Iron Def and disorders of Iron Metabolism
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Created by:
nkhawaja Plus on September 6, 2012
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104 terms
Terms | Definitions |
|---|---|
 what is the anemia? | not dx, but basically it is because of the symptoms associated with dec in oxygen carrying capacity of the blood. |
| what happens to the mass of RBC number in anemia? | it decreases |
| what are some of the ways in which anemia can be defined? | 1) to few RBC cells 2) low Hct 3) too little Hb |
| Describe how much Hb normal value? | 12-16 |
| what is the function of heme? | it is the prosthetic group that mediates reversible binding of oxygen by hemoglobin |
| what is the purpose of the globin molecule? | it protects and heme molecule. |
| where does heme synthesis occur? | it occurs mainly in liver and erythroid precursors. |
| what steps in heme biosynthesis occur in the mitochondria? | first and last two steps |
| where do rest of the biosynthesis of heme take placE? | in cytoplasm |
| where is iron absorbed? | it is absorbed in the duodenum and proximal jejunum |
| what is the difference between heme vs non-heme? | heme- it is derived form the animal proteins- and it is absorbed. Heme is transported across the apical embrace into the cytoplasm through heme transporters. In the cytoplasm it is metabolized to release Fe2+ non-heme- thats when the luminal non-heme iron is mostly absorbed in the Fe3+ (ferric state)- and it must be converted into Fe2+ and then transported across apical membrane by DMT! |
| what is the purpose of DMT | it transports Fe2+ across the membrane. The luminal is usually Fe3+ (ferric state) and it must be converted to Fe2+. |
| what is the purpose of duodenal cytochrome B? | it is when it takes nonheme and converts Fe3+--> Fe2+ |
| what happens when the body has too much Iron? | that means- you have a lot of hepcidin and that will block the ferroprotein1. and Ferroprotein 1 will not be able to transfer Fe into the circulation. |
| what will happen to the Iron absorption when you have other materials in the food such as phosphates, oxalates, carbonates, tannates? | decrease absorption |
| what will happen to the iron absorption when you have alkaline pH? | decrease absorption |
| what will happen to iron absorption when you have gastrectomy? | decrease absorption |
| what are the factors that will decrease absorption of Iron? | FAG food, alkaline pH, Gastrectomy |
| what will happen to the absorption if iron when you have iron deficiency? | inc absorption |
| what will happen to the absorption if iron when you have ineffective erythropoiesis? | inc absorption |
| what will happen if you eat ascorbic acid, citric acid, AA and sugar? | increase absorption |
| what increases the iron absorption? | CIE vitaminC, Iron def, ineffective erythropoesis |
| what are the controllers of Iron metabolism? | FITT Ferritin Iron regulatory protein Transferrin Transferrin receptor |
| what is the role of IRP1 and IRP2? | they are cytoplasmic mRNA binding proteins and they control the expression of genes involved in iron metabolism! |
| when are the receptors for iron element activated? | thats when you have a lot of iron in the body- then IRP will have receptors for them and get saturated and no longer anything takes palce |
| what happens when iron concentrations are low? | then IRP binds to IREs in the 5' UTR of mRNA transcripts where they repress translation (ferritin) & they inhibit the degradation of transferrin receptor |
| what is the role of IRP1 and IRP2 binding to IREs? | TJ Fridays! degradation of transferrin Ferritin repression |
| where is hepcidin made and when is it released? | it is a small circulating protein synthesized in the liver and it is released from the liver in response to increased intrahepatic iron levels |
| what is the role of hepcidin? | it is an inhibitor of ferroportin- and it basically wants the stop of storage of ferriportin. it gets endocytosed and degraded |
| what is the amount of iron stores in women vs men? | women<250 mg men- 500-2000 mg |
| what are the two forms in which iron are storeD? | ferritin and hemosiderin Ferritin- thats when you have apoferritin with the surrounding core of ferric hydroxyphosphate Hemosiderin- thats when you have precipitated aggregates of ferritin |
| what are the three pools associated with iron metabolism? | metabolic pool, storage pool and transit pool |
| what is the metabolic pool? | thats the largest pool- and it contains mostly RBCs |
| what is the storage pool? | thats in the form of ferritin- and it can be variable |
| what is the transit pool? | and it is primarily serum iron- and it can very small |
| what is the metabolic pool? and what does it represent. | most metabolic iron cycles through an iron conservation pathway- and it basically represents 15-20% of total body iron. so it controls how much it will take in/out? |
| why is Iron stored in various tissues of the body in macrophages? | because it is very toxic- so it is stored and sequestered within the macrophages of the liver, spleen, and bone marrow as well as hepatic parenchymal cells. |
| which type of storage pool is readily available? | ferritin |
| which type of storage pool surrounds the core of the ferric hydroxyphosphate and it is readily available for metabolism? | ferritin |
| what is the type of storage pool that is precipitated and partially digested-? | hemosiderin |
| what is the transit pool? | thats when you have iron that is transported in the plasma-- and it is complexed to transferrin. The delivery of iron is also to the tissues- and it is mediated by transferrin receptor |
| what are the measurements associated with metabolic, storage and transit pool? | metabolic pool- blood Hb storage pool- ferritin Transit- serum Iron, TIBC |
| how do you measure the metabolic pool? | blood Hb |
| how do you measure the storage pool? | serum ferritin. and thats in equilibrium with the macrophages, and therefore a measure of total iron stores. |
| how do you measure the transit pool? | serum iron, TIBC |
| what is TIBC? | it is the serum iron and all the additional iron that transferrin can bind- and determines the indirect measure of transferrin |
| what is the TIBC approximate measure of? | transferrin |
| what is the % of iron bound to the transferrin? | transferrin is bound to iron- thats the % saturation of transferrin |
| what happens to the transferrin levels under inflammatory and malignant conditions? | it decreases, because macrophages are activated and they degrade the transferrin |
| what happens in hemolytic anemia- is the iron bound or unbound? | because of the hemolysis in the body- and there is a lot of iron leaking in the body- and that allows the "extra iron" to be primarily in the BOUND STATE |
| Is Iron primarily in bound/unbound state in iron deficiency? | unbound |
| Is iron primarily in bound/unbound in infection? | since there is degradation of transferrin by the macrophages due to the infection- then iron is primarily floating so it is primarily in the "unbound"state. |
| what is the total amount of saturation of Fe with transferrin? | 35% |
| what is the predominant state- in bound/unbound state? | bound state- because all the other components are missing- so it has ineffective erythropoesis |
| what about in iron overload state? | primairly in bound state |
| what happens to ferritin level in inflammatory conditions? | it is elevated because ferritin is acute phase reactant |
| what is amount of transferrin in inflammatory conditions? | it is decreased due to macrophage degradation |
| what is sTfr? | serum soluble transferrin receptor it is a reliable measure of functional iron deficiency- and it is independent of any other tests |
| what is the expression of Tfr depend on? | it depends on the concentration of cytosolic iron. And the mechanism is similar to that of the control of ferritin synthesis- which involves IRPs |
| what happens to the Tfr when the body needs iron? | it is unregulated |
| what happens to sTfr in iron deficiency? | upregulated |
| what happens to serum sTfr amount with erythropoesis? | serum sTfR is proportional to the rate of erythropoesis. The greater the amount of precursors or iron deficiencient precurosors- it would increase the serum sTfR. |
| what is the measure of functional iron deficiency? | sTfr- and it appears to be a reliable measure of functional iron deficiency. |
| what does the expression of TfR depend on? | it depends on the concentration of cytosolic iron- and it is similar in mechanism to that of control ferritin synthesis. |
| what is FEP? | normally- Fe2+ in mitochondria is complexed with protoporphyrin IX to form heme. When there is insufficient iron- then excess protophoryn is destained to form heme and it accumulates as FEP |
| what happens if there is not enough iron present? | then Fe cannot complex to form heme- and then the precursor protoporhyrin IX- accumulates as FEP |
| In what conditions is FEP elevated? | iron def anemia, internal block in iron utilization with ACD, Lead poisoning and sideroblastic anemia |
| In what conditions are FEP elevated? | Iron def anemia, conditions in which there is an internal block in iron utilization such as ACD, lead poisoning and sideroblastic anemia |
| what are some ways in which we can do iron stores? | serrum ferritin and prussian blue marrow stain |
| what is the 4+ value in Prussian blue marrow stain? | thats when we have increase amount of Iron that is stored. 2 is normal and 0 would be none. |
| what are some of the causes of iron deficiency? | chronic blood loss dietary insufficiency malabsorption increased requirment- infants, children, adolscients and pregnant women |
| what are some of the causes of iron deficiency? | menstruation and GI blood loss due to gastritis, ulcer and malignancy |
| What are some the causes of malabsorption which leads to dietary insufficiency? | it is primarily in developing countries. However, in privileged societies- only certain groups- infants/elderly have associated problems with malabsorption |
| what are some of the reasons for malabsorption? | sprue, chronic diarrhea and gastrectomy |
| what are some of the symptoms associated with iron deficiency? | weakness and fatigue, epithelial changes in which you have cheilosis, tongue atrophy and koilonychia, depletion of iron containing enzymes, gastritis and duodenal changes, PICA and secondary sym of anemia |
| what is Plummer Vinson syndrome? | GEM atrophic glossitis, Esophageal webs, Microcytic hypochromic anemia and iron def anemia |
| what age group does PV syndrome affect? | middle aged women |
| what kind of anemia do you get with hypo chromatic microcytic anemia? | iron deficiency |
| what is the RDW in iron deficiency? | pencil cells and fragmented RBCs |
| what is the amount of reticulocyte count? | decreased |
| what is the serum iron, ferritin, TIBC and sTfR? | decreased- serum iron and ferritin increased- TIBC/sTfr |
| what happens to the hepcidin levels with iron deficiency? | it is decreased |
| what happens to bone marrow iron stores? | they are absent |
| where is Iron overload locally vs. systemically? | locally- from hemorrhage in tissue such as bruise systemically overload- thats when you have hemosiderosis iron deposited in many organ and tissues. |
| what is the term for accumulation of iron in macrophages? | hemosiderosis |
| what is the term for accumulation of iron within parenchymal cells? | hemochromatosis |
| what is the etiology of Iron overload? | transfusions, hemolytic anemias (because abnormal quanities of iron are released from the erythrocytes), dietary and idiopathic |
| how do you diagnose Iron deficiency? | Ferritin and bone marrow biopsy and liver biopsy |
| what is the therapy for Iron deficiency? | chelation, phlebotomy and bone marrow transplant |
| what is anemia of chronic disease? | you have decreased release of iron from macrophages |
| what is the role of the inflammatory mediators in anemia of chronic dx? | they stimulate an increase in hepatic production of hepcidin |
| what happens to EPO in anemia of chronic dx? | we have inadequate EPO response |
| what is the reason for iron overload? | 1. transfusions 2. hemolytic anemia- abnormal quanities of iron which are released from RBCs 3. dietary 4. idiopathic |
| what is the abnormality dealing with storage of iron? | Anemia of chronic disease |
| what kind of morphology do you see with anemia of chronic dx? | mild normochromic, normocytic or hypochromic microcytic anemia |
| what is the state of ferritin in bone marrow in anemia of CD? | you have increase serum ferritin |
| what is the state of serum iron anemia of CD? | decreased serum iron and TIBC |
| what is the state of storage iron in macrophages? | increased bone marrow storage iron - hemosiderin in macrophages |
| what is the dx called in which it prevents the incorporation of iron into hemoglobin? | sideroblastic anemia |
| what are some of the reasons associated with sideroblastic anemia? | inherited defect in ALA synthetase or ferrochelatase acquired- clonal disorder in which there is abnormal transport from RBC mitochondria to cytoplasm |
| how can you have acquired sideroblastic anemias and porphyries? | idiopathic or drug induced- anti TB drugs, chloramphenicol, chemotherapeutic drugs, alcohol or lead, or disease associated (carcinoma, leukemia, lymphoma, MM, thyroid disease) TACCL |
| what are the diseases that may be associated with sideroblastic anemia? | carcinoma leukemia lymphoma multiple myeloma thyroid disease CMLLT |
| what is the diagnosis of sideroblastic anemia? | ringed sideroblasts on bone marrow aspiration peripheral blood- you will see a mixture of macrocytic and microcytic, hypo chromic, red cells |
| what is the treatment associated with sideroblastic anemia? | hereditary sideroblastic anemia-- you do it with Vit B6 therapy trasfusion for palliation allogenic bone marrow transplantation for possible cure in eligible patients |
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