| Term 
 
        | What is ferroreductase use for? |  | Definition 
 
        | It converts Fe3+ to Fe2+ to allow it to be absorbed. |  | 
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        | Term 
 
        | Three essential nutrients needed for hematopoiesis. |  | Definition 
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        | Term 
 
        | Three major hematopoietic disorders that can be treated pharmacologically. |  | Definition 
 
        | Anemia, Thrombocytopenia, Neutropenia |  | 
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        | Term 
 
        | An anemia with symptoms resembling pernicious anemia but does not respond to B12. |  | Definition 
 
        | Achrestic anemia encompasses various types of megaloblastic anemia. |  | 
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        | Term 
 
        | A group of anemias characterized by BM suppression with the replacement of hematopoietic cells by fat. This causes pancytopenia which can be accompanied by granulocytopenia and thrombocytopenia |  | Definition 
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        | Term 
 
        | A group fo anemias involving autoantibodies against red cell antigens. |  | Definition 
 
        | Autoimmune Hemolytic Anemia. |  | 
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        | Term 
 
        | Anemia which has bone marrow failure which leads to slow or no functional marrow cell regeneration. |  | Definition 
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        | Term 
 
        | Anemia with shortened survival of mature RBCs and an inability of the bone marrow to compensate for the decreased life span. |  | Definition 
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        | Term 
 
        | An anemia caused by the loss of whole blood. Leads to hypovolemia shock. |  | Definition 
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        | Term 
 
        | An X-linked anemia with ringed sideroblasts, hypochromic, microcytic RBCs, poiklocytosis, weakness and later iron overload. |  | Definition 
 
        | Hereditary Sideroblastic Anemia (Hereditary Iron-loading anemia) |  | 
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        | Term 
 
        | You are looking at a peripheral blood smear and see a reduction of red cell hemoglobin and increased central pallor. How would you classify this anemia? |  | Definition 
 | 
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        | Term 
 
        | Anemia characterized by varying degrees of ertythorocytic hypoplasia without leukopenia or thrombocytopenia. |  | Definition 
 | 
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        | Term 
 
        | No central pallor, increased MCV and increased MCHV |  | Definition 
 | 
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        | Term 
 
        | Pernicious anemia is a subtype of what type of anemia? |  | Definition 
 | 
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        | Term 
 
        | Decrease in Hb content, decreased packed red cell volume and decreased RBCs in blood. |  | Definition 
 | 
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        | Term 
 
        | Autosomal recessive hemolytic anemia which is caused by abnormal RBCs, increased blood viscosity, vasoocclusion and arthralgias. |  | Definition 
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        | Term 
 
        | The general group of iron anemias |  | Definition 
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        | Term 
 
        | Toxic agents such as snake venom cause this type of anemia |  | Definition 
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        | Term 
 
        | 3 causes of thrombocytopenia |  | Definition 
 
        | Low platelet production, increased platelet breakdown in bloodstream (intravascular), increased breakdown of platelets in spleen or liver (extravascular) |  | 
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        | Term 
 
        | What do cellular respiration, krebs cycle, lipid metabolism, gene regulation, DNA replication and repair all have in common? |  | Definition 
 | 
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        | Term 
 
        | What does Divalent Metal Transporter 1 do? |  | Definition 
 
        | DMT1 actively transports ferrous Fe across the intestinal mucosa. |  | 
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        | Term 
 
        | What does Heme Carrier Protein 1 do? |  | Definition 
 
        | HCP1 absorbs the heme-complexed Fe |  | 
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        | Term 
 
        | What is the basolateral transporter of iron in intestinal epithelial cells? |  | Definition 
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        | Term 
 
        | This complex is the storage form of iron which is a water soluble complex with a Fe(OH)3 core covered by an apoferritin (AF) shell. |  | Definition 
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        | Term 
 
        | Plasma protein responsible for transporting Fe in the blood. |  | Definition 
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        | Term 
 
        | Describe the process of receptor-mediated endocytosis of iron into RBCs in the bone marrow. |  | Definition 
 
        | Tf-(Fe3+)2 complex binds to the TfR on an erythroid cell which is endocytosed. |  | 
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        | Term 
 
        | What transports ferrous iron into the cytosol? |  | Definition 
 | 
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        | Term 
 
        | If AF synthesis is inhibited, what is the level of free Fe (high or low?) |  | Definition 
 
        | Low levels of free Fe inhibits AF synthesis and Fe binding equilibrium shifts towards Tf-binding. |  | 
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        | Term 
 
        | If you notice that AF synthesis has been stimulated, what can you presume? What is the purpose of this reaction? |  | Definition 
 
        | If AF synthesis increases, there are high levels of free Fe. This increase of AF allows it to sequester more Fe to protect organs from toxicity. |  | 
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        | Term 
 
        | Hypochromic, microcytic anemia with low MCV and MCHC. |  | Definition 
 
        | Iron deficiency anemia. Seen in infants, kids while growing, or pregnant or lactating women. Also people with gastrectomies or severe small bowel disease. |  | 
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        | Term 
 
        | Generally what are Negative Fe Balance, Fe deficient erythropoiesis, and Fe deficiency anemia? |  | Definition 
 
        | The three stages of Fe deficiency anemia. |  | 
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        | Term 
 
        | A patient comes to you complaining of lassitude, chest pain, difficutly concentrating and shortness of breath. They appear a bit pale as well. What type of anemia are you considering to be most likely? |  | Definition 
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        | Term 
 
        | Are oral Fe preparations as effective as parenteral? |  | Definition 
 
        | Yes, unless there is a GI issue, or are getting treatment with EPO as well due to chronic kidney disease. |  | 
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        | Term 
 
        | How long does Oral Iron Therapy usually last? |  | Definition 
 
        | 3-6 months after correction ofthe cause of Fe loss. This is to ensure replenishment of the Fe stores. And probably so that  Pfizer execs can maintain their christmas bonuses. |  | 
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        | Term 
 
        | What are three oral Fe treatments? Which is the best tolerated? |  | Definition 
 
        | Ferrous sulfate, ferrous gluconate, and ferrous fumarate. Gluconate salts are better tolerated than sulfate salts. (Everyone like sugar better than sulphur) |  | 
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        | Term 
 
        | What type of toxicity is produced by parenteral iron therapy? How can this be avoided? |  | Definition 
 
        | Dose-dependent toxicity. If formulated as a colloid containing particles with a core of iron oxyhydroxide surrounded by a core of carbs, the release of Fe is slower, thus reducing toxicity. |  | 
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        | Term 
 
        | Name three parenteral preps for Fe therapy. Which one can also be administered IM in addition to IV? |  | Definition 
 
        | Iron dextran, Sodium ferric gluconate complex, and Iron sucrose. Iron dextran can be administered IM as well as IV |  | 
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        | Term 
 
        | One of the last members of the KKK is your patient and as per law, you had to treat him. He suffered from Fe anemia and was on oral therapy. He came into the office one day VERY concerned. What was his complaint? |  | Definition 
 
        | Black stools, due to Fe toxicity. Not clinically significant but if he has a GI bleed it could be missed. |  | 
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        | Term 
 
        | IV administration of parenteral Fe therapy could have the very bad adverse effect of... |  | Definition 
 | 
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        | Term 
 
        | Your the chief resident of the busiest ED in New York and you see a 3 year medical student quickly fumbling through med drawers looking for deferoxamine. What is he trying to treat? |  | Definition 
 
        | Deferoxamine is used to treat acute Fe toxicity (esp in children). It is an iron chelator administered IM/IV and strongly binds ferric Fe to inactivate it. It CANNOT remove Fe from Hb or chytochromes. |  | 
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        | Term 
 
        | What drug used for Iron poisoning can give you hypotension, allergic reactions, neurotoxicity or ARDS? |  | Definition 
 | 
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        | Term 
 
        | Your patient has sickle cell anemia and has had several blood transfusions in the past 9 months. He is showing signs of Iron overload. What is the drug you prescribe? |  | Definition 
 
        | Deferasirox. It is a Tridentate iron chelator. It can increase serum creatinine concentration and give you a fever... but its better than being dead. |  | 
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        | Term 
 
        | This molecule is a porphyrin-like ring with a central cobalt atom attached to a nucleotide. |  | Definition 
 | 
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        | Term 
 
        | What is needed to turn N5-methyltetrahydrofolate into Tetrahydrofolate? |  | Definition 
 | 
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        | Term 
 
        | What is needed to turn Homocystine into methionine? |  | Definition 
 | 
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        | Term 
 
        | Methionine biosynthesis and Succiny-CoA synthesis both need what cofactor? |  | Definition 
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        | Term 
 
        | Your patient arrives with neurologic symptoms. Labs reveal a megaloblastic, macrocytic anemia and hypercellular bone marrow. What is the treatment? |  | Definition 
 | 
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        | Term 
 
        | What is a rare but interesting toxicity of B12. |  | Definition 
 
        | Hypokalemia and thrombocytosis (esp after megalobalstic conversion) |  | 
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        | Term 
 
        | You are a huge dork and ask what are the best sources for pteroylgutamic acid? |  | Definition 
 
        | The best source for FOLIC ACID are greens, liver and kidney (I'm not sure who exactly eats kidney) |  | 
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        | Term 
 
        | What needs to happen to folic acid before it can feed into the folate cycle? |  | Definition 
 
        | FA is reduced by DHF-Reductase to DHF-Acid which then feeds into the folate cycle. |  | 
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        | Term 
 
        | Most dietary folate is in the form of N5-methyltetrahydrofolate. What does it need to be converted to in order to be absorbed? What is the cofactor that is needed.? |  | Definition 
 
        | It is demethylated by alpha-1-glutamyl transferase. This reaction required B12 |  | 
        |  | 
        
        | Term 
 
        | The conversions of dUMP to dTMP, serine to glycine, production of purines, methionine synthesis all require what? |  | Definition 
 | 
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        | Term 
 
        | What is the key symptomatic difference between a B12 deficiency and a Folic Acid deficiency? |  | Definition 
 
        | It will cause a megaloblastic anemia but WITHOUT neurological symptoms in the case of Folic Acid deficiency |  | 
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        | Term 
 
        | What drugs (3) can cause megaloblastic anemia? |  | Definition 
 
        | Barbituates, phenytoin, and methotrexate. |  | 
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        | Term 
 
        | Explain how leucovorin can replace Folic Acid during treatment with methotrexate. |  | Definition 
 
        | Methotrexate blocks DHF-reductase. Leucovorin can be completely absorbed in the GI and then broken down into its THF cofactors INSIDE the cell, thus bypassing the DHF-R step. |  | 
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        | Term 
 
        | How does Leucovorin potentiate 5-FU? |  | Definition 
 
        | Leuvovorin is metabolized to Methylene-THF which stabilizes 5-FU binding. |  | 
        |  | 
        
        | Term 
 
        | Oh no! You're a career-couple and choose to have children too late life, who was born with a rare dihydrofolate reducatase deficiency. Whats the treatment? |  | Definition 
 
        | Leucovorin. It bypasses the step which needs this enzyme. |  | 
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        | Term 
 
        | Is EPO cleared by dialysis? |  | Definition 
 
        | Short answer: No. Long answer: No, it's not. |  | 
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        | Term 
 
        | Between Darbepoetin Alpha and Methyoxypolyethylene glycol epoetin Beta, which drug is heavily glycosylated? |  | Definition 
 | 
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        | Term 
 
        | Between Darbepoetin Alpha and Methyoxypolyethylene glycol epoetin Beta, which one has less frequent doses? |  | Definition 
 
        | Methoxypoly...umm...Methoxypoly ethel beta.....Screw it, Mircera is dosed less frequently. |  | 
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        | Term 
 
        | When EPO or a similar drug binds the receptor on RBC progenitors, what pathway is stimulated? |  | Definition 
 
        | JAK/STAT pathway. This leads to more erythroid proliferation and reticulocyte release. |  | 
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        | Term 
 
        | Your patient has low hematocrit and hemoglobin. What class of drugs could you administer to remedy this? |  | Definition 
 
        | ESAs. Fe and Folate supplementation is needed to support the increased erythropoiesis |  | 
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        | Term 
 
        | What are common adverse effects of ESAs? What are patients at risk for if they are in chronic renal failure? |  | Definition 
 
        | HTN and thrombotic complications are more common. If in ARF, the risk of thrombosis increases AND faster tumor growth if you have a head/neck cancer. |  | 
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        | Term 
 
        | Don't give your patient on chemo methoxy polyethylene glycol epoetin beta. |  | Definition 
 
        | Just don't do it. You might kill them. |  | 
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        | Term 
 
        | Name a lineage specific growth factor for granulocytes. |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | What is the MOA for Myeloid Growth Factors? |  | Definition 
 
        | Stimulation of JAK/STAT pathways |  | 
        |  | 
        
        | Term 
 
        | What four pathways get stimulated by G-CSF? |  | Definition 
 
        | 1. Stimulation of neutrophil progenitors 2. Activates phagocytosis activity of neutrophils
 3. Prolongs mature neutrophil survivial
 4. Mobilization of PBSCs to increase their blood concentration.
 |  | 
        |  | 
        
        | Term 
 
        | Name a granulocyte and macrophage CSF. |  | Definition 
 | 
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        | Term 
 
        | Name 5 effects of GM-CSF. |  | Definition 
 
        | 1. Stimulation of granulocytic+erythroid+megakaryocyte progenitors. 2. stimulates neutrophils 3. With IL-2, stimulates T-cell proliferation. 4. Local factor of inflammation 5. Sort of mobilizes PBSCs |  | 
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        | Term 
 
        | In what situations would you use Myeloid Growth Factors? |  | Definition 
 
        | Neutropenia, pancytopenia, stem cell transplantation. |  | 
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        | Term 
 
        | What adverse effect of Myeloid Growth factors can actually lead to the termination of treatment? |  | Definition 
 
        | Leukocytosis (if neutrophil level goes above 100,000/mm3) |  | 
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        | Term 
 
        | What is an obvious adverse effect of Filgrastim and pegfilgrastim? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Out of Filgrastim, Pegfilgrastim and Sargramostim, which drug can be administered SC? |  | Definition 
 | 
        |  | 
        
        | Term 
 
        | Of the two Mp1 agonists (Romiplosim & Eltrobopag) which one is a peptide and which is a small molecule? |  | Definition 
 
        | Romiplostim is a peptide. |  | 
        |  | 
        
        | Term 
 
        | What does IL-11 receptor stimulation lead to? |  | Definition 
 
        | JAK/STAT pathway stimulation |  | 
        |  | 
        
        | Term 
 
        | How does Romiplostim stimulate the JAK/STAT pathway? |  | Definition 
 
        | Romiplostim stimulates Mp1 which stimulates JAK/STAT. This leads to ONLY an increase in platelet count. |  | 
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        | Term 
 
        | What are the two major effects of IL-11? |  | Definition 
 
        | Increases platelet numbers and other progenitors such as neutrophils. |  | 
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        | Term 
 
        | Why can only badass docs administer Eltrombopag? |  | Definition 
 
        | It can only be administered by a registered physician. |  | 
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