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PHARMACOLOGY > Anemia and blood components > Flashcards

Anemia and blood components Flashcards

1
Q

A remarkable process that produces more than
200 billion new blood cells per day in the normal
person and even greater numbers of cells in
persons with conditions that cause loss or
destruction of blood cells

A

HEMATOPOIESIS

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2
Q

Hematopoietic machinery resides primarily in the
bone marrow in adults and requires a constant
supply of three essential nutrients:

A

○ Iron
○ Vitamin B12
○ Folic acid

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3
Q

proteins regulate the proliferation and differentiation of hematopoietic cells

A

Hematopoietic Growth Factors

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4
Q

deficiency in oxygen-carrying
erythrocytes, is the most common deficiency and
several forms are easily treated

A

anemia

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5
Q

So children with microcytic anemia as well as low

reticulocyte count most often have

A

defect in your
erythroid maturation and ineffective
erythropoiesis

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6
Q

Most common cause of chronic anemia

particularly in the pediatric population

A

IRON DEFICIENCY ANEMIA

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7
Q

iron deficiency anemia would present with

A

pallor, easy
fatigability, dizziness, exertional dyspnea and
generalized symptoms of tissue hypoxia.

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8
Q

The cardiovascular adaptations of chronic

anemia would include

A

tachycardia, increased

cardiac output, vasodilation

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9
Q

typical microscopic finding in px with Iron deficiency

A

microcytic hypochromic

anemia.

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10
Q

T or F
In the absence of adequate iron, small
erythrocytes with insufficient hemoglobin are
formed

A

T

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11
Q

also an essential
component of myoglobin, cytochromes, and other
proteins with diverse biologic functions

A

iron containing heme

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12
Q

Forms the nucleus of the iron-porphyrin heme
ring, which together with globin chains forms
hemoglobin.

A

iron

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13
Q

T or F

free inorganic iron is extremely toxic

A

T

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14
Q

peptide produced primarily by liver cells, serves as a key central regulator of the
system

A

Hepcidin

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15
Q

Nearly all of the iron used to support hematopoiesis is reclaimed from

A

catalysis of the
hemoglobin in senescent or damaged
erythrocytes.

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16
Q

The absorption of iron involves two mechanisms:

A

Intestinal epithelial cells actively absorb inorganic
iron via the divalent metal transporter 1 (DMT1)
and heme iron via the heme carrier protein 1
(HCP1).

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17
Q

Iron that is absorbed or released from absorbed

heme iron in the intestine (1) is actively transported into the blood by

A

ferroportin

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18
Q

Iron that is absorbed or released from absorbed

heme iron in the intestine (1) is stored into the blood by

A

ferritin

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19
Q

in the blood, iron is transported by __________ to erythroid precursor in the bone marrow for synthesis of Hgb in RBC

A

transferrin

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20
Q

The transferrin-iron complex binds to

A 
transferrin receptors (TfR) in erythroid precursors
and hepatocytes and is internalized.
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21
Q

Hepatocytes use several mechanisms to take up

iron and store the iron as

A

ferritin

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22
Q

Macrophages that phagocytize senescent erythrocytes (RBC) reclaim the iron from the RBC
hemoglobin and either

A

export or store

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23
Q

hepcidin ______ ferroportin

A

inhibits

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24
Q

high hepatic iron stores ________ hepcidin synthesis

A

increases

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25
Q

what inhibits hepcidin

A

low hepatocyte iron and increased erythroferrone

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26
Q

absorbed iron can be oxidized to ferric iron by the

A

ferroxidase hephaestin

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27
Q

Excess iron is stored in ___________

as ferritin

A

intestinal epithelial cells

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28
Q

shell of a specialized storage protein

A

apoprotein

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29
Q

ferritin is a water-soluble complex consisting of a core of_________ covered by a shell of a specialized storage protein called apoferritin.

A

ferric hydroxide

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30
Q

average american diet (iron)

A

10-15mg elemental iron

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31
Q

Normal individual would absorb ___% iron

A

5-10 (1-2mg per day)

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32
Q

iron is absorbed in the

A

Duodenum and proximal jejunum (active transport)

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33
Q

for a dietary iron to be easily absorbed, it should be converted into

A

ferrous state (in an acidic environment)

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34
Q

ferrous form would then bind with _______ for transport in the bone marrow wherein it is incorporated into the hgb of mature erythrocyte

A

transferrin

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35
Q

GI absorption of iron is increased in

A

Iron deficiency states

erythropoeisis occurs at a more rapid rate

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36
Q

Iron crosses the luminal membrane of the

intestinal mucosal cell by two mechanisms:

A

Active transport of ferrous iron by the
divalent metal transporter DMT1

Absorption of iron complexed with heme

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37
Q

total iron absorption in pregnant women

A

3-4mg/day

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38
Q

Transported in the plasma bound to transferrin, a

β-globulin that can bind _____ molecules of ferric iron

A

two

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39
Q

Transferrin receptors—integral membrane
glycoproteins present in large numbers on
proliferating erythroid cells—bind and internalize
the transferrin-iron complex through the process

A

of receptor-mediated endocytosis

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40
Q

In endosomes, the ferric iron is released, reduced
to ferrous iron, and transported by ______ into the
cytoplasm, where it is funneled into hemoglobin
synthesis or stored as ferritin.

A

DMT1

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41
Q

The transferrin-transferrin receptor complex is

recycled to the cell membrane, where the_______ dissociates and returns to the plasma.

A

transferrin

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42
Q

T or F

Inhibition of hepcidin would enhance iron absorption via ferroportin

A

T

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43
Q

menstruating women lose about __ mg of iron w each menstrual perion

A

30

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44
Q

iron administration preferred for pxs with CKD

A

parenteral

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45
Q

helps to increase GI tolerance and decrease the side effect and increase the bioavailability of most of these iron preparations

A

sustained release and enteric coated preparations

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46
Q

helps in increasing the absorption of iron

A

acidic env (vit c)

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47
Q

treatment with oral iron should be continued for ____ months after correction of the cause of the iron loss

A

3-6

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48
Q

In an iron-deficient individual, about ______

of iron can be incorporated into hemoglobin daily

A

50–100 mg

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49
Q

mg of elemental iron that should be given daily to corrects iron deficiency most rapidly

A

200-400mg

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50
Q

initially, if the dose of iron is adequate, your reticulocye count would begin to increase by

A

3rd-4th day and peak by 7th-10th day of therapy

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51
Q

the magnitude of the marrow response to iron therapy is

A

proportional to the severity of the anemia and the amount of iron delivered to marrow precursors

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52
Q

T or F

An increase in the reticulocyte count is not observed for at least 4 to 7 days after beginning therapy

A

T

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53
Q

An increase of _________ in the concentration

of hemoglobin by that time should be considered a positive response.

A

20 g/L or more

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54
Q

occult blood test or guiac test

A

to determine if the black stool is secondary to iron or bleeding (+) bleeding

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55
Q

would inhibit serum iron absorption by increasing the pH of the stomach and decreasing the solubility of the ferrous salt,

A

PPI

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56
Q

drugs that would enhance the absorption of iron

A

ascorbic acid, chloramphenicol

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57
Q

is a tatracycline that would decrease absorption of iron.

A

doxycycline

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58
Q

other drugs that would decrease absorption of iron

A

cephalosporin, fluoroquinolone, levodopa, levothyroxine, methyldopa

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59
Q

three traditional forms of parenteral iron:

A

○ Iron Dextran ○ Sodium ferric gluconate complex ○ Iron sucrose

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60
Q

colloidal iron preparation embedded within a carbohydrate polymer

A

ferric carboxymaltose

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61
Q

stable complex of ferric oxyhydroxide and dextran polymers

A

Iron dextran

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62
Q

mg elemental iron per mo solution of Iron dextran

A

50mg

63
Q

iron dextran adverse effect

A

headache, light-headedness, fever, arthralgias, nausea and vomiting, back
pain, flushing, urticaria, bronchospasm,
and, rarely, anaphylaxis and death

64
Q

colloidal iron preparation embedded within a carbohydrate polymer

A

Ferric Carboxymaltose

65
Q

○ superparamagnetic iron oxide

○ nanoparticle coated with carbohydrate

A

ferumoxytol

66
Q

in ferumoxytol, carbohydrate shell is removed in the _____________

A

reticuloendothelial system

67
Q

t or f

A 
Ferumoxytol may interfere with magnetic
resonance imaging (MRI) studies.
68
Q

acute iron toxicity in children

A

necrotizing gastroenteritis with

vomiting, abdominal pain, and bloody diarrhea followed by shock, lethargy, and dyspnea

69
Q

what should be done to flush out unabsorbed pills

A

Whole bowel irrigation

70
Q

a potent iron-chelating
compound, can be given intravenously to bind iron that has already been absorbed and to
promote its excretion in urine and feces.

A

Deferoxamine

71
Q

CHRONIC IRON TOXICITY (Iron overload)

A

Hemochromatosis

72
Q

a disorder
characterized by excessive iron
absorption in patients who receive many
red cell transfusions over a long period of
time (eg, individuals with β-thalassemia)

A

Hemochromatosis

73
Q

Chronic iron overload in the absence of anemia is

most efficiently treated by

A

intermittent phlebotomy

74
Q

less efficient or
ineffective as well as more complicated,
expensive, and hazardous, but it may be the only
option for iron overload that cannot be managed
by phlebotomy
VITAMIN B12 (COBA

A

Iron chelation therapy using parenteral
deferoxamine or the oral iron chelators
deferasirox or deferiprone

75
Q

serves as a cofactor for
several essential biochemical reactions in
humans.

A

cobalamin (vit b12)

76
Q

Deficiency of vitamin B12 leads to

A

megaloblastic anemia
gastrointestinal symptoms
neurologic abnormalities.

77
Q

Sometimes called extrinsic factor

A

vit b12

78
Q

a protein
secreted by the stomach that is required for
gastrointestinal uptake of dietary vitamin B12

A

intrinsic factor

79
Q

active form of b12 in humans

A

Deoxyadenosylcobalamin and

methylcobalamin

80
Q

Ultimate source of vitamin B12 is

A 
microbial synthesis (meat 
(especially liver), eggs, and dairy products. )
81
Q

average american diet b12

A

5-30mcg daily (1-5mcg

absorbed)

82
Q

avidly stored, primarily in the liver, with an average

adult having a total vitamin B12 storage pool of

A

3000–5000 mcg

83
Q

the intrinsic factor–vitamin B12

complex is subsequently absorbed in the

A

e distal ileum
by a highly selective receptor-mediated transport
system.

84
Q

Once absorbed, vitamin B12 is transported to the
various cells of the body bound to a family of
specialized glycoproteins,

A

transcobalamin I, II, and III.

85
Q

Excess vitamin B12 is stored in the

A

liver

86
Q

B12 is converted to coenzyme B12–

essential for

A 
hematopoiesis, 
maintenance of myelin (reason for 
causing neurologic abnormality when 
B12 is deficient) throughout the entire 
nervous system and production of 
epithelial cells
87
Q

is responsible for
transporting absorbed B12 to the cell membranes and delivering it to other
organ

A

transcobalamin

88
Q

elimination of b12

A

urine and stool

89
Q

Two essential enzymatic reactions in humans

that would require B12:

A

Methyltransfer (methylcobalamin would
serve as intermediate for the transfer of methyl from N5-methyltetrahydrofolate to
tetrahydrofolate and is necessary for the production of methionine from homocysteine.)

Isomerisation of L-Methylmalonyl-CoA (In the absence of B12 there is an
increase/accumulation of methylmalonic
acid in urine.)

90
Q

Methylcobalamin serves as an intermediate in the
transfer of a methyl group from N5-
methyltetrahydrofolate to homocysteine, forming

A

methionine

91
Q 
measures 
absorption and urinary excretion of 
radioactively labeled vitamin B12 used to further define the mechanism of 
vitamin B12 malabsorption when this is 
found to be the cause of the 
megaloblastic anemia
A

Schilling test

92
Q

serves as a

cofactor for the synthesis of purine and dTMP.

A

THF

93
Q

T or F

Folic acid can correct the neurologic manifestation in b12 deficiency

A

F

94
Q

The accumulation of folate as N5-
methyltetrahydrofolate and the associated
depletion of THF cofactors in vitamin B12
deficiency

A

“methylfolate trap”

95
Q

The most characteristic clinical manifestation of

vitamin B12 deficiency is

A

megaloblastic,

macrocytic anemia

96
Q

The neurologic syndrome associated with vitamin

B12 deficiency usually begins with

A

paresthesias in peripheral nerves and weakness and
progresses to spasticity, ataxia, and other CNS
dysfunctions

97
Q

The most common causes of vitamin B12

deficiency are:

A 
○ Pernicious anemia
○ Partial or total gastrectomy 
○ Conditions that affect the distal ileum
■ Malabsoption syndromes
■ IBD
■ Small bowel resection
○ Strict vegans eating a diet free of meat and dairy products may become B12 
deficient
98
Q

VITAMIN B12 DEFICIENCY CAUSES

A

● Inadequate dietary supply
● Inadequate secretion of intrinsic factor (classical
pernicious anemia)
● Ileal disease
● Congenital absence of TcII (transcobalamin)
● Rapid depletion of hepatic stores by interference
with reabsoption of vitamin B12 excreted in bile
● Appearance of abnormal amounts of TcI and TcIII
in plasma
● Inadequate supply of folic acid as CH3H4PteGlu1

99
Q

Results from defective secretion of
intrinsic factor by the gastric mucosal
cells

A

PERNICIOUS ANEMIA

100
Q

Almost all cases of vitamin B12 deficiency are

caused by malabsorption of the vitamin;

A

HYDROXOCOBALAMIN

101
Q

○ Hydroxocobalamin is preferred

because

A

it is more highly protein-bound
and therefore remains longer in the
circulation

102
Q

are usually
sufficient to treat pernicious anemia who
refuse/cannot tolerate injection

A

Doses of 1000mcg of B12 daily

103
Q

Initial therapy should consist of _________ of
vitamin B12 intramuscularly (IM) daily or every
other day for 1-2 weeks to replenish body stores

A

100-1000 mcg

104
Q

Maintenance therapy consists of

A

100-1000 mcg

IM once a month for life

105
Q

If neurologic abnormalities are present,
maintenance therapy injections should be given
every

A

1-2 weeks for 6 months before switching to

monthly injections

106
Q

Folic acid (pteroylglutamic acid) is composed of

A

heterocycle (pteridine), p-aminobenzoic acid, and

glutamic acid

107
Q

Various numbers of glutamic acid moieties are attached

to the petroleum portion of the molecule, resulting in

A

mono glutamates, tri glutamates, or polyglutamates.

108
Q

Folic acid undergoes reduction, catalyzed by the
enzyme dihydrofolate reductase (“folate reductase”), to
give

A

dihydrofolic acid.

109
Q

subsequently transformed to folate
cofactors possessing one-carbon units attached to the
5-nitrogen, to the 10-nitrogen, or to both positions

A

Tetrahydrofolate

110
Q

Average American Diet: folates

A

500-700mcg of folates daily

50-200mcg usually absorbed

111
Q

Intake of folates for pregnant women

A

300-400mcg daily

112
Q

richest source of folate

A

yeast, liver, kidney and green

vegetables

113
Q

Folate is stored in the

A

liver and other tissues

114
Q

Folate is absorbed in the

A

proximal jejunum.

115
Q

Tetrahydrofolate cofactors participate in

A

one-carbon

transfer reactions.

116
Q

In this reaction, the enzyme thymidylate synthase
catalyzes the transfer of the one-carbon unit of
N5, N10-methylenetetrahydrofolate to
deoxyuridine monophosphate (dUMP) to form
dTMP

A

dTMP CYCLE

117
Q

The cofactor is oxidized to dihydrofolate, and for

each mole of dTMP produced,

A

1 mole of

tetrahydrofolate is consumed.

118
Q

DNA synthesis requires continued

regeneration of tetrahydrofolate by

A

reduction of
dihydrofolate, catalyzed by the enzyme
dihydrofolate reductase

119
Q

dihydrofolate reductase
• The tetrahydrofolate thus produced can then
reform the cofactor N5 , N10-
methylenetetrahydrofolate by the action of

A

serine
transhydroxymethylase and thus allow for the
continued synthesis of dTMP.

120
Q

The combined catalytic activities of
dTMP synthase, dihydrofolate reductase, and serine transhydroxymethylase are referred to as
the

A

dTMP synthesis cycle.

121
Q

Methotrexate inhibits

A

dihydrofolate

reductase

122
Q

Metabolite of 5-fluorouracil inhibits

A

thymidylate synthase

123
Q

required for the
vitamin B12-dependent reaction that generates
methionine from homocysteine

A

N5 -Methylenetetrahydrofolate

124
Q

Drugs which inhibit dihydrofolate

reductase.

A

(Methotrexate, Trimethoprim (TMP),

Pyrimethamine; Phenytoin)

125
Q

Folic acid supplementation to prevent folic acid
deficiency should be considered in high-risk
patients

A 
o pregnant women 
o patients with alcohol dependence 
o hemolytic anemia 
o liver disease 
o certain skin diseases 
o patients on renal dialysis
126
Q

Glycoprotein hormones that regulate the proliferation and differentiation of hematopoietic progenitor cells in the bone marrow

A

HEMATOPOIETIC GROWTH FACTORS

127
Q

○ first growth factors to be identified
○ stimulate the growth of colonies of
various bone marrow progenitor cells in
vitro

A

● Colony-stimulating factors

128
Q

Stimulates RBC

production

A

Erythropoietin

129
Q

stimulates Neutrophil

A

Granulocyte colony-stimulating factor

130
Q

Thrombopoietin receptor agonists

A

(romiplostim and eltrombopag)

131
Q

The preparation for Recombinant human

erythropoietin (rHuEPO) will include

A

alpha , beta

, omega and zeta

132
Q

is producing your
mammalian cell expression system and it is given
3x/week.

A

is producing your
mammalian cell expression system and it is given
3x/week.

133
Q

After intravenous administration,

erythropoietin has a serum half-life of

A

4–
13 hours in patients with chronic renal
failure.

134
Q

○ 1x/week
○ modified form of erythropoietin
○ more heavily glycosylated as a result of
changes in amino acids
○ has a twofold to threefold longer half-life
than epoetin alfa
○ administered weekly

A

● Darbepoetin alpha

135
Q

● Methoxy polyethylene glycol epoetin beta is administered

A

Single IV/SQ at 2 weeks or monthly

interval.

136
Q

isoform of erythropoietin covalently
attached to a long polyethylene glycol
polymer

A

Methoxy polyethylene glycol epoetin beta .

137
Q

● Stimulates erythroid proliferation and
differentiation by interacting with erythropoietin
receptors on red cell progenitors
● Induces release of reticulocytes from the bone
marrow.

A

Erythropoeitin

138
Q

Normally, an inverse relationship exists between
the hematocrit or hemoglobin level and the serum
erythropoietin level.
○ EXCEPT

A

Anemia of CRF

139
Q

Nonanemic individuals have serum erythropoietin

levels of

A

less than 20 IU/L.

140
Q

T or F

As the hematocrit and hemoglobin levels fall and
anemia becomes more severe, the serum
erythropoietin level rises exponentially.

A

T

141
Q

Patients with moderately severe anemia usually

have erythropoietin levels in the

A

100–500 IU/L

range,

142
Q

How would you maintain the anemia of the

patient with CRF?

A

by giving Supplements with

Erythropoietin

143
Q

Erythropoeitin clinical manifestations

A

● Anemia secondary to chronic Kidney disease .
● Patients undergoing myelosuppressive cancer
chemotherapy who have a hemoglobin level of
less than 10g/dl.
● Used illegally by endurance athletes to enhance
performance .
● In patients treated with an ESA , an increase in
reticulocyte count is usually observed in about 10
days .
● An increase in hematocrit and hemoglobin levels
in 2-6 weeks.

144
Q

enhance the expression of your multiple hypoxia
inducible genes such as your Vascular
endothelial growth factor as well as
erythropoietin.

A

hypoxia inducible factor (HIF)

145
Q

Most Common AE erythropoeitin

A

hypertension and thrombotic
complications

uncommon:
There have been small number of cases of pure
red cell aplasia (PRCA) accompanied by
neutralizing antibodies to erythropoietin

146
Q

GCSF

A

○ Filgrastim (rHuGCSF)
○ Tbofilgrastim
○ Pegfilgrastim
○ Lenograstim

147
Q

Has the ability to mobilize hematopoietic
stem cells, to increase their
concentration in peripheral blood

A

GCSF

148
Q 
use of peripheral blood 
stem cells (PBSCs) rather than bone 
marrow stem cells for autologous and 
allogeneic hematopoietic stem cell 
transplantation
A

GCSF

149
Q

Multipotential hematopoietic growth
factor that stimulates proliferation and
differentiation of early and late
granulocytic progenitor cells as well as
erythroid and megakaryocyte
progenitors.

A

GMCSF

Sargramostim (rHuGMCSF)

150
Q

Stimulate the function of mature

neutrophils

A

GMCSF

151
Q

GMCSF Acts together with ________ to
stimulate T-cell proliferation and appears
to be locally active factor at the site of
inflammation

A

interleukin-2

152
Q

clinical uses of Myeloid growth factors

A 
Cancer Chemotherapy induced Neutropenia
● Congenital Neutropenia. 
● Cyclic Neutropenia. 
● Myelodysplasia. 
● Aplastic anemia. 
● Autologous stem cell transplantation.
153
Q

megakaryocyte growth factors

A 
● Thrombopoietin
1. Romiplostim. 
2. Eltrombopag.
3. Avatrombopag
● IL11
○ Oprelvekin
● Fostamatinib
154
Q

is a tyrosine kinase inhibitor
prodrug approved for use in patients with chronic
immune thrombocytopenia who have had an
inadequate response to other therapies

A

Fostamatinib

PHARMACOLOGY (13 decks)

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