Nutritional
Anemias
Spenser Parker, Katie
Gardner, Juliette Soelberg,
McKell Compton
Case Study
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Patient SH
31 yr. old female
23rd week of gestation, 3rd pregnancy
Chief complaint:
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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
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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
CBC
 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
Anemia
Erythropoiesis
 Occurs in bone marrow
 Erythrocytes derived from precursor cells, erythroblasts/
normoblasts
 Abnormal erythroblasts called megaloblasts
 Erythropoietin stimulates uncommitted stem cells to differentiate
into proerythroblasts
 Hgb is 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
 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
Heme (Fe+porphyrin)
(globin+heme)
Hemoglobin
Iron
 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: 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: 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
Absorption
 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
 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
Etiology
1.
2.
3.
4.
5.
6.
Inadequate ingestion
Inadequate absorption
Inadequate utilization
Increased requirement
Increased blood loss or excretion
Defects in release from stores
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 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
1. Plasma ferritin
2. Plasma iron
3. Total circulating transferrin
4. Saturation of circulating transferrin
5. Saturation of ferritin with iron
6. Soluble serum transferrin receptor (STFR)
Diagnosis
 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
Normal Levels:
Ferritin: Males:12-300 ng/mL Female:10-150
ng/mL
Serum Iron: Male (80-180 mcg/dL) Female (60160mcg/dL).
Total Iron-Binding Capacity (TIBC): 250-460
mcg/dL.
Transferrin: Male (215-365 mg/dL) Female (250380 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
 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
 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 irondeficiency 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
 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
 Transferrin saturation (%)= Serum iron level x (100%)
TIBC
 Percentage of transferrin and other mobile ironbinding 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
 Hematocrit (Hct)-measure of the percentage of total blood volume
that is made up by the RBCs.
 Decreased levels of Hct indicate anemia.
 Hct can 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
 Hgb levels 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 be anemic.
 RBC alters with pregnancy, high altitudes, and
hydration status.
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
 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
Pathophysiology
 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
 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
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
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
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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 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
Continued
 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
Continued
 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
 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 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 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
 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
 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
 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 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
 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
B12 Deficiency
Pathophysiology
 B12
is freed from protein (by way of gastric
secretions)
 B12 binds to R-protein
 R-protein hydrolyzed in sm. Intestine
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 IF
Intrinsic factor bind to B12
binds to specific membrane receptor on
illeul brush border
 B12 is absorbed
 B12 binds to transcobalamins (TCI, TCII, etc)
Etiology
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
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Addisonian Pernicious
Anemia
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gastrectomy
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celiac
tropical sprue
strictures, lesions, resection
specific malabsorptions
competition for B12
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blocking
binding
sm. intestine disorders
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total
subtotal
antibody to IF
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hereditary, defective,
autoimmunity
bacteria(H. pylori)
pancreatic disease
HIV
S/S
Gastrointestinal Tract
 Decr. gastric secretions
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decr. breakdown of
protein-->lower amt
of B12
incr. bac count
Other
fatigue
diarrhea
shortness of breath
nervousness
Central/peripheral
nervous system
 paresthesia
(demylination)
 reduction of senses
 decr. muscle
coordination
 decr. memory
 incr. risk for
osteoporosis
Diagnosis
 Radio
assays measure B12 and folate
together
 IF antibody
 dU suppression test
 serum homocysteine & serum methionine
 anti-parietal cell antibodies
 low holoTCII (early sign)
Schillings Test
Not popular because...
Note:
 expensive
 normal absorption of Vit B12 : Ileum
 complicated
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
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PA from lack of IF: abnormal results in
1st and normal in 2nd
PA from malabsorption (intestinal):
abnormal in both
Results altered by:
 renal insufficiency
 laxatives (alter absorption)
 elderly, diabetes,
hypothyroid (altered
excretion)
 inadequate collection of
urine
 stool in urine
Medical Treatment
Usual treatment

>/= 100mcg injected once a week
(reduced until maintenance of monthly
injections)
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** 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
 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
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Type 1 Diabetes, autoimmune thyroid
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Pregnancy
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Elderly
HIV
Eating Disorder
vegans
h. pylori
disease/bariatric surgery
Supplementation
 oral
supplements can increase amt of B12
(no evidence of PA)
 Though absorbed mainly in Ileum, B12 is
passively absorbed throughout the entire
intestine
 rarely will oral supplementation not work
Folate
Deficiency
Anemia
Folate Deficiency Anemia
A
megaloblastic anemia
 Reflects a disturbed DNA synthesis

Results in changes in blood cell structures
and functions
Pathophysiology
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Folate is absorbed in the SI
It binds to protein and is transported as 5methyl tetrahydrofolate (THFA)
Folate is activated when it donates its methyl
group to vitamin B12
Methylfolate Trap


Without B12 folate cannot be activated and is
trapped as the inactive methyl THFA
B12 deficiency can result in a folate deficiency
Etiology
 Poor
folate absorption
 Increased folate requirement
 Prolonged inadequate diet of folate
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
 Pregnancy

and lactation
Extra tissue demand, especially in 3rd
trimester of pregnancy
 Infancy
 Increased

hematopoiesis
Hemolytic anemia
Symptoms
 Fatigue
 Dyspnea
 Sore
 Same
clinical signs as
vitamin B12 deficiency
tongue
 Diarrhea
 Irritability
 Forgetfulness
 Anorexia
 Glossitis
 Weight loss
Diagnosis
 RBC

Indices
Folate deficiency results in an increased
Mean corpuscular volume (MVC)
 Low
serum folate and red blood cell
folate level
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
Serum folate (<3 ng/ml)
RBC folate (<140-160 ng/ml)
 Elevated
formiminoglutamic acid in urine
Folate vs. B12 Deficiency
 Compare:
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Serum folate
Red blood cell folate
Serum vitamin B12
Vitamin B12 bound to TCII
 These
are measured simultaneously
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

Stage 1: Serum folate depletion

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Stage 2: Cell (erythrocyte) folate depletion


< 160 ng/ml
Stage 3: Damaged folate metabolism and
folate-deficient erythropoiesis


<3 ng/ml)
Characterized by slowed DNA synthesis
Stage 4: Clinical folate deficiency anemia

Manifested by and elevated MCV and anemia
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
MNT

One fresh, uncooked fruit/vegetable or juice
daily

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Sources of folate with > 100 mcg
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Orange juice has 135 mcg of folate
Chicken or pork liver
Black beans
Soybean nuts
Spinach
Fortified cereals
RDA is 400 mcg daily for adults
Other
Anemias
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
 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 Anemia




Deficiency usually occurs in infants
who are fed cow’s milk or a copperdeficient 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


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
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
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 (PyridoxineResponsive) Anemia

Has four primary characteristics




Mircrocytic and 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 heme synthesis)
Buildup of iron containing immature red blood
cells (sideroblasts)
Sideroblastic (PyridoxineResponsive) Anemia
 Patients

will have:
Cardiovascular problems
 Iron
overload
 Respiratory problems
 Splenomegaly
 Hepatomegaly
 Occasionally seen is bronze colored skin
Sideroblastic (PyridoxineResponsive) 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


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 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 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 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
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 Anemia
 Athletes
that have low hemoglobin
concentrations would benefit from



Iron rich foods
Protein
Avoiding





Coffee
Tea
antacids
H2 blockers
Tetracycline
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
 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

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 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
 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 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 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 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
Thalassemais
 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
Thalassemais
 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
Sources



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:
http://www.springerlink.com.erl.lib.byu.edu/conte
nt/h36027236338n15l/fulltext.pdf. 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 Study
Nutritional assessment
 Anthropometric:



Current: 5’5” 145 lbs (165 cm 65.9 kg)
Prepregnancy: 135 lbs (61.4 kg)
Prepregnancy: BMI 22.5%
Nutritional assessment
 Biochemical:





Low Hgb, RBC and hematocrit
Low red blood cell indices
Low ferritin
High transferrin
High total iron binding capacity (TIBC)
Nutritional assessment
 Clinical:




Vaginal bleeding and some abdominal
pain
Tired, shortness of breath
Skin pale without rash
Everything else was non remarkable
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 assessment

Genetic:



Mother had cancer
Father had heart problems and high blood
pressure
Grandmother had arthritis
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
 PES

Statement
Increased iron requirement related to
pregnancy as evidenced by low ferritin
values.
One-day Sample diet
Diet Rationale