Essay Sample on Managing Diabetes

Diabetes mellitus (DM) is a chronic disease characterized by abnormal glucose metabolism or difficulty in metabolizing fats carbohydrates and proteins (Daflapurkar, 2014). According to Daflapurkar, the condition often results from low levels of insulin production or the cells developing a limited sensitivity to the action of insulin. Eventually, the glucose levels in the blood rise and impacts on all vital organs of the body. As Gulli, Chatela& Stratford (2015) indicates, without treatment, the glucose levels in the blood may become too high which may impact on both the length and quality of life. The patient may become blind; develop cardiovascular complications, Diabetic Peripheral Neuropathy as well as kidney failure. What is more, in extreme cases can cause coma and death. When properly treated, on the other hand, people with diabetes may lead a relatively normal life. According to Bermudes, Keck, & McElroy (2017), it is estimated that almost 20 million Americans (7 percent to 8 percent of the total population) suffer from diabetes with statistics diabetes will be among the major public health burdens in the near future. This implies that there is need to define ways to adequately address the condition. This study identifies the pathophysiology of symptoms associated with diabetes and diabetic peripheral neuropathy and describes the pharmacological basis of medications. Additionally, it identifies the effectiveness of Metformin and Duloxetine used in treatment. Moreover, education on diabetes self-management is equally provided.

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Pathophysiology of Symptoms: Diabetes and Diabetic Peripheral Neuropathy

Diabetic peripheral neuropathy refers to the presence of symptoms and signs of peripheral dysfunction among people living with diabetes after other factors have been excluded (Boulton, &Vileikyte 2011). According to the scholars, peripheral neuropathy may also affect the neuromuscular system as a whole. Unfortunately, Boulton, &Vileikyte argue that to careful clinical examination is necessary to fully diagnose peripheral neuropathy based on the symptoms. That is, it is essential to analyze a number of biochemical the mechanism once the cells become exposed to high glucose levels. According to Yagihashi, Mizukami & Sugimoto (2011), high levels of glucose facilities the formation of C-reactive protein (CRP) which as opposed to ordinary inflammatory marker, binds to endothelial cell receptors resulting into numerous molecular effects. Some of these effects include inhibiting endothelial nitric oxide synthesis (eNOS) as well as the stimulation of tissue factor production in addition to the production of ant-fibrinolytic factors such as plasminogen activator (PAI)-1 (Shrikhande& McKinsey 2012). This allows for the irreversible chemical reactions that lead to the formation of the advanced glycosylation end products. This process continues leading to the formation of reactive oxidative species like superoxide. Further elevation of ambient glucose levels increases glycosylation since sugars become attached to the amino acids on lipids and on proteins as well as on nucleic acids leading to the alteration of the metabolic activities and other functions of the macromolecules. What follows next is the inducement of monocytes and endothelial cells by receptors on macrophages to increase the rate at which inflammatory cytokines and adhesive molecules are produced.

In diabetes, alterations in the metabolism of Nitric Oxide (NO) also result into hyperglycemia and insulin resistance which also leads to the development of a pro-inflammatory state and eventually turns into the formation of atheroma through a well-developed molecular and cellular pathways (Shrikhande& McKinsey 2012). According to the scholar, this leads to the thickening of basement membranes which produces a burning pain similar to the pain in Jeff's case as presented in the patient information in unit four case analysis. Further, this might damage the nerve endings which may also cause a lot of pain. According to Shrikhande& McKinsey (2012) disturbed action potentials that are often produced when nerve endings are damaged are interpreted by the Central Nervous System (CNS) as pain. Similarly, it will result into vascular smooth muscle cell dysfunction. What is more, when kidney tissues filter the blood in the process of urine formation, they fail to reabsorb excess sugar back to the blood stream due to high levels of sugar in the tissues. According toShrikhande& McKinsey, this makes the sugars to be present in the urine where they draw a lot of water from the body resulting into frequent urination as evidenced by Jeff in the case analysis in unit four.

Pharmacological Basis of Medications and Congruence with Practice Guidelines

This section analyses the actions of lisinopril, metformin and duloxetine drugs on diabetes patients. The lisinopril tablets are often prescribed for the treatment of various conditions such as the treatment of hypertension among pediatric patients who are 6 years old and in adult patients in the treatment of patients in controlling high blood pressure, preventing the risk of serious cardiovascular events such as strokes and heart failure.Lisinopril tablets work by blocking angiotensin converting enzyme (ACE) compound in the body that often make blood vessels to tighten by producing angiotensin II as a natural response for controlling blood pressure. Unfortunately, the tightened blood vessels increase the pressure. By blocking ACE actions, production of angiotensin II lowers allowing blood vessels to relax and widen lowering the blood pressure. Some of the practice guidelines for taking lisinoprilincludes taking its doze at bedtime due to dizziness associated with it. Patients using the drug should also avoid the consumption of salt substitutes such as Lo-Salt due to high concentrations of potassium in the salts.

Metformin drug is also used in collaboration with other practices such as proper diet and carryingout exercises as well as other medications to control blood sugar levels and for treating type 2 diabetes (Harper 2015). According to Harper, metformin drug works by increasing sensitivity to insulin and by decreasing the amount of glucose that the body absorbs from the food. The drug is also characterized by loss of appetite making individuals to naturally eat fewer calories. The main clinical guideline for using metformin drug entails ensuring that the patient undertakes adequate exercises and avoids alcohol so as to increase the effectiveness of the drug. Also, it is highly recommended that monotherapy is prescribed together with metformin by the clinicians for the initial pharmacologic therapy.

Duloxetine drug, on the other hand, is a selective serotonin and norepinephrine reuptake inhibitor (SNRI) used in the treatment of a number of health conditions including the treatment of depression and anxiety. However, it is mostly to relieve pain among patients suffering from peripheral neuropathy as well as patients suffering from arthritis and chronic back pain. The drug works by affecting neurotransmitters where duloxetine prevents the reuptake of serotonin and epinephrine from the nerves where they have been released therefore terminating their acts on adjacent nerves and so reducing pain. According to theAmerican Psychiatric Association (2016), main clinical practices and standards of care for administering Duloxetine include ensuring adequate treatment for pain causing condition.

Effectiveness of Metformin and Duloxetine

By assessing the patient's response (Jeff) between visit one and visit and visit two in the case analysis module, it is evidenced that Metformin drug is relatively effective in lowering the blood pressure. This is because, when assessing the patient's physical data, it found that in visit one, his blood pressure was relatively high (BP 158/92, T 98.1F, P 78, R 20). Similarly, Jeff's lab report on his basic chemistry panel revealed that his sugar levels were extremely high (Glucose: 190). However, after his treatment plan that involved metformin 500 mg, the blood pressure dropped slightly within a period of four weeks (BP 140/84T 98.9F, P 82, R 18). The treatment plan involved after the second visit incorporated twice the amount of dosage of metformin which is likely to lower the sugar levels drastically. Duloxetine drug, on the other hand, does not seem to achieve desired results. This is because the patient continues to report headaches and continues to feel worried. However, as Pop-Busui et al., (2017) observes, duloxetine needs relatively longer time for the realization of a positive patient outcome.

Diabetes Self-Management Education

According to Haas, et al., (2012) Diabetic Self-management Education (DSME) has developed are a number of standards that can be implemented to ensure patients such as Jeff adopt behaviors necessary in managing his diabetic condition. The first standard is concerned with establishment and documentation of organization's structure with specific goals and mission statements for the promotion of diabetes care. The second standard entails the establishment of governing bodies which includes advisory groups and committees to promote quality. Standard 3 entails the determination of diabetes educational needs so as to help in channeling adequate resources to promote quality care. Similarly, the fourth standard entails coordination practices aimed at overseeing planning the implementation and evaluation of the diabetes education. The fifth standard entails providing DSME with certified diabetic educators with necessary skills. Finally, standard 6 involves having a written curriculum with present evidence and practice guidelines to serve as the framework in disseminating the Diabetic Self-management Education.

References

American Psychiatric Association.(2016). American Psychiatric Association practice guidelines for the treatment of psychiatric disorders. Arlington, Virg: American Psychiatric Association.

Bermudes, R. A., Keck, P. E., & McElroy, S. L. (2017). Managing metabolic abnormalities in the psychiatrically ill: A clinical guide for psychiatrists. Washington, DC: American Psychiatric Pub.

Boulton, A. J. M., &Vileikyte, L. (2011).Painful diabetic neuropathy in clinical practice. London: Springer.

Daflapurkar, S. B. (2014). High risk cases in obstetrics. Place of publication not identified: Mcgraw-Hill.

Harper, D. (2015).Dr Dawn's Guide to Digestive Health

Haas, L., Maryniuk, M., Beck, J., Cox, C. E., Duker, P., Edwards, L., ...& McLaughlin, S. (2012). National standards for diabetes self-management education and support. The Diabetes Educator, 38(5), 619-629.

Gulli, B., Chatelain, L., Stratford, C., & American Academy of Orthopaedic Surgeons. (2015). Emergency: Care and transportation of the sick and injured. Sudbury, Mass: Jones and Bartlett Publishers.

Pop-Busui, R., Boulton, A. J., Feldman, E. L., Bril, V., Freeman, R., Malik, R. A., ... & Ziegler, D. (2017). Diabetic neuropathy: a position statement by the American Diabetes Association. Diabetes care, 40(1), 136-154.

Shrikhande, G. V., & McKinsey, J. (2012). Diabetes and peripheral vascular disease: Diagnosis and management. New York: Humana Press.

Yagihashi, S., Mizukami, H., & Sugimoto, K. (2011). Mechanism of diabetic neuropathy: where are we now and where to go?. Journal of Diabetes Investigation, 2(1), 18-32.