Nutritional anemias
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Nutritional Anemias. Spenser Parker, Katie Gardner, Juliette Soelberg , McKell Compton. Case Study. Patient SH 31 yr. old female 23 rd week of gestation, 3 rd pregnancy Chief complaint:

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Nutritional anemias

Nutritional Anemias

Spenser Parker, Katie Gardner, Juliette Soelberg, McKell Compton

Case study

Case Study

  • Patient SH

  • 31 yr. old female

  • 23rd week of gestation, 3rd pregnancy

  • Chief complaint:

    • Fell on ice and has had abdominal pain and vaginal spotting. Questioned if she was beginning premature labor

  • Dx: microcytic, hypochromic anemia 2o to iron deficiency

  • Discharged the following day on 40 mg ferrous sulfate TID

Basic terms

Basic terms

  • Anemia: a deficiency in the size or number of RBC or the amount of Hgb they contain that limits the exchange of oxygen and carbon dioxide

  • Macrocytic: larger-than-normal RBC

  • Microcytic: smaller-than-normal RBC

  • Megaloblastic: large, immature, abnormal, RBC

  • Hypochromic: deficient Hgb content and pale color of RBC

  • Normochromic: sufficient Hgb content of RBC

  • CBC: complete blood count

Nutritional anemias


  • Includes:

    • Total blood cell (TBC) count

    • Hemoglobin

    • Hematocrit

    • RBC indices (measurements of the volume, size, distribution and Hgb content of RBC)

    • WBC count and differential count

    • Blood smear

    • Platelet count and mean platelet volume (MPV)

Iron deficiency a nemia

Iron Deficiency Anemia


  • Occurs in bone marrow

  • Erythrocytes derived from precursor cells, erythroblasts/ normoblasts

  • Abnormal erythroblasts called megaloblasts

  • Erythropoietin stimulates uncommitted stem cells to differentiate into proerythroblasts

  • Hgbis apparent and increases in quantity as nuclear size shrinks

  • Reticulocyte matures into an erythrocyte within 24 to 48 hours

  • Erythrocyte loses its capacity for Hgb synthesis and oxidative metabolism


Hemoglobin synthesis

Hemoglobin Synthesis

  • Hgb: the substance that reversibly binds oxygen

  • Each hemoglobin molecule consists of two parts

    • 1. a protein “globin” part, composed of four polypeptide chains

    • 2. Four disk-shaped pigment molecules called “hemes”. Each heme has an iron molecule in the center. Fe++(ferrous iron) + porphyrin= Heme

  • Each heme molecule is capable of carrying one molecule of oxygen

  • Ferric iron carries an extra positive charge and forms methemoglobin, forming an unstable type of hgb not capable of binding oxygen

  • Nutritional anemias

    Heme (Fe+porphyrin)Hemoglobin (globin+heme)

    Nutritional anemias


    • Adult body contains 2 major pools of iron

      • 1. functional iron in hgb, myoglobin, and enzymes

      • 2. storage iron in ferritin, hemosiderin, and transferrin (transport protein in blood)

    • Iron is highly conserved by the body

    • 90% is recovered and reused everyday

    • The rest is excreted mainly in the bile

    • Dietary iron must meet this 10% gap to maintain iron balance or else iron deficiency result

    • Dietary iron exists in two chemical forms: heme and nonheme

    Heme iron

    Heme Iron

    • Heme iron: in hemoglobin, myoglobin, and some enzymes from animal sources

      • absorbed across brush border after digested from animal sources.

      • the ferrous iron is enzymatically removed from the ferroporphyrin complex

      • the free iron ions combine with apoferritin to form ferritin

      • iron stores are moved into blood at the basolateral membrane involving an active transport mechanism

    Nonheme iron

    Nonheme Iron

    • Nonheme iron: mainly in plant foods but also in some animal foods

      • must be in a soluble (ionized) form to be transferred across the brush border

      • acid of gastric secretions enhance the solubility and change the iron to the ionic state either as ferric (+3) or ferrous (+2) oxidation state

      • divalent metal transporter 1 (DMT1) transports ferrous iron across the border

      • the ferrous (+2) form is absorbed more readily, ferric iron (+3) has to be reduced by ferric reductase to be absorbed

      • the ferrous iron is then bound to apoferritin and goes through the same process as with heme iron to enter the blood



    • Efficiency of absorption is controlled by intestinal mucosa allowing certain amounts of iron to enter blood from the ferritin pool according to the body’s needs

    • Hepcidin produced by liver acts on mucosa cells and inhibits absorption of iron.

    • Another signal from body to the absorbing cells may be transferrin saturation.

    • A low %TIBC of transferrin would stimulate absorbing cells to transport iron across the basolateral membrane to the blood. If iron concentration is excessive, absorbing cells would be down regulated and less iron would be absorbed

    • When circulating % transferrin saturation is low, the new intestinal cells (intestinal cells are sloughed off every 5 to 6 days) will have more receptors for iron absorption

    Iron deficiency anemia

    Iron Deficiency Anemia

    • World’s most common nutritional deficiency disease

    • Iron deficiency results in decreased production of hemoglobin (Hgb)

    • Which in turn results in microcytic, hypochromic anemia

    • This anemia is the last stage of iron deficiency, representing a long period of iron deprivation



    • Inadequate ingestion

    • Inadequate absorption

    • Inadequate utilization

    • Increased requirement

    • Increased blood loss or excretion

    • Defects in release from stores

    Inadequate absorption

    Inadequate Absorption

    • Medications that cause GI bleeding (aspirin, NSAIDS)

    • Diarrhea (decreases intestinal transit time/absorption)

    • Achlorydria (production of gastric acid is not present or low)

    • Celiac disease

    • Atrophic gastritis

    • Partial or total gastrectomy

    • Drug interference (antacids, cholestyramine, cimedtidine [Tagamet], pancreatin, ranitidine [Zantac], tetrcycline, and antiretroviral medications [especially the necleoside reverse transcriptase inhibitors, Combivir, Epivir, Retrovir, Zerit and the protease inhibitor Crixivan])

    Stages of deficiency

    Stages of Deficiency

    • Stages of negative iron balance

      • I: Moderate depletion of iron stores; no dysfunction

      • II: Severe depletion of iron stores; no dysfunction

      • III: Iron deficiency; dysfunction

      • IV: Iron deficiency; dysfunction and anemia

    Measurements of iron deficiency

    Measurements Of Iron Deficiency

    • Plasma ferritin

    • Plasma iron

    • Total circulating transferrin

    • Saturation of circulating transferrin

    • Saturation of ferritin with iron

    • Soluble serum transferrin receptor (STFR)



    • Diagnosis requires more than one method of iron evaluation

    • Preferably the first three measurements

    • Should also include an assessment of cell morphology

    • Serum or plasma ferritin level is the most sensitive parameter of negative iron balance (decreases only in presence of true iron deficiency, as with transferrin saturation)

    Laboratory tests

    Laboratory Tests

    • Normal Levels:

      • Ferritin: Males:12-300 ng/mL Female:10-150 ng/mL

      • Serum Iron: Male (80-180 mcg/dL) Female (60-160mcg/dL).

      • Total Iron-Binding Capacity (TIBC): 250-460 mcg/dL.

      • Transferrin: Male (215-365 mg/dL) Female (250-380 mg/dL)

      • Transferrin Saturation: Male 20% to 50% Females 15% to 50%

      • Hematocrit: Male 42%-52% Female 37%-47%

      • Hemoglobin: Male14-18g/dL Female12-16g/dL

    Laboratory tests ferritin

    Laboratory Tests: Ferritin

    • Most sensitive test to determine iron-deficiency anemia

    • Major iron-storage protein, normally present in the serum in concentrations directly related to iron storage

    • Decreases in ferritin levels indicate a decrease in iron storage associated with iron deficiency anemia

    • Ferritin level below 10mg/100mL is diagnostic of iron deficiency anemia

    • Only when protein depletion is severe can ferritin be decreased by malnutrition

    • Ferritin can act as acute-phase reactant protein and may be elevated in conditions not reflecting iron stores

    Laboratory tests serum iron

    Laboratory Tests : Serum Iron

    • Serum iron: measurement of the quantity of iron bound to transferrin (globulin protein transporting absorbed iron from the plasma to the bone marrow to be incorporated into Hgb).

    • Decreased serum iron level is characteristic of iron-deficiency anemia.

    • Serum iron levels may vary significantly during the day

    • Blood specimen should be drawn in the morning

    • Refrain from eating for appx. 12 hrs to avoid high iron measurement by eating food with a high iron content

    Laboratory test tibc and transferrin

    Laboratory Test: TIBC and Transferrin

    • TIBC is a measurement of all proteins available for binding mobile iron.

    • Transferrin represents the largest quantity of iron-binding proteins.

    • Thus TIBC is an indirect yet accurate measurement of transferrin.

    • Ferritin not included in TIBC (binds only stored iron)

    • TIBC is increased in 70% of patients with iron deficiency.

    • During iron overload, TIBC is less reflective of true transferrin levels

    Laboratory test tibc and transferrin saturation

    Laboratory Test: TIBC and Transferrin Saturation

    • Transferrin saturation (%)= Serum iron level x (100%)TIBC

    • Percentage of transferrin and other mobile iron-binding proteins saturated with iron is helpful in determining the cause of abnormal iron and TIBC levels.

    • Decreased TIBC saturation or transferrin saturation level is characteristic of iron-deficiency anemia (decreased below 15%)

    • Increased intake or absorption of iron leads to elevated iron levels (TIBC is unchanged and the percent of transferrin saturation increases)

    Laboratory tests iron related cbc

    Laboratory Tests: Iron-related CBC

    • Hematocrit (Hct)-measure of the percentage of total blood volume that is made up by the RBCs.

      • Decreased levels of Hct indicate anemia.

      • Hctcan be altered by dehydration, increased RBC size, pregnancy due to chronic hemodilution, living at high altitudes.

    • Hemoglobin (Hgb)-measure of the total amount of Hgb in the blood. Oxygen carrying capacity of the blood determined by the Hgb concentration

      • Decreased levels of Hgb indicate anemia

      • Hgblevels can be altered during pregnancy, living in high altitudes, being a heavy smokes.

    • Red Blood Cell Count (RBC)- count of the number of circulating RBCs in 1 mm3 of peripheral venous blood.

      • When the value is decreased by more than 10% of the expected normal value, the patient is said to beanemic.

      • RBC alters with pregnancy, high altitudes, and hydration status.

    Laboratory tests hemoglobin

    Laboratory Tests: Hemoglobin

    • Hgb concentration by itself unsuitable as a diagnostic tool in cases of suspected iron deficiency anemia

      • It is affected only late in the disease

      • It cannot distinguish iron deficiency from other anemias

      • Hemoglobin values in normal individuals vary widely

    Laboratory tests protoporphyrin

    Laboratory Tests: protoporphyrin

    • The iron-containing portion of the respiratory pigments that combine with protein to form hemoglobin or myoglobin can be used to assess iron deficiency

    • The zinc protoporphryin (ZnPP)/heme ratio is measured

    • This can be affected by chronic infection

    • Can produce a condition that mimics iron deficiency anemia when iron is adequate



    • Depleted iron stores, inadequate iron delivery to bone marrow, impaired iron use within the marrow causes reduced hgb synthesis

    • Iron deficiency anemia present when the demand for iron exceeds the supply

    • Develops slowly through four overlapping stages

      • Stage I: Early negative iron balance

      • Stage II: Iron stores are depleted. Erythropoiesis proceeds normally with the hgb content of RBCs remaining normal

      • Stage III: Decreased circulating iron levels; thus transportation of iron to bone marrow is diminished resulting in damaged metabolism and iron deficiency erythropoiesis (decreased levels of erythron iron)

      • Stage IV: more small hemoglobin-deficient cells enter the circulation in sufficient numbers to replace the normal mature erythrocytes that have been removed from the circulation

    Signs and symptoms

    Signs and Symptoms

    • More severe epithelial disorders:

    • Red, sore, painful tongue

    • Brittle, thin, spoon shaped (koilonychia) nails

    • Mouth: atrophy of lingual papillae- glossitis; burning; redness; angular stomatitis; and a form of dysphagia

    • Stomach: gastritis, may result in achloryhdria

    • Skin may appear pale

    • Inside of lower eyelid may be light pink instead of red

    • Cardiovascular and respiratory changes can lead to cardiac failure

    • Fatigue, shortness of breath

    • Decreased work performance/exercise tolerance

    • Anorexia

    • Pica

    • Pagophagia (ice eating)

    • Slow cognitive and social development in children

    • Growth abnormalities

    • Reduction in gastric acidity

    • Reduced immunocompetence

    • Mental confusion, memory loss, disorientation in elderly population

    Screening strategies

    Screening Strategies

    • Physical signs may not appear until stage III or IV

    • Important to screen those individuals who are at risk

    • Measurement of serum ferritin levels may best reveal stages I and II negative iron balance

    • Serum TIBC may also be as good an indicator

    Risk for iron deficiency anemia

    Risk for Iron Deficiency Anemia

    • Infants

    • Adolescent girls

    • Childbearing years/pregnancy for women

    • Older Adults

    • Those living in chronic poverty

    • Female athletes (esp. involve in endurance sports)

    Treatment of iron deficiency anemia

    Treatment of Iron Deficiency Anemia

    • Treatment should focus on underlying disease leading to the anemia. Repletion of the iron stores, not merely alleviation of the anemia

    • Chief treatment: oral administration of inorganic iron in the ferrous form

      • Most widely used preparation is ferrous sulfate

      • Other salts absorbed to about the same degree are ferrous forms of lactate, fumarate, glycine sulfate, glutamate, and gluconate

      • Iron best absorbed when stomach is empty (although this can cause gastric irritation)

      • GI side effects: nausea, heartburn, diarrhea, constipation, epigastric discomfort and distention

      • If this happens, patients should take iron with meals, though this will reduce absorbability



    • Health professional generally prescribe oral iron for iron deficiency for 3 months (taken 3 times daily)

    • Depending on the severity of the anemia and tolerance of iron supplementation, a daily dose should be 50 to 200 mg for adults and 6 mg/kg for children

    • Ascorbic acid increases both iron absorption and iron gastric irritation

    • Absorption of 10 to 20 mg of iron per day permits RBC production to increase to about 3x the normal rate and increase hgb concentration .2g/dL

    • Increased reticulocytosis is seen within 2 to 3 days, hgb level will begin to increase by day 4 of treatment

    • Iron supplementation should be continued for 4 to 5 months to allow for repletion of body iron reserves



    • If iron supplements don’t correct the anemia:

      • 1. patient may not be taking the medication as prescribed, most likely because of side effects

      • 2. bleeding may be be continuing at a rate faster than erythroid marrow can replace the blood cells

      • 3. the supplemental iron may not be absorbed 2° to steatorrhea, celiac disease, or hemodialysis.

  • In these circumstances parenteral administration of iron in the form of iron-dextran may be necessary

  • Bioavailability of iron

    Bioavailability of Iron

    • Rate of absorption depends on iron status of individual

    • The lower the iron stores, the greater the rate of absorption will be.

    • Iron absorption averages about 5 to 15% from diet of both heme and nonheme iron in a person with normal iron stores

    • Absorption in iron deficiency often increases iron absorption to about 20 to 30%

    • Absorption can be as high as 50% in iron deficiency anemia although not common

    Bioavailability of iron1

    Bioavailability of Iron

    • Efficiency of iron absorption determined somewhat by food that it is derived from

    • Heme iron is much better absorbed than nonheme iron

    • About 3 to 8% of nonheme iron is absorbed

    • About 15% of heme iron is absorbed

    • The ferrous form of nonheme iron is better absorbed than ferric iron

      • Not all ferrous compounds are equally available. Ferrous pyrophosphate used in breakfast cereals is used often because it doesn’t add a gray color to food but it is poorly absorbed

    • Ascorbic acid improves iron absorption (reduces ferric to ferrous iron and forms a chelate with iron remaining soluble throughout lower SI)

    Bioavailability of iron2

    Bioavailability of Iron

    • Animal proteins enhance absorption by an unknown mechanism

    • Gastric acidity enhances solubility and bioavailability of iron from foods; administration of alkaline substances can interfere with nonheme absorption

    • High phytate, oxalates, and tannin content in foods inhibit absorption of nonheme iron (avoid tea and coffee with meals)

    • Increased intestinal motility decreases contact time and removes chyme from highest intestinal acidity, decreasing absorption

    • Poor fat digestion leading to steatorrhea also decreases iron absorption

    Food sources of iron

    Food Sources of Iron

    • Best source of dietary iron is liver.

    • Followed by seafood, kidney, heart, lean meat, and poultry

    • Dried beans and vegetables are the best plant sources

    • Other foods: egg yolks, dried fruits, dark molasses, whole grain and enriched breads, wine and cereal

    • Milk devoid of iron

    • Corn poor source of iron

    • Iron skillet used for cooking add to total iron intake

    Intake of iron

    Intake of Iron

    • RDA:

      • Men and postmenopausal women: 8 mg/day

      • Women of childbearing age: 18 mg/day

      • Teenage boys: 11 mg/day

    • Median iron intakes of most women are lower than the RDA, and the median intakes of men generally exceed the RDA.

    • Foods that supply the greatest amount of iron in US diet include ready to eat cereals fortified with iron; bread, cakes, cookies, doughnuts, and pasta (all fortified with iron); beef; dried beans and lentils; and poultry.

    • Iron fortification of cereals, flours, and bread has added significantly to the total iron intake of the US.

    • Concern about potential iron overloading from fortified breakfast foods was raised because analyzed values of iron content were greater than labeled values

    Iron overload

    Iron Overload

    • Concern with excessive iron intake is related to its role in coronary heart disease and cancer

    • Excessive iron can contribute to an enriched oxidative environment that favors

      • oxidation of LDL cholesterol

      • arterial vessel damage

      • other adverse effect affecting the cardiovascular system

    Iron overload1

    Iron Overload

    • Major cause of iron overload is hereditary hemochromatosis

    • Overload is linked to a distinct gene that favors excessive iron absorption when iron is available in the diet

    • Frequent blood transfusions or long term ingestion of large amounts of iron can lead to abnormal accumulation of iron in the liver

    • Saturation of tissue apoferritin with iron is followed by the appearance of hemosiderin (storage form for iron but contains more iron than ferritin and is very insoluble)

    • Hemosiderosis (iron storage condition) associated with tissue damage is considered hemochromatosis

    • This tissue damage can result in progressive hepatic, pancreatic, cardiac, and other organ damage

    • Absorb 3x more iron from their food than normal

    Iron overload treatment mnt

    Iron overload Treatment/MNT

    • Treatment for significant iron overload:

      • Weekly phlebotomy for 2 to 3 years may be required to eliminate all excess iron

      • May also involve iron depletion with intravenous desferrioxamine-B

      • Calcium disodium ethylenediaminetetraactic acid can also be used

  • MNT:

    • Ingest less heme iron compared with nonheme iron

    • Avoid alcohol and vitamin C supplements because both enhance iron absorption

    • Avoid foods highly fortified with iron, iron supplements, or multiple vitamins/mineral supplements that contain iron

    • RDA should not be exceeded

  • B 12 deficiency

    B12 Deficiency



    • B12is freed from protein (by way of gastric secretions)

    • B12binds to R-protein

    • R-protein hydrolyzed in sm. Intestine

      • Intrinsic factor bind to B12

    • IF binds to specific membrane receptor on illeulbrush border

    • B12is absorbed

    • B12binds to transcobalamins (TCI, TCII, etc)



    Not enough B12 in diet

    • strict vegan

    • chronic alcoholism

    • poverty

    • religion

      Inadequate use

    • B12 antagonist

    • enzyme deficiency

    • abnormal binding proteins

    • inadequate binding proteins

      Increased Requirement

    • hyperthyroidism

    • hematopoiesis

    • infancy

      Increase excretion

    •  liver disease

    • renal disease

    • inadequate binding protein

    Poor Absorption

    • Gastric disorders

      • Addisonian Pernicious Anemia

        • hereditary, defective, autoimmunity

    • gastrectomy

      • total

      • subtotal

    • antibody to IF

      • blocking 

      • binding

    • sm. intestine disorders

      • celiac

      • tropical sprue

      • strictures, lesions, resection

    • specific malabsorptions

    • competition for B12

      • bacteria(H. pylori)

    • pancreatic disease

    • HIV

    Nutritional anemias


    Gastrointestinal Tract

    • Decr. gastric secretions

      • decr. breakdown of protein-->lower amt of B12

      • incr. bac count


    • fatigue

    • diarrhea

    • shortness of breath

    • nervousness

    Central/peripheral nervous system

    • paresthesia(demylination)

    • reduction of senses

    • decr. muscle coordination

    • decr. memory

    • incr. risk for osteoporosis



    • Radio assays measure B12and folatetogether

    • IF antibody

    • dUsuppression test

    • serum homocysteine & serum methionine

    • anti-parietal cell antibodies

    • low holoTCII (early sign)

    Schillings test

    Schillings Test


    • normal absorption of VitB12 : Ileum absorbs more vitamin than body needs and excretes excess in urine

    • Abnormal/impaired absorption: no vitamin will appear in urine

      Stage 1:

    • take radioactive B12 without IF

      Stage 2:

    • take radioactive B12 with IF

    • PA from lack of IF: abnormal results in 1st and normal in 2nd

    • PA from malabsorption (intestinal): abnormal in both

    Not popular because...

    • expensive

    • complicated

      Results altered by:

    • renal insufficiency

    • laxatives (alter absorption)

    • elderly, diabetes, hypothyroid (altered excretion)

    • inadequate collection of urine

    • stool in urine

    Medical treatment

    Medical Treatment

    Usual treatment

    •     >/= 100mcg injected once a week (reduced until maintenance of monthly injections)    

    •    ** 1000mcg orally (1% will absorb by diffusion--effective even without IF)

    • Nasal gel

    • Sublingual tablets

    • Initial dose increases when deficiency due to illness

    Medical nutrition therapy

    Medical Nutrition Therapy

    • High protein diet (1.5g/kg)

    • Green leafy vegetables (iron, folic acid)

    • Liver

    • Beef, pork, eggs, 

    • DGA:

    • over age 50 consume B12 in crystalline (fortified cereals, supplements)

    High risk groups

    High Risk Groups

    • Type 1 Diabetes, autoimmune thyroid

    • Pregnancy

    • Elderly

    • HIV

    • Eating Disorder

    • vegans

    • h. pylori

    • disease/bariatric surgery



    • oral supplements can increase amt of B12(no evidence of PA)

    • Though absorbed mainly in Ileum, B12is passively absorbed throughout the entire intestine

    • rarely will oral supplementation not work

    Folate deficiency anemia

    Folate Deficiency Anemia

    Folate deficiency anemia1

    Folate Deficiency Anemia

    • A megaloblastic anemia

    • Reflects a disturbed DNA synthesis

      • Results in changes in blood cell structures and functions



    • Folate is absorbed in the SI

    • It binds to protein and is transported as 5-methyl tetrahydrofolate (THFA)

    • Folate is activated when it donates its methyl group to vitamin B12

    • MethylfolateTrap

      • Without B12 folate cannot be activated and is trapped as the inactive methyl THFA

      • B12 deficiency can result in a folate deficiency



    • Poor folate absorption

    • Increased folate requirement

    • Prolonged inadequate diet of folate

    Poor absorption

    Poor Absorption

    • Caused by

      • Medications

        • Ex. Phenytoin, methotrexate, sulfasalazine, barbituates

      • Chronic alcoholism

      • Disease

        • Crohn’s disease, celiac disease, tapeworm, tropical sprue and other digestion problems

      • Surgery affecting the upper third of the small intestine

    Increased requirement

    Increased Requirement

    • Pregnancy and lactation

      • Extra tissue demand, especially in 3rd trimester of pregnancy

    • Infancy

    • Increased hematopoiesis

      • Hemolytic anemia



    • Same clinical signs as vitamin B12 deficiency

    • Fatigue

    • Dyspnea

    • Sore tongue

    • Diarrhea

    • Irritability

    • Forgetfulness

    • Anorexia

    • Glossitis

    • Weight loss



    • RBC Indices

      • Folate deficiency results in an increased Mean corpuscular volume (MVC)

    • Low serum folate and red blood cell folate level

      • Serum folate (<3 ng/ml)

      • RBC folate (<140-160 ng/ml)

    • Elevated formiminoglutamic acid in urine

    Folate vs b 12 deficiency

    Folate vs. B12 Deficiency

    • Compare:

      • Serum folate

      • Red blood cell folate

      • Serum vitamin B12

      • Vitamin B12 bound to TCII

    • These are measured simultaneously

    Course of folate deficiency

    Course of Folate Deficiency

    • Folate stores are depleted within 2-4 mo. of a deficient diet

    • Folate deficiency occurs in four stages

    • 2 involved in depletion, 2 marked by deficiency

    Stages of folate deficiency

    Stages of Folate Deficiency

    • Stage 1: Serum folate depletion

      • <3 ng/ml)

    • Stage 2: Cell (erythrocyte) folate depletion

      • < 160 ng/ml

    • Stage 3: Damaged folate metabolism and folate-deficient erythropoiesis

      • Characterized by slowed DNA synthesis

    • Stage 4: Clinical folate deficiency anemia

      • Manifested by and elevated MCV and anemia

    Medical treatment1

    Medical Treatment

    • 1 mg folate to be taken orally every day for 2-3 weeks to replenish stores

      • This will correct megaloblastosis caused by either folate deficiency OR B12 deficiency

    • 50-100 mcg of folate daily will maintain stores

    • Symptomatic improvement is seen within 24-48 hrs of supplementation

    Nutritional anemias


    • One fresh, uncooked fruit/vegetable or juice daily

      • Orange juice has 135 mcg of folate

    • Sources of folate with > 100 mcg

      • Chicken or pork liver

      • Black beans

      • Soybean nuts

      • Spinach

      • Fortified cereals

    • RDA is 400 mcg daily for adults

    Other anemias

    Other Anemias

    Copper deficiency anemia

    Copper-Deficiency Anemia

    • Copper is essential for the proper formation of hemoglobin

    • 90% of copper in serum is incorporated into ceruloplasmin

    • Copper in ceruloplasmin has a role of oxidizing iron before it is transported in the plasma

  • Copper proteins are needed for the use of iron by developing erythrocyte

  • Rda s for copper

    RDA’s for Copper

    • Adolescents and adults for both genders have been established at .9 mg/day

    • 340 to 440 mcg/day for young children

    • 200 to 220 mcg/ day for infants

    • Net absorption of copper is 25% to 60%

    Copper deficiency anemia1

    Copper-Deficiency Anemia

    • Deficiency usually occurs in infants who are fed cow’s milk or a copper-deficient infant formula

    • Children or adults that have a malabsorption syndrome

    • Receiving long term TPN that does not supply copper

    • Copper deficiency leads to iron unable to be released leading to low serum iron and hemoglobin levels

    Anemia of protein energy malnutrition

    Anemia of Protein-Energy Malnutrition

    • Protein is essential for the proper production of hemoglobin and red blood cells

  • Protein-Energy Malnutrition (PEM)

    • Is a reduction in cell mass and thus a reduction in oxygen requirements

    • Fewer red blood cells are then required to oxygenate the tissue

    • Blood volume stays the same so there is a reduced number of red blood cells with a low hemoglobin level (hypochromic, normocytic anemia)

  • Anemia of protein energy malnutrition1

    Anemia of Protein-Energy Malnutrition

    • Can mimic an iron deficiency and is actually a physiologic (non harmful) rather than harmful anemia

    • In acute PEM loss of active tissue mass may be greater than reduction in red blood cells then leading to polycythemia

    • The body responds to this red blood cell production which is not a reflection of protein and amino acid deficiency but an oversupply of red blood cells

    Anemia of protein energy malnutrition2

    Anemia of Protein-Energy Malnutrition

    • Iron released from normal red blood cell destruction is not reused but stored

    • Iron deficiency anemia can reappear with rehabilitation

    • A diet lacking in protein usually is deficient in iron, folic acid, and less frequently vitamin B12

    • Dietitian plays a key role in assessing the diet for typical amounts of these nutrients

    Sideroblastic pyridoxine responsive anemia

    Sideroblastic (Pyridoxine-Responsive) Anemia

    • Has four primary characteristics

      • Mircrocyticand hypochromic red blood cells

      • High serum and tissue iron levels

      • Presence of an inherited defect in the formation of sigma-aminolevulinic acid synthetase (enzyme involved in hemesynthesis)

      • Buildup of iron containing immature red blood cells (sideroblasts)

    Sideroblastic pyridoxine responsive anemia1

    Sideroblastic (Pyridoxine-Responsive) Anemia

    • Patients will have:

      • Cardiovascular problems

      • Iron overload

      • Respiratory problems

      • Splenomegaly

      • Hepatomegaly

      • Occasionally seen is bronze colored skin

    Sideroblastic pyridoxine responsive anemia2

    Sideroblastic (Pyridoxine-Responsive) Anemia

    • Diagnosis is confirmed when finding sideroblasts in the bone marrow

    • The anemia responds to administration of pharmacologic doses of pyridoxine or vitamin B6

  • Treatment consists of 25 to 100 times the RDA of pyridoxine phosphate

  • Blood transfusions are given which is then done with deferoxamine an iron-chelating agent is given to eliminate iron stores

  • Vitamin e responsive anemia

    Vitamin E-Responsive Anemia

    • Hemolytic anemia occurs when defects in red blood cell membranes lead to oxidative damage and results in lysis

      • Vitamin E is involved in protecting the membrane against oxidative damage

  • Vitamin E intake in developing countries are limited, results from multiple studies suggest that poor overall nutritional status and higher prevalence of other oxidative stressors, such as malaria or HIV, predispose populations for deficiency

  • Vitamin e responsive anemia1

    Vitamin E-Responsive Anemia

    • Signs of Vitamin E deficiency

      • Early hemolysis of red blood cells

      • Peripheral neuropathy

      • Ataxia

      • Muscle weakness

      • Retinal damage leading to blindness (retinitis pigmentosa)

      • Infertility

      • Dementia

    Vitamin e responsive anemia2

    Vitamin E-Responsive Anemia

    • Children and the elderly are more vulnerable age groups

    • Men may be at higher risk for deficiency than women

      • Premature Infants need vitamin E since the production of Vitamin E doesn’t happen for a baby until right before scheduled birth

    Vitamin e responsive anemia3

    Vitamin E-Responsive Anemia

    • Since iron is a biologic oxidant a diet high in either iron or PUFA’s increases the risk of vitamin E deficiency

      • PUFA’s are incorporated into the red blood cell membranes and are more susceptible to oxidative damage

  • This anemia is becoming more and more uncommon since there is a ratio of Vitamin E to PUFA given in infant formula

    • Recommendation is .7 IU per 100 kcal and at least 1 IU of Vit. E per gram of linoleic acid

    • Supplemental vitamin E appears to be most highly bioavailable when finely dispersed in a fortified food source or as a powder

    • High doses of Vitamin E results in intraventricular hemorrhage, sepsis, necrotizing enterocolitis, liver and renal failure, and death

  • Non nutritional anemias

    Non-Nutritional Anemias

    Sports anemia

    Sports Anemia

    • Hypochromic Microcytic Transient Anemia

    • First thought the cause was soldiers as a result of mechanical trauma to the erythrocytes during long marches and was called march hemoglobinuria

    • There is an increased red blood cell destruction, decreased hemoglobin, serum iron, and ferritin concentrations in the early stages of vigorous training

    Sports anemia1

    Sports Anemia

    • Athletes that have low hemoglobin concentrations would benefit from

      • Iron rich foods

      • Protein

      • Avoiding

        • Coffee

        • Tea

        • antacids

        • H2blockers

        • Tetracycline

    Sports anemia2

    Sports Anemia

    • No athlete should take iron supplements unless there is a true iron deficiency

    • Female athletes who are vegetarian involved in endurance sports or undergoing growth are at a risk for iron deficiency and should be periodically monitored

    Anemia of pregnancy

    Anemia of Pregnancy

    • Related to increase blood volume

    • Usually resolves itself at the end of pregnancy

    • Demands of iron do increase during pregnancy so inadequate iron intake could play a role

    Anemia of chronic disease

    Anemia of Chronic Disease

    • Pro-inflammatory cytokines have a negative effect on erythropoiesis development leading to anemia in multiple diseases including:

      • Chronic infections

      • Chronic inflammatory diseases

      • Myelodysplastic syndromes

      • Malignancy

  • Mechanisms unclear but thought to be related to inflammatory cytokine-mediated pathogenesis, which includes

    • Defective production of erythropoietin

    • Reduced bone marrow response to erythropoietin

    • Defective reticulo-endothelial release of iron causing iron-deficit erythroblast by IL-1 and TNF

  • Anemia of chronic disease1

    Anemia of Chronic Disease

    • Important to not confuse this with iron deficiency since this is mild and normocytic, so not to give iron supplements when inappropriate

    • Recombinant erythropoietin therapy usually corrects this anemia

    Sickle cell anemia

    Sickle Cell Anemia

    • Chronic hemolytic anemia also known as hemoglobin S disease affects 1 of 600 blacks in US as a result of homozygous inheritance of hemoglobin S

    • Results in defective hemoglobin synthesis and produces sickle shaped red blood cells that get caught in capillaries and do not carry oxygen

    Sickle cell anemia1

    Sickle Cell Anemia

    • Characterized by episodes of pain resulting from occlusion of small blood vessels by the abnormally shaped erythrocytes

    • Hemolytic anemia & vasoocclusive disease results in:

      • Impaired liver function

      • Jaundice

      • Gallstones

      • Deteriorating renal function

    • Frequently occur in abdomen causing acute severe abdominal pain

    Sickle cell anemia2

    Sickle Cell Anemia

    • Important not to mistake this with iron deficiency since patients with sickle cell have usually excessive iron stores

    • Zinc can increase oxygen affinity of both normal and sickle shaped erythrocytes so supplements are usually beneficial

    Sickle cell anemia3

    Sickle Cell Anemia

    • Special care and attention should be given to the diet for those with sickle cell anemia:

      • Dietary intake is usually low since there is pain in the abdomen

      • Children need to make sure they have adequate amounts of calories to maintain growth and development

      • Also have metabolic increase rate since the constant inflammation and oxidative stress

      • Diets must have enough calories and provide foods high in folate, zinc, copper, and even vitamins A,C,D, and E

      • Multivitamin that containing 50 to 150% RDA of folate, zinc, and copper is recommended

      • 2 to 3 quarts of water each day is very important

      • Also patients may need higher than RDA of protein

      • Low in absorbable iron, so iron rich foods should be excluded

      • Alcohol and ascorbic acid should be avoided since they increase iron absorption



    • Affects most people in Mediterranean region

    • Severe inherited anemia’s characterized by microcytic, hypochromic, and short lived red blood cells resulting in defective hemoglobin synthesis

    • The ineffective erythropoiesis leads to an increase in plasma volume, progressive splenomegaly, and bone marrow expansion thus resulting in facial deformities, osteomalacia, and bone changes



    • There is an increase in iron absorption which causes iron to be deposited into tissues which results in oxidative damage

      • Accumulation of iron causes dysfunction of the heart, liver, and endocrine glands

      • Patients require transfusions to stay alive, they must also have regular chelation therapy to prevent buildup of iron from damaging their tissues

    • Malnutrition is common and an important factor in the stunted growth in patients



    • Kheansaard W, Mas-Oo-di S, Nilganuwong S, Tanyong DI. Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in rheumatoid arthritis. Available at: Accessed January 25, 2012.

    • Dror DK, Allen LH. Vitamin E deficiency in developing countries.Food and Nutrition Bulletin. 2011;32:124-143

    • Krause Chapter 31

    Case study1

    Case Study

    Nutritional assessment

    Nutritional assessment

    • Anthropometric:

      • Current: 5’5” 145 lbs (165 cm 65.9 kg)

      • Prepregnancy: 135 lbs (61.4 kg)

      • Prepregnancy: BMI 22.5%

    Nutritional assessment1

    Nutritional assessment

    • Biochemical:

      • Low Hgb, RBC and hematocrit

      • Low red blood cell indices

      • Low ferritin

      • High transferrin

      • High total iron binding capacity (TIBC)

    Nutritional assessment2

    Nutritional assessment

    • Clinical:

      • Vaginal bleeding and some abdominal pain

      • Tired, shortness of breath

      • Skin pale without rash

      • Everything else was non remarkable

    Nutritional assessment3

    Nutritional assessment

    • Dietary:

      • Patient states that appetite is good

      • Hasn’t taken prenatal vitamins because they make her nauseous

      • *Women require an extra 1000 mg of Iron during pregnancy (Nutrition through the life cycle textbook)

    Nutritional assessment4

    Nutritional assessment

    • Genetic:

      • Mother had cancer

      • Father had heart problems and high blood pressure

      • Grandmother had arthritis

    Nutritional assessment5

    Nutritional assessment

    • History:

      • Two pregnancies

      • Smokes (.5/day for 15 years)

      • Has had routine prenatal care

      • She is more tired with this pregnancy

      • Shortness of breath is common with pregnancies but has started earlier this time

    Nutritional diagnosis

    Nutritional Diagnosis

    • PES Statement

      • Increased iron requirement related to pregnancy as evidenced by low ferritin values.

    One day sample diet

    One-day Sample diet

    Diet rationale

    Diet Rationale

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