Questions and Answers
Which of the following statements about iron deficiency is CORRECT?
What are the two primary red cell indices that are reduced in iron deficiency anemia, leading to microcytic and hypochromic red blood cells?
Which protein is primarily responsible for transporting iron to tissues, including erythroblasts in the bone marrow?
What is the main source of iron released into plasma transferrin, after red blood cells reach their lifespan?
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What is the main difference between iron deficiency anemia and anemia of chronic disease?
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Which of the following is NOT a characteristic of iron deficiency anemia?
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Which of the following statements about iron transport is CORRECT?
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What is the primary function of caeruloplasmin in relation to iron metabolism?
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Which protein undergoes a reduction in synthesis during iron overload?
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How does iron deficiency affect the binding of iron regulatory protein (IRP) to iron response elements (IREs)?
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Which complex is primarily responsible for the storage of iron within macrophages?
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What happens to the levels of ferritin and ALA-S during iron deficiency?
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Which of the following is a characteristic of haemosiderin compared to ferritin?
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What is the consequence of iron overload in relation to parenchymal cells?
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How are the levels of protein synthesis for iron metabolism linked to body iron status?
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Study Notes
Iron Deficiency and Anaemia
- Iron is abundant in the Earth’s crust but its deficiency is the leading cause of anaemia, affecting around 500 million globally.
- High prevalence in low-income regions, notably sub-Saharan Africa and South Asia, where poor dietary quality and parasitic infections exacerbate iron loss.
- Anaemia due to iron deficiency presents as microcytic, hypochromic, characterized by low mean corpuscular volume (MCV) and mean corpuscular haemoglobin (MCH), resulting in small, pale red blood cells.
- Main differential diagnoses for microcytic, hypochromic anaemia include iron deficiency, anaemia of chronic disease, and thalassaemia.
Iron Transport and Storage
- Iron transport and storage are facilitated by three key proteins: transferrin, transferrin receptor 1 (TfR1), and ferritin.
- Each transferrin molecule can bind up to two iron atoms, delivering iron primarily to erythroblasts in the bone marrow for haemoglobin synthesis.
- After red blood cells age, they are degraded in macrophages, releasing iron back into plasma, which associates with transferrin.
- Dietary iron absorption occurs predominantly in the duodenum and jejunum, constituting a minor portion of plasma transferrin iron.
- Excess iron beyond haemoglobin synthesis is also recycled into transferrin from erythrocytes.
- Ferritin, a water-soluble protein containing 20% iron by weight, acts as a store for iron and is not visible through light microscopy.
- Haemosiderin is an insoluble iron complex, containing around 37% iron, visible after staining; it arises from the partial digestion of ferritin.
Iron Regulation Mechanisms
- Synthesis levels of ferritin, TfR1, δ-aminolaevulinic acid synthase (ALA-S), and divalent metal transporter 1 (DMT-1) closely relate to iron status.
- Iron overload causes ferritin levels to rise while decreasing TfR1 and DMT-1, whereas iron deficiency leads to low ferritin and ALA-S and increased TfR1.
- Iron regulatory proteins (IRPs) bind to iron response elements (IREs) on mRNAs for ferritin, TfR1, ALA-S, and DMT-1, regulating protein synthesis based on iron levels.
- Upstream binding of IRP to IREs decreases protein synthesis, while downstream binding stabilizes mRNA, enhancing translation.
- Elevated plasma iron levels lead to increased iron transfer to organs, causing tissue damage and pathological conditions associated with iron overload.
- Free iron in plasma (non-transferrin bound iron) poses a toxicity risk to various organs.
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Description
Learn about the global prevalence of iron deficiency, its impact on anaemia, and the characteristics of microcytic and hypochromic anaemia.
