Drugs for Cytopenia: Hematopoietic growth factors

Drugs for Cytopenia: Hematopoietic growth factors | Quizalize

145 questions

Hematopoietic growth factors are best defined as:

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The primary site of hematopoiesis in healthy adults is the:

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Hematopoietic stem cells are characterized by:

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Progenitor cells differ from stem cells because they:

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Correct order of hematopoietic development:

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Colony-stimulating factors were named because they:

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Function of bone marrow in hematopoiesis includes:

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Hematopoietic growth factors exert effects by:

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A lineage-committed progenitor cell:

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Hematopoietic stem cells:

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Marrow stromal niche provides:

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Extramedullary hematopoiesis occurs when:

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Hematopoietic growth factors most essential during:

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Multipotent progenitor cells give rise to:

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Common myeloid progenitor gives rise to all EXCEPT:

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Common lymphoid progenitor produces:

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Growth factor signaling results in:

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Bone marrow failure results in cytopenias because:

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Significance of receptor expression:

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Hematopoietic growth factors clinically useful because they:

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Primary function of hematopoietic growth factors:

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Colony-stimulating factors named because they:

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First hematopoietic growth factor isolated was:

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Recombinant erythropoietin (epoetin alfa) produced using:

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Serum half-life of erythropoietin:

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Darbepoetin alfa differs because it:

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Methoxy-PEG-epoetin beta is administered:

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EPO stimulates proliferation via:

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Endogenous erythropoietin is produced in the:

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Main physiologic trigger for EPO synthesis:

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In normal individuals, serum erythropoietin levels are typically:

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A patient with severe anemia typically has EPO levels in the:

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In chronic renal failure, EPO levels are:

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Patients most likely to respond to ESA therapy have endogenous EPO levels:

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ESAs increase reticulocyte count in approximately:

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Hemoglobin response to ESAs typically occurs within:

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Target hemoglobin for ESA therapy should NOT exceed:

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ESA therapy requires concurrent supplementation with:

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ESAs are routinely used in:

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ESA use in cancer should be limited because of increased risk of:

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ESAs should NOT be used when cancer therapy is given with:

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Most common adverse effect of erythropoietin:

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Serious ESA-associated thrombotic risk increases when Hb:

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Pure red cell aplasia (PRCA) is associated with:

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PRCA was most commonly linked to:

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After regulatory changes, PRCA incidence decreased when Eprex was:

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ESAs are ineffective when:

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Darbepoetin is typically administered:

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Methoxy-PEG-epoetin beta should NOT be used in:

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Illegal use of erythropoietin in athletes increases risk of:

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Filgrastim (rHuG-CSF) is produced using:

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Filgrastim is best described as:

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Sargramostim (GM-CSF) differs from filgrastim because it:

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Pegfilgrastim is created by:

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Major advantage of pegfilgrastim:

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Serum half-life of G-CSF and GM-CSF is approximately:

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Lenograstim differs from filgrastim because it is:

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Tbo-filgrastim is:

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Sargramostim consists of:

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Pegfilgrastim dosing frequency is:

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G-CSF acts primarily on:

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A unique biologic effect of G-CSF is:

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GM-CSF differs from G-CSF because it:

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Both G-CSF and GM-CSF signal through:

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G-CSF increases neutrophil survival by:

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GM-CSF additionally stimulates:

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G-CSF improves neutrophil function by:

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GM-CSF is less favored for PBSC mobilization because it:

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G-CSF and GM-CSF effects on relapse risk:

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GM-CSF at inflammation sites:

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G-CSF after chemotherapy results in:

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Full neutrophil recovery goal:

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Standard G-CSF dosing for neutropenia:

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Pegfilgrastim prophylaxis dose:

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GM-CSF dosing for neutropenia treatment:

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G-CSF should be started:

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G-CSF reduces:

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GM-CSF may show less reduction in FN because:

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G-CSF recommended when FN risk is:

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G-CSF NOT associated with:

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G-CSF mobilizes PBSCs by:

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Target CD34+ infusion for engraftment:

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Standard PBSC mobilization dosing:

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Plerixafor works by:

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Plerixafor added when:

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Plerixafor requires adjustment in:

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Most common G-CSF adverse effect:

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GM-CSF toxicity more likely includes:

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Splenic rupture risk is associated with:

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GM-CSF capillary leak presents with:

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Primary endogenous regulators of platelet production:

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Platelet transfusion failure may occur because:

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Recombinant thrombopoietin development halted due to:

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Thrombopoietin receptor is known as:

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Oprelvekin is:

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Oprelvekin production system:

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Half-life of IL-11 after SC dosing:

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Romiplostim differs from native TPO because it:

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Romiplostim elimination route:

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Romiplostim half-life is:

100

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Romiplostim indication:

101

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Eltrombopag differs from romiplostim because it is:

102

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Eltrombopag also treats thrombocytopenia in:

103

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Peak platelet response for TPO agonists occurs at:

104

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IL-11 approved for secondary prevention in:

105

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IL-11 dosing for chemotherapy thrombocytopenia:

106

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IL-11 initiation timing:

107

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IL-11 continued until platelets:

108

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IL-11 does NOT significantly improve:

109

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Minimal platelet target for TPO agonists:

110

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Main advantage of romiplostim vs recombinant TPO:

111

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Eltrombopag binding site on Mpl:

112

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Required before starting eltrombopag:

113

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Eltrombopag carries risk of:

114

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Romiplostim avoided in:

115

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IL-11 cardiovascular toxicity includes:

116

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IL-11–induced anemia caused by:

117

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Hypokalemia is associated with:

118

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Rebound thrombocytopenia after TPO agonists due to:

119

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Marrow fibrosis with TPO agonists is:

120

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IL-11 does NOT cause:

121

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Romiplostim dosing frequency:

122

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Eltrombopag should be stopped if:

123

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TPO agonists used after failure of:

124

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IL-11 toxicity BEST described as:

125

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Romiplostim increases platelets by:

126

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Eltrombopag contraindicated in:

127

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TPO agonists may worsen thrombosis in:

128

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IL-11 avoided in patients with:

129

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Earliest platelet rise after romiplostim:

130

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Erythropoietin stimulates erythropoiesis by:

131

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First response to EPO signaling:

132

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G-CSF increases neutrophils by:

133

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Unique G-CSF mechanism:

134

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GM-CSF mechanism differs because it:

135

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GM-CSF enhances immunity by:

136

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IL-11 increases platelets by:

137

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IL-11 differs from TPO agonists because it:

138

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Romiplostim mechanism:

139

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Romiplostim avoids antibody formation because:

140

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Eltrombopag mechanism difference:

141

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Both romiplostim and eltrombopag:

142

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Pegfilgrastim prolonged activity due to:

143

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EPO signaling increases reticulocytes by:

144

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Shared mechanism among all hematopoietic growth factors:

145

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