Anemia, Pharmacotherapeutics, PharmD, RGUHS

anemia

1. ANEMIA
By :
Vivek giri

2. DEFINITION
Anemiasareagroupofdiseasescharacterizedbya
decreaseineitherthehemoglobin(Hgb)orthe
volumeofredbloodcells(RBC’s)inbloodtothe
levelsthatarerequiredforadequatetissue
oxygenationorwhichresultsindecreasedoxygen-
carryingcapacityoftheblood.
Anemiasareoftenasignofunderlyingpathology.
Thereforearapiddiagnosisofthecauseofthe
anemiaisessential.

3. Anemiascanresultfrom:
1)InadequateRBCproduction.
2)AcceleratedlossofRBCmass.
3)Manifestationofahostofsystemicdisorderssuchas
infection,chronicrenaldiseasesormalignancy.
ThetermAnemiaisnotdiagnosisbutratheran
objectivesignofdiseases.
WHOdefinesAnemiainadultashemoglobinlevels
lessthan13g/dlinmales,lessthan12g/dlinfemales
andlessthan13g/dlinpediatrics.

4. MATURATION AND DEVELOPMENT
OF RBC

5. ETIOLOGY
Etiologybasicallyconsistofthreemechanism:
1)ReducedHemoglobinsynthesiswhichmaybedue
tolackofnutrientsorbonemarrowfailure.This
leadstoeitherreducedproliferationofprecursorsor
defectivematurationofprecursorsorboth.
2)Increasedhemoglobinlossduetohemorrhage(red
cellloss)orheamolysis(redcelldestruction)
3)Decreasedredcellproductioni.e.disturbancein
stemcellproliferationordifferentiation.

6. A
N
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OF

7. SIGNS AND SYMPTOMS
TheNon-Specificsignsandsymptomsare:
1)Tiredness
2)Pallor(Unnaturallackofcolorintheskin)
3)Fainting
4)Exertionaldyspnoea(Difficultrespiration)
5)Tachycardia
6)Palpitation
7)WorseningAngina
8)Worseningcardiacfailure
9)ExacerbationofIntermittentClaudication.(paininleg
musclesbecausethebloodsupplyisinadequate.)

8. Iron deficiency Anemia (IDA)
Irondeficiencyisthemostcommonnutritionaldeficiencyin
developinganddevelopedcountriesanditisestimatedthatover500
millionpeopleworldwidehaveIDA*
Hemoglobinconsistofproteincomponentwith2alphaand2beta
chains.
Eachchainlinkedtoahemegroupconsistingofaporphyrinring
structurewithanironatomchelatedatitscenterwhichiscapableof
bindingoxygen.
Ironstoresare600-1200mgformalesand100-400mgforfemales,
only0.5-1.0mg/dayislost;another0.5-1.0mgislostdailyduring
menstruation.
DailyrequirementofIron0.9mginmales,2mgfemales,inpregnancy
itis3-5mgandininfantitis0.5mg.
*DatafromtheThirdNHANES(NationalHealthandNutritionExaminationSurvey)

9. Etiology of IDA
Irondeficiencyresultsfromprolongednegativeironbalance
orfailuretomeetincreasedphysiologicironneed.Thespeed
ofirondeficiencydevelopmentdependsonanindividuals
initialironstoresandbalancebetweenironabsorptionand
loss.Multipleetiologicfactorsareusuallyinvolved.
1)Bloodloss(Menstruation,Gastrointestinalpepticulcer,
Trauma)
2)Decreasedabsorptionduetomedication(e.g..Drugslike
Tetracycline)orGastrectomyorregionalenteritis.
3)Increasedrequirement(Infancy,Pregnancyorlactating
females)
4)Impairedutilization(Heredity,decreasedironuse)

10. PathophysiologyofIDA
Diminishedtotalbodyironcontent,developinginstagesoveraperiodof
negativeironbalance
Irondepletion–StageOne
Irondeficienterthyropoiesis–StageTwo
Irondeficiencyanemia–StageThree
StageOne
Ironstorageisexhausted-indicatedby
decreaseinserumferritinlevelsNo
anemia–RBCmorphologyisnormal.
StageTwo
Insufficientirontoinsertinto
protoporphyrinringtoformheme–
Protoporphyrinaccumulatesincelland
complexeswithzinctoformZPPNo
anemia,nohypochromia,butslight
microcytosismaybedecreased
StageThree
Alllaboratorytestsforironstatusbecome
abnormal,Mostsignificantfindingis
microcytic,hypochromicanemiaandthere
ishyperplasiaoferythroids.

11. Signs of IDA
1)Pale skin and mucous membrane
2)Painless glossitis (Inflammation of the tongue)
3)Angular stomatitis (Inflammation of the mucousmembrane
of the mouth)
4)Koilonchia (Spoon shaped nails)
5)Dysphagia
6)Pica (Unusual cravings)
7)Atrophic Gastritis
8)Poikilocytes (misshapen red cells appear on the blood smear
as cigar-or pencil-shaped forms)
Chronic Iron
deficiency

12. Symptoms
1)Faintness
2)Fatigue
3)Dizziness
4)Irritability
5)Malaise
6)Palpitation
7)Headache
8)Shortnessofbreath
9)Angina
10)Ankleedema

13. Treatment of IDA
Aimoftreatmentistocorrecttheanemiaandreplenishiron
stores.
TreatmentofIDAconsistofdietarysupplementsand
administrationoftherapeuticironpreparation.Itisbest
absorbedfrommeat,fishandpoultry.Beveragesaffectiron
absorption.
Inmostcasesoraladministrationofirontherapywithsoluble
ironsaltsisappropriate.
ORAL THERAPY
Ironsulphate,succinate,lactate,fumarate,glycinesulphate,
glutamateandgluconateareabsorbed
Thepresenceofmucopolyssacharideschelatorsubstance
preventstheironfromprecipitatingandmaintainstheironin
solubleform.

14. Thedoseofironreplacementtherapydependsonthe
patientsabilitytotoleratetheadministerediron.
Thegeneralrecommendationisapproximatelyadministered
of200mgofelementalirondailynormallyin2to3divided
dosestominimizetolerability.
Ifpatientcannottoleratethisthansmalleramountof
elementalirone.g.single325mgtabletofironsulphateis
sufficient.
Ironispreferablyadministeredatleast1hourbeforemealto
avoidfood-druginteraction.
Manypatientmaytakeironwithfoodbecausethey
experiencenauseaanddiarrheawhenadministeredonempty
stomach.

16. Adverse Drug Reaction (ADR)
ADRtotherapeuticdoseofironareGastrointestinalinnature
1)Discolorationoffeaces
2)Constipationanddiarrhea
3)Nauseaandvomiting
Drug Interaction
Drugswhichdecreaseironabsorption
1)Aluminum,magnesiumandcalciumcontainingantacids
2)Tetracyclineanddoxycycline
3)Histamine(H2)antagonist
4)Protonpumpinhibitor
5)Cholestyramine

17. Drugs affected by Iron
1)Levodopa↓(chelateswithiron)
2)Methyldopa↓(decreasesefficacyofmethyldopa)
3)Levothyroxine↓(decreasedefficacyoflevothyroxine)
4)Penicillamine↓(chelateswithiron)
5)Fluoroquinolones↓(formsferricion–quinolonecomplex)
6)Tetracyclineanddoxycycline↓(whenadministeredwithin2
hoursofironsalt)
7)Mycophenolate↓(decreasesabsorption)

18. Causes of treatment failure for IDA
1)Poorpatientadherence
2)Inabilitytoabsorbiron
3)Incorrectdiagnosis
4)Continuedbleeding

19. PARENTERAL IRON THERAPY
Parenteraltherapyistakenwhen:
1)Evidenceofironmalabsorption
2)Intolerancetoorallyadministerediron
3)Longtermnonadherence
4)Patientswhocannottakeoralirontherapy
5)Patientswithsignificantbloodlosswhorefuseirontherapy.
PREPARATIONS
1)IronDextran;50mgiron/ml
2)Sodiumferricgluconate;2.5mgiron/5ml
3)Ironsucrose;20mgiron/ml

21. TRANSFUSIONS
Transfusionofallogenicbloodisindicatedinacutesituations
ofbloodlosswhenhemodynamicsupportisneeded.
BloodtransfusioninchronicanemiacanelevateHb
concentration
Anexceptiontothistreatmentoptionispatientswhohave
developedlowHctvaluesoverextendedtimeperiods.These
patientsoftendemonstratecardiaccompromiseafter
transfusiondespiteHctlevelsisinthe20%range.These
patientsshouldreceiveirontherapy,followedbytransfusion
onlyifnecessary.

22. PATIENT CARE
Takeironproductswithoraftermeals–reducestheincidence
ofnausea.
Patientshouldbetoldthattheirfaecesmaybeofcomedark
colored.
Discussaboutthelengthoftreatmentandadherencetothe
therapy.

23. Megaloblastic Anemia
Macrocyticanemiaisdividedintotwotypes:
1.Megaloblasticanemia
2.Nonmegaloblasticanemia
Thetwomajorcausesare:
1.Folatedeficiency
2.VitaminB12deficiency
Perniciousanemiaisaspecificdiseasecausedby
malabsoptionofVit.B12.
ImportanttodistinguishB12fromfolatedeficiency.

24. Stages of B12deficiency
Stage B12conc. Mean corpuscular Hb Signs &
vol. Symptoms
Normal Normal Normal Normal None
-ve bal. ” ” ” ”
Depletion of
Stores Slight ↓ ” ” Possible
B12 def. Moderate ↓ ↑ ” ”
Erythropoiesis
B12 def.
Anemia Severe ↓ ↑ ↓ Probable

25. Etiology of Vitamin B12Deficiency
Thethreemajorcausesare:
1.Inadequateintake
2.Malabsorptionsyndrome
3.Inadequateutilization
Deficiencyoccursfrominadequateintakeormalabsorption.
TheonlydietarysourceofVit.B12(cyanocobalamin)is
fromfoodofanimalorigin.Itispresentinmeat,fish,eggs,
cheeseandmilk.Dailyrequirementsarebetween0.5-1.0μg.
Malabsorptionoccursifthedistilileumisremovedduring
stagnantloopsyndrome,tropicalsprueandfishtapeworm
infestation.
Drugsalsocausemalabsorption.

26. Pathophysiology of Vitamin B12
VitaminB12workscloselywithfolateinthesynthesisof
buildingblocksforDNAandRNA.
Itisawatersolublevitaminobtainedexogenouslyby
ingestionofmeat,fish,poultry,diaryproductsand
fortifiedcereals.

27. Most circulating
cobalamin complex
Free cobalamin
Binding complex
Cobalamin–R-Protein
complex
Release of cobalamin
Stomach
Dietary cobalamin
Complex secreated
into circulation
Mucosal cell receptors
(cubilin) in distal ileum
Cobalamin-Intrinsic factor
complex
Pepsin and HCL
R-Protein
Cobalamin -R-Protein complex
from Bile
Degradation by pancreatic
enzymes
Intrinsic factor

28. Gastrectomy –Vit. B12deficiency
Vit. B12deficiency Deposition of
methyltetrahydrofolate prevent DNA
synthesis
Defect in methylation reaction, needed for
myelin formation leads to neuropathy.
Alternate mechanism involves diffusion.

29. Investigation
Vit. B12
MMA, Hcy conc. and renal function
Schilling test and hematology
Clinical manifestations
•Macrocytosis
•Anisocytosis(cells of unequal size)
•Poikilocytosis(misshapen red cells)
•Thrombocytopenia
•Enlarged Spleen (spleenomegaly), Slight fever
•Mild jaundice and progressive neuropathy

30. Symptoms
Apathy
Weakness
Fatigue
Palpitation
Breathlessness
Sore tongue
Glossitis
Burning of mouth
Nausea
Heart burn

31. Treatment
Goals
1.Reversal of hematologic manifestations
2.Replacement of body stores
3.Prevention or resolution of neurologic manifestations
Dietary intake
Oral administration of Vit.B12 (1-10µg/day cyanacobalamin)
Parenteral administration (100-1000ug deep sc)
Intranasal administration(400µg 3 times a week)

32. Adverse effect
1.Hyperuricemia and hypokalemia
2.Rebound thrombocytosis precipitate thrombotic events
3.Fluid retention in pateints with compromised CV status
4.Rare case of anaphylaxis with parenteral administration

33. FOLIC ACID Deficiency
Most common Vitamin deficiency
Critical in early pregnancy
The four major causes are:
1.Inadequate intake of folic acid
2.Decreased absorption
3.Hyper utilization
4.Inadequate utilization
5.Drugs (Azathioprine, methotrexate, phenytoinetc…)
Etiology of Folic acid Deficiency

34. Pathophysiology
GI cells and RBC
Methyltetrahydrofolate
monoglutamate
Folate
Monoglutamate
Polyglutamate
Dietary Folate
Dihydrofolate
Enzymes in the gut
Absorption
Methylation/ Reduction
Specific carrier
Methyl
Folate
Polyglutamate
DHF Reductase

35. Polyglutamate prevents folate leaking out of cell
Folate –coenzyme for DNA and RNA synthesis
Defective DNA synthesis affect GI cells and RBC –sore
tongue and anemia
Daily requirement-50-100µg
In pregnancy additional 400µg/day recommended
Average amount of stores-5-10mg

36. Clinical manifestation
1.Megaloblastosis
2.Glossitis
3.Diarrhea
4.Weight loss
5.Fatigue
6.Pallor
7.palpitation
8.Chronic folate deficiency predisposes patients to
thrombosis, depression and neoplasia

37. Investigation
1.Serum/erythrocyte Folate level
2.Increased plasma Hcy conc., RFT
3.Peripheral blood-large oval red cells
4.Anisocytosis and poikilocytosis
5.Hypersegmented neutrophils, thrombocytopenia

38. Therapy consist of :
1.Administration of exogenous folic acid
2.Replace body stores
3.Resolve signs and symptoms
Dietary intake
Oral preparations (1mg daily)
Parenteral administration(5mg/ml im/iv/sc)
Treatment

39. Hemolytic Anemia
Hemolytic anemia decreases the life span of
erythrocytes
If the rate of destruction of the erythrocytes
exceeds the rate of production, then anemia
results
Wide range of hemolytic anemia with both
genetic and acquired disorders

40. Classification of Hemolytic Anemia
1.Abnormalitiesofredbloodcellinterior
a.)Enzymedeficts
b.)Hemoglobinopathies
2.RBCmembraneabnormilities
a.)Heridityspherocytosis
b.)Paroxyysmalnocturnalhemoglobinuria
c.)Spurcellanemia
3.Extrensicfactors
a.)Splenomegaly
b.)Antibodyimmunehemolysis
c.)Microanglopathichemolysis
d.)Infections,toxinsetc.
Intra-
corpuscular
Extra-
corpuscular
Hereditary
Acquired

41. Etiology
1. Sickle cell anemia:
It is due to abnormal hemoglobin called hemoglobin S (HbS),
normal hemoglobin is usually HbA
α chains are normal and βchains are abnormal. HbShas
valinesubstituted for glutamicacid as the 6
th
amino acid in
the βpolypeptide compared with HbA
The molecules of HbSpolymerize into long chain and
precipitate inside the cells because of this RBC’s attain sickle
shape and become more fragile leading to hemolysis
Hemolysedsickle cell aggregate and block the blood vessels
leading to infarction.

42. 2. Thalassaemias
It is also known as Cooley’s anemia or Mediterranean anemia
(more common in Thailand and Mediterranean countries)
Due to inherited abnormalities of hemoglobin
It is of two types
1.α Thalassaemias
2.β Thalassaemias(more common)
Defective synthesis of globingenes
Production of αand βchains become imbalanced
Precipitationofpolypeptide Precipitationof
polypeptide
chainintheimmatureRBC chaininthematureRBC
Disturbanceintheprocess Hemolysis

43. αThelassaemia (fetal life) βThelassaemia
αchains are less, absent or βchains are less, absent or
abnormal with excess of abnormal with excess of
γchains. αchains.
Defective Erythropoiesis and Hemolysis
G6PD deficiency:
G6PD is an erythrocyte enzyme that is indirectly involved in the
production of reduced Glutathione.
Glutathione is produced in response to and protects the red cells
from oxidizing reagents.

44. Pathophysiology
Normal120dayslifespanofRBC(comesfromitsinherent
flexibilityinpassingthroughthemicrovasculatureandspleen
withoutdisruptionofcellmembraneorsesquestrationand
phagocytosisbyreticuloendothelialcells)
Hemolysis RBClifespanlessthan120daysdueto
1.Membranedefects
2.Alterationinhemoglobinsolubilityorstability
3.Changesinintracellularmetabolicprocess
Thesechangescanbeintrinsicorextrinsicinorigion
IntracorpuscularchangesExtracorpuscularchangesare
aregeneticallydeterminedcauseofhemolyticanemia
(directeffectonmembrane)

45. Hereditaryspherocytosis:RBC’slosetheirflexiblebiconcave
characteristicsandbecometightspheresdestroyedby
reticuloendothilialcells,causingpigmentbilestones,mild
jaundiceandsplenomegaly.
SicklecellandThelassaemia:Alterationinhemoglobin
solubilityandstabilitycelldeformationhemolysis
Someredcellsinpatientswithsicklecelldiseasecontainfetal
hemoglobin(HbF).Thesecellsdonotsickle.
G6PDDeficiency
G6PD deficiency i.e. decrease in G6PD
Decrease production of NADPH in erythrocytes
NADPH is needed to keep glutathione in reduced form
Hemoglobin in reduced from and helps erythrocytes deal with
oxidative stress

46. Clinical Manifestation
Acute haemolyticanemia:
1.Malaise
2.Fever
3.Abdominal pain
4.Dark urine and jaundice
5.Haemoglobulinaemia
6.Hyperbilinaemia
7.Reticulocytosis
8.Increased urobilinogenlevels in urine
Chronichaemolyticanemia:
1.Splenomegaly
2.Normochromicandnormocyticanemia

47. Investigation
1.Sicklecelldisease:abnormalhemoglobin electrophoresis
Theproportionofhemoglobinsisausefulmonitoringparameter.
2.Thalassaemia:Hemoglobinelectrophoresis
3.G6PDdeficiency:
Treatment
1. Sickle cell anemia:
Patients with sickle cell disease have a high evidence of
Pneumococcal infections
Penicillin V (Phenoxymethyl penicillin): 250mg twice a day
usually for adults
Erythromycin being used for patients allergic to penicillin.

48. Administrationofpneumococcalvaccineandhaemophilus
influenzavaccineisnowcommon
IncreasedproportionofHbFanddecreasedproportionofHbSon
thecirculation
DrugsthatmayincreasefetalHbproduction
1.5-Azacytidine
2.Cytarabine
3.Vinblastin
4.Hydroxycarbamide(Hydroxyurea)Cytotoxicity
5.Eruthropoietin
6.Shortchainfattyacids(Valproateetc.)
Transfusionsandexchangetransfusionshavealsousedto
decreasetheproportionofHbs.Thisislimitedbytheusual
complicationsofchronicinfusions.

49. Ironoverloadtheriskofbloodbornevirustransmissionand
sensitization.
Strongopioidsarerequiredforpainrelief.Morphineisamore
logicalchoiceofopioids.
2.Thalassaemia:
Noeffectivetreatmentforthalassemia
DesferrioxamineandDeferiproneareroutinelyneeded.
Bindswithfreeironand Oral,butitisreportedtocause
Ironboundtoferritin(serumreversibleneutropeniasogiven
Ferritinreaches1000ug/l) topateintswhoareintolerantto
Desferrioxamine

50. Splenectomy
DrugsincreasesHbF:combinationofdrugs
Hydroxycarbamide(hydroxyurea)anderythropoietin
3.G6PDdeficiency:
Nospecifictreatment
Duringacuteepisodesthepatientshouldbekeptwell
hydratedtoensuregoodurineoutputthuspreventingHb
damagingthekidney
Bloodtransfusion

51. Patient care
1.SickleCell
Encouragetotaketheirprophylacticpenicillinandfolicacid
therapyregularly
Opioidaddictionarepreventedbygivinganalgesic
treatmentsrecognizethatthecrisesareextremelypainfuland
patientrequireseffectiveanalgesia
2.Thalassaemia
Needtoeducatethepatientregardingthecytotoxicnatureof
hydroxycarbamide(hydroxyurea)
3.G6PDdeficiency
Patientscanbegivenalistofdrugstoavoid
Drugtherapydoesnotplayalargepartinthemanagement.

52. Anemia of CHRONIC DISEASE
Itisanhypoproliferativeanemiathathastraditionallybeen
associatedwithinfections,inflammatory,hepaticdiseaseor
neoplasticdiseaselastingformorethan1to2months.
ACDisaresponsetostimulationofthecellularimmune
systembyvariousunderlyingdiseaseprocesses.ACD
commonlydevelopsinAIDSpatients,especiallythosewith
opportunisticinfectionsormalnutrition,HIVinfects
hematopoieticcells,whichcanleadtoabnormal
hematopoiesisandbonemarrowsuppression.Inaddition,the
drugsusedtotreatAIDSandassociatedillnesscancausebone
marrowsuppression.
Etiology

54. Pathophysiology
In this anemia RBC’s have shortened life span
Bone marrows capacity to respond to EPO is inadequate to
maintain normal Hb concentration
This anemia may be due to a block in release of iron from the
endothilial cells of the marrow
Cytokinins such as IL1, γinterferron and tumor necrosis
factor released during these illness may inhibit the production
or action of EPO or the production of RBCs

55. Signs and Symptoms
1.Fatigue
2.Breathlessness
3.Swollen feet
4.Chest pain
5.Decreased mental activity
Laboratory findings
1.Serum iron level
2.Bone marrow examination

56. Treatment
Recovery from the anemia usually occurs with resolution of
the underlying process. During inflammation Iron(Fe) therapy
is ineffective by either oral or parenteral route.
Exogenous EPO (recombinant human EPO or epoetin alpha)
has been used to stimulate erythropoiesis in patients with
chronic disease.
The epoetin alpha 150 units/kg given subcutaneously three
times weekly is effective.
Most patients tolerate epoetin alpha therapy well.
Iron deficiency can occur in patients treated with epoetin
alpha

57. However close monitoring of iron level is necessary during
epoetin alpha therapy
Oral iron supplementation should be given if transferrin
saturation drops to 20% or the serum ferritin level drops
below 100u/L
More common toxicities of epoetin alpha are fever, bone pain
and fatigue.

58. Aplastic Anemia
It is group of disorders characterized by pancytopeniain
peripheral blood, vairiablehypocellularityin bone marrow,
absence of underlying malignentor myeloproliferative
disease.
ETIOLOGY
1.Congenital –rare
2.Acquired-virus or chemical
Other etiologies
Hepatitis, infectious mononucleosis, dengue and influenza
Regular exposure to irradiation
Major component of inherited conditions

59. Causes
Damage to the bone marrow's stem cells causes
aplastic anemia. When stem cells are damaged,
they don't grow into healthy blood cells.
The cause of the damage can be acquired or
inherited. Acquired aplastic anemia is more
common, and sometimes it's only temporary.
Aplastic anemia that's inherited is rare.
In more than half of the people who have aplastic
anemia, the cause of the disorder is unknown.
Some research suggests that stem cell damage
may occur because the body's immune system

60. Acquired Causes
A number of diseases, conditions, and
factors can cause aplastic anemia,
including:
Toxins, such as pesticides, arsenic, and
benzene
Radiation and chemotherapy (treatments
for cancer)
Medicines, such as chloramphenicol (an
antibiotic rarely used in the United States)
Infectious diseases, such as hepatitis,
Epstein-Barr virus, cytomegalovirus (si-to-

61. Autoimmune disorders, such as lupus and
rheumatoid arthritis
In some cases, cancer from another part of
the body can spread to the bone and cause
aplastic anemia.

62. Inherited
Causes
Certain inherited conditions can damage
the stem cells and lead to aplastic anemia.
Examples include Fanconi anemia,
Shwachman-Diamond syndrome,
dyskeratosis congenita, and Diamond-
Blackfan anemia

63. RISK FACTORS OF APLASTIC
ANEMIA
Aplastic anemia is a rare, but serious blood
disorder. In the United States, about 500–
1,000 people develop this type of anemia
each year. The disorder is two to three
times more common in Asian countries.
People of all ages can get aplastic anemia.
However, it's most common in adolescents,
young adults, and the elderly. Men and
women are equally likely to have it.
risk for aplastic anemia is higher if :

64. Taken certain medicines or had radiation or
chemotherapy treatment (treatments for
cancer)
Been exposed to toxins
Certain infectious diseases, autoimmune
disorders, or inherited conditions

65. SIGN AND SYMPTOMS
Low numbers of red blood cells, white
blood cells, and platelets cause most of the
signs and symptoms of aplastic anemia.
Signs and Symptoms of Low Blood Cell
Counts
The most common symptom of a low red
blood cell count is fatigue (feeling tired or
weak). Not having enough hemoglobin in
the blood causes fatigue. Hemoglobin is an
iron-rich protein in red blood cells that
carries oxygen to the body.

66. Alowredbloodcellcountalsocancause
shortnessofbreath;dizziness,especially
whenstandingup;headache;coldnessin
yourhandsorfeet;paleskin,gums,and
nailbeds;andchestpain.
Ifyoudon'thaveenoughhemoglobin-
carryingredbloodcells,yourhearthasto
workhardertocirculatethereduced
amountofoxygeninyourblood.Thiscan
leadtoarrhythmias,heartmurmur,an
enlargedheart,orevenheartfailure.

67. White blood cells help fight infections.
Signs and symptoms of a low white blood
cell count include fevers, frequent
infections that can be severe, and flu-like
illnesses that linger.
Platelets stick together to seal small cuts
on blood vessel walls and stop bleeding.
People who have low platelet counts tend
to bruise and bleed easily, and the bleeding
may be hard to stop.

68. TypesCommonofbleedinglinkedtoalow
plateletcountincludenosebleeds,bleeding
gums,pinpointredbleedingspotsonthe
skin,andbloodinthestool.Womenalso
mayhaveheavymenstrualbleeding.
ParoxysmalNocturnalHemoglobinuria
Aboutone-thirdofpeoplewhohave
aplasticanemiahaveaconditioncalled
paroxysmalnocturnalhemoglobinuria
(PNH).Thisisaredbloodcelldisorder.Most
peoplewhohavePNHdon'thaveanysigns

69. OTHER SIGN SYMPTOMS
Aplasticanemiacancausesignsand
symptomsthataren'tdirectlyrelatedto
lowbloodcellcounts.Examplesinclude
nausea(feelingsicktoyourstomach)and
skinrashes.
Shortness of breath
Swelling or pain in the abdomen or swelling
in the legs caused by blood clots
Blood in the urine
Headache
Jaundice

70. Pathogenesis
It involves destruction inhibition or
impairment of stem cells, development of
abnormal micro cells or lack f hemopoietic co
factores.
Exogenous agents(virus,drug,metabolites)
inter the body
attaches to hemopoietic stem cells
agent-stem cell combination stimultus auto
immune procesm cells
distroy stem

71. Recovery may occurs with termination of
immune process and regeneration of patient
stem cells .
If auto immune process continues
immunosuppressive therapy alone may be
effective or followed by marrow
transplantation .
Drug included marrow aplasia –dose related
or idiosyncratic.
Chloramphenicol best drug given by oral,
I.M,I.V and topical administration.

72. Treatment
Treatments for aplastic anemia include blood transfusions,
blood and marrow stem cell transplants, and medicines.
These treatments can prevent or limit complications,
relieve symptoms, and improve quality of life.
In some cases, a cure may be possible. Blood and marrow
stem cell transplants may cure the disorder in people who are
eligible for a transplant. Removing a known cause of aplastic
anemia, such as exposure to a toxin, also may cure the
condition.
Needs of Treatment
People who have mild or moderate aplastic anemia may not
need treatment as long as the condition doesn’t get worse.
People who have severe aplastic anemia need medical
treatment right away to prevent complications.
People who have very severe aplastic anemia need emergency
medical care in a hospital. Very severe aplastic anemia can
be fatal if it's not treated right away.

73. Blood Transfusions
People who have aplastic anemia may need blood transfusions
to keep their blood cell counts at acceptable levels.
A blood transfusion is a common procedure in which blood is
given to you through an intravenous (IV) line in one of your
blood vessels. Transfusions require careful matching of
donated blood with the recipient’s blood.
Blood transfusions help relieve the symptoms of aplastic
anemia, but they’re not a permanent treatment.
Blood and Marrow Stem Cell Transplants
A blood and marrow stem cell transplant replaces damaged
stem cells with healthy ones from another person (a donor).
During the transplant, which is like a blood transfusion, you
get donated stem cells through a tube placed in a vein in your
chest. Once the stem cells are in your body, they travel to your
bone marrow and begin making new blood cells.
Blood and marrow stem cell transplants often cure aplastic
anemia in people who are eligible for this type of transplant.

74. Medicines
If you have aplasticanemia, your doctor may prescribe medicines to:
•Stimulate your bone marrow
•Suppress your immune system
•Prevent and treat infections
Medicines To Stimulate Bone Marrow
Man-made versions of substances that occur naturally in the body can
stimulate the bone marrow to make more blood cells. Examples of
these types of medicines include erythropoietin (e-RITH-ro-PO-e-tin)
and colony-stimulating factors.
These medicines have some risks. You and your doctor will work
together to decide whether the benefits of these medicines outweigh
the risks. If this treatment works well, it can help you avoid the need
for blood transfusions.

75. Medicines To Suppress the
Immune System
Three medicines—often given together—can
suppress the body’s immune system. They are
antithymocyte globulin (ATG), cyclosporine,
and methylprednisolone.
People who have aplastic anemia may need
long-term treatment with these medicines.
Medicines that suppress the immune system
can have side effects. They also may increase
the risk of developing leukemia (lu-KE-me-ah)
or myelodysplasia (MI-e-lo-dis-PLA-ze-a;
MDS). Leukemia is a cancer of the blood cells.

76. Ongoing Care
Treatment for aplastic anemia may cause side
effects or complications.
People who have aplastic anemia may be at
higher risk for infection due to low white
blood cell counts. For example, you may want
to:
Stay away from people who are sick and avoid
large crowds of people.
Avoid certain kinds of foods that can expose
you to bacteria, such as uncooked foods.
Wash your hands often.
Brush and floss your teeth and get regular
dental care to reduce the risk of infection in

77. dose regimen
I.V ALG (10 mg/kg) for five alternate days.
I.V methyl prednisolone (8mg /kg/day) or
2mg/kg/day over 9 days.
Oral prednisolone (1.25mg/kg/day) from day
10 -15 declining to 0.1mg /kg /day from days
3-4.

78. Acetaolamide dapsone quinidine
aspirin diclofenac
sulfonamide
Captopril indometacin
Carbamazpine phenytoin chloramphenicol
oxyphenbutazone