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8/19/2019 Anemias (1)by Dr.Hydi 3rd MBBS-2016.pptx
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AnemiasBy
Dr.Hydi Ahmed
Associate professor of ClinicalPathology
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Normal Hemopoiesis
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ANAEMIADefnition: “Reduction in the
concentration o haemoglobin in theblood below the lower limit o normalor a particular age and sex o anindiidual in a particular enironment!
Value of Haemoglobin less than13.5 g/dl in males, less than 11.5 g/dlin females and less than 15.0 g/dl in
new borns would indicate anaemia
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AD"#$ RE%EREN&E' (% RED )#((D&E##'
_________________________________________________
Male %emale
*************************************************+aemoglobin ,g-dl. /012 3 /412
//12 3 /212
+aematocrit 5 6&7 ,8. 9 ;2< 0=3 9>
R)& count,?// ;@2> ; @2
M&7 ,.
Mean &ell +Ameoglobin
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'CM6$(M' AND 'IN' (% ANAEMIA
'Bmptoms o Anaemia:#eel o haemoglobin at which patient deelops
sBmptoms depends on the rate o deelopment oanaemia1 I haemoglobin has been alling slowlBsBmptoms occur lateand i haemoglobin alls rapidlBsBmptoms occur earlB1 6atient maB present with generaliFed weaGness andeasB atigabilitB1 6alpitation and breathlessness occur i anaemia is
seere or patient has underlBing heart disease1 Anorexia and indigestion are common'igns o Anaemia: 6allor is the main sign1 "sual sites to looG or pallorare the nail bed hands sGin lower conHunctia1 oilonBchia,spoon shaped nails. is seen in iron
defciencB anameia )one deormities occur in thalassaemia maHor #eg ulcers are a eature o sicGle cell anaemia 'Bstolic Murmur maB be audible in pulmonarB area Mild Haundice maB occur in haemolBtic anaemia1 DiJerent other signs and sBmptoms can be ascribedto a specifc cause o anameia
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A''I%I&A$I(N (% ANAEMIA
/1 inetic &lassifcation oAnaemias
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INE$I& A''I%I&A$I(N (%ANAEMIA'
I1 ANAEMIA' D"E $( E?&E''I7E )#((D #(''
,i. Acute blood loss anaemia,ii. &hronic blood loss anaemia
II1 ANAEMIA' D"E $( 6R(D"&$I(N %AI#"RE
,i. +aematenic defciencB: Iron %olic Acid and)/
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III ANAEMIA' D"E $( E?&E''7IE RED &E##' DE'$R"&$I(N ,+AEM(#C$I& ANAEMIA.
/1 +AEM(#C'I' D"E $( RED )#((D &E##'A)N(RMA#I$C ,Intracarpuscular Deect. &ongenitala1 Red blood cells membrane deects: +ereditarB'pherocBtosisb1 EnFBme deects: 1=6D DefciencBc1 +aemoglobinopathies: $halassaemia5 'icGle &ell
Anaemia AcKuiredd1 6aroxBsmal Nocturnal +aemoglobuniria
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M(R6+(#(I& A''I%I&A$I(N (% ANAEMIA'
&auses o MicrocBtic and +Bpochromic Anameias ,M&7 3 #ess than > .1/ 1-Iron DefciencB Anaemia
1
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IR(N DE%I&IEN&C ANAEMIA
Iron defciencB anaemia is the most commoncause o anaemia in eerB countrB o world.
It is the most important cause o a microcBtichBpochromic anaemia in which all the three redblood cell indices ,the M&7 M&+ and M&+&. arereduced and the blood flm shows
small,microcBtic. and pale ,hBpochromic. redcells
$he important causes o microcBtic hBpochromicanaemia are:
)i(Iron defciencB anaemia)ii($halassaemias
)iii('ideroblastic anaemia
)i(Anaemia o chronic disorder
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$he causes o a hBpochromic microcBtic anaemia1 $hese includelacG o iron ,iron defciencB. or o iron release rommacrophages to serum ,anaemia o chronic inammation or
malignancB.1 %ailure o protoporphBrin sBnthesis ,sideroblasticanaemia. or o globin sBnthesis ,Alpha or )eta $halassaemia..
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&A"'E' (% IR(N DE%I&IEN&C ANAEMIA
I1 &+R(NI& )#((D #('':,i. "terine )leeding:
;Menorrhagia ,excessie menstrual bleeding.1 ; 6ostmenopausal bleeding1,ii. astrointestinal )leeding:
; 6eptic "lcer ; )leeding +aemorrhoids
; +ooGworm inestation
; Aspirin or other nonsteroidal anti;inammatorB
drugs ingestion
II1 IN&REA'ED DEMAND:Increased iron demand during inancB
adolescence6regnancB lactation and in menstruating women
III1 MA#A)'(R6$I(N:luten Induced EnteropathB5 astrectomB
I71 DIE$RC:
EspeciallB egetarian diet
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INI&A# %EA$"RE' (% IR(N DE%I&IEN&CANAEMIA
$he patient deelop the general sBmptoms and signs o
anaemia and also show a painless glossitis brittle ridgedor spoon shape nails ,GoilonBchia. dBsphagia ,as a resulto pharBngeal webs..
6atients also show unusual dietarB craing, perertedappetite e1g1 claB eating.
In children the iron defciencB is particularlB signifcant asit can cause irritabilitB poor cognitie unction decline inpsBchomotor deelopment and learning 1 &hild with irondefciencB anameia can also show behaioral problems
oilonBchia: tBpical Lspoon’ shaped nails
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R(N DE%I&IEN&C: #A)(RA$(RC DIAN('I'
heral )lood %indings)i(oglobin is decreased
)ii(ells indices )MVC;MCH;MCHC( are ased
)iii(lood Cells Morphology: Microcytic and chromic red cell morphologB with pencil d poiGilocBttes1 Red cells morphological
es are proportional to degree o anaemia
)i(let count is often oderately raised ularlB in cases o localiFed bleeding site ,reactie bocBtosis
)(es of #or infestation there can $e %osinophilia
hemical %indings)i(iron is decreased
)ii($otal Iron )inding &apacitB ,$I)&. is increased)iii(%errritin is decreased
)i(transerrin saturation is decreased
Marrow %indings )i(roid +Bperplasia5 ErBthroblasts are small ,micronormoblasts. and
ragged cBtoplamic outlines
)ii(tain: Iron will be absent in stores as well as in erBthroid series
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Red )lood &ells MorphologB: MicrocBtic and +Bpo chromic redcell morphologB with pencil shaped poiGilocBttes.
Red cells morphological changes are proportional to degree oanaemia.
Pencil Shape Red cell
( ' & '
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MEA#()#A'$I& ANAEMIA'$his is a group o anaemias due to
impaired DNA sBnthesis theerBthroblasts in the bone marrow showa characteristic abnormalitB 3maturation o nucleus being delaBedrelatie to that o cBtoplasm, megaloblast.
In megaloblast the nuclear chromatinmaintains an open stippled lacBappearance despite normalhaemoglobin ormation in thecBtoplasm o the erBthroblasts as theBmature
$wo main defciencies lead tomegaloblasstic anaemia
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7I$AMIN ) /< AND %(#A$E ; &(M6ARI'(N
7I$AMIN ) /< %(#A$E
&(N$EN$' IN%((D 7egetables 36oor
Meat 3 Rich
7egetables 3 RichMeat 3 Moderate
E%%E&$ (%&((IN
/ ;0 8 loss = 3 @ 8 loss
'I$E (%A)'(R6$I(N
Ileum Duodenum eHunum
NE"R(#I&A#MANI%E'$A$I(N'
An Importanteature
Absent
MA#N"$RI$I(N "nusual Most commoncause o %olatedefciencB
(N'E$ Rapid (nset,$aGes weeGs.
'low ,$aGesBears.
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6A$+(ENE'I' (% +(O )/< AND %(#A$EDE%I&IEN&C 6R(D"&E MEA#()#A'$I& ANAEMIA
G o 7itamin )/< or %olate causes slowing o DNA sBnthesis in deelopithroblasts with an accumulation o cells in premitotic phase o cell cBc neutropeina and thrombocBtopenia also appears to result rom ineJe abnormal precursor cells in the marrow due to impaired DNA sBnthe
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&A"'E' (% 7I$AMIN )/< DE%I&IEN&C
/1Decreased intaGe o 7itamin )/
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&A"'E' (% %(#A$E DE%I&IEN&C
/1 Decreased intaGe o %olic Acid:Nutritional DefciencB
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INI&A# %EA$"RE' (% MEA#()#A'$I& ANAEMIA
lossitis: tongue is bee
red and painul
Angular stomatitis
$he onset is usuallBinsidious with graduallB
progressie sBmptoms andsigns o anaemia1 $he patientmaB be mildlB Haundiced,lemon Bellow tint. due to theexcess breaGdown ohaemoglobin resulting romineJectie erBthropoiesis inthe bone marrow
lossitis sore tongue and
stomatiitis Mild sBmptoms o
malabsorption with loss oweight maB be present due to
epithelial changes #ethar breathlessness and
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7itamin )/< DefciencB:
/;7I$MAIN ) /< NE"R(6A$+C :
)/< defciencB maB cause a progressieneurtopathB aJecting the peripheral sensorB neres$heneuropathB is sBmmetrical and aJects the lowerlimbs more than the upper limbs1 $he patientnotices tingling in the eet diPcultB in walGing andmaB all oer in the darG1 RarelB optic atrophB orpsBchiatric sBmptoms ,Megaloblastic Madness. arepresent
&'N"ERA# $")E DE%E&$'upplementation o maternal diet with olic acidduring6regnancB reduces the incidence o neural tube
deect '&ARDI(7A'&"#AR DAMAE:
#ab Diagnosis o Megloblastic
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#ab Diagnosis o MegloblasticAnemia/16eripheral blood fnidngs
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&..)one Marrow %indings in Megaloblastic Anaemia a1 ERC$+R(6(IE'I' : ; Megaloblasts All the nucleated series o erBthroid cellsshow
megaloblastic change ; $heir abnormal appearance is due to disturbance o cellgrowth and maturation resulting rom intererence with DNAsBnthesis1 ; &ells are larger than erBthroblasts
; Dissociation o &Btoplasmic and Nulcear maturation:Maturation o nucleus lags behind that o cBtoplasm 1+aemoglobiniFation o cBtoplasm taGes place while nucelus is immature
; DBserBthropoiesis : Increase in the proportion o moreprimitie cells b1 #E"&(6(IE'I' ; 'hit to right is obsered ; iant MetamBelocBtes are seen
c1 MEAARC(6(IE'I'; Me aGar oc tes are normalor decreased
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01 'pecial $ests:
/1 'erum 7itamin )/
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Macrocytic Anemia (Meg.):
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Megaloblastic Anemia:
+Bpersegmented Neutrophils
Oal macrocyte
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!etic"locyte co"nt
More than
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%/
Anemia of chronic disease (Anemia
of chronic disorders (ACD)
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Denition of anemia of chronic
disorders
$he anaemia of chronic disease (ACD) is acommon normochromic or mildlyhypochromic anaemia that occ"rs in
patients 0ith a systemic disease . 't ischaracteri1ed by a red"ced ser"m ironand iron$binding capacity2 and normal orraised ser"m ferritin 0ith ade3"ate iron
stores .'t is not d"e to marro0replacement by t"mo"r2 bleeding2haemolysis or haematinic deciency2
altho"gh these often complicate it.
Conditions associated 0ith anaemia of chronic
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Conditions associated 0ith anaemia of chronic
disorders.
/;&hronic infections:
4specially osteomyelitis2 bacterial endocarditis2t"berc"losis2abscesses2 bronchiectasis2 chronic"rinary tract infections2osteomyelitis2 H'5
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*%
Anemia of chronic disease (ACD) $ pathogenesis (#.
I; Inhibition o erBthropoiesis
• +hortened red cell life span2 moderately %8$*89
(from #%8 to :8$/8 days)
•
!elatie bone marro0(erythropoiesis) fail"re$ Cyto;ines released from in7ammatory cells(N$α2
'
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*,
Anemia of chronic disease (ACD) $Diagnosis
• +ymptoms of the "nderlying disease
• +ymptoms of the anemia
• he anemia is "s"ally mild or moderate ( Hb >$##g?dl)
$ lo0er al"es are obsered in %8$*89 of patients
• he anemia is most often normochromic andnormocytic (MCHC and MC5 are normal) ormicrocytic.
. 4rythrocyte sedimentation rate (4+!) $ "s"allyraised
• !etic"locytes $ most often normal
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*@
Anemia o chronic disease
,A&D. ;laboratorB eatures,
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Adantage o anemia in chronicdisorders
-ithdra0al of iron by increased storage ofthe metal 0ithin the retic"loendothelialsystem acts to limit the aailability of iron tomicroorganisms or t"mor cells and therebyinhibit their gro0th and proliferation
$ Decreased hemoglobin red"ces theoygen transport capacity of the blood and
decreases the oerall oygen s"pply2 0hichmay primarily a=ect rapid proliferating(malignant) tiss"es and micro$organism
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+AEM(#C$I&
ANAEMIA'
+AEM(#C$I& ANAEMIA'
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+AEM(#C$I& ANAEMIA'
$he distinguishing eature o all haemolBtic anaemias is
the increased rate o red cells destruction
N(RMA# RED &E## DE'$R"&$I(NRed cells destruction usuallB occurs ater a mean liespano /
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red cell breaGdown; Extraascular: $his taGes place extraascullar acrophages o the reticuloendothelial sBstem
cualar +aemolBsis: (ccurs in some pathological disorders
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IN$R(D"&$I(N $( +AEM(#C$I& ANAEMIA'
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IN$R(D"&$I(N $( +AEM(#C$I& ANAEMIA'
+aemolBtic anaemias are defned as those
anaemias which result rom an increase in therate o red cell destruction1 )ecause oerBthropoietic hBperplasia and anatomicalextension o bone marrow red cells
destruction maB be increased seeral; oldbeore the patient becomes anaemic-compensated haemolBtic disease1 $he normaladult marrow ater ull expansion is able toproduce red cells at six to eight timesproided this is LeJectie1 $hereorehaemolBtic anaemia is not seen unless the redcells lie span is less than 0 daBs.
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A''I%I&A$I(N (% +AEM(#C$I& ANAEMIA'
+ereditarB +aemolBtic Anaemias are the
result o Lintrinsic red cell deects
whereasAcKuired haemolBtic anameias are usuallBthe result o anextracarpuscular deect or
enironmental change1 6aroxBsmal Nocturnal+aemoglobinuria ,6N+. is an exceptionbecause it is an acKuired disorder but the6N+ cells hae an intrinsic deect
#A)(RA$(RC %INDIN' IN +AEM(#C$I&
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ANAEMIA'
$he laboratorB fndings in haemolBtic
anaemia are conenientlB diided in threegroups/1 %eatures o Increased +aemoglobin)reaGdown
i1 aundice and +Bperbilirubenemiaii1 Reduced plasma +aptoglobin and
+aemopixiniii1 Increased serum #D+i1 +aemoglobinemia1 +aemoglobinuriai1 Methhemoglobinemiaii1 +aemosidrinuria
Eidence o
Intraascular +aemolBsis
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+AEM(#()IN DI'(RDER'(R+AEM(#()IN(6A$+IE'
oglobin disorders result rom:
uced sBnthesis o normal Alpha or )eta globin chain
Alpha $halassaemias)eta $halassaemias
thesis o an Abnormal +aemoglobin
rBstaline +aemoglobin ,+b' & D E ( etc. ,$hese are produced due to amino acid substitutionstable +aemoglobin
$+A#A''AEMIA
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$+A#A''AEMIA“$he $halassaemias are a heterogeneous group o geneticdisorders o haemoglobin sBnthesis all o which result
rom reduced rate o production or absence o productiono one o the globin chains o haemoglobin!
According to globin chain which isproduced in reduced amount thalassaemias are diided into two important groups:
,i. )eta , S. $halassaemias: Due to reduced sBnthesis or absence o sBnthesis o )eta globin chains1
,ii. Alpha , T . $halassaemias: Due to reducedsBnthesis or
absence o sBnthesis o alpha globin chains1
; In )eta thalassaemia the beta chain sBnthesis isdecreased or absent but there will be unimpairedsBnthesis o Alpha chains;In some thalassaemias no globin chain is sBnthesiFed atall and hence are called UU or U11 thalassaemias
whereas in others some amount o globin chain isroduced but at a reduced rate these are desi nated as
INI&A# AND ENE$I& A''I%I&A$I(N
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INI&A# AND ENE$I& A''I%I&A$I(N(% $+A#A''AEMIA'
I1 )E$A ,S. $+A#A''AEMIA': ,Deects in transcriptionprocessing or translation o beta; globin mRNA
/1 )eta $halassaemia MaHor:.;+omoFBgous state;'eere anaemia5 reKuires regular blood transusions
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II1A#6+A $+A#A''AEMIA': Deect is mainlBdeletion o genes
,i. Alpha $halassaemia 'ilent &arrier, ; -
.AsBmptomatic5 no red cells abnormalitB
,ii. Alpha $halassaemia trait , ; -; . or ,;;- .
AsBmptomatic liGe beta thalasseamia trait
,iii. +b+ Disease ;;-; 'eere resembles beta thalassaemia intermedia
,i.+Bdrops %etalis ,; ; - ; ;.#ethal in utero
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In )eta $halassaemia MaHor there is a totallacG or a reduction in the sBnthesis ostructurallB normal beta; globin chains with
unimpaired sBnthesis o Alpha chains.
INI&A# %EA$"RE' (% )E$A
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INI&A# %EA$"RE' (% )E$A$+A#A''AEMIA MA(R
/1'eere anaemia with ailure to thrie on 0;4
months o age ater birth
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$he acial appearance o a child with betathalassae'
mia maHor: 'Gull is bossed with prominent rontal
and parietal bones5 the maxilla is enlarged
$he sGull ?; raB in )eta $halassaemiaMaHor: $here is a Lhair 3on;end
appearance as a result o expansion
o the bone marrow into cortical bone
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ient reKuires regular bloodns to sustain an acceptablebin leel1 )ut iron oerload
repeated transusions is ineit;ss chelation therapB ,remoal o en1 Each 2 ml o transusedtains about
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#A)(RA$R(C DIAN('I' (% )E$A$+A#A''AEMIA MA(R
ripheral blood flm will show seere microcBtic and
ochromic blood picture with marGed poGilocBtosisgmented red cells5 target cells.
eticulocBtes count is increased1
eripheral blood shows normoblasts
)eta $halassaemia MaHor
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)eta $halassaemia MaHor
MicrocBtic and hBpochromic blood
pictureMarGed anisocBtosis&
6oiGilocBtosisNucleated R)&
%ragmented red ells
#A)(RA$R(C DIAN('I' (% )E$A $+A#A''AEMIA MA(R
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91 +aemoglobin electrophoresis shows accentuatedband o +b%,%etal +aemoglobin.
21 %etal +aemoglibin estimation bB alGalidenaturation method will show eleated +b%
=1 DNA AnalBsis bB 6olBmerase &hain Reaction ,6&R.to looG or molecular lesion ,mutation or deletion.
41 6renatal Diagnosis: During pregnancB etus canbe diagnosed bB taGing &horionic 7illus'ample,&7'. o etus and then to do 6&R to fndout that whether etus is normal or he is haingmutations which can lead to beta thalassaemia
maHor or minor1
#A)(RA$R(C DIAN('I' (% )E$A $+A#A''AEMIA MA(RU11contd
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Normal +aemoglobin Electrophoretic 6attern
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)eta $halassaemia MaHor
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$halassaemics receiing blood transusion at a thalassaemia center
)E$A $+A#A''AEMIA MIN(R ,$RAI$.
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)E$A $+A#A''AEMIA MIN(R ,$RAI$.
It is a heteroFBgous state1 $he person is carrBingabnormal genes rom one parent and normal rom
other1It is a common usuallB sBmptom less abnormalitBcharacteriFed bB a hBpchromicmicrocBtic blood picture,M&7 and M&+ erB low. with manB target cells andminimal anisocBtosis1 $he red cell count,R)& count. is high ,More than 2 ?//
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ood flm in )eta $halasaemia
aHor: MicrocBtic and +Bpochromic th ragmented red cells target
lls and nucleated red cells,normoblasts.
lood %ilm in Iron DefciencBnaemia: MicrocBtic and hBpochromic bloodicture with pencil; shape cells
lood flm in )eta $halasseamiaMinor ,$rait.: MicrocBtic and Bpochromic blood picture with manB
arget cells and absence o anisocBtosis
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