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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)
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ETIOLOGY
1. Diminished erythropoiesis due to
nutritional def or BM failure
2. Blood loss
3. Increased hemolysis, hereditary or
acquired
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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
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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)
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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
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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
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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
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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 )
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ANEMIA IN ADULT FEMALE
Increased requirement during
menstruation
Pregnancy
Lactation
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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
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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)
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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%
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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.
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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
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TRANSPORT AND STORAGE PROTEINS
Transferrin : Transport of iron and other minerals
Ferritin : Storage
Hemosiderin : Storage
IRON COMPOUND IN THE BODY
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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
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Sources of folate
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Folate : deficiency/toxicity
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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
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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
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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
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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
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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
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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
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SOURCE OF COBALT
RDA 1.4 - 2.0 ug/day
Liver, kidney,
Oysters, clams
Poultry
Milk
PYRIDOXINE (VIT. B6)
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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
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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)
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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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