Diabetes mellitus

Can use dot points, headings, tables and diagram where appropriate.

Case Scenario

Diabetes mellitus causes significant impairment in personnel function, emotional and
physical health and economic functioning of the individual. Management of diabetes mellitus
requires specific management approaches appropriate (Wong, Constantino, & Yue, 2015. The
following essay is a discussion of Melanie, a patient who presents with diabetes mellitus type 2.
The discussion is broken into various parts.
Part 1 questions
Risk factors of T2DM are; an age of above 45 years, the family history of T2DM and body
weight exceeding 120% of the desired body weight. Melanie Johnson is aged 63 years. Melanie’s
mother and sister have been diagnosed with T2DM. Genetic factors account for about 10% of the
heritability of diabetes type 2.Genetics play a role both in the impaired production of insulin and
peripheral insulin resistance at the cellular level. Transcription factor 7–like 2 is the most
common genetically inhered factor responsible for the development of T2DM. The patient’s
Body Mass Index is 36.73. Studies have found an association between obesity, overweight,


hypertension and high low-density lipid profile and the risk of T2DM. Socioeconomic status has
also been linked to BMI and thus the risk of T2DM. Generally, the people from low socio-
economic class eat foods that are glucose and fat intensive. Foods that are not nutrient intensive
are universally cheap and therefore affordable to individuals of low social, economic class.
Further, people from low socio-economic class cannot access health care services that available
for the prevention of T2DM and associated complications (Mendham, Duffield, Marino, &
Coutts, 2015). In the pathogenesis of T2DM, insulin resistance is characteristic. In normal
physiology of blood sugar regulation, insulin reduces the blood glucose levels by increasing
permeability and thus entry of glucose into the cells. Fat accumulation and presence of cytokines
in the blood reduce the sensitivity of insulin receptors on the surface of cells to insulin hormone.
Peripheral insulin resistance leads to the reduced entry of glucose into cells.
Further, increased fat breakdown to glucose in T2DM increases the level of blood glucose.
Besides, the imbalance between glucagon-secreting cells and the insulin-secreting cells
contributes to the pathogenesis of diabetes type 2. In other words, the amount and rate of
glucagon exceed the rate of insulin secretion. Combinations of impaired insulin production and
insulin resistance at the cellular level contribute to the pathogenesis of diabetes type 2. Correctly,
the low insulin secretion in the presence of insulin resistance at cellular levels renders body
system unable to reduce sufficient production insulin to reduce the high level of insulin in the
body (Ding, Chong, Jalaludin, Comino, & Bauman, 2015).
One of the complications of ofT2DM is cardiovascular complications. Specific
cardiovascular complications include hypertension, thrombotic abnormalities and accumulation
of lipids in smooth muscles and around adipose tissue and other organs. Diabetes type2 patient is
at risk of developing cardiovascular complications due to the presence of low-density lipids, high


concentrations of high-density lipids and increased levels of triglycerides. The decline in
cognitive functioning is another complication of diabetes type 2.Imaging studies among people
with diabetes typically have shown cerebrovascular lesions in the brain. Brain imaging in T2DM
has indicated a reduction in the size of temporal, frontal and hippocampus portions of the brain.
The clinical manifestation of decline in judgment, making, and concentrating, memory typical
for Alzheimer’s Disease are observed; as a result brain morphological changes in prolonged
T2DM among elderly individuals aged 60 years and above.
The high levels of the T2DM treatment include the elimination of risk factors,
symptomatic control, and prevention of complications. Prevention of complications involves the
control of blood pressure at 140/90 mmHg and less, performing physical activities to maintain
BMI within the desired range, and dietary modifications to increase nutrient fast foods. The
control of symptoms includes maintaining the glycosylated hemoglobin below 6% and the level
of blood glucose below 7.0 mmol/Litre. Symptomatic control of the glycemic levels in T2DM is
achieved through pharmacological interventions to lower blood glucose (Willer, Harreiter, &
Pacini, 2016).
The onset of T2DM occurs among adults whereas T1DM occurs during childhood and at
puberty. The onset of T2DM has been found to start at 30 years of age and above. However,
T2DM has shown the onset in childhood as well. T2DM is associated with overweight and
obesity whereas T1DM is not associated with obesity. Increase in body fat content causes insulin
resistance that causes T2DM. T1DM is caused by insufficient insulin while T2DM caused by
lack of insulin sensitivity on the surface of cells. T2DM progression is slow and takes years to
manifest whereasT1DM onset is rapid and acute and take weeks to manifest with symptoms.
T2DM prevalence is high and ranges from 90 to 95 % whereas the prevalence of T1DM is low


and ranges 5 to 10% of diabetic cases. T1DM is diagnosed by presenting symptoms of
polyphagia, polydipsia, and polyuria while T1DM is diagnosed based on the blood glucose and
glycosylated hemoglobin in the body (Wong, Constantino, & Yue, 2015).
One of the reasons for the raised Blood Glucose level is the reduction of sensitivity of
insulin receptors. Under the normal physiology of blood glucose control, insulin binds to the
receptors on the surface of the cell. Binding of insulin molecules to the receptors on the cell
surface initiates chemical reactions in the cells and opens up channels through which glucose
molecules into the cell is facilitated. In cases where the patient presents with T2DM, insulin
receptors on the surface of cells are not sensitive to insulin produced. Therefore, the presence of
insulin does not result in a reduction in blood glucose levels. Secondly, impairment in a
production of insulin is by insulin-secreting cells of the pancreas results in increased blood
glucose levels in the case of Melanie. In type 2 diabetes mellitus, the combination of insulin
insensitivity and impaired glucose production by the pancreas is responsible for the
manifestation of symptoms. In the presence of glucose resistance at the level of the cells, the
body does not have an effective mechanism to regulate blood glucose levels. The impaired
secretion of glucose implies that there is not enough insulin concentration to reduce levels of
blood glucose (Inzucchi, Bergenstal, Buse, Diamant, Ferrannini, Nauck, & Matthews, 2015).
Part 2 Questions
Kenacort-A 40 is a corticosteroid. The drug produces its physiological effects by
inhibiting immigration of leucocytes and fibroblasts from their site of production to the site of
inflammation. The drug reverses increased permeability of capillary walls to water and other
molecules during the process of inflammatory body response. Side effects of Kenacort-A 40
include sinusitis, the formation of mobile blood clot, the increase of blood pressure, a collapse of


circulatory systems, enlargement of the heart muscle, and interference with the hypothalamus-
pituitary-adrenal hormonal axis. Kenacort-A 40 causes delayed wound healing and increased
intracranial pressure. Treatment with Kenacort-A 40 requires several and specific nursing
To begin with, patients should be assessed for hypersensitivity to corticosteroids. Part of
history taking should include sensitivity to corticosteroid since the drug should not be
administered to a patient who is hypersensitive to the medication (Cheng, Zamir, Dunlop,
Stawell, Hall, Symons, & Lim, 2015). Metformin reduces blood glucose levels through
inhibition of glucose production by the liver. Metformin reduces glucose absorption in the
intestines after digestion of carbohydrates. Metformin increases the entry of glucose into body
cells and subsequent utilization, therefore, reducing peripheral resistance to insulin. Metformin
side effects include diarrhea, nausea, vomiting, gastric discomfort and indigestion (Zinman,
Wanner, Lachin, Fitchett, Bluhmki, Hantel, & Broedl, 2015). Metformin is known to cause lactic
acid metabolic acidosis. As a result of the physiological effects of the drug, the body’ metabolic
reactions produce lactic acid, which reduces the blood pH to acid levels. Therefore, nursing
management for a patient on metformin such as Melanie should be monitored for symptoms
associated with metabolic acidosis such as hypotension and hypothermia. Also, metformin is
known to cause renal impairment. Patients on treatment with metformin should be monitored for
impaired renal functioning through fluid input and output. Glipizide is a drug that increases
production of insulin and sensitivity of the hormone on cells. Specifically, glipizide increases
secretion of insulin hormone from the pancreatic beta cells.
Additionally, glipizide inhibits the production of glucose from glycogen stored in the
hepatic cell. The side effects associated with glipizide are; abdominal pain, constipating,


diarrhea, flatulence, dermatological reactions, hypoglycemia, erythema, nervousness, depression,
anxiety, and drowsiness. Nursing management includes assessment for risk of developing
hypoglycemia. Hypoglycemia is one of the side effects associated with the drug (Del Prato,
Camisasca, Wilson, & Fleck, 2014). Therefore, nurses managing a patient on glipizide should
observe for a factor that can trigger hypoglycemia such excessively heavy physical activities that
require metabolism of large amounts of stored glucose.
Additionally, patients on glipizide should be assessed for a random blood glucose level
before the administration of the drug. Through collaborative teamwork, nurses should ensure,
glipizide has received adequate instructions on the performance of physical activities and
nutrition. Generally, nutrient and physical activities are part of the self-care management
approaches for diabetes patients. The patient should recover education on the appropriate food
nutrients should be included in their diet as a way of maintaining blood glucose levels, within the
normal ranges (Newman, 2014).
The two tests that Melanie underwent are blood glucose level tests and hemoglobin 1Ac
testing (Hb1Ac). BGL is a measure of the amount of glucose contained per volume unit of blood.
Hb1Ac is the measure of the fraction of blood sugar that is bound to the hemoglobin molecule. In
other words, Hb1Ac is the amount BGL that is available across the lifespan of red blood level,
which is 120 days. The two tests, therefore, measure the fraction of the blood glucose level that
is in circulation and available for metabolism and the excess that causes symptoms of type 2
diabetes mellitus. Before the surgery, Melanie had been fasting. Therefore, the blood glucose
levels reduced below the normal ranges and reduction was further exacerbated by anti-diabetic
drugs. The body has a feedback mechanism when the level of blood glucose reduces or increases
beyond the normal ranges. In Melanie’s case, the body responded to the reduced blood glucose


level by an increase in the secretion of glucagon. Glucagon hormone increases the level of blood
glucose by increasing the breaking down of glycogen. Glycogen also stimulates the conversion
of amino acids into glucose. In Melanie’s case, the glucagon inhibited the secretion of insulin
that could reduce blood glucose levels further. As a result, the blood glucose level increased to
22.9 mmol/L and HbA1c: 110% respectively. However, after surgery, with regular dietary intake
and prescribed anti-diabetic drugs, the patient BGL and Hb1Ac returned to BGL 8.8 mmol/L and
Hba1c: 8% respectively (d’Emden, Shaw, Jones, & Cheung, 2015).
Part 3 Questions
Symptoms are manifested by lack of insulin in insulin-dependent diabetes. However,
Melanie, the patient in the case scenario, present with T2DM. Noninsulin-dependent diabetes
implies that the diabetes symptoms are manifesting as a result of insulin resistance or to another
factor, but insulin is available in sufficient concentrations and amounts in the blood circulation.
Early onset of diabetes type 2 is caused by insulin resistance that occurs before or at the age of
19 years old. However, Melanie is 63 years of age.
Teach-back is a method used to evaluate the effectiveness of patient education offered
during clinical visits. The patient is asked to describe what they need to do as part of self-care
about specific conditions. The nurse asks the patient questions based on the education given the
patient during prior clinical visits. In a study to assess the effectiveness of teach back” method
for the patient education method, the patient’s level of knowledge was assessed before and after
the method had been applied. The study results indicated a strong correlation between the teach
back” method for the patient education and ability to remember details about clinical self-care
education on a condition. I would teach Melanie on the producer of assembling the requirement
for BGL testing, the disinfection of pricking site, switching the BGL machine, pricking and the


collection of the capillary blood sample into the BGL strip and inserting the strip into the BGL
machine and on normal ranges of BGL. In order to evaluate the effectiveness of the instructions
given, I will ask the patient to describe the procedure of testing blood glucose levels using BGL
machine. I will identify the need for reminding the patients on certain aspects of the procedure.
After that, I will repeat the aspects the patients cannot describe. I would use demonstration charts
and handouts.
In conclusion, Melanie, in the case scenario, presents with T2DM. The patient needs
general preventive, symptomatic and complications management. The pharmacological
management is appropriate and requires particular nursing consideration. BGL and Hb1Ac are
critical parameters for use in measuring the levels of blood glucose and the severity of the
condition. According to literature, the teach-back method is appropriate to ensure that Melanie is
capable of effectively using BGL in self-monitoring of body glucose.



Cheng, N. M., Zamir, E., Dunlop, A., Stawell, R., Hall, A. J., Symons, R. C. A., … & Lim, L. L.
(2015). Intravitreal triamcinolone: Efficacy and complications of different methods of
drug delivery. Investigative Ophthalmology & Visual Science, 56(7), 1286-1286.
d’Emden, M. C., Shaw, J. E., Jones, G. R., & Cheung, N. W. (2015). Guidance concerning the
use of glycated haemoglobin (HbA1c) for the diagnosis of diabetes mellitus. The
Medical Journal of Australia, 203(2), 89-90.
Del Prato, S., Camisasca, R., Wilson, C., & Fleck, P. (2014). Durability of the efficacy and
safety of alogliptin compared with glipizide in type 2 diabetes mellitus: a 2‐year study.
Diabetes, Obesity and Metabolism, 16(12), 1239-1246.
Ding, D., Chong, S., Jalaludin, B., Comino, E., & Bauman, A. E. (2015). Risk factors of incident
type 2-diabetes mellitus over a 3-year follow-up: Results from a large Australian sample.
Diabetes research and clinical practice, 108(2), 306-315.


Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., … &
Matthews, D. R. (2015). Management of hyperglycemia in type 2 diabetes, 2015:
Diabetes care, 38(1), 140-149.
Kautzky-Willer, A., Harreiter, J., & Pacini, G. (2016). Sex and gender differences in risk,
pathophysiology, and complications of type 2 diabetes mellitus. Endocrine reviews,
37(3), 278-316.
Mendham, A. E., Duffield, R., Marino, F., & Coutts, A. J. (2015). A 12-week sports-based
exercise programme for inactive Indigenous Australian men improved clinical risk
factors associated with type 2 diabetes mellitus. Journal of science and medicine in
sport, 18(4), 438-443.
Newman, R. (2014). General practice management of type 2 diabetes–2014–15. Melbourne, VIC,
Australia: The Royal Australian College of General Practitioners and Diabetes
Wong, J., Constantino, M., & Yue, D. K. (2015). Morbidity and mortality in young-onset type 2
diabetes in comparison to type 1 diabetes: where are we now?. Current diabetes reports,
15(1), 566.
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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