Type 2 Diabetes Assignment

Running head: TYPE 2 DIABETES ASSIGNMENT 1
Type 2 Diabetes Assignment
Student’s Name
Institutional Affiliation

Running head: TYPE 2 DIABETES ASSIGNMENT 2
Type 2 diabetes consists of a series of dysfunctions evident by hyperglycemia and
following a combination of resistance to insulin action in the muscles, liver together with
destroyed pancreatic beta cell activity resulting to ‘absolute’ insulin insufficiency. A resistance
to Insulin seems to precede, and results to raised insulin production to keep standard blood
glycemic levels (Kautzky-Willer, A., Harreiter, J., & Pacini, G. (2016). However, in vulnerable
patients, the beta cells of the pancreas cannot maintain the increased demand for hormone
insulin, and a slowly advanced deficiency of insulin progresses.
Type 2 diabetes mellitus is accountable for around 86% of all patients with diabetes in
Australia and by sheer members, accounts for more than half of the sum of public health and cost
responsibility associated with type 2 diabetes. The risk factors related to type 2 diabetes mellitus
include obesity (BMI greater than 30), inactivity, and sedentary lifestyle (excessive alcohol
intake, and chronic cigarette smoking). Abnormal cholesterol and triglyceride levels are a risk
for type 2 diabetes mellitus (Rewers, M., & Ludvigsson, J. 2016). Increasing age and genetic
factors are also a risk for type 2 diabetes development. Other causes of diabetes are, genetic
defects of beta cell function, pancreatic disease, and extravagant production of endogenous
hormonal antagonists to insulin.
Pathophysiology
Poor blood glucose control can cause vascular complications. These may be
macrovascular diseases, such as peripheral artery disease, cerebrovascular accident, coronary
artery disease, and microvascular disease retinopathy, polyneuropathy, and nephropathy.

Running head: TYPE 2 DIABETES ASSIGNMENT 3
Optimal control of elevated levels of blood glucose can help prevent the complications and
symptoms resulting from hyperglycemia. Also, treatment of lipid disturbances and hypertension
significantly reduces the incidence and severity of vascular disease.
Macrovascular disease develops in type 2 diabetes mellitus thus promoting an early and
premature increase of long-term cardiovascular problems in type 2 diabetes. A series of
metabolic and hemodynamic factors have been considered to have an impact on accelerated
cardiovascular complications (Neal et al., 2017). Macrovascular complications of type 2 diabetes
mellitus result from excess free fatty acid, elevated blood glucose levels and insulin resistance.
Hyperglycemia, insulin resistance, and excess lipids cause elevated protein kinase activation,
oxidative stress and receptor activation for progressive glycation final products. These factors act
on the endothelium.
Reduced nitric oxide, the increment in endothelia, and elevated angiotensin ii promote
vasoconstriction that leads to hypertension and growth of smooth muscle cell in the vessels.
Diabetic retinal complication is the common cause of loss of sight in individuals between
30 and 65 years of age, in developed countries. The effective treatment is retinal
photocoagulation, especially if it’s administered at an early phase when a person has no
symptoms. Hyperglycemia usually elevates blood flow in the retina and metabolism and has
effects on the endothelial cells of the retina and loss of pericyte, resulting in vascular
autoregulation impairment.
Following unregulated flow of blood at first dilates the capillaries but also raise the
release of vasoactive substance and proliferation of endothelial cell, leading to closure of
capillaries. This results in persistent retinal hypoxia and provokes growth factors release,

Running head: TYPE 2 DIABETES ASSIGNMENT 4
including vascular endothelial growth factor (VEGF), that plays a significant role in provoking
the damaging change in growth of endothelial cells (promoting new vessel structure) and raised
vascular permeability (promoting retinal exudation and leakage).
Macular edema should be suspected in diabetic patients if there is visual acuity
impairment, even if this is related with only moderate peripheral non-proliferative retinal disease
and there is no other pathology. Macular edema can only be excluded on slit lamp retinal
biomicroscopy. If macular changes are observed by direct ophthalmoscopy or retinal
photography, referable maculopathy should be suspected. Acute visual loss happens with
vitreous hemorrhage or retinal detachment.
Neuropathy is a common and early complication found in around 30 percent of patients
with diabetes. Although in some of the individuals it can result in serious disability, and usually
it has no symptoms in most patients. Like retinopathy, it occurs as a result of metabolic
imbalance, and occurrence is linked to the time of diabetes existence and the level of metabolic
regulation. There are facts that the central nervous system function is altered by chronic
diabetes; the effect of diabetes is primarily evident in the peripheral nervous system.
Diabetic nephropathy is a significant cause of complications and death and is now amidst
the major reason of end-stage renal disease (ESRD) (as cited in Wanner et al., 2016). Diabetic
nephropathy is found with other macrovascular and microvascular complications, and treatment
is often tough. The advantages of prevention of ESRD are crucial. The first pathological changes
coincide with the onset of microalbuminuria and involve making the glomerular basement
membrane thicker and compilation of matrix matter in the mesangium. Afterwards, nodular
deposits are typical, and glomerulosclerosis become worse as heavy protein in the urine occurs
until glomeruli are increasingly lost and renal activity deteriorates (Fitchett et al., 2016).