Clin App

Clinical Application
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Abstract
A review of the symptoms indicates that the patient is experiencing vitamin B12 deficiency that is responsible for her anemic condition. In essence, she had inadequate amounts of gastric intrinsic factor, which makes it difficult for her to absorb sufficient amounts of vitamin B12. In addition, she had developed parietal cells antibodies that also hinder the vitamin’s absorption. This set of circumstances explain her vitamin deficiency. Of interest is the fact that the vitamin plays an important part in red blood cells production. With low amounts of red blood cells in the blood, the patients is forced to increase the heart rate and breathing rate as a way of compensating for the low oxygen amounts. The conditions explain the patient’s diagnosis as having suffering from pernicious anemia. The diagnosis can be borne by a blood smear whose results would indicate red blood cells poikilocytosis and anisocytosis, and neutrophils hypersegmentation. Still, additional tests in the form of determining indirect bilirubin and lactate dehydrogenase levels, and Schilling test would be required to confirm the diagnosis before treatment using vitamin B12.

Clinical Application
Part A.
Based on the presented symptoms and the woman’s age age, it can be accepted that the woman is suffering from pernicious anemia brought about by vitamin B12 (cobalamin) deficiency. Firstly regarding the progressive shortness of breath, weakness and fatigue, she has inadequate gastric intrinsic factor that is required for vitamin B12 absorption.

This, in turn, reduces red blood cells productions to ensure that inadequate amounts of oxygen are transported throughout the blood to cause the symptoms (Bope & Kellerman, 2016; National Health Service, 2016). Secondly regarding the mild diarrhea as a gastrointestinal symptom, vitamin B12 absorption is hindered by the development of parietal cells antibodies (Krause, Cirino & Gotter, 2016). The antibodies target and bind her H+/K+ ATPase gastric enzymes thereby destroying the proton pumps. Once the proton pumps are destroyed, the body has problems in acid secretion and experiences megaloblastic changes. Finally, she has reported neurological impairment seen in the numbness and loss of balance. These are symptoms associated with vitamin B12 deficiency (Pelley & Goljan, 2011).
The woman is suffering from a deficiency of vitamin B12 that is characterized by neurological impairment, glossitis, and anemia. These effects occur via DNA synthesis difficulties. The vitamin is an important cofactor for deoxythymidine synthesis from deoxyuridine. The vitamin reduces tetrahydrofolate and forms methylcobalamin by accepting the methyl group from methyltetrahydrofolate. The reduced tetrahydrofolate is of interest in purine synthesis since it acts as a single-carbon donor. In this respect, the vitamin deficiency causes a decrease in the quantity of available tetrahydrofolate, which reduces purine production to impair the synthesis of DNA. The impaired synthesis of DNA causes corresponding megaloblastic alterations in the bone marrow’s contingent of blood cells to cause a matching reduction in red blood cells production even as they are subjected to intramedullary hemolysis, which destroys the cells in great quantities. In essence, pernicious anemia presents antibodies that terminate the parietal cells to result in the intrinsic factor responsible for vitamin B12 production lacking, resulting in the vitamin deficiency. These set of circumstances are responsible for the noted symptoms, explaining the pernicious anemia diagnosis since the symptoms are likely to be the result of vitamin B12 deficiency (Auth & Kerstein, 2013; Bope & Kellerman, 2016).
Part B.
The peripheral blood smear results would vary depending on the length of time in which the woman has suffered from the vitamin B12 deficiency. Given that she is very symptomatic, it can be expected that her anemic condition is extreme or full blown. The peripheral blood smear would show significant red blood cells poikilocytosis and anisocytosis, and neutrophils hypersegmentation. In fact, the morphological changes noted for the peripheral blood smears would match those visualized in cases of leukemia. The destruction of red blood cells is expected since the vitamin B12 deficiency destroys the available red blood cells while also impeding their production (Medscape, 2016b; McPherson & Pincus, 2011).
Once the peripheral blood smear results have been presented, additional tests would be required to confirm the diagnosis. These would include determining indirect bilirubin and lactate dehydrogenase levels, showing elevated amounts in vitamin B12 deficiency cases as a result of intramedullary hemolysis. Besides that, the amount of vitamin B12 found in the serum is expected to be low. Also, high amounts of homocysteine and methylmalonic in the serum would be indicative of vitamin B12 deficiency. The tests can conclude with Schilling test to explain the precise source of the pernicious anemia by examining the vitamin deficiency mechanism through absorption of a vitamin B12 sample that has been radioactively labeled (McPherson & Pincus, 2011).
Part C.
The patient has exhibited tachycardia, paresthesias, and impaired proprioception symptoms. Firstly, the tachycardia symptoms are likely as a reflection of her profound pernicious anemia condition. In this case, the anemic condition and presentation has caused a severe reduction in the amount of red blood cells availability, and by extension it has decreased the concentration of hemoglobin in the blood. This has resulted in marked reduction in the blood’s capacity to transport oxygen to all parts of the body, thereby causing an increase in the heart rate to improve oxygen availability. By pumping more blood at a faster rate, the body is able to overcome the oxygen deficiency and meet its needs. In reality, the blood has an oxygen concentration problem and the body overcomes this challenge by increasing cardiac output to improve oxygenation. Over time, the heart is placed under a lot of stress that could result in its failure (Auth & Kerstein, 2013; Bope & Kellerman, 2016; Medscape, 2016a). Secondly, the paresthesias and impaired proprioceptions are neurological signs resultant of the peripheral nerves (for paresthesias) and posterolateral spinal columns (impaired proprioception) being demyelinated. The vitamin B12 deficiency causes a lack of methionine, making it responsible for the demyelination. After a while, the reported demyelination causes neuronal cell demise. As such, it can be accepted that the tachycardia, paresthesias, and impaired proprioception symptoms can be approached as neurologic symptoms and effectively treated through administration of vitamin B12 to address the noted deficiency (Auth & Kerstein, 2013; Bope & Kellerman, 2016; Medscape, 2016a). Overall, the patient’s pernicious anemia condition should be treated by administering vitamin B12 once the diagnosis has been confirmed through the peripheral blood smear, determining indirect bilirubin and lactate dehydrogenase levels, and Schilling test (McPherson & Pincus, 2011; Medscape, 2016a).

References
Auth, P. & Kerstein, M. (2013). Physician Assistant Review (4th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.
Bope, E. & Kellerman, R. (2016). Conn’s Current Therapy 2016. Philadelphia, PA: Elsevier.
Krause, L., Cirino, E. & Gotter, A. (2016). Pernicious Anemia. Retrieved from http://www.healthline.com/health/pernicious-anemia#Overview1
McPherson, R. & Pincus, M. (2011). Henry’s Clinical Diagnosis and Management by Laboratory Methods (22nd ed.). Philadelphia, PA: Elsevier Saunders.
Medscape (2016a). Pernicious Anemia Clinical Presentation. Retrieved from http://emedicine.medscape.com/article/204930-clinical
Medscape (2016b). Pernicious Anemia Workup. Retrieved from http://emedicine.medscape.com/article/204930-workup
National Health Service (2016). Vitamin B12 or folate deficiency anemia. Retrieved from http://www.nhs.uk/Conditions/Anaemia-vitamin-B12-and-folate-deficiency/Pages/Introduction.aspx
Pelley, J. & Goljan, E. (2011). Biochemistry (3rd ed.). Philadelphia, PA: Mosby Elsevier.