Pathophysiology of Type II Diabetes

Running head: TYPE II DIABETES 1
TYPE II DIABETES
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Introduction
The paper will focus on the case scenario of Bill McDonald who is 58 years old with
Type II diabetes. Bill has a history of smoking and heavy consumption of alcohol for 35
years but he stopped a year ago following the diagnosis. His mother passed at the age of 65
years due to heart failure and diabetes. Bill also has a sedentary life. With regard to Bill’s
case scenario, the paper will comprehensively discuss the pathophysiology of Type II
diabetes in relation to the manifestations experienced by Bill. Secondly, the paper will
analyse the potential approaches of management including medical and nursing strategies for
a patient who is hypertensive diabetic. Lastly, the essay will provide an education plan for the
patient.
Pathophysiology of Type II Diabetes
Type II diabetes is one of the chronic medical conditions affecting the process of
sugar (Glucose) metabolism in the body, which is an essential energy sources in the body. Its
common symptoms include frequent thirst and urination, unintended loss of weight, slow-
healing wounds and sores, frequent infections, and development of darkened skin areas such
as the neck or the armpits. Some of its risk factors include obesity, prediabetes, overweight,
physical inactivity, sedentary lifestyle, age of above 45 years, family history of diabetes,
prediabetes, gestational diabetes, and smoking (Baynes, 2015).
High dietary intake of fat and physical inactivity results in obesity which increases
insulin resistance while genetic factors decreases insulin secretion. Consequently, these two
mechanism results in relative insufficiency of the action of insulin thus leading to Type 2
diabetes. Other factors which contribute to the increase of visceral fat include excessive
intake of sugars, smoking, heavy consumption of alcohol, aging, genetic factors, and lowered
energy consumption following lack of exercise. The two major pathophysiological

TYPE II DIABETES 3
mechanisms that lead to type II diabetes are insulin resistance and impaired secretion of
insulin (DeFronzo, Eldor, & Abdul-Ghani, 2013).
Impaired insulin secretion is the reduction in the responsiveness of glucose which
induces Impaired Glucose Tolerance (IGT). Impaired secretion of glucose results in lipo-
toxicity and glucose toxicity which decreases the pancreatic beta cell mass. In the early stages
of the onset of the disease, the patient presents with increased postprandial level of blood
glucose secondary to the increased resistance of the insulin hormone (Paneni, Beckman,
Creager, & Cosentino, 2013). The increased deterioration of the pancreatic beta cell function
results in uncontrollable and permanent rise of the blood glucose. According to the case
study, Bill’s latest HbA1c is 7.2 % which is an indication of significant elevation of his blood
glucose. Additionally, his range of Fasting glucose of 4.5 to 7.0 mmol/L is an indication
diabetes (Lewis, Collier, & Heitkemper, 2017).
In the insulin resistance, the insulin secreted by the body does not provide adequate
action compared to the concentration of blood glucose. Failure of the insulin hormone to
regulate the sugar levels in the blood results in Type II diabetes. Elevated blood glucose
levels result in the damage of blood vessels resulting in complications such as heart disease,
hypertension, atherosclerosis, stroke, eye damage, neuropathy, hearing impairment, kidney
damage, slow healing of cuts, wounds, and blisters, sleep apnea, and skin conditions (Hinkle
& Cheever, 2013).
The elevated levels of blood sugar causes damage to the vessels supplying blood to
the kidney thus impairing its ability to purify the blood properly. This may also result in
kidney failure. Impaired functioning of the kidney results in increased retention of more salt
and water resulting in fluid imbalance which is evidenced by the presence of peripheral
edema, ankle swelling, and weight gain (Ozougwu, Obimba, Belonwu, & Unakalamba,