Diabetes Case Study: Epidemiology, Pathophysiology, and Management

This case study explores the epidemiology, pathophysiology, and management of type 2 diabetes, including risk factors, complications, and nursing care.

Running head: ASSIGNMENT 2
Diabetes case study
Name of the Student
Name of the University
Author Note

1ASSIGNMENT 2
Introduction- Diabetes mellitus is an umbrella term that refers to a group of metabolic
diseases. The condition primarily occurs when the pancreas do not produce adequate amount of
the hormone insulin, and/or the cells present in the body demonstrate a failure to respond
adequately to the insulin that has been produced (Ta, 2014). Type 2 diabetes mellitus (T2D) is
characterized by insulin resistance or a lack of insulin, and its common symptoms include
frequent urination, increased thirst, and unexplained loss in body weight. Other common signs
and symptoms also encompass tiredness, fatigue, increased hunger, and development of ulcer or
sores. This assignment will explain the epidemiology, pathophysiology, and management of type
2 diabetes.
Epidemiology- Epidemiology refers to the study of the determinants of health, and the
distribution of a particular disease in the population. According to reports from the World Health
Organisation (2016) an estimated for 22 million individuals live with diabetes mellitus on a
global scale. The prevalence of diabetes is thought to increase at a rapid rate with reports by the
International Diabetes Federation stating that roughly 381 million individuals were affected with
the metabolic syndrome in 2013 (Seclen et al., 2015). This number is expected to get doubled by
the year 2030. The prevalence of T2D accounts for more than 85-90% of all diseases, and high
rates of increase in the overall prevalence of the conditions can be accredited to a plethora of risk
factors, which commonly include being obese, or overweight, and increase longevity. Diabetes
mellitus has been found common all across the world. According to Guariguata et al. (2014) T2D
is more prevalent in developed countries, and largest increase in prevalence rates are observed in
middle and low income countries, including Africa and Asia, where the condition is expected to
affect most people within the next two decades. Risk factors that significantly contributed to the
high rates of incidence include urbanization, sedentary lifestyle, lack of physical activity, intake

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of food containing less nutrient and high energy, Western diet consumption, and low
socioeconomic status. According to estimates from the World Health Organisation the condition
resulted in death of almost 1.5 million people in 2012, thus being identified as the eight leading
contributor of death. In addition 2.2 million deaths that occurred all across the world were also
accredited to an increase blood glucose level, which in turn were associated with comorbidities
that increased the likelihood of the affected people to suffer from premature death (WHO, 2016).
Roughly 1 million adults in Australia that accounts for 5% of the entire population had
been diagnosed with diabetes in 2014-2015. The prevalence was found to be similar among
women and men, and rates of diabetes among females were less, in comparison to their male
counterparts who were aged 55 years and onwards (AIHW, 2016). The rates were also similar
across inner regional, outer regional, major cities, and remote areas. In addition, the condition
also affected more people belonging to lower socio-economic section of the society, in
comparison to the high socio economic group. Insulin treatment began for an estimated 164000
people having T2D in the year 2016, which was equal to roughly 61 cases/100000
population, thereby accounting for one individual among 1500 Australians (AIHW, 2018).
Furthermore, as much as 91% of insulin treatment associated T2D cases were found
among people aged beyond 40 years, with a steady increase in the rates in 80-84 year age group.
There were approximately 980,000 cases hospitalization for T2D in 2015-2016, with the rates
being 1.4 times fewer for females. Most adult individuals aged between 45-64 years have been
found more likely to acquire T2D (AIHW, 2018).
Pathophysiology- Impaired secretion of the insulin hormone encompasses a decrease in
responsiveness of glucose, which in turn is observed prior to the clinical onset of the metabolic

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syndrome. More specifically it can be suggested that impaired glucose tolerance often gets
induced by a lessening in the early-phase insulin secretion, which is glucose responsive, which in
turn is concomitant with a decrease in extra secretion of insulin, after consumption of meal that
results in postprandial hyperglycaemia. Conduction of an oral glucose tolerance test in such
cases provides an indication for over-response among people who demonstrate markedly high
amount of insulin resistance (Kahn, Cooper & Del Prato, 2014). Therefore, a decrease in
secretory response during early phase is an essential predictor of the disease and considered
imperative for the basic pathophysiological changes that occur when diabetes onsets in a person.
Impairment of insulin secretion is typically progressive and its progress involves lipotoxicity and
glucose-toxicity. Hence, the beta-cell dysfunction acts as a major factor across the broad
spectrum of prediabetes that eventually gives rise to the development of T2D.
According to Zaccardi et al. (2016) there exists a feedback loop in all human beings that
operates with the aim of ensuring maintenance of blood glucose level and integration of glucose
homeostasis. This feedback loop typically depends on cross talk between insulin sensitive tissues
that are located in the body and the beta-cells of the pancreas (Chevalier & Fénichel, 2015).
Insulin hormone that is released in relation to stimulation of the beta-cell often mediates uptake
of amino acids, glucose, and fatty acids by tissues, which are insulin sensitive, which in turn
feedback the information to islets of Langerhans, about the requirement for insulin. Under
circumstances that involve insulin resistance, which is commonly observed among people who
are overweight or obese, the insulin output is increased by the beta-cell, in order to maintain
optimal levels of glucose tolerance (Kautzky-Willer, Harreiter & Pacini, 2016).
Diminished function of the beta-cells is also recorded among people who are considered
to be at an increased risk of developing the metabolic syndrome, in addition to first degree

4ASSIGNMENT 2
relatives of individuals having T2D. Insulin resistance encompasses the condition where the
hormone insulin present in the body fails to exert an action, proportional to glucose
concentration present in the circulating bloodstream. This impairment of the action of insulin in
main target organs like the muscles and liver has been identified as a prevalent
pathophysiological characteristic of the condition. During progression from normal levels of
glucose to abnormal glucose tolerance, most often an increase is observed in the levels of
postprandial blood glucose (Møller et al., 2014). This eventually leads to the development of
fasting hyperglycaemia, which can be accredited to failure in hepatic gluconeogenesis.
Consumption of a diet that contains high amount of calorie, sedentary lifestyle, physical
inactivity, and administration of steroids often brings about induction of insulin resistance that
subsequently increases the levels of glucagon hormone, and also leads to an elevation of the
levels of glucose dependent insulinotropic polypeptide (GIP), which are a common feature of
glucose tolerance (Christensen et al., 2014). However, it has also been found that during insulin
resistance the response of postprandial glucagon-like peptide 1 remains unaltered. The
pathophysiology of the condition also involves several genomic factors such as, single nucleotide
polymorphism (SNP), which increases the risk for the metabolic syndrome. Some of the most
potent SNPs that are associated with T2D include FSADS1, PPARG, TCF7L2, and KNJ11.
While FSADS1 found to bring about an alteration in the metabolism of unsaturated fatty acids,
TCF7L2 reduces the beta cell responsiveness does leading to impairment in insulin processing
and lowering insulin secretion (Xia et al., 2016).
Management and nursing care- The primary goal of diabetes management in the patient
should focus on restoration of carbohydrate metabolism to normal levels. Other objectives of the
management would focus on providing treatment for preventing the onset of complications,

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which can result from the metabolic syndrome (Garber et al., 2016). Relying on personal
perceptions based on symptoms of hypoglycaemia or hyperglycaemia is often considered
unsatisfactory, taking into consideration the fact that mild or moderate hyperglycaemia does not
bring about the manifestation of any obvious symptoms in the patients. Control of T2D can be
effectively improved by encouraging the patience to use home based glucose metres that will
help in keeping a regular check on the blood glucose level. Regular self-monitoring of the blood
glucose level will prove beneficial in in keeping a check on the amount of blood sugar, thereby
lowering the chances of long term complications.
Following consultation with physician, the patient must be provide access to a blood
monitoring device that she feels comfortable to use by self. Self-testing will form an essential
part of management, since it will provide the patient adequate information about the direction
and speed of glucose alterations (Young et al., 2017). In addition to self-monitoring of the blood
glucose level, the patient must also undergo HbA1c level measurement in the laboratory, after an
interval of three months that will help in providing an overview of the average diabetic control,
over a prolonged duration. Several categories of anti-diabetic medications have gained attention
in recent years, owing to their efficacy in controlling blood glucose levels. The patient will be
administered metformin that has been recognised as the mainstay treatment for T2D based on its
effectiveness in reducing mortality. According to Pernicova and Korbonits (2014) metformin
will inhibit mitochondrial respiratory (complex I), besides activating AMP-activated protein
kinase (AMPK) and inhibiting cyclic adenosine monophosphate (cAMP). In addition to the oral
medication the patient will also be subjected to insulin injections that will facilitate keeping a
control over the levels of glucose in the bloodstream.

6ASSIGNMENT 2
There is mounting evidence for the fact that an increase in exercise levels proves
effective in yielding better management of blood glucose (Kurdiova et al., 2014). Exercise based
lifestyle modification reduces fat content in the body and subsequently lowers the levels of blood
lipid. In addition, moderate aerobic exercise will also prove beneficial in lowering the levels of
HbA1c, thus resulting in an improvement in insulin sensitivity. The patient will also be asked to
participate in resistance based training, under the guidance of the physiotherapy, and a
combination of moderate exercise along with this training regimen will prove most effective in
treating the condition (Colberg et al., 2016).
Adherence to a diabetic diet that promotes a loss in body weight is imperative in this case
scenario (Asif, 2014). Based on evidences, the patient will be recommended to follow a diet that
contains a low carbohydrate content. Incorporating food items in the diet that are a rich source of
fibres and reducing the consumption of sugar (Feinman et al., 2015). In addition, owing to the
fact that vegetarian diets have been associated with a reduction in risk for T2D, the patient will
be advised to consume moderate quantity of animal products (Evert et al., 2014). Another
important management strategy for diabetes would also encompass providing culturally
appropriate education to the patient.
According to Coppola et al. (2016) poor knowledge and awareness among patients about
chronic health disorders often increases their susceptibility to the conditions, and also makes it
difficult from them to recuperate from the illnesses. Hence, patient education will involve
providing a sound understanding of the risk factors that increase the likelihood of suffering from
T2D (Powers et al., 2017). In addition, the patient will also be advised to refrain from smoking
that damages the kidneys and the heart, while raising the levels of glucose in the blood.
Furthermore, patient education would also encompass advising the patient to show compliance to

7ASSIGNMENT 2
the prescribed medications, and recommending them to immediately seek assistance from
healthcare providers if unpleasant side effects.
Some common complications and comorbidities that are associated with T2D include
cardiovascular complications, cognitive dysfunction, and vascular dementia. Cardiovascular
diseases that are thought to be at an increased risk due to T2D are namely, stroke and ischemic
heart disease. In addition, acute complications most often encompass hyperglycaemia,
hypoglycaemia, nonketotic hyperosmolar coma and diabetic coma (Gregg et al., 2014).
Furthermore, according to Gregg, Sattar and Ali (2016) immune dysfunction also gets
manifested as autoimmune disease and/or poor immune response that becomes difficult to
manage. Microangiopathy also creates an impact on the vital organs like eyes, kidneys, lungs,
and feet. In addition, diabetic foot ulcer and retinopathy are common complications that lead to a
deterioration of the health symptoms (Hirsch, 2015).
Conclusion- To conclude, T2D primarily occurs due to insufficient production of the
hormone insulin from the Beta cells located in the islets of Langerhans in pancreas. In other
words the condition is characterized by combination of inadequate insulin secretion and
peripheral insulin resistance. When left untreated the symptoms of in bringing about a decrease
in the beta cell mass of the pancreas and progression of this impairment creates a substantial
impact on the long term regulation of blood glucose level. Medication administration, lifestyle
modifications and patient education will also form an essential part of diabetes management care
plan.

8ASSIGNMENT 2
References
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