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Hematology/Oncology > Hematopoiesis > Flashcards

Hematopoiesis Flashcards

1
Q

what are pluripotent stem cells

A

have ability to salvage all of the elements of hematopoiesis in recipient after the recipient’s bone marrow contents have been wiped out by irradiation or chemotherapy

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2
Q

morphologically what subset of cells do pluripotent stem cells belong to

A

blasts

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3
Q

how frequent are pleuripotent stem cells

A

less than 1 in 20 million

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4
Q

what are pleuripotenet stem cells criticl for

A

bone marrow transplant and gene therapy methods

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5
Q

how are bfu and cfu defined

A

responsiveness to handful of growth factors

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6
Q

what is TPO

A

thrombopoietin

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7
Q

what is EPO

A

erythropoietin

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8
Q

what are the percent of blasts

A

less than 4 percent

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9
Q

what percent is eryhtropoeisis

A

20-30

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10
Q

what percent is myelopoesis

A

60-70

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11
Q

what percent is lymphopoeisis

A

10-20

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12
Q

what are the stages of blasts maturing to neutrophils

A

blast to promyelocyte to myleocyte to metamyelocyte to bands and neutrophils

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13
Q

when in the maturation process do blasts lose ability to divide

A

when they are myelocytes

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14
Q

describe the number of mature species to less mature species as blasts mature

A

more matures ones than less mature ones

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15
Q

what is granulopoeisis termed

A

myelopoesis

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16
Q

what is a key regulator in granulopoeisis

A

GM-CSF and GCSF

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17
Q

what is difference in gmcsf and gcsf in blast maturation

A

gcsf acts primarily on neutrophils (gmcsf also acts on eosinophils)

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18
Q

what is maturation of blasts to erythroblasts

A

blast to pronormoblast to basophilic erythroblast to polychromatophilic erythroblast to normochromic erythroblast

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19
Q

what stimulates epo production

A

hypoxia sensed by renal peritubular cells

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20
Q

how many cell divisions in normal maturation of erythroid precursors

A

5

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21
Q

how are platelets produced

A

huge factory cells - megakaryocytes extend snakelike tubes (proplatelets) into highly fenestrated blood vessels in bone marrow (sinuses)

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22
Q

describe megakaryocytes

A

polyploid (not 2N but 16 to 32 haploid genomes) - nuclei divided multiple times

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23
Q

where does gmcsf come from

A

bone marrow stromal cells

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24
Q

where does gcsf come from

A

bone marrow stromal cells

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25
Q

where does epo come from

A

renal peritubular cells

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26
Q

where does tpo come from

A

hepatocytes

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27
Q

what does tpo regulate

A

blasts maturing to megakryocytes

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28
Q

where is tpo produced

A

hepatocytes at constant rate

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29
Q

what does a low platelet count allow tpo tp do

A

more tpo to bind to megakaryocytes stimulating thrombopoeisis

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30
Q

describe the epo and tpo receptors

A

transmembrane dimer with 2 copies of relatively inactive kinase attached to cytoplasmic tails

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31
Q

what is synonymous with tpo-r

A

cmpl

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32
Q

descibe how the jak-2kinase receptors work

A

binding of the cytokine to the receptor swings cytoplasmic tails together; kinases phosphorylate each other and then can phosphoylate other things downstream

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33
Q

how does bone marrow differ as you age

A

cellularity decreases

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34
Q

what are rhe requirments of red blood cell production

A

heme synthesis, globin synthesis, dna synthesis, regulation

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35
Q

what does heme synthesis require

A

iron, b6, succinyl coA, glycine

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36
Q

what does glycine require

A

b12 and folate

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37
Q

what does globin synthesis require

A

normal globin genes (alpha and beta) and amino acids

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38
Q

what does dna synthesis require

A

deoxynucleoside triphosphates

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39
Q

what do deoxynuceloside triphosphates require

A

ribonucleotide reductase and thymidine

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40
Q

what does thymidine require

A

b12 and folate

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41
Q

how is red blood cell production regulated

A

erythropoeitin

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42
Q

what does erythropoeitin require

A

normal kidneys and normal bone marrow micro environment

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43
Q

what are the 3 ways to become anemic

A

not making enough red blood cells, losing red blood cells from blood stream, or both

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44
Q

what does iron deficiency result in

A

cells without much hemoglobin

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45
Q

what is the appearance of an iron deficient rbc

A

smaller, center is large, hypochromic or microcytic

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46
Q

when will you see the terms anisocytosis and poikilocytosis

A

is a manual lab is done

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47
Q

what does anisocytosis mean

A

variation in size

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48
Q

what does poikilocytosis mean

A

variation in shape

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49
Q

what are anisocytosis and poikilocytosis characteristic of

A

severe anemia - but they are not specific

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50
Q

what will you see before anisocytosis and poikilocytosis in mild or moderate anemia

A

hypochromia

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51
Q

what is RDW

A

red cell distribution widthe- can get found using automated machine - red cell size distribution (if increased - correlated with morphologic anisocytosis

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52
Q

what can anemia suggest

A

iron def, but need other tests

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53
Q

what can microcytosis suggest

A

iron def but need more test

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54
Q

what can hypochromia suggest

A

iron def but need another test

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55
Q

what form is dietary iron typically

A

Fe3+, oxidized or ferric state

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56
Q

what form must iron be in to be taken up into the enterocytes

A

must be reduced to ferrous state Fe2+

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57
Q

how is iron converted from ferric to ferrous state

A

ascorbate used by duodenal cytochrome b (duodenal reductase)

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58
Q

what is ascrobate

A

plain old vitamin C

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59
Q

what is ascorbate turned into

A

dehydroascorbate

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60
Q

once taken up into the enterocytes what does iron need to do

A

be reoxidized for transport by serum oxidases

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61
Q

why must iron be transported with something

A

free iron would be a bad thing; augment bacterial growth and catalyze formation of superoxide radicals from oxygen

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62
Q

what handles iron transport in plasma

A

transferrin

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63
Q

what are the requirements for iron to be transferred by transferrin

A

must be ferric iron

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64
Q

what happens to transferring iron complex

A

turns over rapidly as it is take up by transferrin receptor on surface of RBC

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65
Q

because dietary iron might not be reliable, what does the body do

A

maintains an extensive reserve storage pool of iron in macrophages located in bone marrow, liver and spleen

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66
Q

what is iron bound to in storage in liver spleen and bone marrow

A

bound to ferritin

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67
Q

what transporters are involved in iron absorption in gut enterocytes

A

DMT-1 and ferroportin

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68
Q

what side is DMT-1 on

A

luminal memvrane

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69
Q

what side is ferroportin on

A

basement membrane

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70
Q

what regulates DMT-1 activity

A

iron dep regulation of its mRNA translation and stability

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71
Q

what regulates ferroportin activity

A

reg peptide called hepcidin

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72
Q

what is another role of ferroportin

A

export iron from macrophages that store iron

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73
Q

what are the two iron transport measurements that can be taken

A

iron transport system measurement and storage pool iron measurement

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74
Q

what are three ways to measure iron transport system

A

serum iron, total amount of transferrin in ciruclation and whether or not it is being utilized at full capacity or not

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75
Q

what is serum iron

A

direct measurement of transferrin bound iron

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76
Q

what is total transferrin in circulation also known as

A

total iron binding capacity

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77
Q

what is the term for whether or not the iron transport system is being utilized at full capacity or not

A

trasnferrin saturation

78
Q

how do you calculate transferrin saturation

A

serum iron/transferrin

79
Q

what is the way to measure storage pool iron

A

serum ferritin because trace amounts of ferritin from storage pool sites leak out into the serum and the concentration is proportional to the total amount in the pool

80
Q

what is the most useful initial measurement of iron metabolism in patients with unexplained anemia

A

serum ferritin

81
Q

what are the two ways iron deficiency can happen

A

increased red cell loss (usually some kind of chronic hemorrhage) or reduced dietary iron

82
Q

in either cause of iron deficiency what is depleted

A

storage pool of iron

83
Q

how can we detect a depletion in storage pool of iron

A

reduced serum ferritin levels

84
Q

in most cases what happens when storage form iron is depleted and how can this be detected

A

move any remaining iron to bone marrow (ramp up production of transferrin); increased iron total binding capacity (TIBC)

85
Q

in most cases, iron intake is not keeping up with iron utilization so what is reduced

A

serum iron

86
Q

serum iron decreased means what

A

transferrin saturation is reduced

87
Q

what happens to the transferrin receptors in iron deficiency and why

A

increase; iron starved macs increase amount of transferrin receptors on their surface

88
Q

how can we measure the increase in transferrin receptors

A

soluble transferrin receptor measurement

89
Q

if dietary iron goes down, what happens to storage form of iron

A

increased transfer of iron from the storage pool by an increase in ferroportin on macropahges in liver, bone marrow and spleen ; ferroportin in small bowel enterocytes is also increased in expression

90
Q

where is hepcidin made

A

liver

91
Q

what does hepcidin do

A

regulates iron uptake and transport

92
Q

what is the expression of hepicidin linked to

A

amount of transferrin bound iron in the plasma

93
Q

what does increasing amount of transferrin bound iron in plasma do to hepcidin

A

increases hepcidin production

94
Q

what does hepcidin do to ferroportin

A

reduces ferroportin expression in macrophages and enterocytes (becomes internalized and degraded)

95
Q

a disease process that increases hepcidin can result in what

A

anemia

96
Q

what does the term thalassemia mean

A

reduced globin production

97
Q

what do defects in the beta chain gene of globin produce

A

red cell appearance of small cells lacking hemoglobin

98
Q

how do the cells differ between iron deficiency and thalassemia, usually

A

thalasemmia red cells are smaller with MCV of under 70 pL, and by showing target forms in the periphery

99
Q

what is normal MCV

A

90 to 100 pL

100
Q

what do target forms mean

A

nothing - not specific - can be thalasemmia but also can be with liver damage

101
Q

what is the morphology of beta thalassemia

A

microcytosis, hypochromia (like iron deficiency); frequent target cells (nonspecific); can be severe if homozygous and can be mild and not clinically obvious if heterozygous

102
Q

what is a reliable clue that your patient with microcytic anemia has thalassemia rather than iron deficiency

A

number of red cells

103
Q

what are the number of red cells like in iron def

A

reduced

104
Q

what are the number of red cells like in thalassemia

A

same or increased

105
Q

what are your labs going to look like with thalassemia

A

microcytic anemia with increased or regular numbers of red cells

106
Q

if you see microcytic anemia with increased or regular number of red cells, what do you need to order

A

hemoglobin electrophoresis test to confirm thalassemia

107
Q

what does hemoglobin electrophoresis test detect

A

abnormal hemoglobin (hemoglobinopathies)

108
Q

what chromosome is the beta globin locus on

A

chromosome 11

109
Q

how many copies of the beta globin gene are on each copy of chromosome 11

A

6

110
Q

what are the 6 copies of the beta globin gene

A

epsilon, g gamma, a gamma, psi beta, delta, and beta

111
Q

what are the copies of the beta globin gene expressed in utero

A

epsilon, g gamma, and a gamma

112
Q

what is psi betas function

A

pseudogene awaiting an evolutionary assignment

113
Q

when is delta expressed

A

fetus with low expression after birth

114
Q

when is beta expressed

A

after birth, in adults

115
Q

what does normal hemoglobin look like

A

alpha2beta2 with traces of alpha2delta2

116
Q

what happens if expression of beta globin gene is impaired by mutation

A

amounts of delta expressed increases

117
Q

what is hemoglobin a

A

alpha2beta2

118
Q

what is hemoglobin a2

A

alpha2delta2

119
Q

what is fetal hemoglobin

A

alpha2gamma2

120
Q

what is the type of hemoglobin seen most if patient has beta thalassemia

A

alpha2delta2 or hemoglobin a2

121
Q

in severe cases of beta thalassemia what hemoglobin will be seen

A

hemoglobin f or alpha2gamma2 along with hemoglobin a2

122
Q

what is hemoglobin f

A

alpha2gamma2, fetal hemoglobin

123
Q

what determines the severity of different forms of beta thalssemia

A

mutation type and heterozygous vs homozygous

124
Q

what is different about hemoglobin a and a2 in electrophoresis

A

a2 moves quite differently than a

125
Q

what chromosome is the alpha gene locus on

A

chromosome 16

126
Q

how many copies of the alpha gene are on each chromosome

A

4

127
Q

what are the 4 copies of the alpha globin gene

A

zeta 2 zeta 1 alpha 2 alpha 1

128
Q

which copies of the alpha globin gene are expressed in utero

A

zeta 2 and zeta1

129
Q

which copies of the alpha globin gene are expressed in adulthood

A

alpha 2 alpha1

130
Q

how many possible haplotypes are there for the alpha globin gene

A

4

131
Q

how many possible genotypes for alpha globin gene are there

A

16, but only 10 functional

132
Q

what is alpha thalassemia 1 trait

A

1 defective allele with almost no clinical findings

133
Q

what is alpha thalassemia 2 trait

A

2 defective alleles

134
Q

what do you see with alpha thalseemia 2trait

A

mild microcytic anemia, excess Hgb Barts (gamma)4 at birth, normal Hgb electrophoresis as adults

135
Q

how do you diagnose alpha thalassemia 2 trait

A

PCR based (electrophoresis and/or sequencing)

136
Q

what is epidemiology of alpha thalassemia 2 trait

A

3 percent of AA

137
Q

what is alpha thalassemia with 3 defective alleles called

A

Hgb H disease (beta4)

138
Q

what are the clinical findings in Hgb h disease

A

variable degree of microcytic anemia

139
Q

what is the mechanism in Hgb H disease

A

excess of beta hemoglobin protein forms tetramer

140
Q

how do you detect Hgb H disease

A

electrophoresis picks up tetramer

141
Q

what can Hgb h disease be misdiagnosed as

A

iron deficiency

142
Q

what is hgb barts

A

gamma4

143
Q

what is seen in four defective alleles alpha thalassemia

A

hgb barts (gamma4); lethal in utero and soon after birth

144
Q

what is epidemiology of four def alleles of alpha thalassemia

A

southeast asia

145
Q

what must happen to ribonucleoside triphosphates for dna synthesis

A

reduced to deoxy form

146
Q

what must happen to UTP for dna synthesis

A

must be methylated to TTP

147
Q

what donates methyl groups in dna synthesis

A

folate derived donors

148
Q

what is cobalamin

A

B12

149
Q

what is the difference between thymidine and uracil

A

thymidine is uracil with methyl group added

150
Q

how many different derivatives of folate take part in nnucleotide synthesis

A

2 - n10 formyl form and n5,n10 methenyl form

151
Q

what does the n10 formyl form of folate take part in

A

purine synthesis

152
Q

what does the n5,n10 metheynl form of folate take part in

A

thymidine synthesis

153
Q

describe the process of purine synthesis

A

thee amino acids (gln, glu, and asp) come in with PRPP and n10formyl thf - you get purines (amp and gmp)

154
Q

how do you get from thf to n10formyl thf

A

nadph and co2

155
Q

what does a folate defiency result in

A

anemia bc you need folate to make dna which is needed for red blood cell synthesis

156
Q

what is needed to convert homocysteine the methionine

A

b12 and n5methyl thf

157
Q

what happens if you lack b12

A

all of your folate gets trapped in the n5 methyl form, making it unavailable for nucleotide synthesis; methyl trap hypothesis

158
Q

what is intermediate between thf and n5 methyl thf

A

n5,10 methylene thf

159
Q

when does methionine serve as methyl donor

A

after converted to s-adenosyl-methionine in the biosynthesis of a key component of myelin (sphingomyelin)

160
Q

what does deficiency in b12 result in

A

anemia as well as characteristic neuro condition known as subacute combined degeneration of the spinal cord

161
Q

what happens if you give folate supplementation to b12 def patient

A

worsens neuro conditions

162
Q

can mammals make b12

A

no

163
Q

how do mammals get all the b12 they can

A

Haptocorrin is first binding agent (protein in saliva) followed by binding of intrinsic factor binding b12 after hc is digested away in jejunum; IF brings it down distal ileum where complex enters blood

164
Q

what makes instrinsic factor

A

parietal cells in stomach

165
Q

what are ways in the pancreas that the b12 shuttle can fail

A

chronic pancreatitis

166
Q

what are ways in the jejunum that the b12 shuttle can fail

A

bacterial overgrowth, parasites, sprue

167
Q

what are ways in the ileum that the b12 shuttle can fail

A

ileum resection and crohns disease

168
Q

what are ways in the food that the b12 shuttle can fail

A

b12 def food or breast milk

169
Q

what are ways in the stomach that the b12 shuttle can fail

A

acid blockin drugs, atrophic gastritis, gastric bypass, partial or total gastrectomy, defect in intrinsic factor, pernicious anemia (lack of intrinsic factor)

170
Q

what happens if you have impaired dna synthesis

A

fewer cells produced, normal/enhaced maturation of cytoplasm, and impaired nuclear maturation due to impaired dna synthesis

171
Q

if dna synthesis is impaired where does the production line get held up

A

after one or two cell cycles where nucles is large but chromatin is not condensed down into darker material called heterochromatin

172
Q

what happens to rna if dna synthesis is imparied

A

degraded and hemoglobins red color begins to predominate - megaloblastic appearance

173
Q

what can cause megaloblastic anemia

A

impaired b12 uptake, impaired folate uptake, drug effect, intrinsic bone marrow dysfunction

174
Q

what is the storage form of folate

A

linking it to series of glutamate residues (polygutamate residues)

175
Q

what causes perncious anemia

A

impaired b12 uptake

176
Q

what drugs can cause megaloblastic anemia

A

nucleoside analogues (HAART), and ribonucelotide reductase inhibitors (hyroxyurea)

177
Q

red blood cell production is rgeulated by what

A

organs outside the bone marrow

178
Q

what is a well known treatable consequence of renal failure

A

anemia

179
Q

how is erythopoietin production regulated

A

oxygen sensors in peritubular cells in renal cortex

180
Q

how do peritubular cells in renal cortex regulate erythropoietin production

A

when they sense low oxygen they secrete erythropoietin

181
Q

what regulates the urge to breathe

A

co2 concentration in bloostream

182
Q

what does chronic and acute inflammatory conditions do to hepcidin production and what is the consequence of this

A

increases it; impair utrilization of bone marrow iron stores as well as uptake or dietary iron (anemia of chronic inflammation if this happens long enough)

183
Q

how does il-6 play a role in anemia of chronic inflammation

A

bacteria love iron; when you are undergoing infection it is good idea to hold onto your iron stores so Il-6 induces liver to make hepcidin

184
Q

what happens to free transferrin in anemia of chronic disease

A

pulled out of ciruclation by hungry red cell precursors

185
Q

what happens to transferrin saturation in anemia of chronic disease

A

increased

186
Q

what happens to tibc in anemia of chronic disease

A

decreases

187
Q

what happens to iron plus transferrin in plasma in anemia of chronic disease

A

decreases

188
Q

what happens to ferritin in plasma in anemia of chronic disease

A

increases

189
Q

what are signs of anemia of chronic disease

A

normocytic anemia, increased ferritin, reduced or normal serum iron, increased bone marrow iron stores

190
Q

what infections, inflammation can cause anemia of chronic disease

A

aids, tb, rheumatoid arthritis, any cancer

Hematology/Oncology (4 decks)

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