genetic) Treatment: regular phlebotomy to remove excess Treatment: iron iron Avoidance of iron supplements and sources of Avoidance iron in the diet, especially heme iron iron Awareness of iron cooking vessels Disorders Associated with Iron Toxicity • • • • • • • Thalassemias Sideroblastic anemias Chronic hemolytic anemia Aplastic anemia Ineffective erythropoiesis Transfusional iron overload Alcoholic cirrhosis Megaloblastic Anemias • • A form of anemia characterized by the presence form of large, immature, abnormal red blood cell progenitors in the bone marrow progenitors 95% of cases are attributable to folic acid or 95% vitamin B12 deficiency vitamin 12 deficiency Static Test for Folate/B12 Status Folate • Measured in whole blood (plasma and Measured cells) and then in the serum alone cells) • Difference is used to calculate the red Difference blood cell folate concentration (may better reflect the whole folate pool) better • Can also test serum in fasting patient B12 • Measured in serum Functional Tests for Macrocytic Anemias • • • Homocysteine: Folate and B12 are Homocysteine: needed to convert homocysteine to methionine; high homocysteine may mean deficiencies of folate, B12 or B6 mean Methylmalonic acid measurements can be Methylmalonic used along with homocysteine to distinguish between B12 and folate deficiencies (↑ in B12 deficiency) deficiencies Schilling test: radiolabeled cobalamin is Schilling used to test for B12 malabsorption used Pernicious Anemia A macrocytic, megaloblastic anemia caused by a macrocytic, deficiency of vitamin B12. deficiency 12. • • • Usually secondary to lack of intrinsic factor Usually (IF) (IF) May be caused by strict vegan diet May Also can be caused by ↓gastric acid secretion, Also 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 colchicine, Symptoms of Pernicious Anemia • • • • Paresthesia (especially numbness and Paresthesia tingling in hands and feet) tingling Poor muscular coordination Impaired memory and hallucinations Damage can be permanent Vitamin B12 Depletion • Stage I—early negative vitamin B12 balance • Stage II—vitamin B12 depletion • Stage III—damaged metabolism: vitamin B12 deficient erythropoiesis deficient Stage IV—clinical damage including vitamin B12 12 anemia anemia Pernicious anemia—numbness in hands and feet; Pernicious poor muscular coordination; poor memory; hallucinations hallucinations • • Causes of Vitamin B12 Deficiency • • • • • • Inadequate ingestion Inadequate absorption Inadequate utilization Increased requirement Increased excretion Increased destruction by antioxidants Treatment of B12 Deficiency • • • • Before 1926 was incurable; until 1948 was treated Before with liver extract with Now treatment consists of injection of 100 mcg of Now vitamin B12 once per week until resolved, then as often as necessary often Also can use very large oral doses or nasal gel MNT: high protein diet (1.5 g/kg) with meat, liver, MNT: eggs, milk, milk products, green leafy vegetables Folic Acid Deficiency • • • • Tropical sprue; pregnancy; infants born to Tropical deficient mothers deficient Alcoholics People taking medications chronically that affect People folic acid absorption folic Malabsorption syndromes Causes of Folate Deficiency • • • • • • • Inadequate ingestion Inadequate absorption Inadequate utilization Increased requirement Increased excretion Increased destruction Vitamin B12 deficiency can cause folate Vitamin deficiency due to the methylfolate trap deficiency Methylfolate Trap • • In the absence of B12, In folate in the body exists as 5exists methyltetrahydrofolate (an inactive folate form) form) B12 allows the B12 removal of the 5removal methyl group to form methyl THFA THFA Stages of Folate Depletion and Deficiency • • • • Stage I—early negative folate balance (serum Stage depletion) depletion) Stage II—negative folate balance (cell Stage depletion) depletion) Stage III—damaged folate metabolism with Stage folate-deficient erythropoiesis folate-deficient Stage IV—clinical folate deficiency anemia Diagnosis of Folate Deficiency • • • • Folate stores are depleted after 2-4 Folate months on deficient diet months Megaloblastic anemia, low leukocytes Megaloblastic and platelets and To differentiate from B12, measure serum To folate, RBC folate (more reflective of body stores) serum B12 body High formiminoglutamic acid (FIGLU) in High the urine also diagnostic the Other Nutritional Anemias • • • • Copper deficiency anemia Anemia of protein-energy malnutrition Sideroblastic (pyridoxine-responsive) anemia Vitamin E–responsive (hemolytic) anemia Copper Deficiency • • • • • Copper is required for mobilization of iron from Copper storage sites storage In copper deficient state, result is low serum In iron and hemoglobin, even when iron stores are normal normal Copper is widespread in foods and needed in Copper tiny amounts tiny Sometimes occurs in infants fed deficient Sometimes formula or cow’s milk, adults and children with malabsorption or on TPN without copper malabsorption Diagnosis is important, since more iron won’t Diagnosis help and may interfere with copper absorption help Sideroblastic Anemia • • • • • • Microcytic, hypochromic form Inherited defect of heme synthesis enzyme High serum and tissue iron levels Buildup of immature sideroblasts—hence the Buildup name name B6 is essential—must replace 25 to 100 times the RDA; may need lifelong replacement the Pyridoxine-responsive anemia, distinguished Pyridoxine-responsive from anemia caused by pyridoxine deficiency from Hemolytic Anemia • • • Oxidative damage to cells—lysis occurs Vitamin E is an antioxidant that seems to be Vitamin protective. protective. This anemia can occur in newborns, This especially preemies. especially Nonnutritional Anemias • • • • • Sports anemia (hypochromic microcytic Sports transient anemia) transient Anemia of pregnancy: dilutional Anemia of inflammation, infection, or Anemia malignancy (anemia of chronic disease) malignancy Sickle cell anemia Thalassemias Sports Anemia • • • Transient—usually in athletes who are runners; Transient—usually from compression of RBCs in feet until they burst, releasing hemoglobin burst, Check lab values Counsel about a proper diet Sickle Cell Anemia • • • • Protein-energy malnutrition common; may have Protein-energy poor intake and increased energy needs poor Be careful not to overdo iron in diet or Be supplements; iron stores are often high due to frequent transfusions; avoid iron rich foods, alcohol, and ascorbic acid which enhance iron absorption absorption Promote foods high in copper, zinc and folate as Promote needs are increased due to constant replacement of erythrocytes of Zinc supplements may be useful Thalassemia • • • Severe inherited anemia affecting mostly people Severe of Mediterranean extraction of Defective globin formation in hemoglobin leads Defective to increased blood volume, splenomegaly, bone marrow expansion, facial deformities, osteomalacia, bone changes osteomalacia, Iron buildup due to transfusions requires chelation Iron therapy to remove excess iron therapy Medical and Nutritional Management of Anemia • • • It is important to be familiar with the It etiology and treatment of nutritional and non-nutritional anemias non-nutritional Many non-nutritional anemias have Many nutritional implications nutritional It is critical to DIAGNOSE before treating It anemias with nutritional or non-nutritional therapies therapies ...
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