(10) nutritional anemia

8/10/2019 (10) Nutritional Anemia

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Nutritional Anemia

dr. Agussalim Bukhari,M.Med, PhD, Sp.GK

Department of Clinical NutritionHasanuddin University

Makassar

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Definition

Anemia is a condition in which a deficiencv inthe size or number of erythrocytes or the amount

of hemoglobin (composed of heme) limits the

exchange of oxygen and carbon dioxide

between the blood and the tissue cellsThe anemias that result from an inadequate

intake of iron, protein, certain vitamins (B12, folic

acid, pyridoxine and ascorbic acid), copper, and

other heavy metals are frequently callednutritional anemias

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Definition of Anemia

A condition in which the hemoglobin level is below

normal standard

Age Hb Ht MCHC

6 mo – 6 yrs 11 33 34

6 – 14 yrs 12 36 34

Adult Male 13 39 34

Adult Female 12 36 34

Pregnant Woman 11 33 34

HEMOGLOBIN CUT-OFF POINT ( WHO 1968 & 1972)



ETIOLOGY

1. Diminished erythropoiesis due to

nutritional def or BM failure

2. Blood loss

3. Increased hemolysis, hereditary or

acquired



Nutritional Anemia

Anemia due to nutritional deficiency whichis critical in erythropoesis (RBC synthesis)

Fe, vit.B.12, vit.B6, Vit.C, Cu and Co,Folic acid and protein (vit. A ?), vit E



ETIOLOGY of Nutritional Anemia

Inadequate intake( Primary)

Malabsorption ( TGI disease )

Increased Utilisation (Malignancy, infection)

Increased requirement (Pregnancy)

Increased excretion ( Liver disease)

Increased Destruction (malaria)



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Koilonychia (Spoon Nail)



Morphologic Classification of

Nutritional Anemia(Based on Blood smear assessments)

Hypochromic Microcytic Anemia

Due to iron deficiency

Hyperchromic Macrocytic Anemia or

Megaloblastic anemiaRelated to B12 and Folic acid

deficiency



Etiologies

Category (MCV) Nutritional causes Other causes

Microcytic (<80 u3) Iron deficiency (common),Pyridoxine def (uncommon),Copper def (uncommon)

Chronic diseases,thalassemias,hemoglobin E disorders,sideroblastic anemia

(Lead toxicity)

Normocytic (80-100u3)

PEM Chronic diseases

Macrocytic (>100 u3) Folic acid def, Vit B12 Def Alcoholism, Liver disease,hemolysis

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ETIOLOGIES

• Microcytic and macrocytic can coexist; patientcan have both iron and folic acid def.

• In these cases MCV may normal and suggest anormocytic anemia but the blood smear shows

dimorphic RBCs

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Diagnostic steps

Patient history

Physical examination

Lab: blood smear, blood count, Ht, MCV, BM

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Microcytic anemia

Common cause is iron def

Iron def: inadequate intake, absorption,

excessive loss/bleeding

Iron def is the most common nutritional anemia

and the most common nutritional deficiency.

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AnatomicLesions

FunctionalChanges

BiochemicalLesions

TissueDepletion

NutritionalInadequacy

Secondary

Inadequacy

PrimaryInadequacy

Nutrients

reserve

THE PATHOGENESIS OF NUTRITIONAL DEFICIENCY DISEASE



PATHOPHYSIOLOGY

Iron in the body: functional and storage form

Iron incorporated into heme and myoglobin

Part of enzymes : COX, catalase, peroxidase

Storage form: ferritin and hemosiderin

Dietary iron: heme iron from animal/meat and

nonheme iron from vegetables and cooking

vessels

Largely absorbed in the duodenum

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Premenopausal women need additional 0.5

mg/day to compensate menstrual loss----1.5 mg

---15 mg RDA

The group with greatest risk:

- (1) 6 mo---4 y.o- (2) Early adolescence

- (3) Menstrual women

- (4) Pregnant women

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• Heme iron 20% bioavailable, nonheme iron 3%

available• Net absorption of the two forms combined is

10%

• Each day, about 1 % RBC is destroyed releasing

about 30 mg of Iron into RES and circulation

• Of 30 mg released, about 29 mg salvaged and

only 1 mg must be replaced

• 1 mg can be absorbed from 10 mg ironcontained-diet (RDA)

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Lab

Lab findingInjury, infection,

chronicinflammation

Iron deficiency PEM

Serum iron Low Low Generally Low

Serum TIBC Normal or Low High Low

Serum Ferritin Normal or slightlyhigh

Low Generally Low

Marrow andliver iron store

Present Absent Low to absent

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Treatment

Fe sulfate 325 mg (60 mg elemental iron) 1-3

x/d with meals

Theraphy should be continued for 4 to 6 mo to

restore normal Hb and iron stores.

IV injection can be given as iron-dextranprovides 50 mg/ml (Imferon) when oral theraphy

is ineffective

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Macrocytic anemia

When caused by defic. of Folic acid or vit B12----

megaloblastic anemias because large, immature

RBC precursors (megaloblasts) accumulate in

the BM

Not all macrocytic anemias are megaloblastic;anemias in alcoholism, liver disease, and

hemolysis, the RBCs are large but megaloblasts

are not present in the BM.

In addition, macrocytosis without anemia can be

caused by cold agglutinins, hyperglycemia, and

marked leukocytosis

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IRON DEFICIENCY IN CHILD

Can be found in both developed and developing

countries

Causes

Limited iron reserve

Accelerated growth

Less varied diets

Delayed food supplement

Increased metabolism

Decreased absorption



ETIOLOGY OF ANEMIA IN CHILD

Baby < 6 Months

• Inadequate iron reserve

•

Delayed of food supplements1 - 2 years child

• GI and respiratory tract infection

• Inadequate intake

5 year Child• Parasite infection ( ankylostomiasis, trichuris,

amubiasis )



ANEMIA IN ADULT FEMALE

Increased requirement during

menstruation

Pregnancy

Lactation



Pregnancy and Lactation

Loss of iron during normal pregnancy• Foetus iron 400 mg

• Delivery 325 mg

• Lactation 175 mg

–Total 900 mg

Need additional iron of 2 mg /day for 460 days to

offset the losses



Pathogenesis of Iron deficiency

in women

Altered metabolism of iron during

pregnancy

Other causes

• Change in blood composition

• alteration in bone marrow

• Growth and development of foetus

• Inadequate intake

• Low iron pool (Consecutive

pregnancy)



Total Iron in the Body

4-5gr (Adult) & 400mg (Baby)

RBC 60%

Ferritin & hemosiderin 30%Myoglobin 5-10%

Haem enzymes <1%

Plasma iron 0.1%



IRON

Human body contains 3 to 5 g iron

Approximately 2 g as Hemoglobin and 8 mg asenzymes

Well conserved by the body ; approximately 90% isrecovered and reused extensively.

Highly reactive element that can interact with oxygento form intermediates able to damage cell membraneor degrade DNA.

Iron must be tightly bound to proteins to preventdestructive effects.



IRON COMPOUND IN THE BODY

METABOLIC PROTEIN

Heme Proteins

Hemoglobin Oxygen transport from lungs to tissues

Myoglobin Transport & store oxygen in muscle

Enzymes - Heme

cytochromes Electron transport

Cytochrom P-450 Oxidative degradation of drugs

Catalase Convert H2O2 to O2 and H2O

Enzymes-Nonheme

Iron sulfur & metalloproteins : Oxidative metabolismEnzymes-iron dependent

Tryptophan pirrolase : Oxidation of tryptophan



TRANSPORT AND STORAGE PROTEINS

Transferrin : Transport of iron and other minerals

Ferritin : Storage

Hemosiderin : Storage

IRON COMPOUND IN THE BODY



Two Types of IRON in Food

Heme-Iron:

In animals product (hemoglobin & myoglobin)

Well absorbedabout 10% of iron consumed

Nonheme-iron :

Mainly in plantsMain source of iron in the diet (~90%)

Absorption variable

affected by other factors



IRON CONT………

95% is associated with proteins e.g hemoglobin & myoglobin

Functions: Respiratory transport of O2 & CO2

(Oxygen binding component of hemoglobin and myoglobin) Co-factor for enzymes

Involved in the immune function and cognitiveperformance

Absorption : Well regulated

Transported : Transferrin

Sources : Meat, seafood, some vegetables



Iron Absorption

Healthy Individuals: 5-10% absorbed

Iron deficiency : Up to 40% absorbed Factors that affect absorption:

enhancing factors:

acid in the stomach

heme iron

high body demand

low body stores

meat protein factor (MPF)

vitamin C

Lactoferrin & Lactalbumin

in breastmilk



IRON ABSORPTION, CONT….

Inhibiting factors

dietary fiber (phytate)

oxalate

Phosphate

tannin in tea

Ca in Milk (?)

Antacids

Calcium helps to remove phosphate, oxalate

and phytate that would combine with iron and

inhibit its absorption



Iron Deficiency and Toxicity

Deficiency:

Decreased blood hemoglobin (anemia)

Low plasma iron

Increased transferrin and reduction in tissue iron

Lethargy

Toxicity

Not common, usually due to a genetic disorder



SOURCE OF IRON

Adequate diet contains no more than 6

mg/1000kcal of iron

Indonesian RDA (2004): Adult male 13 mg/day,

female 26 mg/day

Dried beans and green leafy vegetables are the

best plant sources

Best sources dietary iron

Liver, heart, kidney, lean meat

oysters, shellfish

Fish

Poultry



Adult Female :

- Menstruation --- loss 30 mg --- need 0.5-1 mg Fe/d

- Pregnancy --- 900 mg for fetus storage, deliveryand lactation, require 2 mg Fe/d

Prevention :1. Fe prophylaxis

2. Improve diet

3. Family Planning

4. Food Fortification

5. Eradication of infection & parasite

infestation

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Children Needs

(mg)

Male Needs

(mg)

Female Needs

(mg)

0-6 bl 0.5 10-12 th 13 10-12 th 20

7-12 bl 7 13-15 th 19 13-15 th 26

1-3 th 8 16-18 th 15 16-18 th 26

4-6 th 9 19-29 th 13 19-29 th 26

7-9 th 10 30-49 th 13 30-49 th 2650-64 th 13 50-64 th 12

60+ th 13 60+ th 12

Menyusui

6 bl ke-1 + 6

6 bl ke-2 +6

Indonesian RDA for Fe (2004)

S



Fe Sources

Meat and alternative

Liver ( 300 mg) : 5.3 mg

Hamburger : 2.3

Soybean (2 cups) : 2.9

Fish 300 mg : 0.3Chicken 300 mg : 0.9

Vegetables Spinach 1 cup : 1.7 mg

Asparagus 1 cup : 1.2 mg

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MEGALOBLASTIC ANEMIA IN CHILD

FOLIC ACID – Synthesis of RNA & DNA

Etiology :

1.Inadequate intake

2.Malabsorption : steatoroe idiopatik, tropical

sprue, celiac disease, other GIT disorders3.Antagonist folic acid : metotrexate, primetamin,

oral contraception

Therapy :

1.Therapy of etiology and diet

2.Folic acid 3 x 5 mg/hr or 3 x 2,5 mg for baby

3.Blood Transfusion when needed

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MEGALOBLASTIC ANEMIA IN ADULT

= An Perniciosa Addison

Etiology :

Malabsorption of Vitamin B12 due to intrinsic

factor deficiency on gaster mucosa

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MEGALOBLASTIC ANEMIA

1.Primary : inadequate intake of B12 & Folic acid

2.Secondary :

a. Malabsorption; lack of intrinsic factor, oral

contraseption – hinder folic acid absorption

b. Increased requirement ; Hb-nopathi,

hemolysis, anticonvulsant

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Therapy

1. Folic acid 5-10 mg/hr

2. Cyanocobalamine 1000 ug 2 x/wk – 250ug/wk-normal

During Pregnancy :

1. Folic acid 10 mg/d2. Severe Anemia ---- transfusion

3. Fe

Prevention in pregnancy

1. 300-500 ug folic acid with

2. 60 mg elemental Fe/d during trimester

III

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C f f l t d fi i



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Cause of folate deficiency



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FOLIC ACID



FOLIC ACID

RDA, 2004 (Adult)

Male 400ug

Female 400ug

Functions

Coenzymes in transport of carbon atomsessential for bio-synthesis of nucleic acids

Essential for normal maturation of RBC

Convert B12 to coenzyme form

Functions as co-enzyme: tetrahydrofolate (THF)

Other enzymatic reaction

Indonesian RDA for Folic acid (2004)



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Indonesian RDA for Folic acid (2004)

SOURCE OF FOLIC ACID



SOURCE OF FOLIC ACID

Green leafy vegetable,

Organ meats (liver),

lean beef,

Wheat, dry beans,lentils, cowpeas

Asparagus, broccoli,

collards, yeast

Small amount is synthesized by

intestinal tract

SOURCE OF FOLATE



SOURCE OF FOLATE

Vegetables (per 100 g): Asparagus 265 ug

Spinach 130 ug

Broccoli 160 ug

Fruits

Orange juice 75 ugRice 20 ug

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Sources of folate



Sources of folate

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Folate : deficiency/toxicity

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http://photos6.flickr.com/7287262_411edfc1a8.jpg



Deficiency : the most common vitamin deficiency in Australia

Causes: low dietary intake

- Destruction in food preparation

- Poor intestinal absorption

Impairment of DNA replication

Immature RBC cannot divide and become megaloblasts

Symptoms: megaloblastic (macrocytic) anemia

At risk: pregnant women, elderly, alcoholics,

Is linked with neural tube defect in foetus

Folate : deficiency/toxicity

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Group of compounds that contain cobaltSource : synthezised only by microorganisms

Found in food of animal originNot in plantsFunctions: coenzyme in only 2 reactions:

Isomerisation of methylmalonyl CoA --- succinylCoA

Methylation of homocysteine (bloop pressurinducer) --- methionine

Converts folate to active formMaintains sheath that surrounds nerve fibres

Vitamin B12 (Cobalamin)

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Vitamin B12 deficiency



Rare in developed countries except among strictvegetarians

Pernicious anemia: megaloblastic (macrocytic

anemia) and neurological disturbancesCauses:

Malabsorption: GI disorders, Drugs (colchisin,

metformin, antiretroviral, ethanol

Lack of intrinsic factor (in stomach)

Inadequate intake (vegans, alcoholics)

Ascorbic acid (reducing agent)

Vitamin B12-deficiency

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B12 Vitamin cont’d

RDA 2.4 ug

Source: (animal only)

Liver, kidney

Eggs, fish

Milk and dairy product

Vegans require supplement

SOURCE OF B12



SOURCE OF B12

Meats / 300 g

Liver : 6.8 ug

Beef : 2.2

Lamb : 1.8Tuna : 1.8

hamburger :1.5

telur (1 butir) : 0.6

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Indonesian RDA for Vit B12 (2004)



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( )

Indonesian RDA for Vit B12 (2004)



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( )

Children Needs (ug) Male Needs (ug) Female Needs (ug)

0-6 bl 0.4 10-12 th 1.8 10-12 th 1.8

7-12 bl 0.5 13-15 th 2.4 13-15 th 2.4

1-3 th 0.9 16-18 th 2.4 16-18 th 2.4

4-6 th 5 19-29 th 2.4 19-29 th 2.4

7-9 th 1.5 30-49 th 2.4 30-49 th 2.4

50-64 th 2.4 50-64 th 2.460+ th 2.4 60+ th 2.4

Ibu Hamil +0.2

Menyusui

6 bl ke-1 + 0.4

6 bl ke-2 +0.4



COPPER (Cu)-DEFICIENCY ANEMIA

Copper is a component of many enzymes

Copper and other heavy metals are essentialfor the proper formation of hemoglobin

Oxidizing iron before it is transported(ceruloplasmin, copper containing protein,

required for normal mobilization of iron from itsstorage site to the plasma)

Iron cannot be released----low serum iron & Hbin the presence of normal iron stores

Plays role in mitochondrial energy production,protection from oxidants, and synthesis ofmelanine and cathecolamine



SOURCE OF COPPER

Most diet provide 2 mg/day

RDA 1.5 – 3 mg/day

Food high in copper

Oysters, shellfish

Liver, Kidneys

Chocolate

Nuts

Dried legumes, Dried foods

Cereals Poultry



COBALT (Co)

A component of vitamin B12 (cobalamin)

This vitamin is essential for maturation of red

blood cells and normal functioning of all cells

Requirement expressed in terms of Vit B12 : 2.4

ug daily

Toxicity : intake of 10 to 20 ug/kg Body weight :

high intake cobalt in animal diet produce

polycytemia, bone marrow hyperplasia,

reticulocytosis, and increased blood volume Deficiency: related to Vit B12 deficiency ---

macrocytic anemia



SOURCE OF COBALT

RDA 1.4 - 2.0 ug/day

Liver, kidney,

Oysters, clams

Poultry

Milk

PYRIDOXINE (VIT. B6)



Active form of vitamin B6 is Pyridoxal

phosphate (PLP), a coenzyme for numerousenzymes involved in practically all reactions in

the metabolism of amino acids and in several

aspects of the metabolism of neurotransmitters,

glycogen, sphingolipids, heme, and steroidsSideroblastic anemia has inherited defect in the

formation of 8-aminolevulinic acid synthetase,

an enzyme involved in heme

synthesis( pyridoxal-5-phosphate is necessary in

this reaction)

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SOURCES OF PYRIDOXINE



SOURCES OF PYRIDOXINE

Ready-to-eat cereals

Potato, baked, I

Banana, IRice, white, cooked, I cup

Chicken, light meat, fried,,3 oz

Pork chop, baked, 3 oz

Baked beans, vegetarian, I cup

Beef, hamburger, broiled, 3 oz

Chicken, dark meat, fried,3 ozTuna. canned. 3 oz

Sunflower seeds, kernels, 7+ cup

Avocado, California, 1 oz

Whole wheat bread. I slice

Up to 3.6

0.63

0.430.30

0.53

0.44

0.34

0.32

0.310.10

0.26

0.08

0.05

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Vitamin B6 is widely distributed in foods, occurring in greatest

concentrations in meats, whole grain products (especially

wheat), vegetables, and nuts. Animal origin has better bioavailability

RDA = 1.3 mg/day

Vitamin K (K-1 and K-2)



ta ( a d )

Source: K-1: green plant leaves

K-2 produced by bacteria in human

intestine

RDA: 55-65 ug

Function: Clotting of Blood. Involved in theformation of prothrombine and blood

clotting factors (II, VII, IX, X)

Deficiency: Hemorrhage rarely seen in Australia.

May occur in newborn (low at birth).

Can be secondary to disease or drug

treatment

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(10) nutritional anemia

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