Transcript Nutritional Anemias

Medical Nutrition
Therapy for Anemia
Anemia
Definition: deficiency in size or number
of red blood cells or amount of
hemoglobin they contain
Defined as a hemoglobin concentration
below the 95th %ile for healthy
reference populations
Not a disease but a symptom of
conditions including extensive blood
loss, excessive blood cell destruction,
or decreased blood cell formation
Classification of Anemia
Based on cell size (MCV)
Macrocytic (large) MCV 100+ fl
(femtoliters)
Normocytic (normal) MCV 80-99 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 (microcytic) erythrocytes
and a diminished level of
circulating hemoglobin
Last stage of iron deficiency
Represents the end point of a long
period of iron deprivation
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 dysfunction
Stage 2: Severe depletion of iron
stores; no dysfunction
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 sensitive—chief
storage form of iron; directly
proportional to iron stored in cells
Tests for Iron Deficiency
Zinc protoporphyrin/heme ratio
(ZPPH) protoporphyrin binds iron
to form heme or zinc to form zinc
protoporphyrin
In the presence of iron deficiency,
ratio will rise (iron deficiency
defined as ratio>1:12,000)
Not affected by hematocrit or
other causes of anemia; specific to
iron deficiency
Tests for Iron Deficiency
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Total iron binding capacity (TIBC)—
capacity of transferrin to bind iron
Transferrin—globulin that binds/transports
Fe from gut wall to tissues
Percent saturation of transferrin (calculate
by dividing serum iron by the TIBC)
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TIBC increases in iron deficiency
As stored iron falls, saturation of transferrin
decreases
Iron Deficiency:
Clinical Findings
Early
Inadequate muscle
function
Growth
abnormalities
Epithelial disorders
Reduced
immunocompetenc
e
Late
Defects in
epithelial tissues
Gastritis
Cardiac failure
Nutritional deficiency anaemia
clinical application
Angular
Cheilosis
Glossitis
Koilonychia
Marrow iron stores
Plummer-Vinson
syndrome
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 sulfate, ferrous lactate, ferrous
fumarate)
Best absorbed on an empty stomach
but if irritation occurs, give with meals
Dosage 50-200 mg of elemental iron for
adults; 6 mg/kg body weight for
children
Generally supplement for 3 months (4-5
months if taken with meals)
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 stores, the greater the rate of
absorption
Vitamin C—binds iron to form a
readily
absorbed complex
Heme sources (meat, poultry, fish)—
about 15% absorbable
Nonheme iron (grains, vegetables,
eggs)—about 3% to 8% absorbable
Supplementation for
Iron Deficiency Anemia
If patient fails to respond
May not be taking supplements
May not be absorbing iron (celiac
disease, steatorrhea, hemodialysis)
May be bleeding
May need IV iron dextran (can cause
allergic reactions)
Rx of iron deficiency:
Children
Elemental iron 3-6mg/kg/day,
contd.. 4-6 months
Check Hb at 4 weeks
Adults
Ferrous
sulphate/gluconate/fumarate
Iron polymaltose complex
Elemental iron 200mg/day
Parental Iron
Normal Hb/PatientHbXwt(kg)X2.2
Diet for Iron Deficiency:
In adults, limit milk intake - 500 mL/day
Avoid excess caffeine
Eat iron-rich foods
Protein
foods
Vegetables
 Meats

 Fish & Shelfish
Dried peas & beans
Greens
 Eggs
Fruits
 Dried fruit
breads
 Juices
 Most fresh fruits
cereal

Grains
Iron-fortified
Dry cereals

Oatmeal
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
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 (IF)
May be caused by strict vegan diet
Also can be caused by ↓gastric acid
secretion, gastric atrophy, H-pylori,
gastrectomy, disorders of the small
intestine (celiac disease, regional
enteritis, resections), drugs that inhibit
B12 absorption including neomycin,
alcohol, colchicine, metformin,
pancreatic disease
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 I—early negative vitamin B12 balance
Stage II—vitamin B12 depletion
Stage III—damaged metabolism: vitamin
B12 deficient erythropoiesis
Stage IV—clinical damage including vitamin
B12 anemia
Pernicious anemia—numbness in hands and
feet; poor muscular coordination; poor
memory; hallucinations
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 vegetables
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 5methyltetrahydr
o-folate (an
inactive form)
B12 allows the
removal of the
5-methyl group
to form THFA
Stages of Folate Depletion and
Deficiency
Stage I—early negative folate
balance (serum depletion)
Stage II—negative folate balance
(cell
depletion)
Stage III—damaged folate
metabolism with folate-deficient
erythropoiesis
Stage IV—clinical folate deficiency
anemia
Diagnosis of Folate Deficiency
Folate stores are depleted after 24 months on deficient diet
Megaloblastic anemia, low
leukocytes and platelets
To differentiate from B12, measure
serum folate, RBC folate (more
reflective of body stores) serum
B12
High formiminoglutamic acid
(FIGLU) in the urine also
diagnostic
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 storage sites
In copper deficient state, result is low
serum iron and hemoglobin, even when
iron stores are normal
Copper is widespread in foods and
needed in tiny amounts
Sometimes occurs in infants fed
deficient formula or cow’s milk, adults
and children with malabsorption or on
TPN without copper
Diagnosis is important, since more iron
won’t help and may interfere with
copper absorption
Sideroblastic Anemia
Microcytic, hypochromic form
Inherited defect of heme synthesis enzyme
High serum and tissue iron levels
Buildup of immature sideroblasts—
hence the name
B6 is essential—must replace 25 to 100
times the RDA; may need lifelong
replacement
Pyridoxine-responsive anemia, distinguished
from anemia caused by pyridoxine deficiency
Hemolytic Anemia
Oxidative damage to cells—lysis occurs
Vitamin E is an antioxidant that seems to
be protective.
This anemia can occur in newborns,
especially preemies.
Non-nutritional Anemias
Sports anemia (hypochromic
microcytic transient anemia)
Anemia of pregnancy: dilutional
Anemia of inflammation,
infection, or malignancy
(anemia of chronic disease)
Sickle cell anemia
Thalassemias
Sports Anemia
Transient—usually in athletes who are
runners; from compression of RBCs in
feet until they burst, releasing hemoglobin
Check lab values
Counsel about a proper diet
Sickle Cell Anemia
Protein-energy malnutrition common;
may have poor intake and increased
energy needs
Be careful not to overdo iron in diet or
supplements; iron stores are often high
due to frequent transfusions; avoid iron
rich foods, alcohol, and ascorbic acid
which enhance iron absorption
Promote foods high in copper, zinc and
folate as needs are increased due to
constant replacement of erythrocytes
Zinc supplements may be useful
Thalassemia
Severe inherited anemia affecting mostly
people of Mediterranean extraction
Defective globin formation in hemoglobin
leads to increased blood volume,
splenomegaly, bone marrow expansion,
facial deformities, osteomalacia, bone
changes
Iron buildup due to transfusions requires
chelation therapy to remove excess iron
Medical and Nutritional
Management of Anemia
It is important to be familiar with the
etiology and treatment of nutritional
and non-nutritional anemias
Many non-nutritional anemias have
nutritional implications
It is critical to DIAGNOSE before
treating anemias with nutritional or
non-nutritional therapies