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48 Cards in this Set
- Front
- Back
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what is the definition of hematopoiesis?
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The process of the differentiation and proliferation of blood cells from a single stem cell in the bone marrow.
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what three types of cells are made via hematopoiesis? what are their processes called?
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RBC- erythropoiesis
WBC- leukopoiesis Platelet- Megakaryopoiesis |
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what is the precursor of all blood cells?
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pluripotent stem cell
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what highlighted signaling molecule regulates erythrocytes? which one does platelets? which ones do neutrophils?
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eryrthrocytes- Erythropoietin
Platelet- IL-11 Neutrophils- GM-CSF and G-CSF |
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what does erythropoiesis required?
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uninterrupted supply of iron
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At what stage of erythropoiesis does erythropoietin necessary? what are the stages of erythropoiesis?
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rubriblast phase
Pluripotent stem cell --> myeloid progenitor --> rubriblast --> rubricyte --> reticulocyte --> erythrocyte |
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what conditions will disrupt the erythrocyte balance?
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kidney or bone marrow dz, iron deficiency, certain vitamin deficiencies and cancer therapy.
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what drug is almost identical to endogenous erythropoietin? what is the only difference between the two? what relevance does this have for blood doping?
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Epoetin alfa: Epogen
difference: carbohydrate modifications of the protein. D/t this difference in structure, you can give an antibody that will detect if someone has been taking erythropoietin supplements. |
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which drug mimic erythropoietin, but has 4 mutated amino acids that change the carbohydrate modificatiosn? why?
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darbopoietin alfa
the changed carbohydrate modifications extend the 1/2 life of the protein 24-26 hrs. |
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what is the MOA of erythropoietin and recombinant forms?
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stimulates cell surface erythropoeitin receptors (JAK-STAT) on RBC progenitor cells in bone marrow. Stimulates/ inhibits the expression of specific genes causing an overall effect of increased RBC production
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what is the TOP therapeutic uses of erythropoietin?
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cancer tx: chemo and radiation therapy
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what are the three adverse effects associated with and increase in hematocrit d/t erythropoietin?
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HTN, thrombotic complications, polycythemia
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what are the three myeloid growth factors? what makes one of them different from the other?
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figrastim (G-CSF) , Pegfilgrastime (G-CSF) and Sagramostin (GM-CSF)
pegfilgrastime is different because it has polyethylene glycol added to filgrastim to prolong its serum half-life. |
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where is the recombinant human form of G-CSF generated? Where is the recombinant human form of GM-CSF generated? (Glycosylated?)
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G-CSF: Bacteria - not glycosylated
GM-CSF: Yeast- partially glycosylated. |
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what is the MOA of G-CSF targeted drugs? GM-CSF targeted drugs?
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G-CSF: stimulate progenitors already committed to the neutrophil lineage which prolongs neutrophil survival.
GM-CSF: Broad biologic actions on erythroid, granulocyte progenitor cells and megakaryocyte progenitors stimulating the activity of neutrophils. |
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what is the purpose for G-CSF as far as stem cell transplantation is concerned?
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increases concentration of hematopoietic stem cells in peripheral blood.
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what is the main therapeutic use of myeloid growth factors? which one is better tolerated G-CSF or GM-CSF?
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neurtopenia- which is the most common dose-limiting toxicity of chemo
G-CSF is better tolerated. |
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which drug is a recombinant human IL-11 produced in e. coli? what is the MOA?
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Oprelvekin (neumega)- MOA: growth factors bind to IL-11 receptors on committed progenitor cells and through the JAK/STAT pathway which increase prolideration and differentiation of megakaryocytes (platelets)
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what is the main therapeutic use of oprelvekin?
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thrombocytopenia
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deficiency in what causes microcytic anemia? macrocytic anemia?
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micro- iron
macro- Vitamin B12 and Folic Acid |
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how do you tx a pt who has anemia d/t chronic kidney dz? what about anemia d/t cancer chemotherapy?
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epo (+iron)- chronic kidney
epo (+/- iron)- cancer chemo |
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what makes up the nucleus of the porphyrin heme ring in hemoglobin?
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iron
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what does hypochromic mean?
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little or no hemoglobin (hemoglobin gives erythrocyte bright-red appearance)
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what are the four causes of macrocytic hypochromic anemia?
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Inadequate ingestion
decreased absorption (Achlorhydria, crohn's, drug interaction) increased requirements (infancy, childhood, pregnancy) blood loss (menstruation and GI bleeding) |
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70% of the body's iron is in _____
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hemoglobin
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what is the normal dietary intake of iron? what regulates the amount of iron absorbed by the intestine?
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dietary intake- 0.5-1 mg daily
amount of iron absorbed by the intestine is regulated by iron stores in mucosal cells. |
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T/F
The body's way of getting rid of iron is through blood letting and urination. |
FALSE
The body cannot expel iron from its body via urination; it can expel iron from blood letting but that is not a body mediated mechanism to excrete iron. |
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what are the three oral iron drugs that you can take if iron deficient?
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ferrous sulfate (hydrated and dessicated--> more chemically stable)
Ferrous gluconate ferrous fumarate |
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what form of iron should be used for iron deficient individuals? why?
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ferrous because ferric is not well absorbed.
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only ____ of the dose of iron can be absorbed in the GI tract. The dose level is at _____ - _____ of elemental iron per day because of absorption and incorporation limits.
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25%
200-400 mg |
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what should you administer w/ iron in order to lower gastric pH?
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vitamin C- aids in absorption
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T/F
Iron is better absorbed on an empty stomach, but the side effects are worse. |
true
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what are the major side effects of oral iron?
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nausea, dyspepsia, abdominal cramps, constipation
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what is the advantage to parental iron? what are the drugs? which one has IV related deaths?
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advantage is correction of the deficiency in a shorter time period
drugs: sodium ferric gluconate complex, iron dextran and iron sucrose IV related deaths- iron dextran |
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which parenteral iron needs to have a test dose before complete administration? why? what sxs are usually associated?
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iron dextran- to avoid toxicity adn anaphylaxis- HSN like flushing, urticaria, bronchospasm or anaphylaxis
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Iron overdose mainly affects which population? what level is associated with death?
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children: 2-10 grams are associated with death
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what are the sxs of iron overdose? tx?
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sxs: necrotizing gastroenteritis w/ vomiting, abdominal pain and bloody diarrhea.
TX: deferoxamine and deferasirox --> iron chelators that are used to bind iron that has already been absorbed. |
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which cells are effected in megaloblastic anemia?
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erythrocytes and other rapidly dividing cells (blood cells, GI mucosal cells)
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where is vitamin B12 stored? what is necessary for absorption? In what cells is Vitamin B12 deficiency most noticeable?
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liver; absorption requires intrinsic factor. most noticable in cells w/ a high turnover.
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what are the 3 causes of Vitamin B12 deficiency?
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decrease absorption (pernicious anemia and crohn's dz)
inadequate uptake inadequate utilization |
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what is the initial manifestation of vitamin B12 deficiency? later?
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anemia- fatigure, parasthesia, ataxia
later- neuropsychiatric abnormalities |
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17 YOWF presents with lingering fatigue and discoordination as well as some loss of memory and slight psychosis, what might she have?
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Vitamin B12 deficiency
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what are the two drugs used to tx Vitamin B12 deficiency?
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cyanocobalamin and hydroxocobalamin
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what is Vitamin B12 required for? what is the end product involved in?
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conversion of 5-methyltetrahydrofolate to THF (tetrahydrofolate)--> activating it.
involved in: synthesis of DNA |
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Can you give your Vitamin B12 deficient pt folate? why?
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NO because Folate will just mask the neurodegenerative effects and mask the vitamin B12 deficiency.
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without vitamin B12 what cannot form?
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THF which means it can't form thymidylate (from dUMP) or purine biosythesis and can't replicate DNA.
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what is the MOA of folic acid?
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synthesis of purines and thymidylates (DNA synthesis), needed for methylation of transfer RNA and needed for amino acid synthesis.
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when do you start getting sxs caused by folic acid?
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only at high doses.
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