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Hematology MLT > Microcytic and Macrocytic Anemias > Flashcards

Microcytic and Macrocytic Anemias Flashcards

1
Q

What amount of ingested iron is absorbed?

A

10%

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2
Q

Iron is stored as ?

A

Ferritin and homosiderin

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3
Q

Absorbed iron is converted from ?

A

Ferric (Fe3+) to Ferrous (Fe2+)

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4
Q

What factors affect iron absorption?

A

GI tract health
Diet (5% daily intake maintains RBCs)
Current iron stores
Erythropoietic need

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5
Q

Identify iron needs in children and adults?

A

Adults 95% iron is recycled for RBC production

Children 70% iron recycled for RBC production

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6
Q

Why are the iron needs of children higher than adulta?

A

Children have a higher iron demands because of growth spurts.

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7
Q

What can cause IDA?

A

Increased iron demans - growth spurts, prenancy, nursing
iron intake - diet / conditions causing iron malabsorbtion
Blood loss - GI bleeding, excessive periods, hemolysis

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8
Q

Unusual symptoms associated with IDA? (3)

A

Pica - eating weird shit
Chelitis - swollen/ swelling around lips
Koileneychea - spooning of nail beds

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9
Q

What is the iron profile in IDA?

A

decreased iron
decreased serum ferritin
decreased iron saturation
TBIC increased (more sites available for binding)

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10
Q

Describe the CBC profile in IDA? (6)

What indices is increased?

A

Decreased RBC count, Hgb, Hct, MCV, MCH, MCHC.

Increased RDW

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11
Q

How many stages are there in IDA? What happens at each stage? At which stage do symptoms start to show?

A 
3
stage 1 - depletion of iron stores 
stage 2 - ineffective erythroporesis
stage 3 - IDA
symptoms appear stage 3
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12
Q

What is the most sensitive indicator of iron stores?

A

Serum Ferritin

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13
Q

Sideroblastic Anemia

A

Iron overload

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14
Q

Describe the pathophysiology of Hereditary Hematochromatosis and what is it responsible for?

A

Faulty mechanism cause iron overload.

Iron loading starts at young age.

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15
Q

What is the gene affected in Hereditary Hematochromatosis? How is this disease inherited?

A

Abnormal HFE gene, responsible for regulating iron storage and absorption.
Autosomal recessive carried on chromosome 6; linked to HLA-A3
inherited homozygously / herterozygously
Homozygotes more prone to iron overload only 10% in hetero

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16
Q

What are some symptoms of Hereditary Hematochromatosis? (6)

A 
Cirrohsis
Hyperpigmentation
Impotence
hair loss
Tender swollen joints
cardiac arrythmias
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17
Q

Describe the iron profile of patients with Hereditary Hematochromatosis? (5)

A 
Increased serum iron 
increased ferritin
increased tranferrin saturation
TIBC normal range
Transferrin normal range
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18
Q

How is Hereditary Hematochromatosis treated?

A

Therapeutic phlebotomy

Desferyl (defroxamine) - iron chelating (binding) agent

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19
Q

What are the Thalassemia syndromes?

A

Globin chain disorder due to lack of alpha or beta globin chain systhesis.

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20
Q

How many alpha thalassemias are there?

A

4 - related to the number of genes deleted.

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21
Q

What is the most severe alpha thalassemia?

A

Bart’s Hydrops Fetalis

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22
Q

Describe the pathology, gene deletions and symptoms in Bart’s?

A 
No alpha chain synthesis
only Hgb Bart's formed ( 4 gamma chains)
has a very high affinity for oxygen
incompatible with life ; severe anemia
still birth/ spontaneous abortion
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23
Q

Describe the pathology, gene deletions and symptoms in hemoglobin H disease?

A 
3 gene deletion; 1 functioning alpha gene
Hgb H  (5 - 40%) formed and little Hgb A 
Hgb H inclusions: golf ball pitted
Symptoms: anemia, splenolmegaly and bone changes
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24
Q

Describe the pathology, gene deletions and symptoms in Alpha thalassemia trait?

A

2 gene deletion ( 4 functional chains)
Some Hgb Bart’s formed
mild anemia
many microcytic and hypochomic cells

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25
Q

Describe the pathology, gene deletions and symptoms in Silent carrier of alpha THA?

A

1 gene deletion (3 functional genes)
Hematologically normal
slightly microcytic
peripheral smear will have some elliptocytes and target cells

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26
Q

Cooleys / Mediterranean Anemia

A

Beta THA Major

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27
Q

Describe the cause of Beta THA major?

A

little / no beta chain synthesis

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28
Q

What hemoglobin is produced in beta THA major?

A

Hgb F

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29
Q

How is beta THA major treated? (4)

A

Transfusion
iron chelation
bone marrow transplant
stem cell transplant

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30
Q

Symptoms of Beta THA Major? (3)

A

Facial changes, bossing/ protrusion of skull
fail to thrive
jaundice

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31
Q

What Hgb is present in elevated amounts in beta THA minor?

A

Hgb A2

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32
Q

What is the genetic defect in beta THA minor?

A

One abnormal beta gene

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33
Q

What are the known clinical manifestation of beta THA intermedia? (3)

A

develops later in life
minor bone changes
larger spleens

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34
Q

What differentiates Alpha THA from IDA?

A

MCV much lower than IDA

RDW more severe.

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35
Q

What differentiates Beta THA minor from IDA?

A

MCV much lower

RBC count is elevated

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36
Q

Except for low MCV, what is a diagnostic clue for Silent Alpha THA?

A

elliptocytes on smear

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37
Q

What are diagnostic clues for beta THA major?

A

High NRBCs

target cells, fragments on smear

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38
Q

Describe what a megaloblastic anemia and what a macrocyctic anemia?

A

meglaoblastic anemia is the result of a B12 or folic acid deficiency and MCV exceeds 110 fL

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39
Q

Explain the role of B12 and Folic acid in DNA synthesis?

A

DNA sythesis depends on TTP (thymidine triphosphate)
TTP needs methyl group from MTH (methyl tetrahydrofolate) or folic acid.
B12 is the cofactor that transfers the methyl group

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40
Q

If TTP is not made what is it replaced by and what does this lead to?

A

DTP, leading to nuclear fragmentation, destruction and impaired cell division.

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41
Q

What are the characteristics of megaloblasts compared to normoblasts?

A

RBC precursors larger
Nuclear structure less condensed (normoblast c: n ratio decreases, nucleus more compact)
Cytoplasm is basophilic and bluer
chromatin open waved (condensed in normoblast)
***Asychronous maturation between nucleus and cytoplasm)

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42
Q

Describe ineffective erythroporesis related to megaloblastic anemias?

Ratio
prcursors
RETIC count
Bilirubin and LDH

A

M:E ratio 1:1 or 1:3
Megaloblastic precursors hemolyse before maturation complete in bone marrow.
Reticulocytopenia (low RETIC count)
Bilirubin and LDH elevated

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43
Q

The peripheral smear in ineffective erythroporesis related to megaloblastic anemias?

A

Peripheral smear lacks NRBCs

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44
Q

Describe WBC changes in peripheral smear in MA?

A

Hypersegmented neutrophils (>5 lobes)

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45
Q

Describe the CBC in MA? (4)

A

Pancytopenia (low WBC count)
Low RBC count
Low PLT count
MCV initially high

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46
Q

RBC inclusions seen in MA?

A

BS

HJB (more fragmented and larger)

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47
Q

What happens to the RDW in MA?

A 
RDW increased
SCHISTOS
TDS
TC
MACRO
MACRO-OVALO
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48
Q

Where is B12 absorbed?

A

Illeum

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49
Q

What is needed for B12 absorbtion?

A

Intrinsic Factor (IF)

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50
Q

Where is B12 stored?

A

Liver; takes years to deplete

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51
Q

What is the MDA for folic acid?

A

200 micrograms

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52
Q

What is the MDA for B12?

A

20 micrograms

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53
Q

Where is folic acid absorbed?

A

Small inntestine

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54
Q

Folic acis is stored long term or short term?

A

short term; takes months to deplete

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55
Q

Describe B12 transport to bone marrow into red cells?

A

Ingested and separated by saliva enzymes
In stomach combines with IF
B12-IF complex transported to ileum
B12 absorbed and IF degraded
B12 transported to plasma; complexes with transcobalamin II (TCII)
TCII transports B12 to circulation and transfers to liver, bone marrow and other tissues

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56
Q

What protein transports B12 into circulation and to liver and bone marrow?

A

Transcobalamin II

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57
Q

How is folic acid transported into tissues?

A

Absorbed in small intestine
reduced to methyl tetrahydrofolate (MTH) by dihydrofolate reductase - moved to tissues when inside - methyl group released to combine with homocystein

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58
Q

Symptoms of MA?

A

Glossitis
Neurologic
Mania (personality changes)
Demyelination of peripheral nerves

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59
Q

Dietary B12 deficiency is rare except?

A

Vegetarians / infants nursed by vegetarian mums who do not supplement diet

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60
Q

Causes of B12 deficiency?

A

Cobalamin/ intestinal malabsorbtion
food malabsorbtion by helobacter pylori
Blind loop syndrome (basteria take b12)
Fish tapeworm - Diphylobothrium latum competes for B12

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61
Q

Causes of folic acid deficiency?

A 
Pregnancy
elderly 
alcoholics
malabsorbtion syndrome - tropical sprue
Drug/ chemo drugs affect DNA synth
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62
Q

What is Pernicious Anemia?

A

Lack Intrinsic Factor needed for B12 absorption

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63
Q

How is B12 deficiency tested for?

A

Radioimmunoassay

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64
Q

What is the test for Folic acid deficiency?

A

Chemiluminescence - measures folate stored

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65
Q

How is B12 deficiency differentiated from Folic acid deficiency in the Lab?

A

Serum methlymalonic acid (MMA) and homocystein.

Both elevated in B12 deficiency, can detect mild B12 deficiency.

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66
Q

How is IF affected in Pernicous anemia?

A

Can be blocked, neutralized, not secreted:
Gastrectomy
Atrophic gastritis
Antibodies against IF

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67
Q

What do IF antibodies do in PA?

A

Block B12-IF complex preventing absorption in ileum

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68
Q

Differentiate anemias that are macrocytic but not megaloblastic?

A

Megaloblastic Features:
Macrocytes are large and oval
lack hypochromia - normochromic

69
Q

Non-megaloblastic RBC morphology?

A

Round hypochromic macrocytes

blue tinged macrocytes seen in neonate response to anemic stress

70
Q

Causes of non-megaloblastic anemia?

A

Alcoholism
Hypothyroidism
Liver Disease

71
Q

Hereditary Spherocytosis is common in what group of people?

A

N. Europe

72
Q

What is the % inheritance of Hereditary Spherocytosis?

A

75% Auto dominant

25% Auto recessive

73
Q

What is deficient in Hereditary Spherocytosis?

A

Membrane proteins Spectrin and Ankyrin
on protein band 3
protein band 4.2

74
Q

Where are spherocytes found in Hereditary Spherocytosis?

A

Peripheral circulation

In spleen only

75
Q

What is wrong with Sperocytes?

A

Cell membrane can only stretch 3% (normal is 117%)
Ion transport both active and passive is disrupted
unable to deform in microvasculature

76
Q

Describe osmotic fragility testing?

A

Cells tested at varying salt concentrations
Normal RBCs reach equilibrium
Solution become more hypotonic (less salt & more water) —> water influx some hemolysis.

77
Q

What do normal RBCs lyse at in Osmotic fragility test?

A

0.85% NaCl

78
Q

What do sperocytes lyse at in osmotic fragility test?

A

0.65% NaCl

79
Q

What membrane proteins are affected in Hereditary Stomatocytosis?

A

Spectrin
Stomatin
Some ankryin

80
Q

What happens to stomatocyte cells?

A

membrane only expand 3%

Na+ and K+ active transport fucked up

81
Q

What is the inhertitance pattern of Hereditary Stomatocytosis?

A

Auto dominant, but rare disorder

82
Q

Stomatocytes are also seen in what kind of individuals?

A

Lacking Rh antigens - Rh Null disease

83
Q

What is the protein deficiency in Hereditary Eliptocytosis? What regions is this associated with?

A

Spectrin

associated with alpha and beta regions

84
Q

What is the inheritance for Hereditary Eliptocytosis?

A

Auto. Dominant

85
Q

4 Subtypes of Hereditary Eliptocytosis?

A

Common Hereditary Sperocytocis (CHE) - Auto Dom
Southeast Asian Ovalocytosis (SAO) - Auto Dom
Spherotic Hereditary Eliptocytosis (SHE) - Auto Dom
Hereditary Pyropoikilcytosis (HP) Auto Recessive

86
Q

Mild CHE

A

No clinical sysmptoms

87
Q

Severe CHE

A

seen in infants more often then changes to mild in adults

88
Q

What is a unique feature of RBCs in SAO?

A

2 bars across RBC centre

Cells spoon shaped

89
Q

What group is affected by SAO?

A

Melanesia / malasian populationn?

90
Q

SHE affects which group of people

A

N. Europeans

91
Q

SHE symptoms?

A

Gall bladder disease and splenomegaly

92
Q

What is a unique feature of HP RBCs?

A

Red cell budding and red cell crenantion

93
Q

Pyruvate Kinase Deficiency is a disorder of what pathway?

A

Embden-Myerhof Pathway

94
Q

Pyruvate Kinase Deficiency prevents what leading to what?

A

Unable to make ATP from ADP for RBC membrane function, which leads to a buildup of 2,3 diphosphoglycerate

95
Q

as well as N. Europeans Pyruvate Kinase Deficiency affects?

A

Amish population of Miffin county PA

96
Q

What is the most common enzyme deficiency in the world?

A

G6PD

97
Q

What is G6PD Deficiency’s mode of inheritance?

A

X-linked recessive

98
Q

G6PD is needed for which pathway?

A

Phosphogluconate pathway

99
Q

What does G6PD do?

A

Keeps gluthione in a reduced state

100
Q

What does lack of G6PD cause?

A

Prevents NADH formation, which is needed to reduce gluthione which prevents oxidative stress.

101
Q

What is a unique feature of G6PD deficiency?

A

Protects against malaria

102
Q

What are the 4 clinical conditions of G6PD deficiency?

A

Drug induced acute hemolyt[ic anemia
Favism
Neonatal jaundice
Congenital non-spherotic anemia

103
Q

Diagnosis of G6PD deficiency what is important?

A

timing critical and not done during a hemolytic episode

104
Q

What is the amino acid substitution in Hgb S?

A

Valine is subbed for glutamic acid at position 6

105
Q

What is the inheretance for Hgb S?

A

Auto Dom on chromosome 11

1 location on each chromosome for normal or abnormal beta chain

106
Q

What are the two types of Sickle Cell?

A

Reversible (blunt ends) and Irreversible (pointy ends)

107
Q

What happens to RBCs containing Hgb S in areas of low O2?

A

Rigid

108
Q

What can induce Sickling?

A

Hypoxia
Acidocis
Dehydration
Exposure to cold

109
Q

Sickle cell life span?

A

10 - 20 days

110
Q

What are the 4 haplo types of Sickle cell?

A

Asian, Benin, Bantu, Senegal and carribean

111
Q

What differentiates the 4 sickle cell haplo types?

A

Different sequence of nucleotides (polymorphisms) on DNA strands, all located in same gene cluster.
Amount of Hgb F present

112
Q

How does Hgb F affect sickle cell?

A

presentation is less severe

113
Q

Clinical considerations of sickle cell?

A 
Chronic hemolytic anemia
Recurrent painful attacks
Bacterial infections
Hypercellular bone marrow
Cholelithiasis (gallstone formation)
114
Q

How does sickly cell affect the spleen?

A 
Splenomegaly
loses ability to clear abnormalities
HJBs evident
splenic atrophy
splenic sequestration (RBCs trapped in spleen)
115
Q

How does sickle cell affect the lungs?

A

Embolisms (Occlusions)

Pnemonia

116
Q

What is a trademark of sickle cell?

A

Painful crisis (sickle cell crisis)

117
Q

How can sickle cell affect males?

A

Priapsm (persistent boner)

118
Q

How does sickle cell affect eyes?

A

Retinopathy
blindness
retinal detachment
lesions

119
Q

What are treatments for sickle cell?

A

Prophylactics
Transfusions for 3 - 5 weeks until Hgb 9-11 g/dL
Hydroxyurea

120
Q

What is the amino acid substitution in Hgb C formation?

A

Lysine subbed for glutamic acid at 6th position of beta chain

121
Q

What is the inheritance in sickle cell trait?

A

Hetrozygous - one normal and one abnormal gene

122
Q

What is the inheritance in sickle cell disease?

A

Homozygous - both genes abnormal

123
Q

The diothnate test is based on what principle?

A

Hgb S precipitates

124
Q

What is the Hgb Distribution in Sickle cell trait?

A

Hgb A 60%
Hgb S 40%
have normal lives but crisis can be triggered

125
Q

What is a unique identifier of Hgb C Disease RBCs?

A

Crystals (bars of gold)

126
Q

What is the Hgb C ratio?

A

Hgb A 60% Hgb C 40%

127
Q

What is a unique identifier of Hgb SC Disease?

A

SC Crystals (Washington monument)

128
Q

What is the hgb distribution in SC Disease?

A

hgb S 50% and hgb C 50%

129
Q

What hgb results from a Hgb sub of lysine for glutamic acid at the 26th position of the beta globin chain?

A

Hgb E

130
Q

What is the 2nd most common Hgb worldwide?

A

Hgb E

131
Q

What is the distribution of Hgb in Hetrozygotes?

A

70% Hgb A and 30% Hgb E

132
Q

What hgb is a beta chain variant?

A

Hgb D punjab

133
Q

What hgb is a alpha chain variant?

A

Hgb G phila

134
Q

What hgb variants have no hematological abnormalities?

A

Hgb D punjab & Hgb G phila

135
Q

What Hgbs migrate in the same position as Hgb S at alkaline electrophoresis at pH 8.6?

A

Hgb G phila

136
Q

What Hgbs migrate in the same position as Hgb C at citrate electrophoresis at pH 6.0?

A

Hgb O arab

137
Q

What are the features of hemoglobin S Beta-THA?

A

No Hgb A

2 bands on electrophoresis one at Hgb S and one and Hgb A2

138
Q

What is the principle of the sickledex tube test?

A

Hgb S is insoluble when combined with a buffer and reducing agent
Therefore it precipitates

139
Q

What is the interpretation of the sickledex tube test?

A

Positive: turbid solution if Hgb S present or any other sickling Hgb present
Negative: solution clear

140
Q

The morphologic classification of anemias is based on?

a. RBC
b. Cause of the anemia
c. Red blood cell indices
d. Reticulocyte count

A

c. red blood cell indices.

141
Q

Which of the following symptoms is specific for IDA?

a. Fatigue
b. Koilonychia
c. Palpitations
d. Dizziness

A

b. Koilonychia

142
Q

Which of the following laboratory tests would be abnormal through each stage of iron deficiency?

a. Serum Iron
b. Hgb and Hct
c. RBC
d. Serum Ferritin

A

d. Serum Ferritin

143
Q

A patient presents with microcytic hypochromic anemia with ragged-looking red blood cells in the peripheral smear and a high reticulocyte count. A brilliant cresyl blue preperation reveals inclusions that look like pitted golf balls. These inclusions are suggestive of?

a. Hgb H disease
b. Beta THA major
c. Hereditary Hemochromatosis
d. Beta THA trait

A

a. Hgb H disease

144
Q

The most cost effective treatment for a patient with Hereditary Hemochromatosis?

a. Desferyl chelation
b. bone marrow transplant
c. Therapeutic phlebotomy
d. stem cell transplant

A

c. Therapeutic phlebotomy

145
Q

List two sets of lab data that can distinguish IDA from Beta thallasemia trait?

a. Serum Iron and RBC
b. Hgb and Hct
c. WBC and RDW
d. Red blood cell indices and platelets

A

a. Serum Iron and RBC

146
Q 
What is the majority Hgb in Beta THA Major?
a. Hgb A
b. Hgb A2
c. Hgb F
c . Hgb H
A

c. Hgb F

147
Q

Of the 4 Alpha THAs, which is incompatible with life?

a. A THA silent
b. A THA trait
c. Hgb H
d. Bart’s Hydrops fetalis

A

d. Bart’s Hydrops fetalis

148
Q

Which of the following Hgbs has the chemical confirmation Beta4?

a. Hgb Barts
b. Hgb Gower
c. Hgb H
d. Hgb Portland

A

c. Hgb H

149
Q

Although there aare many complications in individuals with THA major. Which of the following is the leading cause of death?

a. Splenomegaly
b. Cardiac complications
c. hepatitis C infections
d. Pathologic fractures

A

b. Cardiac complications

150
Q

Which of the following inclusions cannot be visualized by the Wright-stained peripheral smear?

a. Basophilic stipling
b. Hgb H inclusion bodies
c. Howell-Jolly Bodies
d. Heinz Bodies

A

d. Heinz Bodies

151
Q

Which of the following functions most affects spherocytes as they travel trough circulation?

a. tend to form inclusion bodies
b. less deformable and more sensitive to low glucose in the spleen
c. they tend to be sequestered in the spleen because of abnormal hemoglobin
d. they form siderotic granules and cannot navigate circulation

A

b. less deformable and more sensitive to low glucose in the spleen

152
Q

Many individuals with hereditary spherocytosis are prone to jaundice because of?

a. Epstein-Barr Virus
b. pathologic fractures
c. gallstone disease
d. skin pigmentation

A

c. gallstone disease

153
Q

Which of the following are characteristics of HP?

a. Elliptocytes with sperocytes intermixed with in peripheral smear
b. Sperhocytes with polychromasia and low MCV
c. Elliptocytes, spherocytes, and budding red blood cells
d. Mostly elliptocytes and few other morphologies.

A

c. Elliptocytes, spherocytes, and budding red blood cells

154
Q

What red blood cell morphology is formed as a result of Heinz bodies being pitted from the RBC?

a. Acanthocytes
b. Bite cells
c. Burr cells
d. Stomatocytes

A

b. Bite cells

155
Q

All of the following statements are correct about G6PD deficiency EXCEPT?

a. It is the most common glycolitic enzyme deficiency assciated with the pentose phosphate pathway
b. It increases formation of heinz bodies
c. it causes Hgb to be oxidized from ferrous to ferric state
d. It is transmitted on a mutant gene on the X chromosome

A

c. it causes Hgb to be oxidized from ferrous to ferric state

156
Q

Which of the following factors contributes to the the pathophysiology of sickling?

a. Increased iron concentration
b. Hypochromia
c. Fava beans
d. Dehydration

A

d. Dehydration

157
Q

Which of the following statements pertains to the the most clinically significant Hgb variants?

a. most are fusion Hgbs
b. most are single amino acid subs
c. most are synthetic defects
d. most are extensions of the amino acid chain

A

b. most are single amino acid subs

158
Q

Which of the following Hgbs ranks second in varient Hgbs worldwide?

a. Hgb S
b. Hgb E
c. Hgb H
d. Hgb C

A

b. Hgb E

159
Q 
Which of the following shows crystal "gold bars' in the peripheral smear?
a. Hgb CC
b. Hgb DD
c Hgb EE
d. Hgb SS
A

a. Hgb CC

160
Q

Which of the following Hgb Seperation methods is used for most newborn Hgb screening?

a. HPLC
b. Alkaline Electrophoresis
c. Isoelectric focusing
d. Acid electrophoresis

A

c. Isoelectric focusing

161
Q

Which Hgbs migrate to the same location at pH 8.6?

a. Hgb F, Hgb H, Hgb Barts
b. Hgb A2, Hgb s, Hgb C
c. Hgb A2, Hgb C, Hgb E
d. Hgb D, Hgb O, Hgb F

A

c. Hgb A2, Hgb C, Hgb E

162
Q

All but one of the following may be seen in the peripheral smear when sickle cell crisis has occurred?

a. Target cells
b. NRBCs
c. Polychromasia
d. Moderate elliptocytes

A

d. Moderate elliptocytes

163
Q

Which Hgbs travel together at pH 8.6?

a. Hgb F, Hgb H, Hgb Barts
b. Hgb S, Hgb D, Hgb G
c. Hgb A2, Hgb C, Hgb E
d. Hgb D, Hgb O, Hgb F

A

b. Hgb S, Hgb D, Hgb G

164
Q

Which Hgbs migrate to the same point at pH 6.0?

a. Hgb A, Hgb O, Hgb A2, Hgb D, Hgb G Hgb E
b. Hgb S, Hgb D, Hgb G
c. Hgb A2, Hgb C, Hgb E
d. Hgb D, Hgb O, Hgb F

A

a. Hgb A, Hgb O, Hgb A2, Hgb D, Hgb G Hgb E

165
Q

Which test clarifies varying degrees of anemia?

A

Microhematocrit

166
Q

A non specific screening test for inflammation?

A

Erythrocyte sedimentation Rate

167
Q

ESR is diagnostic in what 3 disease states?

A

Multiple myeloma
Temporal Arteris
Polymyalgia rheumatic

168
Q

Which test is an indicator of the bone marrow’s ability to produce RBCs?

A

reticulocyte count

169
Q

How many RBCs screen in a reticulocyte count?

A

1000

Hematology MLT (5 decks)

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