NU104 Unit 4 Mechanism Write-Up Example

Large Cells, Too Few of Them: A Mechanism Write-Up of Folate Deficiency Anemia in a Composite 66-Year-Old Man, From an Empty Diet and Daily Drinking Through Stalled DNA Synthesis to Breathlessness on the Stairs

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Purdue University Global

NU104: Pathophysiology for Nursing

Unit 4 Mechanism Write-Up

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[Date]

The patient is a composite; laboratory values are typical for the condition and bracketed where illustrative.

The Patient

[Walter], a composite 66-year-old retired machinist, lives alone since his wife died two years ago. He eats one meal a day, usually toast or canned soup, and drinks four to six beers most evenings. His daughter brought him in because two flights to his apartment now leave him winded and he looks "gray." He is pale, his heart rate is [104] at rest, and his tongue is smooth and sore. His hemoglobin is [8.9] g/dL, and his red cells are large, with a mean corpuscular volume of [114] fL. His serum folate is low, and his vitamin B12 level is normal.

Step One: Not Enough Folate Coming In

Folate is found mainly in leafy green vegetables, legumes, citrus fruit and fortified grain products. The body stores only enough to last a few months, far less than its store of vitamin B12, so a poor diet empties folate stores relatively quickly. Walter's diet supplies very little. Alcohol makes the shortfall worse in several ways: it displaces food, reduces folate absorption in the small intestine, and increases folate loss through the kidneys (Green & Datta Mitra, 2017). Chronic drinking also disturbs how the liver stores and handles folate, so even the folate Walter does absorb is used less efficiently (Medici & Halsted, 2013). His deficiency is therefore the result of low intake and reduced absorption acting together.

Step Two: DNA Synthesis Stalls in the Marrow

Folate, in its active form, carries one-carbon units needed to make thymidine, one of the four building blocks of DNA. Without enough folate, cells cannot make DNA fast enough. Most cells divide slowly enough to cope, but the bone marrow produces about two million red cells every second, so it is among the first tissues to show the effect.

In the developing red cell, the nucleus depends on DNA synthesis to divide, while the cytoplasm, which makes hemoglobin, depends on RNA and protein synthesis that continue normally. The two fall out of step. The cytoplasm keeps growing while the nucleus lags, so precursors become abnormally large, with an immature-looking nucleus. These large precursors are called megaloblasts (Rogers, 2023).

The cell grows on schedule but cannot divide on schedule, which is why the anemia is made of big cells rather than small ones.

Step Three: Fewer, Larger, More Fragile Red Cells

Many megaloblasts never mature. They die in the marrow before release, a process called ineffective erythropoiesis, which explains why the marrow can look very active while the blood contains too few red cells. The cells that are released are large, oval and fragile, and they survive in the circulation for a shorter time than normal. The result is a macrocytic anemia: Walter has fewer red cells, each one larger than normal, and a hemoglobin well below the normal range. White cells and platelets can be affected for the same reason, and neutrophils with too many nuclear lobes are a typical finding on the blood smear.

Step Four: Less Oxygen Delivered

Oxygen delivery to tissues depends on cardiac output and on the oxygen content of arterial blood, and almost all of that content is carried bound to hemoglobin. With his hemoglobin roughly two-thirds of normal, each liter of Walter's blood carries roughly a third less oxygen, even though his lungs work normally and his oxygen saturation is normal. A pulse oximeter would read [98] percent, because it measures the share of hemoglobin carrying oxygen, not the amount of hemoglobin available.

Step Five: The Body Compensates, Then Shows the Strain

The body responds in predictable ways. The heart rate rises to move the smaller oxygen supply around faster, giving Walter a resting pulse over 100. Blood is redirected away from the skin toward vital organs, contributing to his pallor. Red cells release oxygen more readily to tissues. These responses keep him comfortable at rest, but exertion asks for more oxygen than his compensated system can deliver, so climbing stairs leaves him breathless. His sore, smooth tongue reflects the same DNA problem in another fast-dividing tissue, the lining of the mouth.

Why B12 Was Checked First

Vitamin B12 deficiency produces the same large red cells, because B12 is needed to regenerate active folate. But B12 deficiency can also damage nerves, causing numbness, poor balance and memory change, and giving folate alone can correct the anemia while nerve damage continues. Before folate treatment begins, B12 must therefore be measured and found normal (Green & Datta Mitra, 2017). Walter's normal B12 and lack of neurologic signs point to folate as the single cause.

Nursing Relevance

Treatment with oral folic acid usually produces a rise in young red cells within a week and a corrected hemoglobin within about two months. For Walter, the lasting fix lies in what caused the deficiency: help with meals, a conversation about alcohol, and attention to the isolation behind both. Nurses watch for fall risk while he remains anemic and short of breath.

References

Green, R., & Datta Mitra, A. (2017). Megaloblastic anemias: Nutritional and other causes. Medical Clinics of North America, 101(2), 297-317. https://doi.org/10.1016/j.mcna.2016.09.013

Medici, V., & Halsted, C. H. (2013). Folate, alcohol, and liver disease. Molecular Nutrition & Food Research, 57(4), 596-606. https://doi.org/10.1002/mnfr.201200077

Rogers, J. L. (Ed.). (2023). McCance & Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.