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Questions and Answers
Which clinical manifestations are indicative of iron overload disorders?
In which part of the body is the highest concentration of iodide found?
What is the primary form of iodine excreted in urine?
Which dietary source is most beneficial for preventing iodine deficiency?
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What effect does prolonged iodine deficiency have on the thyroid gland?
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Which of the following factors decrease iron absorption in the intestine?
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What is the primary regulatory mechanism for iron absorption in the body?
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Which form of iron is primarily responsible for transport in the blood plasma?
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Where does the majority of iron absorption occur in the digestive system?
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Which of the following best describes the functional forms of iron in the body?
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What role does transferrin play in iron transport?
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What role does the enzyme ferric reductase play in iron absorption?
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Which clinical condition is characterized by microcytic and hypochromic red blood cells?
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How does the body's handling of iron differ from other minerals?
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Which of the following is NOT a good dietary source of iron?
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What can result from parenterally administered iron in cases of overload?
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Which form of iron is primarily associated with storage in the body?
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What is the primary blood iron form in erythrocytes?
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What proportion of transferrin is typically unsaturated?
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In iron deficiency anemia, what changes occur in plasma iron and TIBC?
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What is hemosiderosis characterized by?
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Study Notes
Trace Elements - Iron
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Dietary Sources: Liver, heart, kidney, spleen, meat, and egg yolk are excellent iron sources. Molasses, dates, legumes, vegetables, and whole grains are also good sources.
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Absorption: Iron absorption is a dynamic process occurring mainly in the duodenum and upper jejunum. The amount of absorbed iron compared to ingested iron is typically low (5%-35%).
Factors Influencing Iron Absorption
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Enhancing Absorption: Ascorbate and citrate increase iron uptake by increasing metal solubility in the duodenum.
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Inhibiting Absorption: Plant phytates (in wheat and some cereals) and tannins (in some teas) decrease iron solubility, hindering absorption.
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Mechanism: A ferric reductase enzyme and duodenal cytochrome b reduce ferric iron to ferrous iron. Ferrous ions are then transported across the enterocyte membrane by DMT1. Iron then leaves the enterocyte and is oxidized by hephaestin, binding to plasma transferrin for distribution.
Regulation of Iron Absorption
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Hepcidin: The liver senses body iron stores and erythroid requirements, producing hepcidin, an inhibitory peptide. This peptide acts on the intestine to reduce iron absorption.
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Dcytb and DMT1: These protein levels are also influenced by iron levels in enterocytes, likely in response to hepcidin's iron efflux action through ferroportin.
Distribution and Functions of Iron
- Forms: The total body iron is approximately 4 grams. Iron exists in two forms:
- Functional (75%): Mostly in the form of hemoproteins like hemoglobin
- Nonfunctional (25%): These are transport and storage forms of iron, which are non-heme metalloproteins.
Iron Transport and Storage
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Transferrin: The transport protein for iron in blood plasma.
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Ferritin: The primary storage form in tissues (liver, kidneys, spleen, bone marrow, and intestinal mucosa).
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Hemosiderin: A form of iron storage when body iron levels are high.
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Lactoferrin: A glycoprotein present in milk that facilitates iron transport and storage in milk.
Blood Iron
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Erythrocytes: Contain hemoglobin that uses iron.
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Plasma Iron: Concentrates at 50-150 µg/dL. Carried by transferrin.
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Transferrin Saturation: Transferrin has a total iron-binding capacity (TIBC) of 250-400 µg/dL. In healthy individuals, about 30% of TIBC is saturated. Unsaturated transferrin is about 60-70%.
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Iron Deficiency Anemia: Plasma iron decreases while TIBC increases in iron deficiency anemia.
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Ferritin Levels: Plasma ferritin levels are very low in iron deficiency, rising in hemosiderosis.
Abnormalities of Iron Metabolism
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Iron Deficiency Anemia: Characterized by microcytic and hypochromic red blood cells, often caused by excess menstrual flow or gastrointestinal bleeding. Treatment involves addressing the cause, and possibly iron dextran injections for those who can't tolerate oral iron.
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Iron Toxicity (Hemosiderosis/Hemochromatosis): Inability to excrete excess iron. Excess iron accumulation in the tissues leads to hemosiderosis, with possible organ damage and symptoms like bronze diabetes. This is often caused by repeated blood transfusions or excessive oral or parenteral iron intake.
Iodine
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Dietary Sources: Seafood, vegetables near the ocean, and iodized salt are good sources.
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Absorption and Distribution: Organic iodine is converted to inorganic iodide before absorption. Inorganic iodine and iodide are absorbed by the skin, lungs, and intestine.
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Thyroid Uptake: About 30-50% of iodine is taken up by the thyroid gland, in the forms monoiodotyrosine (MIT), diiodotyrosine (DIT), triiodothyronine (T3), and tetraiodothyronine (T4) via thyroglobulin.
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Other Tissues: The rest of the iodine (50%-70%) is mostly present in body fluids in organic combinations with hormones like T3 and T4 and inorganic forms like iodide (I⁻).
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Excretion: About 70% of iodine is excreted in the urine as inorganic iodine. Another 30% is in the feces, from unabsorbed iodine in the diet and iodine secretion in saliva, bile, and intestinal secretions.
Iodine Deficiency
- Goiter: Prolonged iodine deficiency leads to thyroid hypertrophy (goiter)
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Description
Explore the essential trace element iron in this quiz. Learn about its dietary sources, absorption mechanisms, and factors that influence its uptake in the body. Test your knowledge on how to enhance and inhibit iron absorption.
