Discuss about the Human Body Systems and their Structure and Function.
The circulatory system plays a fundamental role in the body, providing the body with the ways to transport oxygen, nutrients, and hormones all throughout the body. Blood circulates all across the body, moving from the heart through the tissues and reverts to the heart via the blood vessels. Blood vessels are of three major types: arteries, capillaries and veins. However, with relevance to the case study, in type two diabetes, the fatty acid deposition in a streaking pattern facilitated by high Arteries can be defined as the largest blood vessel and in term of diabetes, its effects are seen predominantly at three particular arteries namely the coronary, cerebral and peripheral arteries (De Nicola et al., 2014). The arteries have three layers, a thick outer layer made up of connective tissues, a middle layer made up of smooth tissues and an inner layer made up of endothelial tissues. This thickness aids in delivering highly pressurized oxygen-rich blood from the heart to peripheral sections of the body, where it is divided into smaller blood vessels which are known as capillaries. The capillaries connect the arteries and the veins by webbing the tiny vessels together then they meet in which oxygen, nutrients and wastes can be exchanged for all body cells. The veins return fresh oxygenated blood from the lungs back to the heart. The function of the blood vessels is to transport both glucose and insulin through the body within the bloodstreamsglucose levels in the blood along the arterial wall produces plaques, it narrows down the arteries and can even lead to blockage of the arteries (Ferrannini & Solini, 2012).
The kidney system serves as the essential functional system in the body that purifies the blood within the body and facilitates the excretion procedure of harmful toxic substances fromn the body. The functional unit of this body system is the nephron that acts like a filter and removes all toxic waste substances from the blood. The nephron is made up of a glomerulus and renal tubular system. There is a capillary tuft inside the glomerulus that receives blood from the afferent arteriole and releases into the efferent arteriole. The glomerulus walls acts as the effective filtration barrier, that under pressure helps in separating blood cells and large molecules from the water and small molecules. The capillary barrier in glomerulus essentially has an inner lining made up of and the outer layer of the epithelial cells, the basement membrane, endothelial cells, the mesangial or supporting tissue that encroaches on it in diabetic glomerular disease (Inzucchi et al., 2015). The changes in the filtration barriers leads to affecting the excretion of the renal protein leading to albuminuria. The changes in the albumin molecules restrict the passage into ultra-filtrate due to the intact glomerular wall. The glomerular ultra-filtrate is modified next by the renal tubule system via the control of the water reabsorption happening in the collecting ducts, distal convoluted tubule, the loop of Henle, proximal convoluted tubule. In diabetes patients, the process of the diabetic neuropathy leads to glomerulosclerosis changing the structural features of the glomerulus facilitated by the increased extracellular deposition inside the renal corpuscle which decreases the surface area available for filtration (Sulo et al., 2013).
The endocrine system goes through the most of the changes due to the type two diabetes, and pancreas plays a fundamental role in this. It is responsible for two major functions: secretes hormones and produces digestive enzymes. The pancreas’ head is located in the duodenal curve and its body is connected to the head via a slight constriction. Within the pancreas, tiny structures called islets of Langerhans which lie between the alveoli secrete hormones into the blood (Hinson et al., 2010). The beta cells within the islets releases insulin immediately after each meal, this insulin with the glucose reaches the bloodstream and runs through the entire body, and insulin has specific receptors in the cells that it eventually binds to. The binding triggers the glucose gates to open allowing the glucose molecules to enter cells (Handelsman et al., 2015). In terms of patients with type 2 diabetes, the insulin production and binding properties are not affected. However, the glucose gates fail to open which restricts the glucose from entering into the cell after the binding takes place(Palmer & Clegg, 2015).
The blood pressure is the power of force that maintains the blood circulation process while the heart is beating. However, Type 2 diabetes is fundamentally associated with increase in the blood pressure or hypotension which has been the case for the Zane as well. As mentioned above the deposition of the plaques narrow down the arteries which in turn enhanced the pressure with which the blood flows. high blood pressure consistently occurs can make the heart muscle tire and be enlarged then. Hypotension also can be affect by endocrine system, particularly the antidiuretic hormone (ADH) may increase blood pressure by constricting the blood vessels. High blood pressure coming with type II diabetes has potentials in developing the chances of kidney disease, retinopathy or visual lost. In addition, peripheral resistance is more likely caused by the narrowing of the blood vessels (Marieb, 2015).
The blood glucose levels are monitored through two particular hormones insulin and glucagon which are produced in Islets of Langerhans. After absorbing food and digestion of carbohydrates in food, the blood glucose level will be higher, which trigger the secretion of insulin in the pancreas via the β cells. The insulin acts as a triggering signal for body to utilize glucose as fuel. Insulin also leads to the glucose being converted into glycogen, a storage molecule produced in the liver. Both of the processes result in pulling the glucose molecules from the blood, helping to reduce the blood sugar levels down in the body of the patient, and also reducing insulin secretion, which leads the body to be returned to homeostasis (Ashcroft & Rorsman, 2012). Glucagon has an antagonistic action increasing the concentration of glucose in the blood. Glucagon triggers the breakdown of the glycogen into glucose in the liver and its release into the blood stream, resulting into the rise in the blood glucose levels. This results into reducing the glucagon secretion levels and reverts the body back to the state of homeostasis. The diabetes leads to a broken or dysfunctional negative feedback loop between the actions of both of the hormones which make it impossible for the body to reduce blood sugar. The pancreas of a diabetic patient produces lesser amount of insulin and this in turn leads to higher concentration of blood glucose levels in the body which disrupts the negative feedback loop and affects the homeostatic procedure (Al-Goblan, Al-Alfi & Khan, 2014).
The balance between water re-absorption and excretion is maintained by the series of negative feedback loop with the help of endocrine system and the autonomic nervous system. During the decrease in the fluid volume, there is an increase in the concentration of sodium in the blood due to the increased osmolarity, which leads to the stimulation of the hypothalamus. The hypothalamus acts as an osmoreceptor, which has been reported to react to changes in osmotic pressure and in turn has a significant impact on the pituitary gland. In response, the posterior pituitary gland releases antidiuretic hormone or vasopressin into the bloodstream and the hormone facilitates water retention by the kidneys. as a result there is an increase in concentration of the urine and an increase in the amount of water that returns to the ECF, thus as a result the volume depletion is corrected (Hinson, Raven & Chew, 2010). with the decreased sodium concentration in the blood, the adrenal cortex is stimulated which then secretes aldosterone. The aldosterone instructs the distal nephrons of the kidney into retaining higher concentration of sodium. In case of diabetes, the increased glucose concentration leads to hyponatremia facilitated by affecting the serum electrolyte balance or homeostasis. The rise in the glucose concentration leads to a marked increase in the osmotic force that draws the water to the extracellular space. This phenomenon dilutes the extracellular sodium and causes a decrease in the plasma sodium concentration. However the external insulin and sulfonylureas are also known to cause hyponatremia by augmenting the effects of vasopressin at the renal collecting ducts. Another signature change in the electrolyte levels of the body due to the diabetes is the changes in the potassium levels of the body. This physiological process is also associated with the enhanced concentration of glucose in the body due to diabetes. The rise in the glucose concentration in the body due to the lack of adequate insulin secretion leads to potassium efflux to the extracellular space and causes hyperkalemia (Hinson, Raven & Chew, 2010).
Another very important impact of the diabetes is the damage that it inflicts on the nerve conduction properties of the patient. The pathogenesis or the process of this phenomenon is diabetic neuropathy. According to the Marieb (2015), long term presence of high blood glucose levels accompanied by the high concentration of trigluycerides causes significant damage to the nervous system of the body. There are four basic types of neuropathy; the first type is the peripheral neuropathy that typically targets the feet and the legs of the patient but in rare cases it may also affect the hands and the arms of the patient. The second type leads to affecting the internal organs of the patient. It leads to problems with heart rate and blood pressure, digestive system, bladder, sex organs, sweat glands, and eyes. The third type is focal neuropathy that is associated with damage to a single nerve, most often in your hand, head, torso, or leg. It leads to different entrapment syndromes like carpel tunnel syndrome. the fourth type is the proximal neuropathy that causes a rare and disabling type of nerve damage in the hips, buttock or thigh. considering the pathogenesis of the process, blood vessels depend on nerve function and the nerves depend on the adequate blood flow in the body. Due to the diabetes the narrowing of the blood vessels leads to abnormalities such as thickening in the capillary basement membrane and endothelial hyperplasia. This results into neuronal dysfunctions facilitated by oxygen tension and hypoxia. as a result the nerve conduction velocities are reduced and adds to the progression of the neural dysfunction (Ahn & Song, 2012).
Diabetes, especially the type two variant is fundamentally associated with polyuria or frequent urination. Polyuria can be defined as the condition where the body urinates far more than usual even leads to a significant increase in the amount of urine. In case of diabetes, the increase in the blood glucose levels lead to enhanced removal of the glucose from the blood from the kidneys. As a result the kidneys of the diabetic results in filtering out higher amount of water causing the patient to urinate more (Liamis et al., 2014). Along with that, the abnormally high concentration of glucose cannot be completely reabsorbed and some of it is released in the urine, which draws more watrev in the urine enhancing the amount of urine and in turn enhancing the need to urinate more; which could have been the case for the patient Zane as well.
Obesity can be considered as one of the most significant contributing factors that enhancing the risk for type 2 diabetes significantly in the patient. According to the authors, it has to be mentioned that the progressive defect in then insulin secretion is coupled with the rise in insulin resistance. Both of these processes have been reported to occur prematurely in the obese patients heightening the chances of type 2 diabetes (Briones et al., 2012). The fat deposition in the obese patients especially the visceral and ectopic fat depots facilitate the development of insulin resistance in the patients which in turn leads to defect in the insulin secretion as well via the feedback loop by the glucose allostasis concept. Hence, the risks of type two diabetes is enhanced in case of patients that are obese or overweight (Al-Goblan, Al-Alfi & Khan, 2014).
References:
Ahn, S., & Song, R. (2012). Effects of tai chi exercise on glucose control, neuropathy scores, balance, and quality of life in patients with type 2 diabetes and neuropathy. The Journal of Alternative and Complementary Medicine, 18(12), 1172-1178.
Al-Goblan, A. S., Al-Alfi, M. A., & Khan, M. Z. (2014). Mechanism linking diabetes mellitus and obesity. Diabetes, metabolic syndrome and obesity: targets and therapy, 7, 587.
Ashcroft, F. M., & Rorsman, P. (2012). Diabetes mellitus and the β cell: the last ten years. Cell, 148(6), 1160-1171.
Brethauer, S. A., Aminian, A., Romero-Talamás, H., Batayyah, E., Mackey, J., Kennedy, L., … & Chand, B. (2013). Can diabetes be surgically cured?: long-term metabolic effects of bariatric surgery in obese patients with type 2 diabetes mellitus. Annals of surgery, 258(4), 628.
Briones, A. M., Cat, A. N. D., Callera, G. E., Yogi, A., Burger, D., He, Y., … & Sorisky, A. (2012). Adipocytes Produce Aldosterone Through Calcineurin-Dependent Signaling Pathways: Implications in Diabetes Mellitus–Associated Obesity and Vascular Dysfunction. Hypertension, HYPERTENSIONAHA-111.
De Nicola, L., Gabbai, F. B., Liberti, M. E., Sagliocca, A., Conte, G., & Minutolo, R. (2014). Sodium/glucose cotransporter 2 inhibitors and prevention of diabetic nephropathy: targeting the renal tubule in diabetes. American Journal of Kidney Diseases, 64(1), 16-24.
Ferrannini, E., & Solini, A. (2012). SGLT2 inhibition in diabetes mellitus: rationale and clinical prospects. Nature Reviews Endocrinology, 8(8), 495.
Handelsman, Y., Bloomgarden, Z. T., Grunberger, G., Umpierrez, G., Zimmerman, R. S., Bailey, T. S., … & Davidson, J. A. (2015). American Association of Clinical Endocrinologists and American College of Endocrinology–clinical practice guidelines for developing a diabetes mellitus comprehensive care plan–2015. Endocrine Practice, 21(s1), 1-87.
Hinson, J., Raven, P., & Chew, S. (2010). System of the body: The endocrine system. (2nd ed.). Sydney: Churchchill Livingstone.
Inzucchi, S. E., Bergenstal, R. M., Buse, J. B., Diamant, M., Ferrannini, E., Nauck, M., … & Matthews, D. R. (2015). Management of hyperglycemia in type 2 diabetes, 2015: a patient-centered approach: update to a position statement of the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes care, 38(1), 140-149.
Liamis, G., Liberopoulos, E., Barkas, F., & Elisaf, M. (2014). Diabetes mellitus and electrolyte disorders. World Journal of Clinical Cases: WJCC, 2(10), 488.
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Palmer, B. F., & Clegg, D. J. (2015). Electrolyte and acid–base disturbances in patients with diabetes mellitus. New England Journal of Medicine, 373(6), 548-559.
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Sulo, G., Igland, J., Vollset, S. E., Nygård, O., Øyen, N., & Tell, G. S. (2013). Cardiovascular disease and diabetes mellitus in Norway during 1994-2009 CVDNOR–a nationwide research project. Norsk epidemiologi, 23(1).
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