Anemias by Dr.Ahmed Noureldin Ahmed

8/14/2019 Anemias by Dr.Ahmed Noureldin Ahmed

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Approach to a ChildWith AnmiaBy

Dr.Ahmed Noureldin AhmedMBBS, DCH, DTM&H (Cairo

PHC Pdiatrician


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Formation of Blood elements

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Formation of RBCs in B.MPleuripotent Stem Cell

Pro- Normoblast

Basophilic NormoblastPolychromatic Normoblast

Orthochromatic NormoblaqstPolychromatic Erythrocyte Erythrocyte


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Developing RBCs1- Early& Late Pro-erythroblast

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2-Basophilic Erythroblast.


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DefinitionAnemia is a decrease in Hb below thereference level for age and sex

Anaemia is diagnosed if the Hb:in an adult male is < 13 gm%in an adult female is < 12 gm%

in a child (3-12yrs is< 11 gm% in a pregnant women is < 11 gm%


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How to diagnose Anaemia ?

History & Physical examinationInvestigation: Blood Indices : (Hb, RBCs ,PCV ,MCV , MCH , MCHC, RDW, Mentzer index Blood film

(shape, size , staining, abnormal cells

special investigation (Iron studies, B.M exam.


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CBC by Coulter Counter Measured Values:

1-RBCs count 2- MCV 3 - Hb in gmCalculated Values:

1- MCH( in pgm/cell =(Hb in gm RBCs x 10 N. 27 32 ( in Mic.hypo Anemia , in Macro An

2-Hct (PCV in % = RBCs x ( MCV/10N. ( M 40-54% , F 37-47% , Children 36-44%

3-MCHC (in gm/dl = (Hb in gm / Hct x 100N. 30-35gmg ( in mic.hypo An , in microspherocytosis

4-RDW= coefficient of variation in RBCs size.N.11.5 14.5 % , ( in IDA , N or in thalassemia trait5-Mentzer index = MCV RBCs


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1- MCVIt is the mean volume of one RBCMCV = (PCV / RBCs X 10

(45/5X 10 = 90)N 80 96(

> 96 in Macrocytosis < 80 in Microcytosis N in Normocytic Anemia


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2-PCV ( HematocritIt is the volume of packed RBCs in 100ml of Blood.

PCV = RBCs x ( MCV/10 = 5 x ( 90/10 = 45% Males : 40- 54 % Females 37- 47%

Children (2-12Yrs 36-44%

PCV below lower limit =Anaemia PCV above upper limit =Polythythaemia


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3-Red Cell Distribution width

(RDWIt is a quantification of anisocytosis ( variation in RBCs size

It is the coefficient of variation of red cellvolume distribution

A normal value is helpful in distinguishingthalassemia minor from IDAas a causeof microcytosisPractically , when it is elevated in a patientwith microcytosis , IDA is more likelycause of anemia ,not thalassemia trait

or N. value points to thalassemia trait.


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Normal Values in ChildrenLower limit of normalHb )3rd centile

Lower limit)3rd centile( & upper limit) 97th centile( of MCVAgeIn yr .

HbIn gm/dl

MCVlower limit

MCVUpper limit

1-4 11.2 72 85

5-7 11.5 75 87

8-10 11.8 76 89

12-14 12 77 90

15-17 1312

78 92

18 1412

80 95


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What abnormal Results of CBCmeans?

High Numbers of RBCsHigh Numbers of RBCs::Low oxygen tension in the blood

Congenital heart Disease

Cor pulmonale Pulmonary fibrosisPolythythaemia Vera

Dehydration Ch.Renal disease withErythropoietin production
http://www.umm.edu/ency/article/anxiety_overview_003211.htmhttp://www.umm.edu/ency/article/anxiety_overview_003211.htm


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Low numbers of RBCs mayindicate

1-Blood loss : a( Anaemia b( haemorrhage2-Bone marrow failure due to:

)radiation, toxin, fibrosis,tumor (3-Erythropoietin deficiency)secondary torenal disease(

4-Hemolysis)RBC destruction(5-Malnutrition) iron, folateB12, B6(

6-Leukaemia

7-multiple Myeloma
http://www.umm.edu/ency/article/tumor_overview_001310.htmhttp://www.umm.edu/ency/article/kidney_disease_overview_000457.htmhttp://www.umm.edu/ency/article/hemolysis_overview_002372.htmhttp://www.umm.edu/ency/article/malnutrition_overview_000404.htmhttp://www.umm.edu/ency/article/folic_acid_folate_overview_002408.htmhttp://www.umm.edu/ency/article/vitamin_b12_overview_002403.htmhttp://www.umm.edu/ency/article/vitamin_b6_overview_002402.htmhttp://www.umm.edu/ency/article/vitamin_b6_overview_002402.htmhttp://www.umm.edu/ency/article/vitamin_b12_overview_002403.htmhttp://www.umm.edu/ency/article/folic_acid_folate_overview_002408.htmhttp://www.umm.edu/ency/article/malnutrition_overview_000404.htmhttp://www.umm.edu/ency/article/hemolysis_overview_002372.htmhttp://www.umm.edu/ency/article/kidney_disease_overview_000457.htmhttp://www.umm.edu/ency/article/tumor_overview_001310.htm


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Classification of Anemia

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Blood Filma Hypochromic Microcytic b Macrocytic& hypersegmented cell(arrow c Megaloblast in B.Md Spherocyte ( arrow e Sickle cell( arrow & target cell f Howell-Jolly bodies g Blister cell inG6PDD


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Normal CBC.


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Normal CBC

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Different types of WBCsBand Cell Basophil

LymphocyteAtypical LymphocyteNeutrophil

Eosinophil
http://www.hoslink.com/images/band1web.jpghttp://www.hoslink.com/images/neut2web.jpghttp://www.hoslink.com/images/lymph3web.jpghttp://www.hoslink.com/images/lymph1aweb.jpghttp://www.hoslink.com/images/Baso_1web.jpghttp://cell%20morphology%20-%20haematology_files/eosin2_t.jpg


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Iron Metabolism70%of the total Fe is circulating in RBCs

25%of the body Fe is stored in R.E.S(Liver,Spleen&Bone marrow

Fe is stored as Ferritin & Hemosiderin

0.1%of the total body Fe is circulating in the plasma bound to TransferrinThere is considerable interchange between the

store and the plasma.


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Iron Absorption: Normally 1mg ( 18 mol Fe is absorbed each day on

ordinary diet . Within the intestinal cells some of Fe combines with

apoferritin to formferritin which is the storage form . Factors affecting Fe absorption: 1- Ferrous Fe is absorbed better than ferric Fe 2- Gastric acidity helps to keep Fe in the ferrous state 3- Inorganic Fe is absorbed better than organic Fe 4- Reducing agents Fe absorption 5- Fe absorption is with low Fe stores and in Fe overload 6- erythropoietic activity ( bleeding , haemolysis , high

altitude absorption 7- Alcohol absorption 8- Phosphate & phytate Fe absorption

Iron Transport in the plasma


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Iron Transport in the plasma* Normal Fe loss is small & normal Fe stores are large.It would take about 3 years to become Fe deficient on acompletely iron-free diet . But if there is any abnormal loss ,itll be much shorter Fe is transported in the plasmain the Ferric form, attached to Transferrin , at a concentration

of about 18mol/L,but it is capable of binding54mol/L

therefore , it is about 1/3 saturated* Free Fe is toxic , so it is all bound to protein.* In the plasma it is bound to transferrin* In the stores it is bound to protein in Ferritin & Haemosiderin * In RBCs it is incorporated in Hb.* There is no significant Fe excretion.* Body Fe stores are determined by control of absorption


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Iron Transport in the plasmaplasma Fe with a transferrin is more

suggestive of IDA than a plasma Fe alone.A very low Ferritin almost certainly confirms

the Dx of IDA, but a normal or high levels donot exclude it.Plasma Fe concentration gives no information

about the state of stores.


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Hb Synthesis


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Foods that affect the bioavailabjlity of nonheme iron

Decreased by:Tannates Phosphates oxalates ( found in cereals

eggs Cheese Tea

Increased by:Citrate Fructose Ascorbic acid ( in red beans,

banana and cauliflower Fruit juice 30 minutes before meals


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Iron Deficiecy AnemiaIDA is the most common anemia of infancy & childhood.

The body of the newborn infant contains 0.5 gm FeThe adults iron content is 5 gm

To make up the 4.5 gm difference , 0.8mg Fe must be absorbed each dayduring the 1st 15 years of life.

An extra amount ( 0.5 - 1 mg / day is required to balance losses.To maintain a positive Fe balance during childhood , 1.5mg Fe must be

absorbed each day from the diet.Because 10 % of dietary Fe is absorbed from the average diet,

8 15 mg Fe daily is necessary for optimal nutrition.During the 1st years of life ,when relatively small amounts of Iron rich

foods are ingested , it is difficult to attain these amountsThe infants diet should include Iron fortified foods ,such as cereals or Iron supplemented formulas , by no later than 6 months of age.

IDA develops when there is an inadequate amount of Fe for Hb synthesis.It is the most common cause of anemia during childhood esp.between 6-24months

IDA


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IDA

Iron stores are enough during the 1st

4mo, thereafter Feneeds to be absorbed to keep the demands for rapidgrowth.

For this reason IDA is common between 6-24 mo

this may occur earlier in cases of less stores of Fe( premature SBW Perinatal blood lossDietary habits play a role ( as exclusive breast feeding < 6

mo without supplementation

IDA affects behaviour , cognitive function,attention andperformance of affected children.


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IDAIn infants, early introduction (at age 6 or 8 months of wholecow's milk into the diet is clearly associated withIDAandpatients consuming larger amounts of milk are at higher risk of anemia . This is due to three factors:

1Cow's milk exerts a direct toxic effect on the intestinal mucosaof infants, leading to prolonged microscopic blood loss in the

stools. 2The caloric value of whole cow's milk is high due to fat content,decreasing the appetite and leading to less intake of potential

iron-rich foods.3The bioavailability of iron in cow's milk is low.

Accordingly, the AAP recommends that cow's milk not be used inthe first year of life. Infants should receivebreast milk or ironfortified formulasfor the first year of life,and iron-fortifiedcereal should be added at the age of 4-6 mo.


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Which Pediatric groupsneed screening for IDA?

1-LBW2-Use of formula not fortified with iron

3-Low socioeconomic status4-Exclusive breast feeding ) without solid or

formula supplementation( beyond 6 mo.5-Teenage females who have heavy menses.

As a rule, the smaller the baby ,the earlier &greater the amount of iron needed.

LBW (1000- 1500 gm needs2-3 mg/kg/day(beginning at 2 mo.of age


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Causes of IDA1-Poor intake

2-Decreased Absorption

3-Increased demands4-Blood loss.IDA resulting from blood loss can occur in

the prenatal , perinatal and postnatalperiod


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Clinical presentationHistory

Dietary HistoryPresence of Pica,Geophagia ( IDA,Lead poisoning

History of Blood lossPrenatal,perinatal and postnatal Hx, Family Hx

Any medication

Symptoms : anorexia, easy fatigability, apathy ,Pica and irritability ( due to deficiency in tissueiron-containing enzymes


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Physical Examination

Mild IDA : (Hb 7 10 gm/dlis relatively asymptomaticModerate IDA :palor , glossitis( atrophy of thepapillae of the tongue , angular stomatitis ,

koilonychia , brittle nail and brittle hair , candidiasisSevere IDA : tachycardia , a systolic ejection murmur at the Lt upper sternal border .

Very severe IDA ( Hb 3gm% :Parotid enlargement ,signs of CHF ( tachcardia, S3 , cardiomegaly ,hepatomegaly , distended neck veins and rales onlung auscultation


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Laboratory Findings1-CBC : Hb , PCV , MCH , MCV,

Mentzer Indez 16

2-Blood Film: Microcytic Hypochromic, Normal Reticulocyte3-Iron Study : Serum Fe , Ferritin , TIBC

%saturation ( Fe/TIBC ,Erythrocyte protoporphyrin


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DiagnosisThe diagnosis of iron deficiency anaemia relieson a good clinical history with questions aboutdietary intake, regular self-medication with

NSAIDs and the presence of blood in the faeces(which may be a sign of haemorrhoids or carcinoma of the lower bowel . In women, a

careful enquiry about the duration of periods, the

occurrence of clots and the number of sanitarytowels or tampons used (normal 3-5/dayshould be made.


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Clinical Hints1- Fe + TIBC + Ferritin = IDA

2- Fe + TIBC +Ferritin = Anemia of Ch.dis.3- Fe + TIBC +Ferritin = Ch.Hemolysis

4-Microcytosis disproportioate to Anemia = Thalassemia.5-Failure of Microcytic anemia to responds to Fe:

a Wrong Dx b Persistent bleeding

c Malabsorption d Non-compliance


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Investigation of UnexplainedHypochromic Microcytic Anemia

1-Blood film :a RBCs morphology b reticulocyte count

2-Iron Studies : serum Fe,TIBC , % saturation(N.1/3 saturated i.e 18mol/L

3-Search for GIT bleeding:a Fecal occult Blood b Endoscopy c Angio.4-Marrow aspiration :a stainable Fe stores

b Ring Sideroblasts5-Urinary Hemosiderin :ch.i.v hemolysis

6-Hb electrophoresis ; HbA2 -thalassemia


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DDx of IDAIDA Thalass.T

raitThalass.Major

Anemia of ch.dis.

MCV or N

RBCs N Fe N TIBC N or N N or N or

%saturat N Ferritin N N or HbA2 - @N @ N N

RDW N N


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Management of IDA

Treatment with multivitamins containingiron is inadequate once the child isanemic. Oral ferrous sulfate , at adose of 3 mg/kg of elemental iron

for mild anemia or 6 mg/kg for severeanemia should be given. It should becontinued for 2-3 months after normalization of blood counts to repletethe total body iron stores. The liquid

can stain the teeth so it should be givenin juice rather than dropped directly intothe mouth. Avoid giving it with milk asmilk interferes with its absorption


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Treatment of IDARegular response to adequate amounts of Fe is a good

diagnostic and therapeutic test!Oral Fe ( sulphate , gluconate , and fumarate provide

inexpensive and satisfactory therapy.

No evidence that addition of trace elements or other hematinics increase response to Fe.Dose: 3 6 mg /kg/day ( elemental Fe for 3-6 months.

Within 4 days after Fe , peripheral reticulocytosis is seen.

Family Education: amount of milk to 500ml/day, amount of iron rich foods , correct faulty habits and treat the cause of IDA.


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Available Fe preparations

1-Ferrous Fumarate Tablets 200mg ( 65mg elementalFe

2-Glucofer(Ferrous gluconate 300mg =35mg elemental Fe

3-Fefol ( Ferrous sulfate 325mg =105 mg elemental Fe

4-Ferrose Syp (150mg Ferrous sulfate =30 mg elemental Fe

5-Fer in sol , Kdiron Drops (Ferrous sulfate 0.6ml = 75 mg ferrous sulfate = 15 mg elemental Fe


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Food Content of IronFood Fe in mg Food Fe in mg

One Apple 0.25mg 1cup Lentils 6.6mgOne banana 0.37mg 1cup Peas 3.25mgGrapefruit(I cup 1.02mg 1cup Soybean 8.84mgGrapes ( Cup 0.42mg 1cup White flour 5.8mgRaisins ( cup 3 mg 1cup Spinach 6.4mg

100gm Meat2.75mg

100gm Shrimp2.33mg100gm Chicken 1.25mg 100gmTuna 1.30mg

Duck 6mg 100gm Sardine 2.5mg

1cup Beans 5.25mg


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HbHb is a tetramer of 4 globin chainscovalently linked to heme and arranged in2 polypeptide chains.Adult haemoglobin)Hb A(consists of two and two globin chains. A haem group is bound toeach globin chain; the haem group has aporphyrin ring with a ferrous atom which can reversibly bind one O2 mol


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Some Types of Hb


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Hb Electrophoresis


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Thalassemia


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Thalassemiasare genetic disorders of Hb synthesis

with reduced production of one or more of the globin chains.

underproduction of Hb and imbalanceglobin chain synthesis with precipitationof excess chainformation of Heinz

bodies.These inclusion bodies increase the

rigidity of RBCs their destruction either in B.M or in the circulation or in both


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Features of - thalassemia

-thalassemia trait(minor 1-CBC MCV , MCH , Hb , RBCs

2-Blood Film Basophilic stippling,target cells poikilocytes.

3-HE HbA2 HbF4-Iron study Normal serum Fe & Ferritin

5-No response to iron therapy.

-thalassemia IntermediaMore severe than thalassemia.trait , but milder than thalassemia.Major


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-thalassemia Major(Cooleys Anemia

1-presents during the 1 st year of life with: FTT , intermittent infections , severe anemia ,

hepatosplenomegaly , bone expansion ( due to extra-medullary hemopoiesis , the classical thalassemia facies

2-X-Ray Hair-on- end arrangement of bone trabeculae3-CBC Hb , MCV , MCH , Reticulocytes , Normal

WBCs & Platelets ( unless hypersplenism is present4-Blood Film Tear drops , target cells , Wafer cells ,

hypochromic microcytic picture

5-TIBC is saturated , serum Fe & Ferritin 6-Hb. E. HbF ( > 70% , HbA2 , or absent HbA


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- Thalassemiaa A child with thalassemia showing typical facial featuresb Hair-on-end appearance .c X-Ray show expansion of the marrow and thinned cortex


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B-thalassmia


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Management1-Hypertransfuse to maintain Hb < 10gm/dl

2-Folic acid supplement3-Splenectomy , if indicated

4-Iron chelation ( desferrioxamine as earlyas possible , ( may cause cataract

5-Genetic counselling

6-HBV vaccination7-Bone marrow transplantation

Si kl ll S d


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Sickle cell SyndromeSickle cell anemia is an autosomal recessive disorder thatresults from a substitution of valine for glutamine in the-globin chain. This substitution results in alteration of the Hb structure.Under deoxygenated conditionsaggregation of Hb into long polymer that distort RBCsinto a sickle shape.

Sickling shortens RBC survival and results in ach.hemolytic anemia. Sickled cells also cause

microvascular obstruction, which leads to tissueischemia and infarction.The sickling process is accentuated by : hypoxia , acidosis,dehydration,high or low temperature.

If only one of the two -globin genes is affected , thepatient has Sickle trait ( heterozygous state

If both - globin genes have the genetic substitution,thepatient is homozygous for Hb S and has Sickle cellanemia.

Newborn screen for sickling is routinely done in all hospitals


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Sickle SyndromesSickle cell Disease

SS = sickle cell anemiaAS = sickle cell traitSickling is precipitated by:Infection dehydration cold acidosis hypoxia

Sickle cell trait( Hb AS55-60%Hb A , 40 % Hb S , 2-3% Hb A2 *Normal life expectancy and usually asymptomatic

Protected against Plasmodium Falciparum Malaria*Rarely can cause Papillary necrosis Nocturia &

painless hematuria, and inability to concentrate the urineBacteruria during pregnancy


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Sickle cell Anemia ( Hb SS

1-a homozygous state ( 85% HbS , 10% Hb F2-Usually presents in childhood withanemia and mild Jaundice

3-Hand and Foot Syndrome (dactylitis is common with painfulswelling of fingers and toes( due to symmetric infarction in

metacarpals,metatarsal, & phalanges

4-In older patients Vaso-occlusive problems occur owing tosickling in the small vessels of any organ.Typical Sickling Crises include:

1-Bone pain commonest 2- Chest pleuriticpain,fever,cough ,pulmonary infiltrates, resemble pneumonia

3-Cerebral hemiparesis,fits 4- kidney papillary necrosis5-Spleen Painful infarcts 6- Penis priapism Attacks of pain with mild fever last from few hours to few days.


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Varieties of Sickle cell Crisis

1-Hemolytic crisisSepsis (Salmonella infection or associated G6PDD ; relatively uncommon.(10% ,it lasts2-3wks.It is marked by abdominal pain , fever , jaundice , tender hepatomegaly,& intransaminases

2-Aplastic CrisisDue to Parvovirus infection or folate deficiency, Reticulocyte

3-Thrombotic CrisisThe commonest . It may affect abdomen , lung , brainInfarcts are precipitated by tissue hypoxia.May be accompanied with fever , fits , dyspnea.

Complications : hyposplenism, aseptic necrosis of bone ,renal failure4-Sequestration Crisis

Most serious esp. in infants ( due to hypovolemia rapid onset hepatosplenomegalyAs the sickled cells traverse the spleen,they cause microvascular obstruction,infarctionand fibrosis of the spleen.( autoinfarction of the spleen


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Long term Problems

1-Susceptibility to infection:Parvovirus and strept.pneumonia fatal meningitis

Salmonella osteomyelitis2-Ch. Leg ulcer :

Due to ischemia3-Gallstones:

From persistent hemolysis4-Aseptic necrosis of femoral head

5-Retinal detachement & proliferative retinopathy Blindness

6-Ch.Renal disease


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Investigations

1-CBC Hb 6 8 gm % , Reticulocytes 10 20% Thrombocytosis , Leucocytosis

2-Blood Film Post-splenectomy features:Howell Jolly bodies Pappenheimer bodies Target cells

Spur cells- Spherocytes - Schizocyte-3-Induce Sickling by Na Metabisulphite

4-Hb E.

Hb SS , no Hb A 80 95%Hb SS and 2 20% Hb F


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Management

1-Steady state anemia No treatment 2-Avoid precipitating factors(infection, dehydration , cold , acidosis , or hypoxia

3-prophylaxis to prevent pneumococcal infections Polyvalentanti-pneumococcal Vaccine , Long term oral penicillin 250 mg BID.

4-Acute attacks

i.v. fluids (to prevent dehydration - O2 - Antibiotics analgesia( acetaminophen & codeine - transfusion in severe anemia5-Folic acid to pregnant women & to patients with severe hemolysis

6-Exchange transfusion in recurrent crisis7-Splenectomy may be life saving in children with splenic sequestratn

8-Hydroxyurea episodes of pain,& the acute chest syndrome( Hydroxyurea has as one of its side effects the ability to increase HbF

-cells with HbF are less prone to sickle.9-Other agents that HbF are 5-azacytidine , Recombinant human Erythropoietin.


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Alfa Thalassemia


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Alfa- ThalassemiaSilent carriers are missing1 alpha gene.They have no clinical abnormalities. Their hemoglobin, and hemoglobinelectrophoresis are normal and their MCVis borderline normal. Those with alphathalassemia trait are clinically normal,but their Hb is slightly low and their hemogram demonstrates MCV. Their

Hb.elecrophoresis is normal unless it isdone in the newborn period at which timeHbBarts is present


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Hb H

The name Hb H disease is a misnomer , it is not a disease, but rather a condition.People with Hb H conditioncan live healthy,

long lives. They are not transfusion dependent. People with Hb H need

to avoid all forms of supplemental iron. Since the bonemarrow of thalassemia patients requires excess folic acid(due to erythroid hyperplasia , most clinicians adviselifelong supplementation of 1 milligram daily of folic acid toavoid relative folate deficiency. During times of severeillness, or in pregnancy, the Hb may drop significantlybelow baseline in Hb H disease, and a transfusion may berecommended. Again, iron is generally not deficient and,thus iron supplementation is not helpful, nor is it

appropriate.

Case Study 1


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Case Study 115year old is to have Hb 10.6gm/dl & MCV 65. She

reports regular menses , lasting 4-5 days eachcycle. She has no specific complaints.She is unawreof a family Hx of anemia. Her diet appears to beadequate.P.E is unremarkable.Nohepatosplenomegaly or jaundice were detected.What is the most appropriate management?

a Start on oral contraceptive and recheck CBC in 2 mob Start an empiric Fe while waiting results of Hb electr.& Fe studies and recheck CBC if Fe is deficientc Check for Hb Barts, if not present starts on Fe tab

and recheck CBC in 2 mo.d Order Hb electr.,if Hb H is not found starts Fe tab,while awaiting Fe studies results and recheck CBC

in 2 mo if IDA was present.

Answer is (b


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Answer is (bThe 2 most likely etiologies of the anemia inthis young lady are :IDA or a form of thala.

She could be managed with a trial of Fe for one month.If a repeat CBC shows nochange , then either alfa or beta thalassshould be considered. Hb elect.would bethe next step if Fe trial fails.

An in HbA2 is very suggestive of -thala.trait( due to mild anemia in this case

If Hb elect is normal or near normal, alfathalassemia is the most likely cause.


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Answer


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Answer

4a. Fe is indicated as a therapeutic trial. But if noimprovement in the Hb results, then a

thalassemia is possible4b. Fe is contraindicated since it will not improvethe Hb and it will add to the potential for irontoxicity

4c. Fe is contraindicated, since it will not improvehis Hb and it will add to the potential for irontoxicity

4d. Despite the presence of thalassemia, irondeficiency is documented by laboratorystudies, so iron supplementation is indicateduntil iron deficiency resolves. Once IDA is nolonger present, iron supplements becomecontraindicated

Q3: Which of the following finding would distinguish


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-thalassemia trait from IDA?a Microcytic RBCsb Absence of anemiac Elevated Hb A2 level

d Normal Transferin saturatione Normal serum Ferritin concentration-------------------------------------------------------------------------------

Q4: Persons who have sickle cell trait have which of the following ? a) Impaired growth and development in childhood b Increased incidence of hematuriac Impaired ability to concentrate urined Increased mortality rate in pregnant womene Increased incidence of splenic infarction with high altitude hypoxia

Al T h


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Always Together .

D Ah d


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Dr.Ahmed.

Noureldin

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Anemias by Dr.Ahmed Noureldin Ahmed

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