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58 Cards in this Set
- Front
- Back
name 4 iron supplements
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1) Ferrous Sulfate
2) Ferrous Gluconate 3) Ferrous Fumarate 4) Iron Dextran |
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name 2 inactive forms of Vit B12
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1) Cyanocobalamin
2) Hydroxycobalamin |
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Name 1 iron chelator
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1) Deferoxamine
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Name 2 active forms of Vit B12
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1) Deoxyadenosylcobalamin
2) methylcobalamin |
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_________inhibits folate reductase
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methotrexate
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name 2 hematopoetic growth factors that are recombinant human EPO
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1) Epoetin
2) Barbepoetin |
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name 3 colony stimulating growth factors
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1) Filgrastim (RHuG-CSF)
2) Sargamostim (RHuGM-CSF) 3) Pegfilgrastim |
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Cardiovascular adaptation to chronic anemia
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1) tachacardia
2) increased Cardiac Output 3) Vasodilation |
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Iron is needed for_______
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Hb synthesis
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B12 is needed for ____________
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DNA synthesis
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Folic Acid is needed for__________
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the synthesis of pyrimidine and purine bases and amino acids
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Trace the cycle of ingested iron
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1) ingested iron is absorbed from the intestinal mucosa into the circulation, where it is bound to transferrin
2) Iron is distributed to tissue for incorporation into Hb, Myoglobin, and enzymes, or it is stored as ferritin 3) after 120 days, erythrocytes are degraded by reticuloendothelial cells, and the iron is retained in the plasma or stored |
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Iron is absorbed in the ______state
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absorbed in the reduced state (+2)
AKA ferrous |
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Iron is stored in the ______state
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stored in the oxidized state (+3)
AKA ferric |
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Given the recycling of Iron and dieary abbundane of Fe, intake is not typically a major concern....It is a concern in these 6 circumstances__________
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1) Children
2) pregnancy 3) menstruation 4) female athletes 5) surgery 6) disease |
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where is iron absorbed?
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1) duodenum and proximal jejunum
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greatest source of Iron________(bioavalability)
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Meat >>>>>plants
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what does transferrin do for iron?
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1)transport -- Rc mediated entry into RBC
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how is iron eliminated?
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1) no mechanism per se
2) mucosal cells in stool, trace amount in urine, bile, and sweat 3)***regulated at the level of absorption and storage |
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causes of microcytic anemia?
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1) iron deficiency
2) thalasemia 3) lead toxicity |
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treatment for iron deficiency (oral)
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1) ferrous sulfate
2) ferrous gluconate 3) ferrous fumarate |
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treatment for iron deficiency (IM or IV)
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Iron dextran (ferric hydroxide + dextran)
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what affects the absorption of the oral preparations of iron?
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1) food decreases absorption
2) Vit C increases absorption |
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treat Acute Iron toxicity
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1) acute iron toxicity typically occurs in children (10 oral tablets can be lethal)
----whole bowell irrigation ----Deferoxamine |
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what is deferoxamine
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1) iron chelator used in acute iron toxicity
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what causes chronic iron toxicity?
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1) genetics
----hemochromatosis 2) acquired ----many RBC transfuscions |
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you can get inactive forms of Vit B12 from what food products?
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1) meat
2) dairy |
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what does the active form of Vit B12 "deoxyadenyslcobalamin" do?
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1) aids in the conversion of methylmalonyl-CoA --> Succinyl CoA
2) Succinyl CoA is used fir a.a. and FA catabolism |
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what does the active form of Vit B12 "methylcobalamin" do?
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1) provides the methyl group for the conversion of homocystine --> methionine
------in this process methylcobalamin is converted to cobalamin 2) cobalamin is converted back to methylcobalamin cia methyl-H4-folate --this converts methyl-H4 folate -->H4 folate ----------------H4 folate donates single carbons to pyrimidines and purines and aa |
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what function does glucoprtein play with B12
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1) glucoprotein is a intrinsic factor secreted by parietal cells of the gastric mucosa
---it facilitates absorption of Vit B12 |
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deficiency of Vit B12 --> the accumulation of ____________
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1) methylmalonyl CoA (goes to methylmalonic acid)
2) homocystine |
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if Vit B12 deficient what is the ROA
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most B12 deficiencies are due to malabsorption, thus parenteral injections are required
----IM daily for 1-2 weeks then 1/month for life |
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which of the B12 supplements are prefered
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1) hydroxycobalamin
----b/c it remains longer in circulation (highly bound to plasma proteins) |
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where is folic acid absorbed at?
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proximal jejunum
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_________may--> folate deficiency
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1) inadequate dietary intake of:
-----organ meats -----beans -----green veggies 2) Alcoholics (or other liver diseases) 3) ***poor diet, reduced absorption, increased metabolism, or decreased storage |
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folic acid is an enzymatic cofactor for________________
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1) DNA synthesis
2) B12 dependant methionine production 3) purine, pyrimidine, and aa synthesis |
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name 1 drug that decreases folate absorption / metabolism
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1) methotrexate (Folate reductase)
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thalasemia is prevalant in the __________population
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prevalant in the mediterranean population
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characteristics of sideroblastic anemia
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1) iron levels are normal but not incorporated into Hb
2) Fe accumulates in the mitochondria |
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causes of B12 DEFICIENCY
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1) PERNICIOUS ANEMIA
2) vegans 3) alcoholics 4) celiac disease |
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causes of Folate deficiency
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1) pregnancy
2) phenytoin 3) malignancy |
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causes of normocytic anemia
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1) Uremia
2) Malignancy 3) RA 4) Aplastic anemia |
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EPO is a __________
--its function is_____ |
1) glycoprotein
2) hematopoetic growth factor (stimulate RBC production) |
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where is EPO produced? what is its stimulus?
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1) kidneys
2) in response to hypoxia |
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how does EPO stimulate RBC
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EPO binds on Rc on RBC progenator --> stimulates proliferation / differentiation
----induces release of reticulocytes from the bone marrow |
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EPO typicslly has an inverse relationship with Hb andHct...when is this not true?
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1) renal disease: (b/c kidney produces EPO) so even if you have anemia the kidney cant keep up with demand
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EPO may need to be given when_____________b/c EPO decreases the need for blood transfusions
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1) cancer chemotherapy
2) HIV therapy 3) Chronic renal failure |
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if you have an EPO deficiency then you can give ____________
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1) Epoetin
2) Darbepoetin (3x longer half life due to sialic acid content) |
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when you give EPO also give____________
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iron & folate
--------to mantain stores |
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G-CSF stands for
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granulocyte colony stimulating factor
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GM-CSF stands for
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granulocyte macrophage colony stimulating factor
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what is the fx of the drugs that have G-CSF and GM-CSF capability?
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1) they are myeloid growth factors
2) they bind to the Rc on various myloid progenators --> stimulate proliferation / dfferentiation 3) stimulates mature Neutrophils ---stimulates phagocytic activity ----prolongs cell survival in circulation *****they are colony stimulating factors used in the tx of neutropenia associated with cancer chemtherapy, and bone marrow transplant |
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which drug has G-CSF capability
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filgrastim
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which drug has GM-CSF capability?
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sargramostim
|
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what is uniwue about pegfilgrastim?
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1) covalent conjugation product of filgastrim and polyethylene glycol that has a much longer half life (42 hours)
2) modification increases the size of the molecule such that it is to large for renal clearabce |
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how is pegfilgrastim eliminated?
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primarily by neutrophil uptake and metabolism
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these 2 forms of B12 are cofactors for methylation reactions?
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1) deoxyadenosylcobalamin
2) methylcobalamin |
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folate is needed for purine base synthesis. if methotrexate is given it will inhibit the synthesis of____________
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1) DNA
2) RNA 3) THYMIDYLATES 4) Proteins |