NURS 215 Week 6 Discussion Board Forum 3 Example

Discussion Board Forum 3: Iron Deficiency Anemia From the Cell to the Bedside

NURS 215 Post-licensure Pathophysiology, Discussion Board Forum 3

Thread by [Student Name]

The patient and classmates are composites; the textbook and the studies cited are real.

Last month, our telemetry unit took a retired machinist, 68, who had chest pressure that came on when he climbed the stairs at home. His troponin was normal, but his hemoglobin was 7.9 g/dL, his mean corpuscular volume was 71 fL and his ferritin was 6 ng/mL. He had known coronary artery disease, but his chest pain turned out to be driven by the blood, not a new blockage.

Grossman and Porth (2014) explain that iron is the center of the heme molecule that binds oxygen. When iron is short, developing red cells in the marrow cannot make enough hemoglobin. They keep dividing while waiting for hemoglobin to accumulate, so they end up smaller (microcytic) and paler (hypochromic) than normal. That is why his MCV was low. His very low ferritin showed that his iron stores were empty, which separates true iron deficiency from other causes of small red cells.

Pasricha et al. (2021) describe hepcidin, a hormone made by the liver, as the main regulator of iron balance. Hepcidin blocks iron absorption in the gut and iron release from storage cells. When iron stores are low, hepcidin falls so the body can absorb more; when inflammation is present, hepcidin rises and iron is withheld from the blood even if stores are adequate. The authors also stress that the cause of iron deficiency should always be sought, and that when iron runs low in a man or in a woman past menopause, a bleeding source in the gut should be looked for.

The link to his chest pain is compensation. With less hemoglobin, each liter of blood carries less oxygen, so the heart increases its rate and output to keep tissues supplied. His heart rate was 104 at rest. In a heart with narrowed coronary arteries, that extra work raises oxygen demand beyond what the vessels can deliver, and angina results. Correcting the anemia relieved his symptoms better than any cardiac medication would have. His heart was not failing him; it was working overtime for blood that could not carry enough oxygen. His colonoscopy, done before discharge, found a slowly bleeding polyp, which was the real diagnosis and the reason his iron had run out.

Reply to Brittany

Brittany, your patient with rheumatoid arthritis had a low hemoglobin but a normal ferritin, and you wondered why oral iron was not ordered. Pasricha et al. (2021) explain that inflammation raises hepcidin, which traps iron inside storage cells and blocks absorption from the gut, so iron is present but unavailable for making red cells. Ferritin also rises with inflammation, so a normal ferritin may hide a true deficiency or may reflect anemia of inflammation. Grossman and Porth (2014) describe this anemia of chronic disease as typically mild and normocytic, while iron deficiency is microcytic. Oral iron is often absorbed poorly when hepcidin is high, which may be why your provider chose to treat the arthritis first. Was her transferrin saturation checked?

Reply to Carlos

Carlos, your patient who stopped taking ferrous sulfate because of nausea and constipation is common, and there may be a better way to dose it. Stoffel et al. (2017) studied iron-depleted women and found that iron given on alternate days was absorbed more efficiently than iron given on consecutive days, because each dose raises hepcidin for about a day and reduces absorption of the next dose. Pasricha et al. (2021) note that this hepcidin response limits the efficiency of high-dose daily iron. Fewer doses may also mean fewer stomach side effects. It could be worth asking the provider whether an alternate-day schedule would help him stay on therapy, while still investigating why he became iron deficient. Did his provider explain the cause of his deficiency?

References

Grossman, S. C., & Porth, C. M. (2014). Porth's pathophysiology: Concepts of altered health states (9th ed.). Wolters Kluwer Health/Lippincott Williams & Wilkins.

Pasricha, S. R., Tye-Din, J., Muckenthaler, M. U., & Swinkels, D. W. (2021). Iron deficiency. The Lancet, 397(10270), 233-248. https://doi.org/10.1016/S0140-6736(20)32594-0

Stoffel, N. U., Cercamondi, C. I., Brittenham, G., Zeder, C., Geurts-Moespot, A. J., Swinkels, D. W., Moretti, D., & Zimmermann, M. B. (2017). Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: Two open-label, randomised controlled trials. The Lancet Haematology, 4(11), e524-e533. https://doi.org/10.1016/S2352-3026(17)30182-5