Type II Diabetes Mellitus

This article provides an overview of Type II Diabetes Mellitus, including its epidemiology, pathophysiology, and management. It discusses the prevalence, complications, and treatment options for this chronic condition.

Running head: TYPE II DIABETES MELLITUS 1
Type II Diabetes Mellitus
Name
Institutional Affiliation.

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Introduction
Type 2 diabetes mellitus is a life-long ailment that alters the normal blood sugar metabolic
processes in a human body. The condition is characterized by relatively low levels of insulin or
resistance to insulin and consequently leading to high blood glucose (Goldstein & Mueller-
Wieland, 2013). This writing will, therefore, focus on the epidemiology of the disease; the most
common onset age, incidence, prevalence, complications in the long term, mortality as well as
morbidity in Australia. The pathophysiology of the disease will also be focused on. This
inscription will also focus on the management practices for the disease, medications used for
remedy, the frequency of conducting self-tests, diet, exercise and monitoring practices most
applicable for individuals with the condition. Complications that could emanate from poorly
controlled levels of blood sugar are to be discussed in the last section of the paper.
Epidemiology.
Based on data recorded in 2014–2015, an estimate of one million Australian adults had type II
diabetes mellitus. This number represented 5% of the total Australian adults (AIHW, 2018). This
data emanated from ABS 2014–15 National Health Survey according to self-reported incidences.
Out of the total male population, 6% had type II diabetes while 5% of female had the disease.
From the age of 55 years onwards, the rates were higher among females than males. The regional
proportions were relatively similar with the percentages being 5% in major cities, 6% in inner
regions and 6% in the outer regional and remote locations (AIHW, 2018). Based on
socioeconomic categories, the prevalence in the lowest socio-economic group was 8% with a 3%
recording in the highest socioeconomic group. It is, however, worth noting that underestimation
of type II diabetes prevalence is likely to occur when data is collected from self-reported cases.
This is mainly because participants may not accurately report or may not completely know their

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diabetes status. Additionally, the unreported state of many cases is another barrier to data
accuracy.
Further information from the national diabetes register (NDR) reveals the rate if insulin use
among type II diabetes patients. The register has it that approximately 16,400 type II diabetes
patients commenced insulin intake in 2016. This proportion equates to around 1 insulin user
among 1,500 Australians (AIHW, 2018). The incidents for type II diabetes treated with insulin
were 1.5 times higher among males in comparison to females. Categorizing by age, it was noted
that patients aged 40 years and above accounted for 91% of insulin-treated diabetes type 2. A
direct proportional steady increase of the rates to age in noted to a climax number of 240 insulin
takers among 100,000 Australians as at the age of 80-84. The rate at this old age is the highest
with it being sighted to double the rate among 50-54 years old patients and eight times higher the
rate of patients at 30-34 years old category (AIHW, 2018). In cases where diabetes was the
underlying cause of death, 55% of the deaths were as a result of type II diabetes mellitus
(Australian Institute of Health and Welfare, 2018).
There are several long-term complications emanating from type II diabetes and are categorized
as micro-vascular and macro-vascular complications. Micro-vascular complications affect the
nerves, kidneys, and eyes (Becker, 2015). Prolonged out of range glucose levels cause
retinopathy and cataracts in eyes, kidney failure, and diabetic neuropathy. Kidney failure is a
situation where the kidneys are unable to properly clean the blood as they are required to and
thus necessitating medical intervention. Macro-vascular complications, on the other hand, affect
the blood vessels, the brain, and the heart. The disease is known to cause plaque build-up in large
blood vessels and eventually lead to stroke, heart attack, or peripheral vascular disease (PVD) if
left unmanaged (Chatham, Forder, & McNeill, 2012).

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Pathophysiology.
The pathophysiology of type is more attributed to insulin resistance as well as impaired secretion
of insulin. Lowered responsiveness to glucose is the basic meaning of impaired insulin secretion
and notable before the clinical onset of type II diabetes (Wass & Stewart, 2011). Lowered
glucose response in the early phase of insulin secretion induces impaired glucose tolerance
(IGT).in addition, after-meal reduced insulin secretion results in postprandial hyperglycemia.
Generally, impaired glucose secretion is progressive with continued impairment involving lipo-
toxicity as well as glucose toxicity. A series of laboratory experiments have revealed that when
left untreated, the aforementioned conditions trigger a decrease in pancreatic beta cells. As a
result, long-term blood glucose control is affected by the aforementioned impairment of
pancreatic beta cells progression (DeFronzo, et al., 2015). Although an increase in postprandial
blood glucose is mainly sighted in patients after the onset of the disease, progressive
deterioration of pancreatic beta cell functioning consequently results in the permanent raising of
blood sugar. The former is predominantly caused by reduced early-phase insulin secretion as
well as amplified resistance to insulin.
The response of insulin is initiated depending on the coupling of glucose and trans-membranous
transport of glucose to the glucose sensors. An increase in glucokinase is then induced by the
glucose sensor complex leading to stabilization of the protein and consequently impairing its
degradation (Holt, Cockram, Flyvbjerg, & Goldstein, 2017). Glucokinase induction is the first
step linking the apparatus responsible for the secretion of insulin with the intermediary secretion.
Type II diabetes patients present significantly reduced Glucose transport inβ –cells. As a result,
the control point for insulin secretion is shifted from glucokinase to the actual glucose transport
system. As the disease progresses, the release of newly synthesized insulin in the second phase is

TYPE II DIABETES MELLITUS 5
impaired. In some patients, however, partial reversal of this impairment is possible by reversing
imparting strict glycemic control. This impairment, commonly known as desensitization, occurs
when insulin is released and as a result, glucose is paradoxically inhibited (Rubin, Strayer, &
Rubin, 2011). This occurrence is directly attributable to sustained hyperglycemia which is caused
by an accumulation of glycogen within the β-cell.
Other defects in the functionality of β-cell in type II diabetes mellitus patients include lowered
conversion of proinsulin to insulin and asynchronous release of insulin. In the first phase of
insulin secretion, an impairment in many cases serves as the marker for type II diabetes among
family members of individuals previously suffering the condition (Sheehan & Ulchaker, 2011).
The pathogenesis of type II diabetes is also largely attributable to insulin resistance. This is a
condition where sufficient action is not exerted by insulin in proportion to its concentration and
the concentration of glucose in the blood (Wiernsperger, Bouskela, & Kraemer-Aguiar, 2010).
Insulin resistance occurs in key target organs such as the muscles and the liver. Its development
and expansion occur before the onset of the disease. A clarification on the interrelation between
insulin resistance and environmental factors (free fatty acids, hyperglycemia, and mechanisms of
inflammation) as well as genetic factors has been brought forth by deep investigations into the
molecular mechanisms of insulin action. There are various genetic factors such as
polymorphisms of thrifty genes e.g. the β3 adrenergic receptor gene which is associated with
visceral obesity and thus promoting resistance to insulin (Lopez-Garcia & Perez-Gonzalez,
2012). Additionally, insulin receptor substrate (IRS)-1 gene polymorphisms and insulin receptors
are known to have a direct effect on insulin signals.
Recently, scientists have put more emphasis on trying to clarify how adipocyte-derived bioactive
substances, also known as adipokines are involved in insulin resistance. As such, it has been

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established that free fatty acids, resistin, TNF- Alpha as well as adiponectin modes' of action
improve resistance. Additionally, a series of clinical tests such as steady-state plasma glucose
(SSPG), homeostasis model assessment for insulin resistance (HOMA-IR), minimal model
analysis, and the insulin sensitivity test have been developed to facilitate in the extent of insulin
resistance (Wiernsperger, Bouskela, & Kraemer-Aguiar, 2010).
Management.
Self-testing and monitoring is an essential part of type II diabetes mellitus treatment. For patients
who are already under insulin treatment, a doctor will recommend the number of times to test in
a day depending on the amount and type of insulin that the patient is using (Joshi, 2015). For
patients taking multiple daily injections, it is more recommendable to test at bedtime and before
meals. For patients taking long-acting insulin, it may be necessary to test only twice per day, that
is at dinner and before breakfast (Thompson, 2010). For patients whose mode of type II diabetes
management is through exercise and diet alone, it may not be necessary to conduct self-tests on a
daily basis. Doctors usually set a blood sugar target range based on several factors (Joshi, 2015).
Such factors include; age, duration of the disease, severity of the disease, presence of diabetes
complications, pregnancy status and presence of other medical complications as well as the
general health of the individual.
Since type II diabetes emanates from difficulties in getting sufficient glucose to the cells and its
subsequent accumulation in the blood, a diet plan for type II diabetes patients should consist of
foods with low sugar content (Oberg, Stoppler, & Cunha, 2018). Such foods include complex
and high fiber carbohydrates and proteins including but not limited to whole wheat, oatmeal,
quinoa, brown rice, vegetables, lentils, and fruits. Foods with low glycemic index are a good
choice for people with type II diabetes as they only cause a modest upsurge in blood sugar. It is

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worth noting that long-term complications of type 2 diabetes can be effectively prevented
through proper glycemic control.
For type II diabetes patients, exercise is another crucial component to include in their treatment
plan. Patients who are physically active and maintain fitness have a higher ability to control their
diabetes by maintaining the correct range of their blood glucose (Leontis, 2019). Subsequently,
such individuals are able to prevent long-term diabetes complications. For individuals with low
insulin production, exercise causes the muscles to use glucose even in the absence of insulin. On
the other hand, exercise increases the effectiveness of insulin by reducing its resistance and
consequently increasing the intake of glucose in the muscles and other body cells among
individuals with insulin resistance.
Increased risk of fungal and bacterial skin diseases come hand in hand with type II diabetes that
is highly controlled (Becker, 2015). Additionally, poor control of the disease increases the
chances of acquiring eruptive Xanthomatosis, another lethal skin condition related to type II
diabetes. Some of the key skin complications that may arise out of poor diabetes control are;
pain, discoloration or redness, itchiness, boils, rashes, blisters, raised patches that could be shiny
or scaly, inflammation of the hair follicles, styes on eyelids, pea-sized bumps that are firm and
yellow in color, and a thick waxy skin (Holt, Cockram, Flyvbjerg, & Goldstein, 2017).
There are also a number of skin conditions that may develop when type II diabetes is poorly
controlled (Sheehan & Ulchaker, 2011). First is glaucoma whose occurrence is initiated by
building up of pressure in the eyes. Cataracts, on the other hand, are caused by cloudiness in the
eye lens. The last condition is retinopathy, an impairment that follows damage of blood vessels
at the back of the eye. The aforementioned conditions are known to cause loss of vision but their
timely diagnosis and treatment can help maintain eyesight.

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Nerve damage, also referred to as diabetic neuropathy is another condition attributable to poor
type II diabetes control. There are two main types of neuropathy; peripheral neuropathy, known
for slowing healing of sores and increasing/decreasing sensitivity, and autonomic neuropathy
(Wass & Stewart, 2011). Generally, the risk of suffering from stroke and heart disease is high
among individuals with type II diabetes. However, uncontrolled state of the disease elevates the
risks greatly. This is because, with time, the cardiovascular system is gradually damaged by high
blood sugar. The most common signs of stroke are confusion, lack of coordination and balance
and weakness or numbness on one side of the body. Dizziness, chest discomfort or pressure, and
sweating are observable signs of a heart attack. Lastly, kidney disease may also be caused by
poorly controlled diabetes (Goldstein & Mueller-Wieland, 2013). It is characterized by loss of
appetite, fluid buildup in the kidneys, weakness and poor concentration.
Conclusion.
In conclusion, this paper has clearly outlined the epidemiology of the disease; the most common
onset age, incidence, prevalence, complications in the long term, mortality as well as morbidity
in Australia. It has also focused on how the disease alters the normal functioning of the body.
Also documented are the management practices for the disease, medications used for remedy, the
frequency of conducting self-tests and monitoring, diet, exercise practices most applicable for
individuals with the condition. The paper has concluded with the most common complications
that arise from poorly controlled type II diabetes mellitus.

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