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Onc Ex 2
| Question | Answer |
|---|---|
| ESAs Iron, B12, Folic acid | Medications for anemia |
| Myeloid growth factor products CDK 4/6 inhibitor | Medications for neutropenia |
| Thrombopoietin receptor antagonists Rituximab | Medications for thrombocytopenia |
| The absence of pluripotent redundant growth factors is [1] for; the absence of non-redundant factors leads [2] | 1. compensated for 2. specific cytopenia |
| Myeloid GF's | GM-CSF G-CSF |
| Thrombopoietic GF's | Interleukin-11 Thrombopoietin |
| Epoetin alfa has [1] amino acid sequence as human erythropoietin | [the same] |
| In epoetin alfa, the glycosylation differences can be | detected |
| The glycosylation differences in epoetin alfa do not change the | kinetics, potency, or immunoreactivity. |
| Epoetin alfa has a [1] binding affinity | high |
| Epoetin alfa has a [1] half life | short |
| The growth factor, GM-CSF, first affects the | trilineage myeloid stem cells and stimulates it |
| G-CSF is [1] and causes [2] | 1. single lineage 2. neutrophils |
| TPO is a [1] GF | pluripotent |
| EPO is [1]; it only impacts the development of cells starting with [2]. | 1. single lineage 2. BFU-E |
| For EPO, receptors are on | immature RBC's starting with BFU-E and on erythrocytes, which are mature. |
| The growth factor, GM-CSF, affects the | GM-CSF |
| For darbepoetin, there is change in [1] amino acids to add glycosylation. The change in amino acids results in [2] more glycosylation sites. | 1. 4 2. 2 |
| Darbepoetin has a [1] binding affinity | moderate |
| Darbepoetin has a [1] half-life compared to Epoetin alfa | longer |
| With ESAs, Hct. may rise quickly after 1st administration due to release of | reticulocytes |
| Takes about [1] days before erythrocyte progenitor cells are continuously released into circulation. | 10 |
| Polycythemia, blood hyperviscosity, stroke, MI, Pure red cell aplasia - development of neutralizing antibodies against erythropoietin HTN May reduce survival in H&N carcinomas Allergic reactions | ESA adverse effects |
| Iron deficiency causes [1] anemia | microcytic hypochromic |
| Intestinal epithelial cells actively absorb inorganic iron via the | divalent metal transporter 1 (DMT1) |
| Intestinal epithelial cells actively absorb heme iron via the | heme carrier protein 1 (HCP1) |
| Iron that is absorbed or released from absorbed heme iron in the intestine is actively transported into the blood by [1] and stored as [2] | 1. ferroportin (FP) 2. ferritin (F) |
| In the blood, iron is transported by [1] to erythroid precursors in the bone marrow for synthesis of Hgb in RBCs; or to hepatocytes for storage as [2] | 1. transferrin (Tf) 2. ferritin (F) |
| High hepatic iron stores [1] hepcidin synthesis, which inhibits [2] | 1. increase 2. ferroportin |
| Low hepatocyte iron and increased erythroferrone [1] hepcidin and [2] iron absorption via ferroportin. | 1. inhibits 2. ferroportin |
| Some IV iron products have BBW for | anaphylaxis |
| Causes of vitamin B12 deficiency | 1. megaloblastic anemia 2. neurological symptoms |
| Vitamin B12 mechanism of action | Cofactor for many essential biochemical reactions, including production of tetrahydrofolate |
| There is usually [1] ug of vitamin B12 absorbed from the [2] ug in diet | 1. 1-5 2. 5-30 |
| Vitamin B12 is stored in the | liver |
| Vitamin B12 is absorbed by active transport across the | gut |
| Folic acid deficiency is commonly caused by | inadequate dietary intake |
| Some meds may cause folic acid deficiency by inhibiting | dihydrofolate reductase |
| Folic acid deficiency causes | inadequate dietary intake megaloblastic anemia |
| GM-CSF products | Sargramostin |
| G-CSF products | Filgrastim Pegfilgrastim Efbemalenograstim alfa Eflapegrastim-xnst |
| Sargramostim is a | glycoprotein produced in yeast |
| The primary effect of Sargramostin is to | stimulate myelopoiesis |
| In Sargramostim, the gene for [1] has been modified so there is a substitution of [2] at position 23, resulting in changed glycosylations. | 1. GM-CSF 2. leucine |
| Sargramostim enhances | migration, phagocytosis, superoxide production, antibody-dependent cell-mediated toxicity of neutrophils, monocytes, and eosinophils |
| Sargramostim acts [1] with other hematopoietic growth factors | synergistically |
| Sargramostim is administered | SQ/IV |
| The half-life of Sargramostim is | 2-3 hours |
| The IV infusion for Sargramostim is | slow |
| From Sargramostim, can get a transient decrease in | absolute leukocyte count |
| From Sargramostim, may get dependent [1] increase in [2] counts. | 1. biphasic 2. leukocyte |
| After discontinuing Sargramostim, leukocyte count returns to baseline in | 2-10 days |
| For Sargramostim, at lower doses, effect is primarily | neutrophilic |
| Adverse effects of Sargramostim | Bone pain, malaise, flu-like symptoms, fever, diarrhea, dyspnea, and rash. Acute reaction to 1st dose. Capillary leak syndrome. |
| Serious adverse effects of Sargramostim | Transient supraventricular arrhythmia, dyspnea, elevation of SCr, bilirubin, and hepatic enzymes |
| Filgrastim is recombinant human [1] and is produced by [2] | 1. G-CSF 2. E.coli |
| Unlike natural G-CSF, Filgrastim is not [1] and carries an extra [2] | 1. glycosylated 2. N-terminal methionine |
| The principle action of Filgrastim is to increase | neutrophil production |
| Filgrastim can also reduce inflammation by inhibiting | IL-2, tumor necrosis factor, and interferon gamma |
| Mobilizes primitive hematopoietic stem cells | Filgrastim |
| Dosage forms of Filgrastim | SQ or IV (over 30 minutes) |
| The half-life of filgrastim is | 3.5 hours |
| Adverse effects, prolonged high doses of filgrastim | mild to moderate bone pain, local skin reactions, acute cutaneous necrotizing vasculitis |
| Adverse effects, prolonged use with filgrastim | marked granulocytosis and mild to moderate splenomegaly |
| Clearance by glomerular filtration is minimized therefore longer half-life than filgrastim | Pegfilgrastim |
| Studies suggest neutrophil-mediated clearance may be self-regulating | Pegfilgrastim |
| Efbemalenograstim alfa-vuxw adverse reactions | nausea, anemia, and thrombocytopenia |
| Eflapegrastim-xnst adverse reactions | fatigue, nausea, diarrhea, bone pain, headache, pyrexia, anemia, rash, myalgia, arthralgia, and back pain |
| Half-life is approximately 14 hours; bone marrow cell cycle arrest lasts for up to 32 hours after a single dose | Trilaciclib |
| Stimulate production of megakaryocytes and platelets in the marrow by activating the TPO receptor | Thrombopoietin Receptor Agonists |
| Eltrombopag | Small-molecule, non-peptide thrombopoietin-receptor agonist |
| Daily, but patients of East Asian ancestry or with moderate to severe hepatic insufficiency, start with a lower dose | Eltrombopag |
| Common adverse effects Eltrombopag | anemia, nausea, pyrexia, cough, fatigue, headache, and diarrhea |
| Serious adverse effects Eltrombopag | hemorrhage, thrombosis, ascites, drug-induced disorder of liver, liver failure, portal vein thrombosis, encephalopathy, cataracts |
| Drug interactions: calcium, antacids, calcium rich foods | Eltrombopag |
| Possible risk to developing fetu and nursing infants | Thrombopoietin Receptor Agonists |
| An Fc-peptide fusion protein (peptibody): 4 copies of a small peptide grafted onto an immunoglobulin scaffold | Romiplostim |
| Romiplostim is given | SQ, weekly |
| Common adverse effects of Romiplostim | headache, dizziness, insomnia, myalgia, arthralgia, extremity pain, abdominal pain, dyspepsia, and paresthesia |
| Serious adverse effects of Romiplostim | acute myeloid leukemia, hemorrhage, increased reticulin in bone marrow, portal vein thrombosis |
| Small molecule thrombopoietin (TPO) receptor agonist | Avatrombopag |
| Avatrombopag dosage form | PO |
| Common adverse effects of Avatrombopag | pyrexia, abdominal pain, nausea, headache, fatigue, contusion, epistaxis, upper respiratory infection, arthralgia, gingival bleeding, petechiae, nasopharyngitis, and peripheral edema. |
| Serious adverse effects of Avatrombopag | portal vein thrombosis, thrombosis |
| Take with food | Avatrombopag |
| Kills B cells | Rituximab |
| Primary adverse effects Rituxumab | Immunosuppression due to targeting of normal mature B cells Hypersensitivity related to chimeric nature of the monoclonal antibody |
| IVIG | Derived from human plasma; contains a mixture of antibodies |
| Antibodies in the IVIG saturate Fc receptors on immune cells, preventing them from recognizing auto-antibody-coated platelets and destroying them. | IVIG |
| Derived from human plasma where donors were exposed to the D-antigen. | Rho(D) immune globulin (anti-D immune globulin) |
| After administration of anti-D immune globulin, the anti-D coated RBCs saturate the Fc receptor sites on macrophages in the reticuloendothelial system of the spleen. This results in preferential destruction of those RBCs. This may spare the destruction of antibody-coated platelets. | Possible MOA for Rho(D) immune globulin (anti-D immune globulin) for treating ITP |
| IVIG adverse effects | rash, chills, HAs, SOB, hypertension (premedication used to treat) |
| Rho(D) immune globulin (anti-D immune globulin) adverse effects | possible severe vascular hemolysis |
| Erythropoietin Growth Factors | Erythropoietin |
Created by:
vlambert1797
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