Implications of Type II Diabetes Mellitus for the Quality of Life

INTRODUCTION

Type II diabetes mellitusis a condition whereby, the body does not generate a sufficient amount of insulin, or the body cells pay no heed to the insulin. Thus, individuals with type II diabetes mellitus, have sugar or glucose accumulation in their blood at significantly high levels1. Consequently, the surplus glucose can affix to proteins within the blood vessels, and as a result varying their standard structure plus function. One consequence of this condition is that the blood vessels turn out to be thicker along with being less elastic, and this makes it difficult for blood to press through them. Some studies even indicate that it is escalating worldwide, and relates with elevated levels of morbidity, as well as mortality due to cardiovascular disease. The aim of this paper is to elaborate on the implications of type II diabetes mellitus for the patient quality of life. This involves looking at accumulation of sugar/glucose in the blood, thickening of blood vessels, kidney disease, and damage and blockage of blood vessels. Moreover, the paper asseses the type II diabetes impaired circulation of blood, amputations of lower limbs, nerve disease, diabetic

1 Kagan, Andrew. Type 2 diabetes : social and scientific origins, medical complications and implications for patients and others. Jefferson, N.C: McFarland & Co, 2010.p 93

eye disease, stroke, and happenings at molecular level.

Type II diabetes mellitus is a set of metabolic diseases categorized by hyperglycaemia, or high levels of sugar in the blood. Type II diabetes mellitus is a non insulin dependent diabetes, since the body insulin levels are normal, or even in some extent higher. But, the target cells do not act in response to the hormone as they ought to, and as a result the blood sugar levels remain abnormally high. The symptoms of Type II diabetes mellitusis normally initialize during the middle ages, when the insulin manufacture has decline. Type II diabetes mellitus makes the fat, liver, and muscle cells not to correctly act in response to insulin, or become insulin resistance. Accordingly, the sugar in the blood does not move into these cells, in order to be stored as intended for energy. Moreover, when sugar is not able to enter the cells, there is the build-up and accumulation of sugar in the blood or d hyperglycaemia2.

2 Ibid

Figure 1: 3 Pathogenesis of Type II Diabetes This table chows the commonness of type II diabetes from the year 1930 till 2011. The figure on the right illustrates what causes Type II diabetes and how it affects the human body. However, the type 2 diabetes typically takes place gradually over time. Hence, most individuals with the disease are overweight at the time of being diagnose. For that reason, the augmented fat makes it harder for these people body to make use of insulin in a proper manner the correct way. Nevertheless, it can also occur in individuals who are thin and most often occurs in the elderly. Notably, family past account, in addition to genes take part in a bigger role in the occurrence of type 2 diabetes. Moreover, the diminished activity level, coupled with poor diet, and surplus body weight in the region of the waist also increase the risk of getting Type II diabetes.

Additionally, Type II diabetes causes acceleration in the thickening of blood vessels. This is known in scientific circles, as arterial occlusive disease is the cause of additional diabetic complications. Consequently, it results in the kidney disease, heart attack, diabetic foot issues and failure of vision. In addition since thickening of the blood vessels cuts off

3 S.g. Korenman and Ronald Kahn, Atlas of clinical endocrinology (Location: Wiley-Blackwell,2000), Volume 2, p 81.

The Hyperglycaemia condition induces augmented polyol pathway movement, or dyslipidaemia formation of highly developed glycation final product, in addition to augmented protein kinase activity. Furthermore, this results in mounting oxidative stress as well as endothelial dysfunction. Consequently, these occurrences have an effect on impaired blood flow plus endoneurial hypoxia that are acknowledge to take part in a foremost role, in resulting of diabetic neuropathy in human. They also add to the inflammatory fibro proliferative reaction, which harms the endothelium, as well as smooth muscle within the arterial wall, such as the instigation of atherosclerotic procedure. A key feature of Type II diabetes mellitus is its elevated intensity of low-density cholesterol, or hypercholesterolemia. Hence, in this condition the arteries of the person with this type of diabetes go through two processes simultaneously. Firstly, there is the solidification of the artery wall by means of calcium, and as a result there is the plugging of the lumen with atharoma or otherwise the plaque. The plaque is composed of lipoproteins, triglycerides and cholesterol, but the LDL cholesterol is harmful, since it acts like saturated fat, hence it builds up on the inner surface of the blood vessel walls5. Various studies have indicated that the thickening of the cellar membrane in endoneurial capillaries in nerves, from diabetic subjects, is as a result, of the reduplication of the basal lamina. Consequently, these alterations add to the overall diffusion expanse for oxygen as well as nutrients to axons plus Schwann cells. Hence, this results in endothelial cell hyperplasia, along with swelling in the direction of the lumen, which is adequate to lead to occlusion plus thrombosis. What is clear though is that the site of the first physiological assault, takes place in the epineurial and transperineurial arterioles, which control endoneurial flow resulting in impaired perfusion followed by structural modifications6.

High blood glucose levels caused due to type II diabetes mellitus over time can result in an augmented accumulation of fatty materials on the entrails of blood vessel walls. Consequently, such deposits may have a negative effect on blood flow, along with increasing the possibility of clogging plus hardening of the blood vessels. This condition is referred to as therosclerosis, and individuals with type II diabetes mellitus have an elevated danger

4 Kagan, Andrew. p 95 5 Ibid. pg 94 6 Ibid. pg 95

These problems brought about by type II diabetes mellitus, damage and blockage of blood vessels comprises heart attack, because of obstruction of blood vessels bringing in blood to the heart. Moreover, individuals with type II diabetes mellitus, have high blood triglyceride levels, and this aid in making HDL cholesterol that is considered helpful in diminished levels. As a result, it makes them vulnerable to atherosclerosis, and since obese individuals run short of standard fat storage room, the triglyceride molecules overrun tissues in which fat does not fit in and this obstructs with usual organ function8.

The blood vessel in Type II diabetics has been shown by various studies, to have uncharacteristic vascular reactivity. Thus, insulin induced vasodilatation of interior carotid artery is distinctly impaired inside patients with type II diabetes. Moreover, the vasolidatory reaction of the interior carotid artery to insulin is also impaired, and this indicates that there is the impairment of the cerebral circulation to counteract vasodilatory stimuli. The endothelium dependent, along with independent blood circulation course, becomes worse in patients with type II diabetes mellitus9.

Even though the risk factors associated with the sequence of constant kidney disease within type II diabetes mellitus has not been made completely clear, the type II diabetes mellitus is also responsible for Kidney damage. Thus, type II diabetes melitus is for the most part the reason for the occurrence of End-Stage Kidney Disease10. Under this condition, the diminutive blood vessels in the kidney come into harm, and as a result, the kidney is not able to clean the blood, as it should be. Consequently, the body retains extra water plus salt than it has to, which then leads to a weight gain along with ankle swelling. Moreover, these patients have protein in their urine, and the waste matters accumulate in their blood. Since, type II diabetes mellitus can lead to damage of the nerves this in turn leads to complicatedness in some of these patients when emptying their bladder. Therefore, the pressure ensuing from the packed bladder can blow up, and as a result damage the kidneys. In addition, if urine stays in the bladder for an extended period, the patient‘s body begin to build

7 Ibid 8 Ibid 9 Ibid. pg 94 10 Leehey, David J, Tarek M Daoud, Holly J Kramer, and Maninder P Chatha. "Progression of kidney disease in type 2 diabetes – beyond blood pressure control: an observational study." BMC Nephrology (licensee BioMed Central Ltd.) 6, no. 8 (2005). para 4

kidney disease is the augmented seepage of albumin within the urine, and the blood pressure becomes too high. As the kidneys functioning collapse, the Blood Urea Nitrogen or BUN intensity will go up simultaneously with the point of creatinine found in blood11. The patient may also undergo nausea, loss of appetite, muscle cramp mainly in legs and increasing fatigue. Furthermore, the patient is likely to experience vomiting, itching, and anaemia.

Lower levels amputations are more common in patients with Type II diabetes, this is more so in their toe, foot and ankle. According to a study across several states in the US, a number of type II diabetic patients experience ipsilateral or subsequent leg contralateral amputation, especially after a separate hospitalization within the twelve months after the amputation. In addition, individuals with type II Diabetes are 12-18 times with additional chances of undergoing a lower limb amputation than those individuals without diabetes12. The reason for this outcome is that Atherosclerotic Peripheral Arterial Disease, commonly known as PAD along with diabetic peripheral neuropathy turn out to be grave complications arising from diabetes and can sometimes results in lower limb complications. Consequently, the messed up sensation, which increases the risk of trauma, and the severe, Type II diabetes can result in stroke, which is due to the obstruction of blood vessels leading to the brain. Thirdly, there is the obstruction of blood vessels within the legs plus feet, and which results in foot ulcers, contagions, in addition to loss of the diabetic patient toe, foot, and even lower leg13. Consequently, this weakness to injury as well as deprived wound healing can result in ulceration, and if not taken care of punctually, the foot ulcers can then be infected for the most part when diabetes management is poor. Soft tissue infection may progress to involve the underlying bone. These entrenched infections are more often than not very hard to treat and mostly require amputation. In the same way, when the extremities of the body are deprive of oxygen due to atherosclerotic Peripheral Arterial Disease, then the tissue demise may take place, resulting in

11 National Kidney Foundation. Diabetes and Kidney Disease. 2011. http://www.kidney.org/atoz/content/diabetes.cfm (accessed November 15, 2011). Para 6 12 Aubert, Ronald. Diabetes in America. Nih, 1995. P 409 13 Ibid

amputation becomes necessary. However, the type II diabetes patient can avoid ulcers and the subsequent amputations when they practice proper foot care, and undergo timely treatment of ulcers during their initial stage. In another study, the occurrence of foot ulcerations, as well as lower limb amputation in type II diabetics has shown to be lower. Nevertheless, the reoccurring levels of ulceration plus danger of amputation is elevated, with soaring mortality15.

When an individual with type II diabetes blood sugar are relatively high for an extended period, they develop a state identified as diabetic neuropathy, or nerve disease. The reason for this condition is that, the cells, which comprise the nerves, are amend in reaction to elevated blood sugar. Consequently, different sets of nerves are affected by the high levels of sugar in the blood. In addition, diabetic autonomic neuropathy is set up in relation with distal symmetrical polyneuropathy. It can be detected using, indirect cardiovascular reflex tests that assess the integrity of complex reflex arcs, and the clinical manifestation of diabetic peripheral neuropathy ranges from an imperceptible reduction in temperature perception in the feet to sudden cardiac death16. Figure 217 : Comparison table

14 Muller, Ilona Statius, Wim J C de Grauw, Willem H E M van Gerwen, and Marie Louise Bartelink. "Foot Ulceration and Lower Limb Amputation in Type 2 Diabetic Patients in Dutch Primary Health Care." Diabetes Care (American Diabetes Association), 2002: p 574. 15 Muller, Ilona Statius, Wim J C de Grauw, Willem H E M van Gerwen, and Marie Louise Bartelink. "Foot Ulceration and Lower Limb Amputation in Type 2 Diabetic Patients in Dutch Primary Health Care." Diabetes Care (American Diabetes Association), 2002: p 574. 16 Abela, George S. Peripheral vascular disease: basic diagnostic and therapeutic approaches. Philadelphia,Pa.: Lippincott Williams & Wilkins, 2004. 17 Yokoyama, et al. 2007

Type II diabetes diminishes or disfigures the nerve role, resulting in a state referred to as neuropathy. Neuropathies, which are a set of disorders that have an effect on the nerves, thus, individuals with type II diabetes have damaged nerves, which are responsible for sensing temperature, heaviness, or pain on the skin. Moreover, they mostly have an effect on the feet plus lower legs and this result in symptoms, such as numbness, otherwise tingling, prickling sensation, cramps and intense feeling to touch. This is referred to as peripheral neuropathy, and it damages the nerves within the upper plus lower body extremities. Diabetic neuropathy can also directly influence the microcirculation by the destruction of the nerve axon spontaneous effect18. Type II diabetic peripheral neuropathy also results in muscle weaknesses, along with the loss of reflexes, notably at the ankles. This results to shifts in gait, foot deformities like hammertoes, and even in extreme cases the fall down of mid foot. Furthermore, the initial region, as well as the number of nuclei in epineurial arteries will be augmenting in nerves in patients with neuropathic diabetic. What‘s more, the distribution of nerves energy of epineurial, plus transperineurial arterioles are diminished, especially for smaller vessels involved in influencing vascular resistance. Therefore, this denervation of blood vessels contribute to both the reduced endoneurial blood flow, as well as the increased epineurial arteriovenous thrusting as observed in diabetic neuropathy patients19.

The resulting chronic hyperglycemia takes part in a larger function, in the progression of six out of the seven categories of diabetic eye disease. These eye illnesses caused by type II diabetes comprises, cataract, glaucoma, and keratopathy. There is also the ischematic optic neuropathy, cranial neuropathy and retinopathy. For instance, studies done by the‖ United Kingdom prospective diabetes” or UKPDS, indicate the progression of retinopathy in patients with type 2 diabetes, there is a strong link with baseline glycaemia, as well as glycaemic exposure, and this development is associated with hyperglycaemia20. Majority of patients with type II diabetes are initially diagnose with diabetes eye diseases, without

18 Andersen, Henning, and F Arnold Gries. Textbook of diabetic neuropathy : 93 tables. Chapter 2; Stuttgart: Thieme, 2003. 19 Ibid 20 Scanlon, Peter, Charles Wilkinson, and Stephen Aldingto. A Practical Manual of Diabetic Retinopathy Management. Chichester: Wiley-Blackwell,, 2009. P 29

hemorrhage, commonly referred to as microaneurons. In addition, there is the seepage of water, as well as proteins into the middle of the retina, or macula resulting in a condition known as macula edema, and which leads to vision loss, even though it could be temporary. However, without treatment, additional permanent vision loss takes place21. Accordingly, type II diabetes can lead to proliferative eye disease, or fresh blood vessel growth, and the retina begins to grow new blood vessels with an intention of replacing the damaged ones under a process known as neovascularization. However, the issue with this process is that these fresh blood vessels, are burdened with holes, and thus they are prone to abrupt bleeding with severe damage to the retina without warning, since they are deformed. Secondly, these new blood vessels in the retina can cause scar tissue inside the retina, along with retinal detachments, plus glaucoma. Therefore, this largely adds to the risk of permissible blindness. Additionally, type II diabetes can also lead to cataract, or clouding of the lens contained by the eye, and which subsequently blurs the vision. Hence, majority of the diabetic eye diseases blindness occurs in individuals who are over 60 years of age, and affects 90-95% of individuals with type 2 diabetes22.

Stroke, or cerebrovascular accident, occurs in people with type 2 diabetes, due to the hindrance of the artery that provides the receptive brain cells. Given that individuals with type 2 diabetes have high blood pressure, then they are vulnerable to stroke. The reason being that, people with type 2 diabetes mellitus have clogged up carotid arteries, and the diabetic‘s propensity towards high blood cholesterol, as well as extreme lipid levels, coupled with high blood pressures, leads to arteriol blockage, resulting in strokes. Hence, individuals with type 2 diabetes are 2-3 times more likely to undergo stroke than those without, mainly due to the obstruction of the artery found in the neck or brain. This is referred to as ischemic stroke, and some of type 2 diabetics will develop stroke, due to the bursting of the blood vessel in the brain, which results in bleeding into or around the brain23.

21 Scheiman, Mitchell, Maxine Scheiman, and Steven Whittak. Low vision rehabilitation: a practical guide for occupational therapists. Thorofare, NJ: SLACK Inc, 2007. P 267 22 Ibid 23 Kothari, V, AI Adler, I M Stratton, S E Manley, HA Neil, and RR Holman. "UKPDS 60: risk of stroke in type 2 diabetes estimated by the UK Prospective Diabetes Study risk engine." Pubmed 33, no. 7 (2002): 1777

the occlusions lead to minute infarcts inside the white material of the brain. In addition, diabetic autonomic neuropathy may possibly add to the occurrence of cerebrovascular disease in individuals with type II diabetes24.

The type 2 diabetes mellitus also relates with a noticeable boost in the threat of coronary heart disease. Furthermore, patients with type II diabetes are more likely to have congenital heart failure than people without due to high levels of hyperglycaemia, increased blood pressure in addition to obesity25. Additionally, Type II diabetes is link to other risk factors for heart diseases, like hypertension, uncharacteristic blood fats, as well as the increased fat in the region of the waist.

Notably, the Type II diabetes mellitus is symptom of a fundamental cellular breakdown, which is improper metabolism of Glucose. Hence, every cell in the body becomes incapable when it comes to transporting glucose originating from blood stream towards their interior. Consequently, the glucose is left over in the blood stream, or in some instances amassed as body fat, or else released in the Urine. When insulin attaches with a membrane receptor, it kicks off a complex flow of biochemical reactions within the cell. Thus, one of these responses, results in Glucose transporters, or GLUT4 molecules to depart their storing region in the cell and journey to the interior surface of the cell plasma membrane. Type 2 diabetics, due to its high regular insulin levels, characteristically have merely 1200 insulin receptors, and even lesser for every cell membrane, which is around half of the standard26. Then there is the glycation, where sugar molecules react with proteins in the human body to create non- purposeful structures, and this is a major feature of type II diabetes complications. The reason is that it interrupts proteins all the way through the body and is related to nerve injury, heart attack, in addition to blindness. Additionally, the oxidative stress turns out to be a major damage resulting from type II diabetes. Such individual‘s go

24 Ibid 25 Nichols, Gregory A, Christina M Gullion, Carol E Koro, Sarah A Ephross, and Brown Jonathan. "The Incidence of Congestive Heart Failure in Type 2 Diabetes.Diabetes Care (American Diabetes Association) 27, no. 8 (2004): p 1879 26 Petersen, Kitt Falk, Sylvie Dufour, Douglas Befroy, Rina Garcia, and Gerald I Shulman. "Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes." New England Journal Of Medicine (NIH) 350, no. 7 (2004): p 665.

This figure shows how glucose reacts with muscle in the human body to create non- purposeful structures causing in type II diabetes. For the most part, measurement of blood glucose levels is the widespread clinical tests applied in diagnosing diabetes. Accordingly, the general fasting glucose examination measures the quantity of glucose within the blood normally after fasting. Consequently, pre-diabetes is ascertained, if the level of glucose in the blood during the period of fasting ranges in the region of 100 to 125 mg/dL. As a result, diabetes is identified when the level of glucose within the fasting blood goes up to around 126 mg/dL or greater than that28.

Based on the above research paper, type II diabetes Mellitus diabetes has quickly developed as the foremost cause in the increase of heart disease across the western nations, along with being the principal reason for non-accident amputation as well as blindness amongst adults. The most obvious and general symptoms associated with type II diabetes mellitus comprises, augmented levels of thirst plus urination. In addition, the individual experiences abnormal weight alterations, tetchiness, fatigue, as well as blurry vision. The clinical abnormalities of type II diabetes comprise hyperglycemia plus glucose contained in the urine. Moreover, the individual develops some form of breath, which remarkably may well smell sweet, possibly due to presence of ketones in the patient‘s blood, or ketosis. Some individuals with type II diabetes also start to have dark outgrowths in their skin, or commonly referred to as skin tags. For these reason, the cost of uninhibited type II diabetes mellitus are harsh. For instance, some of the patients become blind others develop kidney failure, with

27 Guilherme, et al. 2008 28 Life Extension Newsweekly. Diabetes. 2011. http://www.lef.org/protocols/metabolic_health/diabetes_01.htm (accessed November 17, 2011). Para 12

At present, majority of the practitioner‘s centre of attention in the treatment of type II diabetes is restricted to blood sugar management, and which is largely concerned with blood sugar control. Despite the fact that, diabetes is distinguish by surplus blood glucose, this cut down approach by practitioners for controlling blood sugar levels, can really speed up the progression of II diabetes, given that it does not deal with the critical aspect of addressing the harm it causes. Therefore, it is crucial that type II diabetics patients, as well as those predisposed to it, realize the methods in which the abnormal levels of glucose in the blood results in damage, and undertake vigorous measures in order to interrupt these processes. For instance, instead of individuals with type II diabetes taking drugs that additionally boost the intensity of insulin inside the blood; they should be made to use therapies, which add to the sensitivity of body insulin receptors within the cell membranes. Nevertheless, the best measures against type II diabetes is improved diet along with exercise. Even though, this type of diabetes has a genetic aspect, many of the research have indicated that diet plus exercise can thwart it.

Diabetes is a very intricate disease. The only way to manage it successfully is by taking the full precautionary measures. A person with diabetes will be requiring a complete team of skilled professionals that may guide him to living a complete and healthy lifestyle. Diabetes Type II Mellitus is not dependant on insulin because it causes the blood to have rather higher levels of glucose. There are many complications associated with Diabetes Type II Mellitus which have been discussed in great detail above. This disease may be controlled by proper drug intake and a healthy lifestyle.

Abela, George S. (2004). Peripheral vascular disease: basic diagnostic and therapeutic approaches. Philadelphia,Pa.: Lippincott Williams & Wilkins. Andersen, Henning, and F. Arnold Gries (2003). Textbook of diabetic neuropathy : 93 tables. Chapter 2; Stuttgart: Thieme. Aubert, Ronald (1995). Diabetes in America. Nih. p. 409 Guilherme, et. al. (2008)

Jefferson, N.C: McFarland & Co. Kothari, V., AI Adler, I. M. Stratton, S. E. Manley, H. A. Neil, and R. R. Holman (2002). "UKPDS 60: risk of stroke in type 2 diabetes estimated by the UK Prospective Diabetes Study risk engine." Pubmed 33, no. 7 (2002): 1777 Leehey, David J., Tarek M. Daoud, Holly J. Kramer, and Maninder P. Chatha (2005). "Progression of kidney disease in type 2 diabetes – beyond blood pressure control: an observational study." BMC Nephrology (licensee BioMed Central Ltd.) 6, no. 8 (2005). para 4 Life Extension Newsweekly. Diabetes (2011). http://www.lef.org/protocols/metabolic_health/diabetes_01.htm (accessed November 17, 2011). Para 12 Muller, Ilona Statius, Wim J. C. de Grauw, Willem H. E. M. van Gerwen, and Marie Louise Bartelink (2002). "Foot Ulceration and Lower Limb Amputation in Type 2 Diabetic Patients in Dutch Primary Health Care." Diabetes Care (American Diabetes Association): p. 574. National Kidney Foundation (2011). Diabetes and Kidney Disease. 2011. http://www.kidney.org/atoz/content/diabetes.cfm (accessed November 15, 2011). Para 6 Nichols, Gregory A., Christina M. Gullion, Carol E. Koro, Sarah A. Ephross, and Brown Jonathan (2004). "The Incidence of Congestive Heart Failure in Type 2 Diabetes." Diabetes Care (American Diabetes Association) 27, No. 8: p. 1879. Petersen, Kitt Falk, Sylvie Dufour, Douglas Befroy, Rina Garcia, and Gerald I. Shulman (2004). "Impaired Mitochondrial Activity in the Insulin-Resistant Offspring of Patients with Type 2 Diabetes." New England Journal Of Medicine (NIH) 350, No. 7: p. 665. Scanlon, Peter, Charles Wilkinson, and Stephen Aldingto (2009). A Practical Manual of Diabetic Retinopathy Management. Chichester: Wiley-Blackwell, p. 29 Scheiman, Mitchell, Maxine Scheiman, and Steven Whittak (2007). Low vision rehabilitation: a practical guide for occupational therapists. Thorofare, NJ: SLACK Inc, p. 267 Yokoyama, et. al. (2007).

Dietitian at Prince Sultan Military Medical City, Riyadh Kingdom of Saudi Arabia ali8668@hotmail.com