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NUTRITIONAL CARE IN

ANEMIA

Nutrition Departement
Faculty of Medicine
University of Sumatera Utara
Classification
Microcytic (small cell)
- Major nutritional cause is iron deficiency
- Minor pirydoxin & copper deficiency

Normocytic anemia
- PEM & various chronic disease

Macrocytic
- Vitamin B12 & folic acid deficiency
Etiology of anemia
Nutritional anemia caused
by Fe, protein , certain vitamin
(B12,folic acid,pyridoxine,vit.C) &
Cu.
Hemorrhage anemia
Genetic abnormalities
Chronic disease states
Drug toxicity
Iron-deficiency anemia is the
most common nutritional anemia
and perhaps
the most common nutritional
deficiency disorder in the world
Iron deficiency anemia
Is charaterized by the production of small RBC and a
diminished level of circulating Hb.
This is the last stage of Fe deficiency,and re presents
the end point of a long period of Fe deprivation.
The condition can arise from.
Inadequte dietary intake secondary to a poor diet
without supplementation.
Inadequate absorption resulting from diarrhea,
achlor hydria, intestinal disease i.e celiac
disease,atrophic gastritis,partial or total
gastrectomy, or drug interference.
Inadequate utilization secondary to chronic
gastrointestinal disturbances
Increased iron requirement for growth of blood
volume, which occurs during infancy, adolescence,
pregnancy, and lactation.
Increased excretion because of excessive
menstrual blood (in females), hemorrhage
from injury, or chronic blood loss from
bleeding ulcer,beleeding
hemorrhoids,esophageal varices,regional
enteritis,ulcerative colitis,parasitic or
malignant disease.
Defective release of iron from stores into the
plasma and defective iron use caused by a
chronic inflammation or other chronic disorder.
Dietary Iron
Heme Fe (meat, fish and poultry) best
absorbed
Non-heme Fe (cereal, vegetables) taken up less
avidly
Heme Fe 20% bioavailable, nonheme only 3%
Ionic Fe (Fe++) also well absorbed
>1/3 of Fe from fortification of flour
Tea inhibits Fe absorption
Factors affecting absorption
Enhancing factors : Inhibiting factors :

- Ascorbic acid - Carbonates


- MFP - Oxalates
(Meat,Fish,Poultry) - Phytates
factor. - Tanin
Megaloblastic anemia
This anemia is charaterized by the presence of
large,immature, abnormal,RBC progenitor in the
bone marrow.
95% of cases are caused by deficiency of Vitamin
B12 & folic acid.
Both vitamins are essential to
The synthesis of nucleoproteins.
Hematologic changes.

Normal body folate stores are depleted within 2 to


4 months in individuals consuming folate-
deficiency diets.
Folic acid deficiency anemia
Dietary Sources

Widely distributed in :
Yeast
Liver and other organ meat
Leafy vegetables
Fresh fruit
Enriched bread and cereal products

Oranges juice the highest contributor of folic acid


to the American diet

Between 50% and 90% of folate in the food


destroyed by prolonged cooking and processing
Treatment
Plasma level should be used to guide therapy

Readily resolved with a 1 mg daily oral


supplement

In the patients with malabsorption,


Initial treatment parental folate
Maintenance oral therapy
Vitamin B12 Deficiency
Most often caused by impaired
absorption

Strict vegetarian (vegans) who consume


no dairy products, eggs or meat
increased risk for deficiencies

The main cause of vitamin B12


deficiency is PERNICIOUS ANEMIA
Pernicious anemia is a megaloblastic ,macrocytic
anemia caused by a deficiency of vit.B12,most
commonly from a lack of IF (Intrinsic Factor)
Vit.B12 deficiency anemia occcurs in
Rarely, strict vegetarians whose diet contain no
vit.B12,except for traces found in plants
contaminated by microorganisms capable of
synthesizing vit.B12.
Antibody to IF in saliva or gastric juices
Small intestine disorders affecting the ileum (i.e celiac
disease,idiophatic steatorrhea,tropical sprue,cancers
involving the small intestine.
Drugs (paraaminosalicylic
acid,colchicine,neomycin,metformin,antiretrovirals)
Long-term ingestion of alcohol or calcium-chelating
agents.
The development of vitamin B12
deficiency
First stage, characterized by a negative vitamin
B12 balance,
During which the plasma vitamin B12 level is
marginal and only vitamin B carries in plasma
(transcobalamins) may be abnormally low

Subsequently, the plasma vitamin B12 level falls


When the level reaches 100 150 pg/ml,
neutrophils begins to appear hypersegmented

Finally, macroovalocytes appear, the MCV is


elevated and the Hb level drops

Anemia develops IN THE LATER STAGES of vitamin


B12 deficiency like Iron Deficiency.
Dietary Sources
Found ONLY in food of animal origin
Most meat and dairy products contain B12
Beef liver : an especially rich sources

RDA
and 2 g / day
During pregnancy 2,2 g / day
During lactation 2,6 g / day
Remission of the sign & symptoms a single
intramuscular injection of 100 to 1000 g of
cyanocobalamins or hydroxocobalamins

Daily administration of 100 g for several


days

For Pernicous Anemia patients & other who


need continued parenteral therapy
injections of 100 g every month
OTHER NUTRITIONAL ANEMIAS
Anemia of Protein Energy Malnutrition.
Protein is essential for the proper production of
hemoglobin and RBCs.
In acute PEM ,the loss of active tissue mass may be
greater than the reduction in the number of RBCs.
The anemia of PEM may be complicated by
Deficiencies of Fe & other nutrients
Associated infection
Parasitic infestation
Malabsorption.
A diet lacking in protein is usually deficient in
Fe,Folic acid,and Vit.B12.
Copper Deficiency Anemia.
Cu is essential for the proper formation of Hb.
Ceruloplasmin, a Cu - containing protein, is required
for
1. Normal mobilization of Fe from its storage sites to
the plasma in Cu deficient state,Fe can
not be released low serum Fe & Hb
level ,even in the presence of normal Fe stores.
2. Use of Fe for the developing RBCs
3. Optimal function of RBCs membrane.
Cu deficient may occurs in
Infants who are fed cows milk or copper-deficient
infant formula
Children & adults who have a malabsorbtion
syndrome or who are receiving long-term total
parenteral nutrition that does not supply Copper.
Sideroblastic (Pyridoxine-Responsive) Anemia.
Is charaterized by a derangement in the final pathway
of Heme synthesis buildup of iron-containing
immature RBCs, which has 4 characteristics.
Microcytic & hypochromic RBCs
High serum and tissue iron levels
The presence of an inherited defect in the formation
of aminolevulinic acid synthetase.
A buildup of iron-containing immature RBCs
(sideroblast).
Aquired sideroblast anemias such as those attributable
to drug therapy (isoniazid, chloramphenicol),Copper
deficiency, hypothermia, and alcoholism are not
responsive to vit.B6 (pyridoxine) administration.
Vitamin E-responsive hemolytic anemia.
Hemolytic anemia occurs when defects in RBC
membranes lead to oxidative damage and
eventually to cell lysis.
Caused by shortened survival of mature RBCs.
Vit.E (anti oxidant) is involved in protecting the
membrane against oxidative damage.
Signs noted in vit.E deficiency is early hemolysis
of RBCs.