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Medical Nutrition Therapy for Anemia


Stage IV clinical damage including vitamin B12 anemia ... Vitamin B12 deficiency can cause folate deficiency due to the methylfolate trap ... – PowerPoint PPT presentation

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Title: Medical Nutrition Therapy for Anemia

Medical Nutrition Therapy for 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

Classification of Anemia
  • Based on cell size (MCV)
  • Macrocytic (large) MCV 100 fl (femtoliters)
  • Normocytic (normal) MCV 8-99 fl
  • Microcytic (small) MCVlt80 fl
  • Based on hemoglobin content (MCH)
  • Hypochromic (pale color)
  • Normochromic (normal color)

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

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 no
  • Stage 2 Severe depletion of iron stores no
  • Stage 3 Iron deficiency
  • Stage 4 Iron deficiency (dysfunction and anemia)

Tests for Iron Deficiency
  • Serum iron poor indicator, highly variable day
    to day and during the day
  • Ferritin - most sensitivechief storage form of
    iron directly proportional to iron stored in

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 ratiogt112,000)
  • Not affected by hematocrit or other causes of
    anemia specific to iron deficiency

Tests for Iron Deficiency
  • Total iron binding capacity (TIBC)capacity of
    transferrin to bind iron
  • Transferringlobulin 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

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

KoilonchiaA 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 sulfate, ferrous lactate, ferrous
  • 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)

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

Restoring Iron Levels
  • Factors to consider
  • Bioavailability of ironthe lower the Fe stores,
    the greater the rate of absorption
  • Vitamin Cbinds iron to form a readily absorbed
  • Heme sources (meat, poultry, fish) about 15
  • 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,
    steatorrhea, hemodialysis)
  • May be bleeding
  • May need IV iron dextran (can cause allergic

  • A genetically determined form of iron overload
    that results in progressive hepatic, pancreatic,
    cardiac, and other organ damage

  • 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

Hemochromatosis Risk Factors
  • Higher risk in people of northern European
  • 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

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

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

Hemochromatosis Diagnosis and Treatment
  • Testing serum ferritin and transferrin
    saturation can reveal excess stores of iron
    followed by HFE (genetic) test and possible liver
  • Treatment regular phlebotomy to remove excess
  • Avoidance of iron supplements and sources of iron
    in the diet, especially heme 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 of
    large, immature, abnormal red blood cell
    progenitors in the bone marrow
  • 95 of cases are attributable to folic acid or
    vitamin B12 deficiency

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

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

Pernicious Anemia
  • A macrocytic, megaloblastic anemia caused by a
    deficiency of vitamin B12.
  • Usually secondary to lack of intrinsic factor
  • 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

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

Vitamin B12 Depletion
  • Stage Iearly negative vitamin B12 balance
  • Stage IIvitamin B12 depletion
  • Stage IIIdamaged metabolism vitamin B12
    deficient erythropoiesis
  • Stage IVclinical damage including vitamin B12
  • Pernicious anemianumbness in hands and feet
    poor muscular coordination poor memory

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
    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

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

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

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

Stages of Folate Depletion and Deficiency
  • Stage Iearly negative folate balance (serum
  • Stage IInegative folate balance (cell
  • Stage IIIdamaged folate metabolism with
    folate-deficient erythropoiesis
  • Stage IVclinical folate deficiency anemia

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

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

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
  • Copper is widespread in foods and needed in tiny
  • Sometimes occurs in infants fed deficient formula
    or cows milk, adults and children with
    malabsorption or on TPN without copper
  • Diagnosis is important, since more iron wont
    help and may interfere with copper absorption

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

Hemolytic Anemia
  • Oxidative damage to cellslysis occurs
  • Vitamin E is an antioxidant that seems to be
  • This anemia can occur in newborns, especially

Nonnutritional Anemias
  • Sports anemia (hypochromic microcytic transient
  • Anemia of pregnancy dilutional
  • Anemia of inflammation, infection, or malignancy
    (anemia of chronic disease)
  • Sickle cell anemia
  • Thalassemias

Sports Anemia
  • Transientusually in athletes who are runners
    from compression of RBCs in feet until they
    burst, releasing hemoglobin
  • Check lab values
  • Counsel about a proper diet

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
  • Promote foods high in copper, zinc and folate as
    needs are increased due to constant replacement
    of erythrocytes
  • Zinc supplements may be useful

  • 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
  • Iron buildup due to transfusions requires
    chelation therapy to remove excess iron

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