Publishedonalmostadoctorfreemedicalstudentrevisionnotes(http://almostadoctor.co.

uk)
Home>Systems>Haematology>Anaemia>SummaryofAnaemias

SummaryofAnaemias

Microcytic
Type
Iron
Deficiency

Aeitology
Bloodloss:GIbleeding(pepticulcer,

Clinicalfeatures

diverticulitis),Menorrhagia,hookworm
(developingcountries)

Brittlehair+nails
Atrophicglossitis
Angularstomatitis

PoorDiet
Malabsorption

Koilonychia
(Rare:postcricoidwebs)

Anaemiaof
chronic
disease

Diseases:infection,colloagenvascular
disease,rheumatoidarthritis,malignancy,
renalfailure,chronicinflammatorydisease
(crohns),TB,endocarditis.

Normochromic,normocyticormicrocytic
anaemia

Investigations
Hb,MCV
RBCmicrocytic,

Management
Treatunderlying

hypocgromic,

anisocytosis,
poikilocytosis.
Serumferritin
SerumIron
TIBC

Oralironferrous
sulphate(SE=
constipation)

serumironlevels
serumiron
bindingcapacity
ornormalserum
ferritin.

Treatunderlying
cause

Disorderofhaem

Withdraw

releaseofironfrombonemarrowto
developingerythroblasts,inadequate
erythropoietinresponsetotheanaemia,RBC
survival.

Sideroblastic

Inherited

Thereisironavailablebutthebodyis

cause.

Ifduetorenal
failurethen
anaemiapartlydue
toerythropoeitin
deficiencythus
recombinant
erythropoietinis
useful.

or
Acquired
2*tomyelodysplasia,
alcohol,
leadorisoniazidpoisoning,
idiopathic,
malignancy,
antiTBdrugs,
malabsorption

Thalassemia

unabletosynthesizeitintotheRBCs

Dyserythropoiesis(defective
developementofeyrocytes)
ironloadingbonemarrow
haemosiderosis(storageofiron
compoundhaemosiderininvarious
placese.g.endocrine,liver,cardiac
damage)

synthesis:
refractoryanaemia
hypochromiccellsin
theperipheralblood

causativeagents
someresponseto
pyridoxine(VitB6)
Maybe
transfusion
dependentand
ironoverloadisa
problem.

ringsideroblastsin
bonemarrow.
(erythrocyteswith
granulesofironintheir
cytoplasm)

Seehaemolyticanaemias

MacrocyticMacrocytosispresenceofabnormallylargeredbloodcellsintheblood
Type

Aetiology

Clinical
Features

Investigations

Management

Megaloblastic

Thepresenceinthebone

Usually

Bloodfilm:

marrowofdevelopingRBCswith
delayednuclearmaturation
relativetothatofthecytoplasm.

asymptomaticas
thefallinthe
levelsofHbin
responsetothe
fallinglevelsof
B12/folateoccur
overalongperiod
oftimetherefore
allowingthebody
toadjust.

hypersegmentedpolymorphs(B12),targetcells(liver
disease).
ESR
Malignancy
LFTs
T4
SerumB12andserumfolate/redcellfolate.

defectiveDNAsynthesis,
WC(leukopenia)maybe
hypersegmented,
platelets
(thrombocytopenia)

Causes:
B12/Folatedeficiency
Drugs(hydroxycarbamide/
hydroxyurea)

Bonemarrowbiopsyifaboveunsignificant:

Megaloblastic
B12/folatedeficiency,cytoxicdrugs
Normoblasticmarrow
liverdamage,myoxedema(coarseningofskindueto
hypothyroidism)
Increasederythropoiesis
e.g.haemolysis

Abnormalerythropoiesis
sideroblasticanaemia,
leukaemia,aplasia.

VitB12
Deficiency

Diet:Ifnoanimalproductsare
consumed(vegan)

Peripheral
neuropathy

Treatcause
IMB12


Imparedabsorption:

Perniciousanaemia,
Gastrectomy(noIFfrom
terminalileum),

dorsalcolumn
degen.

injections
NBconfirm
whetherB12or
folatedeficient
asfolatewill
correctHbin
B12deficiency
butwillnottreat
neuropathy

(Rarely
dementia)

illealdisease/resection,coeliac
disease.

Pernicious
anaemia

Autoimmuneconditionwhere

General:

Macrocyticanaemia

IM

thereisatrophyofthegastric
mucosa,withfailureofIntrinsic

Glossitis
Angular

MCV>110withhypersegmentedneutrophilnuclei
inseverecasesleucopoeniaandthrombocytopenia.

Hydroxocobalamin

Factor(andacidproduction)
B12absorption.

stomatitis
Mildjaundice

Hb

x2weeklyfor3
weekstoreplenish

usuallyolderpeople,

weakness+
tiredness

WCC+Platelets
SerumB12<50ng

bodystores,3
monthlyforlife.

commoninwomen,fairhair
blueeyes.

Dysponea
Diarrhoea

Redcellfolate
Serumautoantibodies.Parietalcellantibodies90%,IF

Prematuregrey
hair

antibodies50%.

Associatedwithother

hypokalaemiawhen
txbeginsoralK+

autoimmuneconditions:
e.g.Thyroid,

Mild
Splenomegaly

SerumBilirubin(breakdownof
haemoglobin,duetoineffectiveerythropoiesisinthe

Vitiligo
Addisons.

Fever

Bonemarrow)

Neurologicalfits

Schillingtest

withverylow
levelsofB12and

(todifferenciatePAfromsmallbowelmalabsorption)

in

Bonemarrowexam
HypercellularBMwithmegaloblasticchanges.

Polyneuropathy
weakness,ataxia,
paraplegia

watchfor

mayberequired

Opticatrophy
dementia,visual
disturbances.

Folate
Deficiency

PoorIntake

Anaemia

Redcellfolate

Txofunderlying

oldage
poverty

symptoms

Serumfolate
jejunalbiopsytolookforsmallboweldisease.

conditon.

alcoholexcess
anorexia

Oralfolicacid5mg
dailyfor4months,

Sources=greenveg,beans,
wholegrains,somebreakfast

higherdosesifdueto
malabsorption.

cereals

Malabsorption
coeliacdisease

Prophylacticfolic
acidisgiventopts

tropicalsprue
Excessutilization

withchronic
haemolysisand

pregnancy,lacatation,
prematurity

pregnantwomen.

chronichaemolyticanaemia,
malignantandinflammatory
diseases,
dialysis

Normocytic
Type

Aeitology

Clinical
features

Investigations

Management

Aplastic
anaemia

Pancytopenia
deficiencyofallcellelements

Resultingfrom
deficiencyof

FBCpancytopeniawithlow/abscentreticulocytes.

TxCause:
Supportivecare

oftheblood,

RBCs,WBCs,

Bonemarrowexamhypocellularmarrowwithfat

Transfusionsof

Aplasia

Platelets.

spaces.

RBC,platelets

hypocellularityofthebone
marrow

Antibiotictx.

Anaemia

likelyhoodof

Poorprognosis:

Congenital

infection

peripheralblood

Idiopathicacquired(50%)
Chemicalse.gbenzenes

Bleeding
Bruising

neurtophilcount<0.5

Drugse.g.cytotoxics,

Bleedinggums

peripheralblood

chemotherapy,

Epistaxis

plateletcount<20x10/L

chloramphenicol,gold,

Mouthinfections

reticulocytecountof

x10/L

insecticides,ionisingradiation
Infectionse.g.viralhepatitis,
HIV

arecommon

<40x10/L

Ifnorecovery:

Bonemarrow
transplantation

Immunosuppressive
txwith
antilymphocyte
gobulinand
ciclosporin(where
BMTisnotpossible
duetoGVHDrisk)

Haemolytic

Thereisincreaseddestructionofred

Jaundice

FBC,

cellsandareductionofcirculating

Hepatospenomegaly

Reticulocytes,

lifespantowhichthebonemarrowis

Bilirubin,

unabletocompensateforthe
increasedloss.

Hx:
familyhistory

LDH,
Haptoglobin,

race

Urinaryurobilinogen.

haematuria

Thismaybe:

drugs
previousanaemia

Bloodfilms:polychromasia,
macrocytosis,spherocytes,

extravascular(within

elliptocytes,fragmentedcellsor

reticuloendothelialsystem)theyare

Istheresignificanthaemolysis:

sicklecells.

removedfromthecirculationasthey
aredefective

Isthereincreasedcellbreakdown:

DirectCoombstest:identifies

or

bilirubin(unconjugated),

RBCscoatedwith

intravascular(withinblood

urinaryurobilinogen,

antibody/complementanda

vessels)e.g.duetotrauma,complement

haptoglobin.

positiveresultususallyindicates

fixationorotherextrinisicfactors.

animmunecause.

Isthereincreasedredcell
production:

Causes:

e.g.reticulocytosis,

Chromiumlabelling:forRBC

polychromasia,

lifespanandthemajorsiteof

RBCmembranedefect:
Hereditaryspherocytosis

macrocytosis,
marrowhyperplasia.

breakdown

Hereditaryelliptocytosis

Isthehaemolysismainlyintra/extra

Haemoglobinabnormlaities:

vascular:

Thalassaemia

E:splenichypertrophy

Sicklecelldisease

RBCmetabolicdefects:

I:methaemalbuminaemia,

Glucose6phosphatedehydrogenase
defieciency

freeplasmahaemoglobin,
haemoglobinuria,

Pyruvatekinasedefeicency

haptoglobin,

Immune:

haemosiderinuria.

Autoimmunehaemolyticanaemia
Haemolytictransfusionreactions
Druginduced
NonImmune:
Paroxysmalnocturalhaemoglobinuria
Microangiopathichaemolyticanaemia
Marchhaemoglobinuria
Other:
Infections(e.g.malaria)
Drugs/chemicals
Hypersplenism
Trauma

Thalassaemia

Multiplegenedefectsrate

Symptomsmay

FBC

Transfusionkeep

ofproductionofoneormore

bemildsevere,

MCV

Hb>9g/dL

globinchains.
Theimbalanceofglobinchain

dependingon
howmany/

Film
Iron

productionleadsprecipitationof

chaingenes
havebeen
deleted

HbA2

desferrioxamine.To

HbF

protectagainst

Hb

cardiacdisease&

Electrophoresis

DM.

globinchainswithinredcellsor
precursors.Thiscelldamage,
deathofRBCprecursorsinthe
bonemarrowandhaemolysis.

Ironchelatorse.g.

dosesof

thalassaemia:reduced

ascorbicacidalso

chainsynthesis
thalassaemia:reduced

ironoutput

chainsynthesis

Splenectomy,if

hypersplenismpx.

Folate
supplements


BMT

Sicklecell
anaemia

Inheritanceoftheglobin

HbASthereare

Hb

Folicacidin

gene.

usuallyno

Reticulocytecount

patientswithsevere

Mayhave:

symptomsunless

Bilirubinmayberaised

haemolysis

sicklecellanaemiaHbSS
sicklecelltraitHbAS

thepatientis
exposedto

Bloodfilmshowssicklederythrocytes

pneumococal

HbSConeShaemoglobinand

extremehypoxia

Dx:

vaccinetoinfection

oneChaemoglobingroup,(the

Vizelectrophoresisshowing8090%HbSSandabsent

risk,dailyoral

Cgroupcausestheredblood
cellstodevelop).

HbACamilder
courseofHbSS

HbA.

penecillin
Exchange

likelyhoodof

transfusionsto

thromboses
occuring.

frequencyofcrises

Hydroxycarbamide

HbSS

(hydroxyurea)raises

symptomsdueto
haemolysisand

theconcoffetalHb

vasoocclusion.

possibleBMT

Asthesickled
cellsarefragile
andhaemolyse
andblocksmall
vessels.

continuedin
largebox
below.
Haemolysis:
mildanaemia(usuallynosymptomsduetohyperdynamiccirculationandalowerO2 affinityofHbSthannormalHb).
jaundice
painfulswellingofhandsandfeet
recurrentsicklecellcrises

butthereisa

recurrenthaemolysisformationofpigmentgallstones

Vasoocclusion:
AvascularnecrosisofBMresultsinthebonemarrowpaincrisis,maybeprecipiatedbyhypoxia,dehydrationorinfection
usuallyaffectsribs,spine,pelvisinadults
handsandfeet(dactylitis)inchildren
mayrequireaddmissiontohospitalforanalgesia

Othercomplications:
Splenicatrophy
resultingininfectionriskwithPneumococcus,SalmonellaspeciesandHaemophilus
Cerebralinfection
causingfitsandhamiplegia
Retinalischaemia,
mayprecipitateproliferativesickleretinopathyandvisualloss.

Other:
renalpapaillarynecrosis
chronicrenalfailure
legulcers
acutechestsyndrome(commonestcauseofdeathinadultswithsicklecell)
fever
cough
dysponea
pulmonaryinfarctsontheCXR
Causedbyinfection,fatembolifromnecroticbonemarroworpulmonaryinfarctionduetosequestrationofsicklecells

Copyright20092013DrTomLeach

SourceURL(modifiedon18/03/201506:04):http://almostadoctor.co.uk/content/systems/haematology/anaemia/summary