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MBHT5001 Diabetes Management

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MBHT5001 Diabetes Management

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Course Code: MBHT5001
University: The University Of Sydney

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Country: Australia

Melanie Johnson is a 63 year old woman who has been admitted to your surgical ward for the drainage of a Bakers Cyst. She was diagnosed with Type 2 Diabetes Mellitus (T2DM) 6 months ago, during a routine workup for surgery. She takes no specific medication for her diabetes, and has been told by her GP to ‘watch what she eats’. She was devastated to discover her diagnosis of T2DM, as she was aware of the risks due to her family history. She has not returned to her GP since her initial diagnosis. She has no other past medical history of note. Melanie says tearfully “I have been trying to eat right and exercise, but I can’t walk because of the pain in my knee and I was feeling down and eating ice cream. I have hardly eaten anything in the last week because I am trying to lose weight and get my blood sugar down”.
Her mother and older sister were both diagnosed with T2DM in their early 50’s.
Melanie tells you she has had the Bakers Cyst for about 2 years. It has been increasing in size over the last 8 months, restricting her movements. The planned surgery is drainage followed by two follow up cortisone injections. On Admission at 0800 – her blood glucose level (BGL) was 22.9 mmol/L; HbA1c: 11%. She has been fasting since midnight. She notes that she is feeling quite “stressed” about the surgery. On admission the following were recorded:
Height: 167cm
Weight: 105kg
Blood Pressure: 140/80 mmHg
Pulse rate: 95 beats/min
Respiratory Rate: 22 breaths/minute
Temperature: 36.7 °C Sp02: 97% 
Part 1
Melanie is distressed that her blood glucose level is elevated and asks you for help in understanding her diabetes. She tells you that she has a friend who is very overweight, eats lots of cake and hardly ever exercises, and he does not have diabetes.
1. Describe the pathophysiology of T2DM with links to Melanie’s case. Include in your answer risk factors for T2DM, the pathogenesis of T2DM, possible complications of T2DM and outline the 3 levels of treatment options for T2DM.
2. Differentiate between T2DM and T1 DM (at least 6 differences).
3. Identify at least 2 reasons Melanie’s BGL is high on admission. Discuss how each reason you identify effects BGLs.
Part 2
The surgery is successful and Melanie comes to see you in the outpatient clinic for cortisone injections (Kenacort-A 40). She has been commenced on metformin (APO-Metformin Tablets) and glipizide (Minidiab Tablets) to help control her diabetes. Her blood test on this visit were BGL 8.8 mmol/L; HbA1c: 8%. 
1. Discuss the three medications Melanie is on. Include in your answer the action, complications/side effects and nursing considerations linked to Melanie’s situation. (500) 2. Discuss the two blood results, one from prior to surgery and one from the clinic visit of Melanie’s BGL and HbA1c. What are they? What do they measure and why have they changed?
Part 3
While Melanie is waiting to see the doctor, she starts talking to you about her condition. She asks if she has insulin dependent diabetes or early onset diabetes. She is also unsure of how to use her BGL machine and BGL strips.
1. Discuss why the terms insulin dependent diabetes mellitus/ non insulin dependent diabetes mellitus and early onset/mature onset are misleading.
2. You need to teach Melanie how to use her BGL machine. Discuss the “teach back” method for patient education (include evidence from peer reviewed sources). Discuss how you would use this method to teach Melanie how to use her BGL machine.

Type 2 diabetes affects the way the body metabolises sugar to produce energy. With type 2 diabetes, two things occur; the body resists insulin or fails to produce enough insulin to maintain normal glucose levels.
Part 1
Pathophysiology of T2DM
Diabetes is a metabolic condition characterised by the hyperglycemic state that results from the insufficient action of insulin (American Diabetes Association, 2014). Insulin resistance as well as impaired secretion of insulin contribute to the development of pathophysiological conditions. The latter develops from a decline in sugar responsiveness observed before the clinical onset of a disease. While the former is as a result of the decrease in sugar-responsive early-stage insulin production, plus a decline in extra insulin production (Caramel & Stagnaro, 2013). Impaired insulin production is progressive and entails glucose toxicity as well as lipotoxicity. When left untreated, the latter causes a decline in mass of the pancreatic β cells. However, continuous impairment of these cells hinders how the blood sugar is controlled. As individuals in early phases after diabetes onset show a rise in postprandial blood sugar due to increased insulin resistance, the progression of the worsening pancreatic beta cells functions causes a permanent increase in blood sugar (Caramel & Stagnaro, 2013).
On the other hand, insulin resistance occurs when insulin in the body fails to put enough to the blood concentration. Insulin resistance starts and stretches before the onset of a disease. However, the mechanism of insulin action shows how insulin resistance, genetic and environmental factors are intertwined. Some of the genetic factors include insulin receptor, insulin receptor substance and gene polymorphism which affects insulin signals as well as polymorphisms of thrifty genes (Chatterjee, Khunti & Davies, 2017). Inflammatory mediators and glucolipotoxicity are essential mechanisms for impaired insulin production plus signaling resistance. Other methods such as presence of visceral obesity and high fasting blood insulin can also be used to check for the extent of insulin resistance
Some of the risk factors that increase the chance of T2DM include being overweight, fat distributing especially when body stores fat in the abdomen and inactivity (Cornell, 2015). Family history including parents and siblings is also a risk factor for T2DM. From the case scenario, Melanie’s mother and sister were diagnosed with diabetes in their early 50s. The risk of T2DM increases with age as a person gets older, particularly after 45years. Melanie was 63 years old meaning that age was also a contributing factor towards her disease. Women having polycystic ovarian syndrome a condition characterised by irregular menstruations, obesity and excess hair growth are also at risk of developing T2DM. 
The potential side effects of T2DM are blood vessel diseases as well as cardiovascular disease. Studies show that T2DM increases the chances of developing heart diseases, angina, atherosclerosis and hypertension. Neuropathy is another complication where excess sugar in the body damages the capillary walls that nourish the nerves, particularly the leg nerves. Poorly controlled blood sugar levels or BSLs can lead to numbness especially in affected limbs. Nephropathy is another T2DM complication wherein the kidney contains blood vessels that filter waste from the blood (Esser, Legrand-Poels, Piette, Scheen & Paquot, 2014). Diabetes can cause damage to the filtering system and lead to kidney failure. Other complications of T2DM include eye and foot injury, skin conditions, hearing problems, and Alzheimer’s disease.
Other than feeding on a healthy diet, close monitoring of BGLs and regular exercise; medications such as metformin and sulfonylureas can also control T2DM. The drugs improve the sensitivity of blood insulin for the body to use insulin more effectively and to help it secrete more insulin (Fontes-Carvalho, Ladeiras-Lopes, Bettencourt, Leite-Moreira & Azevedo, 2015). From the case scenario provided, Melanie was prescribed Metformin and Glipizide to help control her diabetes.
Differences between T1DM and T2DM
In T1DM, the immune system attacks the hormone secreting pancreatic β cells thus lowering the state of the body to secrete enough insulin as well as control blood sugar levels. Since the body does not secrete enough insulin, a patient needs supplemental insulin when diagnosed with T1DM (Cornell, 2015). On the other hand, when T2DM starts, cells become resistant to the effect of insulin and with time, they stop producing enough insulin-making the body not to utilise glucose effectively. Therefore, the cells cannot take up sugar, which later binds in the blood a process known as insulin resistance (Cornell, 2015). When BGLs are high, the cells get overexposed to insulin and becomes unresponsive to insulin.
Reasons why Melanie’s blood glucose level was high on admission
On admission, Melanie’s blood sugar level was 22.9mmol/l meaning that she had diabetes. Some of the commonly known causes of high BGLs include not taking diabetic medications like witnessed in the case scenario by Melanie and high carb bedtime snacks which are not mentioned in the case scenario. Somogyi effect and dawn phenomenon are other effects of high BGLs.
i). The dawn phenomenon
In the dawn phenomenon, the body uses sugar for energy, so it’s essential to have sufficient energy to be able to wake in the morning (Lovshin & Zinman, 2013). At night the body starts churning out stored glucose to prepare for the next day. So, if Melanie has been fasting for a whole week, what would be the source of her energy? The body also releases hormones that lower sensitivity to insulin. These events may occur as the diabetes medication tablets taken the previous days are wearing off. However, we know that Melanie was not taking diabetes medication before.
ii). Somogyi effect
Somogyi effect or rebound hyperglycemia is another possible cause of high blood sugar levels. Somogyi effect derives its name from a doctor who wrote on the impact. When blood glucose levels drop very low in the middle of the night while a person is asleep, the body releases hormones to rescue the person from dangerously low blood sugar levels.  The hormones then prompt the liver to release stored glucose in more substantial amounts than as usual (Marso et al., 2016). This system is not ideal for a diabetic person, as the liver expels more glucose than required thus causing high blood glucose level in the morning. From the case scenario, Melanie knew that she had diabetes due to her family history and never bothered to take medications. She also fasted for a week to get her blood glucose level down but due to the Somogyi effect discussed above, she was tested to have high blood glucose levels of 22.9mmol/l on admission to the surgical unit.
Part 2
Medications prescribed to Melanie
i). Metformin
Metformin is a drug prescribed to persons with T2DM for boosting the sensitivity of body tissues for it to utilise insulin more efficiently (Morrison & Kleemann, 2015).  The medication also lowers sugar production in the liver. As the drug may not lower enough blood glucose on its own, a doctor can recommend other therapies like lifestyle changes which involve things such as losing weight or becoming more active. From the case provided, Melanie was 105 kg and had fasted for one week to get her blood glucose level down. It is through the same fasting as well as an exercise which makes metformin more effective in lowering the high blood sugar levels.  Metformin has a range of complications or side effects, but nausea and diarrhea are the common ones (Patel et al., 2016). Such problems go away as the body gets used to medications. Assuming that metformin and lifestyle changes do not work to control blood sugar levels, infected medicines can be used as an alternative.
ii). Cortisone injection (Kenacort-A40)
Kenacort 40 Mg is an injection used to relieve symptoms including swelling and pain. From the case study, Melanie was admitted to the surgical ward to drain the Baker’s cysts she has been diagnosed with two years ago. As her knee had swollen to the point that she could barely move, the cortisone injection was used to relieve pain and the swelling. Kenacort is used to treat symptoms such as itching, swelling, and redness of the skin (Perry et al., 2015).  The medicine should be used with caution especially in people with diabetes, kidney diseases or liver disease.  Cortisone injection causes several complications which include easy bruising of the skin, irritation, itching, tingling in arms/legs, headache, blurred vision and anxiety among others (Perry et al., 2015). It is not mentioned whether all of these side effects were evident in Melanie’s case.
Kenacort should be used with caution especially in persons with already existing hyperlipidemia because of increased risk of elevating in serum triglycerides as well as LDL cholesterol levels. Close monitoring of cholesterol levels and serum triglyceride is necessary for such patients. Besides, appropriate dose adjustments with suitable alternatives are essential in some cases based on clinical condition. Kenacort also interacts with other diseases involving the renal, osteoporosis, liver diseases, and myocardial interactions; hence, it is always necessary to consult a doctor before commencing the drugs.
iii). Glipizide
Glipizide is an oral tablet used to treat T2DM. The drug helps release insulin from the pancreas and move glucose from the bloodstream to the cell where it belongs thus decreasing the BSLs. Some of the common complications of Glipizide are low blood sugar as well as digestive problems including nausea, constipation or diarrhea. Serious side effects of Glipizide include low blood sugar, allergic reactions, low blood cell count, low blood sodium level and liver problems (Rajeev, Cuthbertson & Wilding, 2016).  Glipizide interacts with medications such as antifungal drugs, antibiotics, drugs containing salicylate and sulfonamide, blood thinner medications, beta blockers and depression drugs among others. Before commencing Glipizide, it is always advisable to inform the doctor in case of other prescribed drugs to avoid complications. Also, a doctor can test for blood sugar levels to check if it is safe to take Glipizide (Rajeev, Cuthbertson & Wilding, 2016).
The two blood tests before surgery and the other from clinic visit.
On admission to the surgical unit, Melanie had a blood sugar level of 22.9mmol/l and Hemoglobin A1c level of 11%. Blood sugar level and HbA1c test are used to monitor blood glucose levels. As Melanie had been fasting for one week, her blood glucose level read at 22.9 mmol/l meaning that she had T2DM, but there was some room for improvement. For people with a BGL of 7.00mmol/l, they should incorporate activities into their week and make some changes to their diet or be prescribed a medicine to lower the BGLs. HbA1c is used to measure hemoglobin levels, and an HbA1c of 11% is an indication that Melanie had T2DM.
After the surgery, Melanie’s blood glucose levels feel from 22.9mmol/l to 8.8mmol/l and HbA1c from 11% to 8%. An indication that the medications (metformin and Glipizide) Melanie was prescribed along with lifestyle changes worked in her favour to reduce blood sugar level.
Part 3
Why insulin-dependent diabetes and early onset are misleading
T2DM is a mild type of diabetes due to its slow onset and its control over both diets as well as oral medication (Wanner et al., 2016). However, the effects of uncontrolled as well as untreated T2DM are the same as those of T1DM.  Such type is also referred to as noninsulin dependent diabetes, a term that’s somehow misleading (Wanner et al., 2016).  A vast number of individuals with T2DM use diet and medications to control this condition. However, insulin injections are at times vital especially when treatment with diet as well as oral medication does not work (Yabe, Seino, Fukushima & Seino, 2015). From the case scenario provided, Glipizide and metformin tablets controlled the condition of Melanie since after taking the medications, her blood sugar levels fell from 22.9mmol/l to 8.8mmol/l
Teach-back method to use BGL machine
For effective teaching as well as evaluation of a patient’s comprehension, it is necessary to use a patient-centred method and that’s where the teach-back method comes in (Wanner et al., 2016). Teach-back approach is used to show patient’s understanding of information the care provider has imparted (Zaccardi, Webb, Yates & Davies, 2015). A
fter going through the teach back session, I would confirm Melanie’s comprehension by asking for an explanation or a demonstration on how to use a BGL machine.  Teach-back approach helps avoid overwhelming information to a person. To use the BGL machine, Melanie first needs to understand what T2DM is and how to use it to check for blood glucose levels Zinman et al., 2015).  Assuming that Melanie takes insulin to manage her BGLs, she must know how to determine the dosage based on the sugar level plus how to maintain low or high blood glucose level.  She must know when blood sugar levels are extreme and when to consult a healthcare provider. As Melanie had baker’s cysts other than T2DM, teaching sessions would include identifying as well as modifying risk factors for such conditions.
Healthy lifestyle choices can help prevent T2DM. As medications are an option for the T2DM, metformin plus other oral diabetes medication can help reduce the risks of T2DM.
American Diabetes Association. (2014). Diagnosis and classification of diabetes mellitus. Diabetes care, 37(Supplement 1), S81-S90.
Caramel, S. C., & Stagnaro, S. (2013). Inherited Real Risk of Type 2 Diabetes Mellitus: bedside diagnosis, pathophysiology and primary prevention. Frontiers in endocrinology, 4, 17.
Chatterjee, S., Khunti, K., & Davies, M. J. (2017). Type 2 diabetes. The Lancet, 389(10085), 2239-2251.
Cornell, S. (2015). Continual evolution of type 2 diabetes: an update on pathophysiology and emerging treatment options. Therapeutics and clinical risk management, 11, 621.
Esser, N., Legrand-Poels, S., Piette, J., Scheen, A. J., & Paquot, N. (2014). Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. Diabetes research and clinical practice, 105(2), 141-150.
Fontes-Carvalho, R., Ladeiras-Lopes, R., Bettencourt, P., Leite-Moreira, A., & Azevedo, A. (2015). Diastolic dysfunction in the diabetic continuum: association with insulin resistance, metabolic syndrome and type 2 diabetes. Cardiovascular diabetology, 14(1), 4.
Lovshin, J. A., & Zinman, B. (2013). Diabetes: clinical inertia—a barrier to effective management of T2DM. Nature Reviews Endocrinology, 9(11), 635.
Marso, S. P., Daniels, G. H., Brown-Frandsen, K., Kristensen, P., Mann, J. F., Nauck, M. A., … & Steinberg, W. M. (2016). Liraglutide and cardiovascular outcomes in type 2 diabetes. New England Journal of Medicine, 375(4), 311-322.
Morrison, M. C., & Kleemann, R. (2015). Role of macrophage migration inhibitory factor in obesity, insulin resistance, type 2 diabetes, and associated hepatic co-morbidities: a comprehensive review of human and rodent studies. Frontiers in immunology, 6, 308.
Patel, T. P., Rawal, K., Bagchi, A. K., Akolkar, G., Bernardes, N., da Silva Dias, D., … & Singal, P. K. (2016). Insulin resistance: an additional risk factor in the pathogenesis of cardiovascular disease in type 2 diabetes. Heart failure reviews, 21(1), 11-23.
Perry, R. J., Camporez, J. P. G., Kursawe, R., Titchenell, P. M., Zhang, D., Perry, C. J., … & Ruan, H. B. (2015). Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes. Cell, 160(4), 745-758.
Rajeev, S. P., Cuthbertson, D. J., & Wilding, J. P. H. (2016). Energy balance and metabolic changes with sodium?glucose co?transporter 2 inhibition. Diabetes, Obesity and Metabolism, 18(2), 125-134.
Wanner, C., Inzucchi, S. E., Lachin, J. M., Fitchett, D., von Eynatten, M., Mattheus, M., … & Zinman, B. (2016). Empagliflozin and progression of kidney disease in type 2 diabetes. New England Journal of Medicine, 375(4), 323-334.
Yabe, D., Seino, Y., Fukushima, M., & Seino, S. (2015). β cell dysfunction versus insulin resistance in the pathogenesis of type 2 diabetes in East Asians. Current diabetes reports, 15(6), 36.
Zaccardi, F., Webb, D. R., Yates, T., & Davies, M. J. (2015). Pathophysiology of type 1 and type 2 diabetes mellitus: a 90-year perspective. Postgraduate medical journal, postgradmedj-2015.
Zinman, B., Wanner, C., Lachin, J. M., Fitchett, D., Bluhmki, E., Hantel, S., … & Broedl, U. C. (2015). Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. New England Journal of Medicine, 373(22), 2117-2128.

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