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246-Online: IRON – The Body’s Most Precious Metal – Kinetics, Laboratory Evaluations, and Pathologies


Contact Hours (Points): 4 [ASCP-BOC Designation: 2 Contact Hrs-Heme + 2 Contact Hrs-Chem]
Iron presents a problem for the body. On the one hand it is absolutely essential to life. It is at the center of the oxygen carrying capacity of hemoglobin as well as cytochromes that provide energy for cells. But at the same time, iron can be toxic to cells; oxidizing lipids in membranes and proteins. Thus the body is challenged to regulate iron in a way that provides for essential needs, maintains a ready store for emergencies, and yet avoids toxic overload. This self-study will review the regulatory and storage mechanisms for iron metabolism, discuss diseases in which iron regulation is disturbed, and the testing performed in the clinical laboratory for the assessment of iron.

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Product Description

IRON – The Body’s Most Precious Metal: Kinetics, Laboratory Evaluations, and Pathologies

Self-Study 246 – Intermediate – Advanced Level

Contact Hours (Points): 4 [ASCP-BOC Designation: 2 Contact Hrs-Heme + 2 Contact Hrs-Chem]

Written by Kathy Doig, PhD, MLS(ASCP)SHCM

Published 2013.

At the conclusion of the course, the learner should be able to articulate the value of classical and modern laboratory tests of iron status in the diagnosis of iron overload and iron deficient conditions, both hereditary and acquired.

Learning Objectives:

  1. Explain why iron must be carefully regulated in the body, including a list of effects of excess iron accumulations.
  2. Trace a molecule of iron from absorption in the intestines through transport and finally to incorporation into heme.
  3. Explain the function and name the location of each of the following proteins:
  • Divalent metal transporter 1 (DMT1)
  • Ferroportin
  • Ferritin
  • Transferrin receptor 1 (TfR1)
  • Hepcidin
  • Hemojuvelin
  • Hemochromatosis receptor (HFe)
  • Transferrin receptor 2 (TfR2)
  • Matriptase-2
  1. Differentiate proteins involved in regulation of body iron from those involved in regulation of intracellular iron.
  2. Describe the process by which the body regulates iron absorption in the intestines, including responses to high and low levels of body iron.
  3. Describe the process by which iron is absorbed into individual cells and how that is regulated in instances of high and low cellular iron.
  4. Discuss the release of iron from transferrin and name the source of plasma ferritin.
  5. Discuss the mechanisms by which anemia develops in iron deficiency, the anemia of chronic inflammation, sideroblastic anemia and iron refractory iron deficiency anemia.
  6. Describe the general mechanism by which iron overload occurs in acquired and hereditary hemochromatosis.
  7. Describe the difference in treatment of acquired vs hereditary hemochromatosis to the pathophysiology and theorize the reason for the difference.
  8. Describe the principle for the assay of each of the following and the clinical significance or applications of each:
  • Total serum iron (SI)
  • Total iron binding capacity (TIBC)
  • Percent iron saturation (% sat)
  • Ferritin
  • Zinc protoporphyrin (ZPP)
  • Reticulocyte hemoglobin (CHr) or reticulocyte hemoglobin equivalent (RET He)
  • Soluble transferrin receptor (sTfR)
  • sTfR/log ferritin
  • Thomas plot
  1. Calculate percent iron saturation when given total serum iron and TIBC.
  2. Plot patient results on a Thomas plot when given the hemoglobin concentration of reticulocytes and sTfR/log ferritin values.
  3. Given results of iron studies in objective #11 and complete blood count values, interpret them to diagnose conditions of iron deficiency, latent iron deficiency, the anemia of chronic inflammation (i.e. functional iron deficiency), sideroblastic anemia and iron overload.
  4. Recommend sequential or follow-up testing based on results of tests listed in #11.

Online 246: Course Taken Online: $48.00 BUY NOW

IMPORTANT: This online course is accessible using the following:

Desktop or Laptop Computer – Download the latest Adobe Reader program.

Kindle Fire – No additional App download is necessary.

Apple iPad (all versions) / Nook / Kindle – Recommend purchase of a PDF Reader App, such as GoodReader, Cloudreaders, or Stanza by Amazon. Once downloaded, launch this App to access the course online site in order to logon to and view your course.

Here’s what satisfied customers say~

“Thank you for sending this to me. This was an incredibly well done course! I have seen other Iron courses, but this one carefully defined the physiology and then the clinical without bogging down in terms that would cause confusion. I have not seen such a well done course in a long time on this topic. I especially liked the fact that she put the cellular regulation of iron acquisition in an appendix. While not required reading for this course, it was an added perk. The glossary was a nice touch. I would imagine this course would be of tremendous value whether the person is a hematologist or a chemist, since it so nicely tied the two disciplines together.”
~Brenda Kochis, PACE Reviewer, Washington State

Basics of Iron Chemistry; Absorption of Iron in the Intestines; Plasma Transport of Iron; Iron Absorption by Individual Cells; The Process of Cellular Iron Absorption; Regulation of Cellular Iron Absorption; Macrophage Salvage of Iron; Hepatocyte Regulation of Body Iron
Serum Iron Assay; Total Iron Binding Capacity (TIBC); Percent Transferrin Saturation (% Sat); Ferritin ; Free Erythrocyte Protoporphyrin (FEP) and Zinc Protoporphyrin (ZPP); Serum (Soluble) Transferrin Receptor (sTfR); Reticulocyte Hemoglobin Content; sTfR/log Ferritin and sTf/log Ferritin; Thomas Plot
Hemochromatosis: Acquired or Secondary Hemochromatosis; Hereditary Hemochromatoses. Iron Deficient Conditions – Acquired Conditions of Iron Restricted Erythropoiesis: Classic Iron Deficiency Anemia. Anemia of Chronic Inflammation; Sideroblastic Anemia; Hereditary Forms of Iron Erythropoiesis-Iron Refractory Iron Deficient Anemia (IRIDA); Harnessing Knowledge of Iron Kinetics to Treat Iron-Related Disease

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