Nutritional Anemia.ppt by Dr Amna Mahmood

nutritional anemia are common types of anemia in developing countries

1. NUTRITIONAL
ANEMIA

2. •Roleofironinnutritionalanemia
•RolevitaminB9andB12innutritional
anemia
•RoleofvitaminKandCinbloodclotting

3. Symptoms of anemia

5. NUTRITIONAL ANEMIA
DEFINITION
Itisadiseasesyndrome
causedbyMalnutrition.
•AcctoWHO–
•Aconditioninwhich
hemoglobincontentofblood
islowerthannormal,asa
resultofdeficiencyofoneor
moreessentialnutrients,
speciallyiron
•

6. Nutritional Anemia
•Deficiencyof
A.Iron
B.Folate
C.VitaminB
12
D.Protein
•Correctedby
supplementation

8. ANAEMIA
•ANAEMIA-InsufficientHbtocarryoutO
2
requirementbytissues.
•WHOdefinition:Hbconc.11gm/dl
•Fordevelopingcountries:cutofflevel
suggestedis10gm/dl

9. INTRODUCTION
Irondeficiency(ID)isoneofthemostfrequent
nutritiondeficiencyallroundtheworld
Itsprevalenceishigherinchildrenandchildbearing
agewomen
Irondeficiencyanemia(IDA)mainlyaffectschild
behavioranddevelopment,workperformanceand
immunity

10. Prevalence
–Widespreadpublichealthproblem
withmajorconsequencesfor
humanhealthandsocio-economic
development
–WHOestimates2billionpeopleare
affectedworldwide
–>50%duetoirondeficiency

12. WHO cut off criteria OF hb%
(in venous blood)
Adultman 13 gm/dl
Adult woman (non
pregnant)
12 gm/dl
Adult woman
(pregnant)
11 gm/dl
Child above 6 yrs12 gm/dl
Child below 6 yrs11 gm/dl

13. Iron requirements (RDA)Females 11 – 14 15
15 – 18 15
19 – 24 15
25 – 50 15
51 + 10
Pregnant 30
Lactating 1
st
6
months
15
2
nd
6
months
15
Category Age
(years)
RDA – Iron
(mg)
Infants 0 – 0.5 6
0.5 – 1 10
Children 1 – 3 10
4 – 6 10
7 – 10 10
Males 11 – 14 12
15 – 18 12
19 – 24 10
25 – 50 10
51 + 10

14. 14

17. •Ironisanessentialmineralforhumandevelopment
andfunction,ithelpsformationofHb-theoxygen
carryingcomponentofRBC
•Ironiscriticalformotorandcognitivedevelopment
inChildhood,andforphysicalactivityinallhumans.
•ThecentralfunctionofIronis“OXYGEN
TRANSPORT”andCellrespiration

19. Causes of IDA
•Increaseddemandforiron
–Rapidgrowthininfancyor
adolescence
–Pregnancy
–Erythropoietintherapy
•Increasedironloss
–Chronicbloodloss
–Menses
–Acutebloodloss
–Blooddonation
–Phlebotomyastreatmentfor
polycythemiavera
•Decreased iron
intakeorabsorption
-Inadequatediet
-Malabsorptionfrom
disease (sprue,
Crohn'sdisease)
-Malabsorptionfrom
surgery (post-
gastrectomy)
-Acuteorchronic
inflammation

20. I. ClinicalIndices
•Pallorof the:
•Conjunctiva,
•Tongue,
•Nailbedand palm

21. Unique Physical Exam
findings
–Koilonychia -Cheilosis
..spooning of the ..fissures at the
corners
fingernails of the mouth

22. Pale conjunctiva
An enlarged spleen
Cold hands and feet
Frequent infections
Shortness of breath
Swelling or soreness of the tongue

23. •Assessment of IDA
I.Clinical and
II.Laboratory indices.
•Laboratory indices are the most
common methods used to assess iron
nutrition status.

24. II. Laboratory Indices
1.Low Hemoglobin
2.Low Hematocrit
3.Low Mean Corpuscular Volume
4.Serum Ferritin <10ng/ml
5.Transferrin Saturation<15%
6.TIBC>350µg/dl
7.Increased free erythrocyte
protoporphiryn

25. Checking Haemoglobin Level

26. TREATMENT
IRON SUPPLEMENT

28. Sources of Iron
Thereare2typesofironinthe
diet;haemironandnon-haem
iron
HaemironispresentinHb
containinganimalfoodlikemeat,
liver&spleen
Non-haemironisobtainedfrom
cereals,vegetables&beans
Milkisapoorsourceofiron,
hencebreast-fedbabiesneed
ironsupplements

30. HIGH RISK FACTORS

31. CLASSIFICATION OF VITAMINS

32. Folic acid (Vitamin B
9)
Awatersolublevitaminusedwidelyinpregnancyandforthetreatment
ofanemia
Itisinvolvedincarbontransferreactionsofaminoacidmetabolism
Essentialforpurineandpyrimidinesynthesis
Vitalforhematopoiesisandredbloodcellproduction

34. THFAwhichis5,6,7,8-tetrahydrofolicacidisinactivebutactsasacarrier
ofdifferentone-carbongroups
Methyl,formyl,formiminohydroxymethyl,methylene,methenyl
3possibilities
AtNno.5
AtNno.10
AtNno.5and10
Theactiveformis5-methyltetrahydrofolicacid

35. •Folic acidis the synthetic (simple)formof folate
Used in nutritional supplements and food
fortification
Only form that can be transported across
membranes
Most oxidized and stable form of folate

36. Main functions of folic acid
•NeededforDNAsynthesisinallcellsofthebodye.gRBCs
•Preventionofneuraltubedefects
•Playsamajorroleinproteinsynthesis
•Metabolismofhomocysteine
•Roleincancerprevention

37. One carbon metabolism
•ItisimportantinAminoacidmetabolismfortransferor
exchangeofonecarbonunits
•Thefollowingonecarbonfragmentsareinvolvedinbiological
reactions
Methyl (-CH
3)
Hydroxymethyl(–CH
2OH)
Methylene (=CH
2)
Methenyl (-CH=)
Formyl (–CH=O)
Formimino (–CH=NH)

43. The Methyl Folate Trap
Theconversionof5,10-methylene-THFto5-methyl-THF
bymethylenetetrahydrofolatereductase(MTHFR)is
irreversible
Theonlywaytouse5-methyl-THFisinthevitamin-B
12-
dependentremethylationofhomocysteinetomethionine
(regeneratingTHF)
Thisreactionisdependenton5-methyl-THFandthe
availabilityofvitamin-B
12

45. Inhumans,thisistheonlyknowndirectlinkofthemetabolismoftwo
vitamins;folicacidandvitamin-B
12
Incasesofvitamin-B
12deficiencyanintracellulardeficiencyofbiologically
activeTHFarises
Thissituationiscalleda‘folatetrap’(ormethylgrouptrap)
becausetheconcentrationof5-methyl-THFcontinuestorisebutduetoit
beingpreventedfromreleasingmethylgroups,a‘metabolicdead-end
situation’develops,whichleadstotheinevitableblockageofthe
methylationcycle

46. Theco-factorsfortheC1-transfersdecreaseleadingtodecreasedreplication&
celldivision
Thedeficiencyfirstaffectsthehighlyproliferatinghaematopoieticcellsinthe
bonemarrowpancytopenia
clinicallynodifferencebetweenvitamin-B
12deficiencyanemiaandfolicacid
deficiencyanemia
Ifsuchananemiaistreatedwithvitamin-B
12,theblockageisimmediately
stoppedandthebloodcountquicklynormalizes
However,iftheanemiaisexclusivelytreatedwithfolicacid,itisconvertedto
dihydrofolateandTHF

47. Long-termtherapyusinghighdosesoffolicacidcould
thereforeconcealtherealcausei.e.pernicious(vitaminB
12-
deficiency)anemiaforalongtime
Theserumfolatecontinuestorise(congestionofnon-
regenerated5-methyl-THF)whiletheintracellularfolate
concentration(erythrocytes)drops
Thissituationinterruptsthemethylationcyclewithnumerous
cellprocessessuchassynthesisofmyelinresultinginserious
neurologicaldamage

48. •Dietary deficiency is the commonest reason for
folic acid deficiency
•They may be due to:
•Inadequate intake as seen in alcoholics
•Over cooking of food
•Impaired absorption due to diseases of the small
intestine
•Drug interference eg., sulfamethoxazole
Deficiency of Folic Acid

49. •Increased demand of folic acid as seen in
•Pregnancy
•Hemolytic anemia
•Other causes
•Loss in patients undergoing hemodialysis
•Impaired synthesis of active form seen I
npatientsreceiving folic acid antagonists
such as methotrexate

50. Clinical Features
•Megaloblastic anemia:
characterized by hyperchromicmacrocytic
anemia
•Megaloblastic changes in bone
marrow and mucosa
•Pallor
•Glossitis

51. Laboratory findings

52. •Bonemarrowshowsmegaloblastic
changescharacterizedbyabnormally
largesizeoferythroidcellswithnormal
cytoplasmicmaturationbutimpaired
nuclearmaturationduetodefective
DNAsynthesis
•Defectiveredcellproduction

53. Biochemical Findings
•Low plasma folic acid levels
(<3ng/ml)
•Low red cell folic acid levels
(<150ng/ml)
•Normal plasma vitamin B12 levels

54. •Folic acid deficiency is associated with increased
excretion of formiminoglutamate(FIGLU) in urine
•Due to impaired conversion of FIGLU to glutamate in
a reaction requiring THF
FIGLU excretion test

55. Vitamin B
12

56. Vitamin B
12(cobalamin)
Themostpotentvitamin
Anti-perniciousanemiavitamin
Complexstructure
CorrinringwithacentralCobaltatom
Corrinringhas4pyrroleunits
CentralCoisattachedinthemiddlethrough
Nitrogenatoms

58. Vitamin B
12(Cobalamin)
•VitaminB
12isinvolvedinthesynthesisofnew
cells,maintainsnervecells,reformsfolate
coenzymes,andhelpsbreakdownsomefatty
acidsandaminoacids
•Vitamin B
12Recommendations
–RDA Adults: 2.4 μg/day

59. Sources and distribution
Extrinsic sources:
–Meat, fish, poultry, and shellfish
–Milk, cheese and eggs
–Fortified cereals
Intrinsic sources:
Intestinal bacteria

60. Biochemical Functions
•Synthesis of methionine from homocysteine
•Isomerization of methylmalonyl CoA to succinly Co

63. Biochemical functions
Converted in the body to two coenzyme forms called cobamines
These are:
A. Deoxyadenosylcobalamin:
•5-deoxyadenosyl group is added to it in the mitochondria
•It is a coenzyme for mitochondrial methyl malonyl-CoA mutase which
converts methyl malonyl-CoA into succinyl-CoA
B. Methylcobalamin:
•Methyl group is added to it in the cytosol
•It is a coenzyme for methionine synthase which plays an important
role in Folic acid metabolism

67. Clinical conditions associated with
vitamin B
12deficiency
1.Pernicious anemia:
An autoimmune disorder
Primary cause is absence of intrinsic factor in the gastric
juice
Hematological symptoms:severe anemia, mild jaundice, diarrhea, anorexia and in
severe cases pancytopenia
Anemia is mainly caused by folic acid deficiency as it is required for purine, pyrimidine
and DNA synthesis which leads to non-maturation of nuclei whereas cytoplasmic growth
and protein development are normal giving rise to large RBCs which undergo hemolysis
ultimately leading to megaloblastic anemia

68. 2. Total gastric resection:can lead to deficiency of intrinsic
factor
3. Pancreatectomy: absorption of B
12is reduced
4. Dietary lack: in strict vegetarians
5. Tape worm infestation: diphyllobothriumutilizes B
12
6. Blind loop syndrome: infestation with gut bacteria leading to
increased utilization
7. Sprue: generalized malabsorption
8. Hereditary malabsorption: unknown mechanism
9. Drugs: Phenphormin, colchicine, neomycin, ethanol etc
interfere with B
12absoprtion
10. Old age: general malabsorption

70. Laboratory diagnosis of B
12deficiency
1. Serum concentration of B
12
2. Schilling’s test
3. Urinary excretion of methylmalonic acid
and homcysteine
4. Antibodies against intrinsic factor
5. Response to B
12therapy

71. Vitamin B
12Deficiency
–Deficiency Symptoms
–Anemia –large cell type (same as Folate)
•Fatigue and depression
•Degeneration of peripheral nerves progressing
to paralysis (irreversible)

73. Vitamin C
•Antiscorbutic factoris the original name for vitamin C
•Vitamin C serves as a cofactor to facilitate the actions of an
enzyme and also serves as an antioxidant

74. Vitamin C
•Vitamin C Food Sources
–Citrus fruits, cantaloupe, strawberries, papayas and
mangoes
–Cabbage-type vegetables, dark green vegetables like green
peppers and broccoli, lettuce, tomatoes and potatoes
•Other Information
–Also called ascorbic acid
–Easily destroyed by heat and oxygen

76. Functions of Vitamin C
1.Formation of collagen:
Conversion of proline to hydroxyproline and lysine to
hydroxy lysine
Helps in formation of triple helical structure of collagen
2.Antioxidant role
3.Found in glandular tissue:
Adrenal cortex and corpus luteum
Synthesis of steroid hormones

77. 4.Reducing Fe
+3
to Fe
+2
Helps in iron absorption from the small intestine
5.Treatment of methaemoglobinemia
6.Degradation of tyrosineto homogentisicacid and maloyl
acetic acid
7.Reduction of folic acid to tetrahydrofolate
It deficiency can lead to megaloblastic anemia

78. 8.Processing of polypeptide hormones:
Oxytocin, ADH and CCK by promoting the activity
of the amidase enzyme
9.Hydroxylation reactions
Dopamine to noradrenaline
Synthesis of carnitine
Formation of bile acids
Microsomal drug metabolic reactions

79. Vitamin C
•Other roles of Vitamin C
–As a Cure for the Common Cold
Some relief of symptoms
Vitamin C deactivates histamine like an antihistamine

80. Summary of biochemical functions of Ascorbic Acid
•Collagen formation
•Bone formation
•Iron and hemoglobin metabolism
•Tryptophan metabolism (serotinin)
•Tyrosine metabolism (homogentisic acid)
•Folic acid metabolism

81. Summary of biochemical functions of Ascorbic Acid
•Peptide hormone synthesis
•Synthesis of corticosteroid hormones
•Sparing action on other vitamins
•Immunological function
•Prevention of cataract
•Prevention of chronic diseases

83. 10-14% people still get scurvy

84. Vitamin C Deficiency
–Deficiency disease is called scurvy
–Symptoms
•Anemia –small cell type
•Atherosclerotic plaques and pinpoint
hemorrhages
•Bone fragility and joint pain

88. •VITAMIN K

89. Sources
•Cabbage, cauliflower, spinach, egg yolk, and liver etc
Bacterial flora
•RDA
70 to 140 mg/day (adequate levels)

90. Absorption
•Bile salts are needed for the absorption of Vitamin K along
with other fat soluble vitamins
•Enter blood through lymph
•Carried in plasma in combination with albumin

91. Biochemical Role of Vitamin K
•PrincipalroleofvitaminKisthepost-translational
modificationofvariousbloodclottingfactors
•Prothrombin,bloodclottingfactorsII,VII,IX&Xare
synthesizedasinactiveprecursorsbyliver.VitKact
ascoenzymeincarboxylationofvariousglutamicacid
residuesthusformingmatureclottingfactors
containinggammacarboxyglutamate(Gla)
•InhibitedbyDicumarol(naturalanticoagulant)&
•Warfarin(synthetic)

93. Biochemical Role of Vitamin K
•Gla residues of prothrombin with 2 -ively charged
carboxylate groups are good chelators of Ca
+2
ions.
Prothrombin-calcium complex binds phospholipids
on surface of platelets converting prothrombin to
thrombin essential for clotting.
•Osteocalcin of bones, Protein S & C also contain Gla
residues. Takes part in degradation of blood clotting
factors)
•Vitamin K also plays role in Electron Transport Chain
as it resembles CoQ

96. Deficiency of Vitamin K
•Unsual
•Broad spectrum antibiotics like certain second generation
cephalosporins (prolong use) decreases bacterial gut
population so decrease Vitamin K synthesis endogenously
leading to hypoprothrombinemia
•Vitamin K deficiency in newborns esp premature
sterile intestine, lacks bacteria to synthesize vitamin K
intramuscular injection of Vitamin K given to newborns as
prophylaxis against haemorrhage
•Fat malabsorption syndrome & diarrhoea due to IBD also leads
to Vitamin K deficiency

97. Deficiency of Vitamin K
•Decrease clotting factors II, VII, IX & X
•Increase PT, CT
•Bleeding tendencies
•Decrease osteocalcin in bones
Fetal Warfarin Syndrome
•Treatment of pregnant women with warfarin for DVT can lead
to fetal bone abnormalities
•Increase dose of Vitamin K is an antidote to overdose of
warfarin

98. 2.Effectsofdeficiency
Biologicallyactiveformsofclottingfactor,ii,vii,ixand
xnotavailable
Increasedprothrombintime(P.T)
Increasedclottingtime(C.T)
Tendencytobleedprofuselyfromminorwoundsor
evenspontaneousbleedingfrommucousmembranes

99. Bleedingfromrespiratorytract,G.I.Turinary
tractanduterus
Prolongeduseofanticoagulants
Decreasedosteocalcinandbonematrixgla
protein

100. THANK YOU
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