Iron Deficiency Anemia Discussion

Iron Deficiency Anemia Discussion

Discussion

Part A

Kathy and her parents will be educated to ensure Kathy eats more iron-rich foods like liver, dark green vegetables, soy products, cereals, dried fruits, whole-grain bread, and eggs. To ensure maximum absorption of the iron, the family will be advised to ensure that Kathy does not consume tea, coffee or milk after taking iron-rich foods (Nihal, 2015). Consuming vitamin C food sources can enhance iron absorption. In addition, the family will be advised to have Kathy take iron supplements such as ferrous sulfate and multivitamins but only under the healthcare provider’s prescription (Nihal, 2015).  The anticipatory guidance for this patient is to have the patient always attend follow-up reviews to assess if Kathy is responding to the treatment. As Nihal (2015) further states, if the patient is not responding to treatment, the patient will be referred to a suitable specialist in order to establish if there might be other causes of iron deficiency anemia for the patient. In case the patient responds to treatment, nutritional counseling will be reinforced and iron treatment continued and have the hemoglobin/hematocrit rechecked. Iron Deficiency Anemia Discussion

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The treatment plan for the patient will include a dosage of elemental iron 30 mg per kg per day for three months. An increase in Hb levels by 1 g per dL (10 g per L) after a month since the treatment commencement will be an indication of adequate response (Mathews & Jason, 2014). In case the hemoglobin levels do not increase as recommended, guidelines recommend further evaluation. Further evaluation starts with a comprehensive history and physical assessment in order to identify the cause of the iron deficiency. In case the indices of Hb and red blood cells are normal, a complete blood count ought to be done 12 months later. However, no further follow-up is required if the patient’s hematocrit level stays normal and she is asymptomatic (Mathews & Jason, 2014).

Part B

Childhood Acute Lymphocytic Leukemia (ALL) and G6PD Deficiency

Childhood acute lymphocytic leukemia (ALL) is the cancer of the bone marrow and blood. It is a common type of cancer among children. The pathophysiology involves stem cells developing into lymphoblast and failing to develop into maturation to become lymphocytes (Terwilliger & Hay, 2017). The lymphoblasts are the leukemia cells. The lymphoblasts do not function like the normal lymphocytes and hence they are unable to fight infections effectively. Additionally, as the number of lymphoblasts increases in the bone marrow and blood, the other blood cells such as platelets, white blood cells, and red blood cells do not develop well. This may cause an infection, easy bleeding or anemia. Symptoms of ALL include fever, bleeding easily, joint or bone pain, loss of appetite, painless lumps within the stomach, groin, neck or underarm, fatigue, petechiae and looking pale (Terwilliger & Hay, 2017). Treatment of ALL includes chemotherapy, radiation therapy, chemotherapy with stem cell transplant, and targeted therapy (Terwilliger & Hay, 2017). Iron Deficiency Anemia Discussion

G6PD deficiency is a genetic disorder that is common in males. G6PD deficiency occurs when the body has inadequate glucose-6-phosphate dehydrogenase (G6PD). G6PD assists red blood cells to work effectively and protects them from harmful substances within the blood. Because in G6PD deficiency the red blood cells lack adequate G6PD and hence lacks protection, the red blood cells start breaking apart a process called hemolysis (Vizzi et al, 2016). Destruction of many cells leads to patients developing hemolytic anemia. Clinical manifestations of G6PD deficiency include fast pulse rate, jaundice, fatigue, paleness, dizziness, dark, tea-colored urine, breath shortness, and an enlarged spleen. Treatment of G6PD deficiency includes removal of the trigger such as treating the infection or discontinuing the use of certain medication. Severe anemia may be treated using an iron supplement or in case it is a very severe transfusion of healthy blood cells may be performed (Vizzi et al, 2016).

References

Mathews S & Jason D. (2014). Iron Deficiency Anemia: Evaluation and Management. Am Fam Physician. 87(2), 98-104.

Nihal O. (2015). Iron deficiency anemia from diagnosis to treatment in children. Turk Pediatri Ars. 50(1), 11–19.

Terwilliger T & Hay M. (2017). Acute lymphoblastic leukemia: a comprehensive review and 2017 update. Blood Cancer J. 7(6), e577.

Vizzi E, Gilberto B, Colman L & Perez H. (2016). Prevalence and molecular characterization of G6PD deficiency in two Plasmodium vivax endemic areas in Venezuela: predominance of the African A-202A/376G variant. Malar J. 15(9). Iron Deficiency Anemia Discussion

 

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