Classification And Diagnosis Of Diabetes Mellitus

Classification And Diagnosis Of Diabetes Mellitus

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Classification And Diagnosis Of Diabetes Mellitus

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Classification And Diagnosis Of Diabetes Mellitus

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Course Code: NURBN2016
University: Federation University is not sponsored or endorsed by this college or university

Country: Australia

Questions 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 T1DM (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.
Questions 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.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?
Questions 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. (100)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.

The current paper is a discussion on the case study of Diabetes Mellitus.  The patient is Melanie Johnson, a 63-year-old female who was diagnosed with type 2 diabetes and had been admitted for drainage of a baker’s cyst. The paper will outline the pathophysiology of type 2 diabetes including the risk factors, pathogenesis, complications and treatment options. Differences between the two classes of diabetes will be outlined. The medications used by Melanie will be discussed including their modes of action, side effects and nursing considerations for their use. The lab evaluation of diabetes will be outlined, especially the two tests that were done on Melanie; HbA1c and blood glucose. The phrases insulin- dependent, non-insulin dependent, early onset, and mature onset diabetes will be discussed with a view of posing why they are misleading terms. The teach-back method will be used to teach the patient how to use a BGL machine.
Diabetes Mellitus: Risk factors and Pathophysiology
Diabetes is a complex endocrine pathology characterized by hyperglycemia due to derangements in pathways of glucose metabolism (Kahn, Cooper, & Del Prato, 2014). Type 2 diabetes mellitus is hyperglycemia due to a combination of factors such as peripheral insulin resistance, inadequate secretion of insulin in response to hyperglycemia and subsequent inappropriate glucagon secretion. It is a disorder due to an interplay of genetics, environment, and lifestyle. There is a large genetic component to type 2 diabetes, with the inheritance of the susceptibility to develop insulin resistance. There is a high concordance in twins proving the genetic linkage. On that note, it is also noted to run in families (Inzucchi & Sherwin, 2011). This was evidenced in Melanie’s case as her mother and elder sister both have diabetes type 2. Genome-wide association studies have identified several genes linked to pancreatic beta cell functions and insulin function.
Environmental and lifestyle factors implicated in diabetes make up the risk factors, most of which are modifiable. Obesity, alcohol, smoking, and aging are the most common. An increase of BMI of increases the risk of developing diabetes by up to 5 times (Inzucchi & Sherwin, 2011). Obesity is linked to insulin resistance in the periphery. The higher the BMI the higher the risk. The patient has a BMI of 37.6, which is termed obese according to the heart foundation standards. This increases her risk considerably. The use of high-fat diets with high simple sugars and a decrease in fibers and starch worsen obesity and increase the risk even further (Tong, Dong, Wu, Li, & Qin, 2011).
Insulin resistance is whereby the insulin concentration in the bloodstream does not exert sufficient action that is occurs in major glucose utilizing tissues such as the liver and muscle. It is seen prior to disease onset. Genes such as insulin receptor and insulin receptor substrate polymorphisms have been linked to this pathology. It is increased in obesity hence sparking research into the role of adipokines and free fatty acids in the pathogenesis (Kahn, Cooper, & Del Prato, 2014).
Impaired insulin secretion is impaired responsiveness of the pancreas to glucose leading to a decrease in insulin secretion. This causes a post-prandial hyperglycemia as the pancreatic beta cells become more desensitized. This decrease in the early- phase secretion of insulin is an important event in type 2 diabetes pathogenesis as without one can have insulin resistance but no diabetes. This might be the reason why Melanie’s friend who is overweight and barely exercises but does not have diabetes. All overweight individuals have some degree of insulin resistance but diabetes develops in those who cannot adequately increase their insulin to meet the extra need (Kahn, Cooper, & Del Prato, 2014).
Diabetes Mellitus: Complications
Glucose is a systemic fuel source hence the effects of diabetes mellitus will affect literally all body systems. The complications are physiologically classified as microvascular or macrovascular complications. Microvascular complications include diabetic retinopathy, nephropathy leading to renal failure, peripheral neuropathy leading to sensory loss, motor weakness and pain, autonomic neuropathy leading to postural hypotension, bowel problems and urinary incontinence, and diabetic foot causing foot ulcers and arthropathy (Walker & Colledge, 2013). Macrovascular complications include impaired coronary circulation causing myocardial infarction, impaired cerebral circulation causing stroke and transient ischemic attacks, and impaired peripheral circulation causing ischemia and claudication. These patients also have an increased risk of infection due to a pre-infection environment in hyperglycemia (Walker & Colledge, 2013).
Diabetes Mellitus: Levels of treatment
Three levels of treatment exist with the first level being the prevention of diabetes, the second one treatment of recognized disease and prevention of complications and the third, treatment of complications. Prevention of T2DM include advice on exercise, smoking cessation, reducing weight and diet modification to include foods with less fat and simple insulin is added (Tong, Dong, Wu, Li, & Qin, 2011). Complications should be screened for and managed accordingly including hypercholesterolemia and hypertension (Kahn, Cooper, & Del Prato, 2014).   sugars. Drug treatment of diabetes include the use of oral hypoglycemic agents and if insulin needs increase then
Differences between type 1 and type 2 diabetes mellitus
The following are the major differences between the two main categories of diabetes (Walker & Colledge, 2013):

Type 1 diabetes mellitus

Type 2 diabetes mellitus

The pathology is due to complete insulin deficiency due to the destruction of pancreatic cells or defective secretion of insulin.

The pathology involved is relative insulin resistance in the periphery with inadequate insulin secretion in response.

It is not often associated with obesity but can occur in those who are overweight.

Obesity is a major risk factor for T2DM due to insulin resistance associated with it.

This type of diabetes cannot be controlled without insulin as they are deficient in insulin.

These patients can achieve diabetic control without medication initially and can use other medications such as oral agents. However, they too can need insulin in later stages of the disease.

Most cases are diagnosed in childhood

Most cases are diagnosed in middle adulthood or old age.

This is an autoimmune disease in which beta cells of the pancreas are a target.

There is no autoimmune reaction in this type of diabetes as the pathology is driven by insulin resistance.

Ketoacidosis is a hallmark of this disease either on the diagnosis or during no-compliance to medication.

No ketoacidosis occurs in type 2 diabetes and most common findings on diagnosis include hypercholesterolemia and hypertension.

Reasons for hyperglycemia on admission
The patient had been fasting since midnight. This means that she developed hyperglycemia of 22.9 mmol/L after a period of fasting. This can be attributed to two phenomena namely the dawn phenomenon and the Somogyi effect (Rybicka, Krysiak, & Okopie?, 2011).
The dawn phenomenon is a normal early morning rise in blood glucose which in type 2 diabetes, is exaggerated.  It occurs in up to 75% of those who have type 2 diabetes. This is thought to be due to the diurnal pulses in the secretion of secondary hormones just before waking up, such as cortisol, growth hormone, cortisol, glucagon, and adrenaline with growth hormones being the main culprit (Monnier, Colette, Dejager, & Owens, 2013). These hormones are counterregulatory to insulin and raise the blood sugar. In the non- diabetic individual, however, insulin is released to balance the blood sugar hence keeping the blood sugar levels within normal. In type 2 diabetes, impaired insulin secretion on the background of insulin resistance causes a persistent rise in blood sugars. This is compounded by fasting which causes the release of a large amount of glucose from the liver (Monnier, Colette, Dejager, & Owens, 2013).
The Somogyi effect is also termed reactive hyperglycemia and occurs in type 2 diabetes. It is due to overcompensation of hypoglycemia by a hyperglycemia. The hypoglycemic effects are not felt during the fast as the patient is asleep. These symptoms such as tremors and confusion go unnoticed. The body compensated by elevating blood sugars leading to a hyperglycemia in the morning (Rybicka, Krysiak, & Okopie?, 2011).
Clinical pharmacology
Melanie was on three medications, namely metformin, glipizide, and cortisone.
Metformin is an oral hypoglycemic agent used in the treatment of type 2 diabetes, belonging to the family of biguanides (Katzung, Masters, & Trevor, 2015). Its mechanism of action is thought to relate to the reduction of hepatic production of glucose by activation of an enzyme; AMP-activated protein kinase (AMPK). Other postulated mechanisms of action include impairing renal gluconeogenesis, slowing down the absorption of glucose from the gut, stimulation of tissue glycolysis and reducing plasma glucagon (Katzung, Masters, & Trevor, 2015). These actions all reduce circulating glucose and are not dependent on functioning beta cells of the pancreas. The most common side effects include nausea, vomiting, diarrhea, and anorexia. Other effects include a reduction in levels of vitamin B12 and persistent diarrhea (Katzung, Masters, & Trevor, 2015). Nursing consideration in those using this drug includes monitoring for side effects, patient education on use and making sure that the patient does not receive the drug in contraindication such as renal failure, liver disease, and allergy.
Glipizide is a second-generation sulfonylurea. It is an insulin secretagogue used in the management of type 2 diabetes mellitus. The mechanism of action is increasing insulin release from the pancreatic beta cells. Other mechanisms include reducing serum glucagon levels. Increase in insulin release is through binding to sulfonyl-urea receptor that is associated with a potassium channel. Binding of the drug leads to inhibition of potassium efflux causing depolarization that opens voltage-gated calcium channels and the release of preformed insulin (Katzung, Masters, & Trevor, 2015). It is contraindicated in those with liver disease due to its hepatic metabolism. Nursing considerations include checking for side effects and making sure contraindications are screened for. Routine measurement of blood glucose to assess the efficacy and appropriate dosing is also recommended.
 It is a glucocorticoid steroid drug used in the treatment of inflammatory conditions (Katzung, Masters, & Trevor, 2015). The mechanism of action is widespread and affects many cells including the effect on metabolic functions, catabolic effects, anti-inflammatory effects among others. The metabolic effects include a homeostatic effect on both insulin and glucagon hence having a net effect of raising blood sugar and stimulation of insulin release. They are anti-inflammatory effects by suppression of cytokine release and function of leukocytes (Katzung, Masters, & Trevor, 2015). This is particularly important since the patient had a baker’s cyst. Side effects are many and prolonged steroid use is not recommended. They affect all body cells. They include peptic ulcers, Cushing’s syndrome, muscle loss and impaired wound healing. Nursing considerations include monitoring for such adverse effects and limiting the use of the drug to short periods or low doses.   
Blood Glucose and HbA1c
Blood glucose levels are measured to ascertain the amount of circulating glucose, hence the homeostatic control of glucose (Kerner & Brückel, 2014). They are used in the diagnosis of Diabetes Mellitus. The normal range of blood glucose in an adult is random blood sugar of 3.2 to 7.8 mmol/L and fasting blood sugar of 3.2 to 6.1 mmol/L (Kerner & Brückel, 2014). The patient had a blood sugar of 22.9 mmol/L which shows a marked elevation after fasting since midnight. This is due to her type 2 diabetes that presents with insulin resistance and impaired secretion leading to hyperglycemia. On follow-up, it had reduced to 8.8 mmol/L due to the treatment she had been initiated on.
HbA1c is another measured parameter in glucose control. It is used to show glycemic control within the past 2 to 3 months (Nathan, McGee, Steffes, Lachin, & DCCT/EDIC research group, 2013). It is a form of glycated hemoglobin. Glucose binds hemoglobin in varying degrees with the normal percentage being 4 to 6%. However, in poorly controlled diabetes, the percentage of glycated hemoglobin increases due to the longer exposure to a hyperglycemic environment. Control of glucose level in diabetics reduces this exposure. The normal range for glycemic control is HbA1c of less than 7% (Nathan, McGee, Steffes, Lachin, & DCCT/EDIC research group, 2013). The patient on admission had a HbA1c level of 11% due to the poor glycemic control. However, this value reduced to 8% on follow-up after initiation of therapy. This still shows poor control as the normal should be below 7%.
Misleading Terms
The terms insulin dependent and early onset diabetes are commonly used to describe type 1 diabetes while non-insulin dependent or mature onset diabetes are used to describe type 2 diabetes mellitus. These terms are, however, very misleading. Although type 1 diabetes is often diagnosed in childhood, instances of it being found in adults are reported hence the term early onset is misleading. The same applies to the term mature onset for type two diabetes mellitus as some are diagnosed in younger patients (Walker & Colledge, 2013).
Type 2 diabetes mellitus is characterized by insulin resistance and impaired secretion and can be managed by diet alone, or with use of oral hypoglycemic drugs. This earned it the name non-insulin dependent. This is misleading as in the later stages of the disease impaired secretion is severe enough o cause beta cell dysfunction and atrophy with a progressive worsening of symptoms that cannot be treated by oral agents alone and insulin is needed (Walker & Colledge, 2013).
“Teach-back” method in patient education
The teach-back method is a patient education method used to evaluate teaching and comprehension. Also termed the “show me” method, the patient is taught and asked to demonstrate what was learned, if the patient can effectively teach the health professional what he was taught, it proves understanding and successful education (Tamura-Lis, 2013).
The patient is to be taught how to use a BGL machine. Most machines come with their own instruction manual for steps such as calibrating the machine. However, some steps are standard when using the machine. The patient should be familiarized with the equipment including the meter, test strips, and lancets. She is then shown how to power on the machine, insert the test strip, aseptically prick her finger, apply the blood drop to the strip and read the results. Also, maintenance of the machines is taught. The patient is then asked to teach the nurse what she has just learned to evaluate understanding. If any portions of her teach back are wrong, they are corrected and the process repeated until she can effectively teach back the correct procedure (Tamura-Lis, 2013).
DeFronzo, R. A., Ferrannini, E., Groop, L., Henry, R. R., Herman, W. H., Holst, J. J., … & Simonson, D. C. (2015). Type 2 diabetes mellitus. Nature reviews Disease primers, 1, 15019.
Inzucchi, S. E., & Sherwin, R. S. (2011). Type 2 diabetes mellitus. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier.
Kahn, S. E., Cooper, M. E., & Del Prato, S. (2014). Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present and future. Lancet, 383(9922), 1068–1083.
Katzung, B. G., Masters, S. B., & Trevor, A. J. (2015). Basic and Clinical Pharmacology (LANGE Basic Science). McGraw-Hill Education
Kerner, W., & Brückel, J. (2014). Definition, classification and diagnosis of diabetes mellitus. Experimental and Clinical Endocrinology & Diabetes, 122(07), 384-386.
Monnier, L., Colette, C., Dejager, S., & Owens, D. (2013). Magnitude of the dawn phenomenon and its impact on the overall glucose exposure in type 2 diabetes: is this of concern? Diabetes care, DC_122127.
Nathan, D. M., McGee, P., Steffes, M. W., Lachin, J. M., & DCCT/EDIC research group. (2013). Relationship of glycated albumin to blood glucose and glycated hemoglobin (HbA1C) values and to retinopathy, nephropathy and cardiovascular outcomes in the DCCT/EDIC study. Diabetes, DB_130782.
Rybicka, M., Krysiak, R., & Okopie?, B. (2011). The dawn phenomenon and the Somogyi effect—two phenomena of morning hyperglycaemia. Endokrynologia Polska, 62(3), 276-284.
Tamura-Lis, W. (2013). Teach-back for quality education and patient safety. Urologic Nursing, 33(6), 267.
Tong, X., Dong, J. Y., Wu, Z. W., Li, W., & Qin, L. Q. (2011). Dairy consumption and risk of type 2 diabetes mellitus: a meta-analysis of cohort studies. European journal of clinical nutrition, 65(9), 1027.
Walker, B. R., & Colledge, N. R. (2013). Davidson’s Principles and Practice of Medicine E-Book. Elsevier Health Sciences.

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