Diabetes mellitus, or simply diabetes, is a disease characterized by high blood glucose levels that is a consequence of the body’s inability to produce or use insulin. It is a state mainly defined by the level of hyperglycemia giving rise to the risk of microvascular impairment (retinopathy, nephropathy, and neuropathy). It is associated with abridged life expectancy, substantial morbidity due to specific diabetes-associated microvascular complications, amplified risk of macrovascular complications (ischemic heart disease, stroke, and peripheral vascular disease), and lessened quality of life (WHO,2018)
Numerous pathogenetic procedures are involved in the development of diabetes.
These comprise of processes, which abolish the beta cells of the pancreas with subsequent insulin deficiency, and others that result in resistance to insulin action. The irregularities of carbohydrate, fat, and protein metabolism are due to scarce action of insulin on target tissues resulting from insensitivity or lack of insulin (WHO Consultation, 1999). Diabetes mellitus may extant with characteristic symptoms such as thirst, polyuria, blurring of vision, and weight loss.
All these symptoms do not always occur altogether or sometimes they can be minor.
2,000 years ago, diabetes has been known as a devastating and lethal disease. In the first century A.D. a Greek physician, Aretaeus, defined the destructive nature of the disorder, which he named “diabetes” from the Greek word for “siphon”. Physicians in ancient times, like Aretaeus, recognized the symptoms of diabetes but were failed to treat it effectively.
In the 17th century a physician, Dr. Thomas Willis from London, used to check whether his patients had diabetes or not by sampling their urine.
If it proved to have a sweet taste, he would diagnose them with diabetes mellitus-“honeyed” diabetes. This method of monitoring blood sugars was used until the 20th century.
Before the discovery of insulin, there were only a few options to treat diabetes. One of those was low-calorie diets that prolonged their lives but left them weak. But in 1921, doctors in Canada treated patients dying of diabetes with insulin and managed to drop high blood sugars to normal levels. Since then, medical revolutions have been continuing to prolong the life span and increase the quality of life in people with diabetes.
In the ’50s, a discovery happened that claimed there were two types of diabetes: “insulin sensitive” (type I) and “insulin insensitive” (type II). It was after two thousand years since Aretaeus spoke of diabetes as “the mysterious sickness”. It had been a long and arduous course of discovery, as generations passed by, many physicians and scientists had added their collective knowledge to find a cure. It was from this prosperity of knowledge that the discovery of insulin emerged in a small laboratory in Canada. Since then, medical innovations have continued to make life easier for people with diabetes.
In the 21st century, diabetes researchers are still in the search of a cure but it is unclear whether they can achieve complete success or not. There is a chance of dramatic discovery like insulin or finding ways out to slow the progress. (Satley, 2008).
An understanding of the pathophysiology of diabetes is based upon knowledge of the fundamentals of carbohydrate metabolism and insulin action. Following the consumption of food, carbohydrates are converted into glucose molecules in the gut. Glucose is absorbed into the bloodstream causes elevated blood glucose levels. This increase in glycemia stimulates the secretion of insulin from the beta cells of the pancreas. Insulin is required by most cells to allow glucose entry. Insulin helps glucose to enter into the cells by combining with specific cellular receptors or transporters, resulting in energy production from glucose. The amplified insulin secretion from the pancreas and the subsequent cellular utilization of glucose results in diminished blood glucose levels. Lower glucose levels then result in lessened insulin secretion.
If insulin production and secretion are changed by disease, blood glucose dynamics will also change. If insulin production is decreased, glucose entry into cells will be inhibited, resulting in hyperglycemia. The same consequence will be seen if insulin is secreted from the pancreas but is not used properly by target cells. If insulin secretion is increased, blood glucose levels may become very low (hypoglycemia) as large quantities of glucose enter tissue cells and little remains in the bloodstream. Several hormones may affect glycemia. Only insulin can decrease the blood glucose level. The counter-regulatory hormones such as glucagon, catecholamines, growth hormone, thyroid hormone, and glucocorticoids all act to increase blood glucose levels, in addition to their other effects (Meley et al, 2006).
Complications due to diabetes are a key reason of disability, reduced quality of life, and death. Diabetes complications can affect several parts of the body manifesting in diverse ways for different people. Diabetes increases patients’ risk for many serious health problems. In men, it is responsible for erectile dysfunction, low testosterone levels, and emotional factors –such as depression, anxiety or stress–that can interfere with sexual feelings. In women, diabetes can be especially hard. Even for those who do not have diabetes, pregnancy brings the risk of gestational diabetes. According to statistics from the American Diabetes Association, heart disease is the leading cause of death in women with diabetes (American Diabetes Association,1995). In addition, women with diabetes are afflicted by depression, their sexual health is at risk, and eating disorders tend to occur more frequently. Diabetes can affect every part of the body, including the feet, the eyes and the skin. These problems act as early indicators of having diabetes. Foot complications can get worse and lead to serious complications, such as neuropathy, skin changes, calluses as well as foot ulcers, poor circulation, and (Aalto, 1997).
Diabetes complications are divided into two major categories:
The most serious microvascular diabetes complications are eye complications. Diabetic patients need to check their eye condition by doing an annual ophthalmic exam. Diabetic retinopathy is the leading cause of blindness in the working population of the Western world. The risk of developing diabetic retinopathy or other microvascular complications of diabetes depends on both the duration and the severity of hyperglycemia (Almdal, 2006).
Diabetic retinopathy is normally classified on two basic facts such as either background or proliferative. General understanding of each feature are needed to interpret eye examination reports and advise patients of disease progression and prognosis. Background retinopathy includes such features as small hemorrhages in the middle layers of the retina. They clinically appear as “dots” and are frequently known as “dot hemorrhages”. The formation of new blood vessels on the retina surface is the main characteristic of Proliferative retinopathy and may lead to vitreous hemorrhage (Watkins, 2003).
Diabetic nephropathy is the leading cause of renal failure in the United States. About 20% to 30% of patients with diabetes develop evidence of nephropathy. As with other complications of diabetes, the initial treatment of diabetic nephropathy is prevention. Like other microvascular complications of diabetes, there are strong associations between glucose control and the risk of developing diabetic nephropathy. Patients should be treated to the lowest safe glucose level that can be obtained to prevent or control diabetic nephropathy (Gross et al 2005). Patients with diabetic nephropathy can have benefited from antihypertensive drugs, as an additional treatment of hyperglycemia, for example, Renin-angiotensin system blockers (Gross et al 2005).
Diabetic neuropathy is referred to by the American Diabetes Association (ADA) as “the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after the exclusion of other causes” (American Diabetes Association, 2007). As with other microvascular complications, the risk of developing diabetic neuropathy is proportional to both the magnitude and duration of hyperglycemia, but some individuals may have a genetic influence that affects the risk of developing such complications.
Polyol accumulation, injury from AGEs, oxidative stress, etc. are assumed to be the underlying causes of the precise nature of peripheral nerve injury from hyperglycemia. Peripheral neuropathy may occur in different forms such as sensory, focal/multifocal and autonomic neuropathies. More than 80% of amputations occur after foot ulceration or injury, which can be a resulting effect of diabetic neuropathy (Boulton et al.,2005).
The central pathological mechanism in macrovascular disease is the process of atherosclerosis, which leads to narrow arterial walls in the body. Chronic inflammation and arterial wall injury in the peripheral or coronary vascular system is a possibility to cause atherosclerosis. (Lehto, 1996).
The development of cardiovascular disease (CVD) is a secondary risk for diabetic patients. Although the precise mechanisms through which diabetes increases the likelihood of atherosclerotic plaque formation are not completely defined, the association between the two is profound (Laing et al 2003). Cardiovascular disease is a major complication and the leading cause of premature death among diabetic patients (Merz et al., 2002). Diabetic patients have a 2 to 6 times higher risk for developing complications such as ischemic heart disease, cerebrovascular disease, and peripheral vascular disease than the general population.
Among macrovascular diabetes complications, coronary heart disease has been associated with diabetes in numerous studies beginning with the Framingham study (Kannel et al., 1979).
The major cardiovascular risk factors in the non-diabetic population (smoking, hypertension, and hyperlipidemia) also operate in diabetes, but the risks are enhanced in diabetic patients. Overall life expectancy in diabetic patients is 7 to 10 years shorter than non-diabetic people due to many complications.
Type II diabetes typically occurs in the setting of the metabolic syndrome, where abdominal obesity, hypertension, hyperlipidemia, and increased coagulability are included. There are other factors that can also promote CVD. Even in this setting of multiple risk factors, type II diabetes acts as an independent risk factor for the development of ischemic disease, stroke, and death (Almdal et al.,2004), Diabetes is also a strong independent predictor of the risk of stroke and cerebrovascular disease, as in coronary artery disease (Lehto et al., 1996).
The increased risk of CVD has led to receiving the patient’s aggressive treatment to achieve primary or secondary prevention of coronary heart disease before it occurs. Studies in Type I Diabetes have shown that intensive diabetes control is associated with a lower resting heart rate and that patients with higher degrees of hyperglycemia tend to have a higher heart rate, which is associated with a higher risk of CVD (Paterson et al., 2007).
Once the clinical macro-vascular disease develops in diabetic patients, they have a poorer prognosis for survival than normoglycemic patients with macrovascular disease. In female diabetic patients, their natural protective mechanisms of vascular disease are deemed.
In addition, the combination of hypertension and diabetes is a serious situation, posing an increased predisposition to cardiovascular morbidity and mortality. As hypertension occurrence and related complications, development is a common risk for diabetic patients; it should therefore be taken as seriously as glycemic control when planning treatment strategies. Hyperlipidemia can occur as a result of poorly controlled diabetes or may occur as an independent risk factor for macrovascular disease. About 25% of patients attending a diabetes clinic will have elevated lipid levels (Jacobson, 1985).
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