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48 Cards in this Set

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  • Back
what is the definition of hematopoiesis?
The process of the differentiation and proliferation of blood cells from a single stem cell in the bone marrow.
what three types of cells are made via hematopoiesis? what are their processes called?
RBC- erythropoiesis
WBC- leukopoiesis
Platelet- Megakaryopoiesis
what is the precursor of all blood cells?
pluripotent stem cell
what highlighted signaling molecule regulates erythrocytes? which one does platelets? which ones do neutrophils?
eryrthrocytes- Erythropoietin
Platelet- IL-11
Neutrophils- GM-CSF and G-CSF
what does erythropoiesis required?
uninterrupted supply of iron
At what stage of erythropoiesis does erythropoietin necessary? what are the stages of erythropoiesis?
rubriblast phase

Pluripotent stem cell --> myeloid progenitor --> rubriblast --> rubricyte --> reticulocyte --> erythrocyte
what conditions will disrupt the erythrocyte balance?
kidney or bone marrow dz, iron deficiency, certain vitamin deficiencies and cancer therapy.
what drug is almost identical to endogenous erythropoietin? what is the only difference between the two? what relevance does this have for blood doping?
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.
which drug mimic erythropoietin, but has 4 mutated amino acids that change the carbohydrate modificatiosn? why?
darbopoietin alfa

the changed carbohydrate modifications extend the 1/2 life of the protein 24-26 hrs.
what is the MOA of erythropoietin and recombinant forms?
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
what is the TOP therapeutic uses of erythropoietin?
cancer tx: chemo and radiation therapy
what are the three adverse effects associated with and increase in hematocrit d/t erythropoietin?
HTN, thrombotic complications, polycythemia
what are the three myeloid growth factors? what makes one of them different from the other?
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.
where is the recombinant human form of G-CSF generated? Where is the recombinant human form of GM-CSF generated? (Glycosylated?)
G-CSF: Bacteria - not glycosylated
GM-CSF: Yeast- partially glycosylated.
what is the MOA of G-CSF targeted drugs? GM-CSF targeted drugs?
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.
what is the purpose for G-CSF as far as stem cell transplantation is concerned?
increases concentration of hematopoietic stem cells in peripheral blood.
what is the main therapeutic use of myeloid growth factors? which one is better tolerated G-CSF or GM-CSF?
neurtopenia- which is the most common dose-limiting toxicity of chemo

G-CSF is better tolerated.
which drug is a recombinant human IL-11 produced in e. coli? what is the MOA?
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)
what is the main therapeutic use of oprelvekin?
deficiency in what causes microcytic anemia? macrocytic anemia?
micro- iron
macro- Vitamin B12 and Folic Acid
how do you tx a pt who has anemia d/t chronic kidney dz? what about anemia d/t cancer chemotherapy?
epo (+iron)- chronic kidney
epo (+/- iron)- cancer chemo
what makes up the nucleus of the porphyrin heme ring in hemoglobin?
what does hypochromic mean?
little or no hemoglobin (hemoglobin gives erythrocyte bright-red appearance)
what are the four causes of macrocytic hypochromic anemia?
Inadequate ingestion
decreased absorption (Achlorhydria, crohn's, drug interaction)
increased requirements (infancy, childhood, pregnancy)
blood loss (menstruation and GI bleeding)
70% of the body's iron is in _____
what is the normal dietary intake of iron? what regulates the amount of iron absorbed by the intestine?
dietary intake- 0.5-1 mg daily

amount of iron absorbed by the intestine is regulated by iron stores in mucosal cells.

The body's way of getting rid of iron is through blood letting and urination.

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.
what are the three oral iron drugs that you can take if iron deficient?
ferrous sulfate (hydrated and dessicated--> more chemically stable)
Ferrous gluconate
ferrous fumarate
what form of iron should be used for iron deficient individuals? why?
ferrous because ferric is not well absorbed.
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.
200-400 mg
what should you administer w/ iron in order to lower gastric pH?
vitamin C- aids in absorption

Iron is better absorbed on an empty stomach, but the side effects are worse.
what are the major side effects of oral iron?
nausea, dyspepsia, abdominal cramps, constipation
what is the advantage to parental iron? what are the drugs? which one has IV related deaths?
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
which parenteral iron needs to have a test dose before complete administration? why? what sxs are usually associated?
iron dextran- to avoid toxicity adn anaphylaxis- HSN like flushing, urticaria, bronchospasm or anaphylaxis
Iron overdose mainly affects which population? what level is associated with death?
children: 2-10 grams are associated with death
what are the sxs of iron overdose? tx?
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.
which cells are effected in megaloblastic anemia?
erythrocytes and other rapidly dividing cells (blood cells, GI mucosal cells)
where is vitamin B12 stored? what is necessary for absorption? In what cells is Vitamin B12 deficiency most noticeable?
liver; absorption requires intrinsic factor. most noticable in cells w/ a high turnover.
what are the 3 causes of Vitamin B12 deficiency?
decrease absorption (pernicious anemia and crohn's dz)
inadequate uptake
inadequate utilization
what is the initial manifestation of vitamin B12 deficiency? later?
anemia- fatigure, parasthesia, ataxia

later- neuropsychiatric abnormalities
17 YOWF presents with lingering fatigue and discoordination as well as some loss of memory and slight psychosis, what might she have?
Vitamin B12 deficiency
what are the two drugs used to tx Vitamin B12 deficiency?
cyanocobalamin and hydroxocobalamin
what is Vitamin B12 required for? what is the end product involved in?
conversion of 5-methyltetrahydrofolate to THF (tetrahydrofolate)--> activating it.

involved in: synthesis of DNA
Can you give your Vitamin B12 deficient pt folate? why?
NO because Folate will just mask the neurodegenerative effects and mask the vitamin B12 deficiency.
without vitamin B12 what cannot form?
THF which means it can't form thymidylate (from dUMP) or purine biosythesis and can't replicate DNA.
what is the MOA of folic acid?
synthesis of purines and thymidylates (DNA synthesis), needed for methylation of transfer RNA and needed for amino acid synthesis.
when do you start getting sxs caused by folic acid?
only at high doses.