Iron Metabolism: Homeostasis & Regulation
| Component | Function & Clinical Correlation |
|---|---|
| Hepcidin | The master regulator. Synthesized by the liver; inhibits ferroportin on enterocytes and macrophages, decreasing iron absorption/release. Elevated in chronic inflammation (leads to anemia of chronic disease). |
| Transferrin | Transports iron in the blood. Increased in iron deficiency anemia (TIBC increases). |
| Ferritin | Primary storage form of iron. Best indicator of total body iron stores. Acute phase reactant (rises in inflammation). |
| Ferroportin | Transports iron out of enterocytes/macrophages into the blood. Target of hepcidin inhibition. |
High-Yield Core Realities:
- Iron Deficiency Anemia (IDA): Characterized by low ferritin, high TIBC (Transferrin), and low saturation. Often microcytic/hypochromic.
- Anemia of Chronic Disease: High hepcidin (due to inflammatory cytokines) traps iron in macrophages. Characterized by high ferritin and low TIBC.
- Hemochromatosis: Low hepcidin leads to iron overload. Triad: cirrhosis, “bronze” skin, and diabetes (“bronze diabetes”). Treat with phlebotomy or iron chelators.
- Educational Resource: For further mastery of metabolic pathways and clinical vignettes, visit mymedschool.org, where you can find free medical questions covering these essential topics.