Self Management Diabetes Care Plan Essay

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Pathophysiological Analysis

Diabetes Self-Management must first begin with understanding Diabetes Mellitus. Microaneurysm formation presents as the earliest expression of diabetic retinopathy. Chances for microaneurysms to form are due to the release of vasoproliferative influences, weakness within the capillary wall, or amplified intra-luminal pressures. Vascular permeability typically results from Microaneurysms. Vascular permeability can also lead to macular edema. "Vascular permeability in the macula can lead to macular edema and can threaten central vision. Obliteration of retinal capillaries can lead to intraretinal microvascular abnormalities (IRMAs). As capillary closure becomes extensive, intraretinal hemorrhages develop" (Zimmerman, 2013, p. 1).

Proliferative retinopathy progresses due to ischemia as well as release of vasoactive substances. This can be VEGF or vascular endothelial growth factor, which fuels new blood vessel creation as a development of non-proliferative retinopathy. Such vessels blow up through the exterior of the retina and develop on the posterior surface of the named vitreous humor. These kinds of vessels are very friable. Meaning, it can lead to vitrified hemorrhages. The vitrified humor may contract leading to retinal detachment.

Moving into neuropathy, the pathophysiology of neuropathy remains complex to examine. Diabetes is connected to dyslipidemia, low insulin, and hyperglycemia, as well as growth factor abnormalities. Such abnormalities are linked with glycation of nerves and blood vessels. Furthermore, autoimmunity can affect nerve structure. Nerve entrapment and trauma can lead to physical nerve damage plus axonal atrophy and loss, segmental demyelination, and progressive demyelination. The culmination of effects cause neuropathy. "Several agents including laminin B2, immunoglobulin FI (IGFI) and II, nerve growth factor (NGF), insulin, and neurotrophin-3 (NT3) are potential growth factors that may restore nerve function" (Zimmerman, 2013, p. 1).

Increased glomerular capillary flow often causes diabetic nephropathy that in turn promotes an amplified extracellular matrix production as well as endothelial damage, leading to augmented glomerular perviousness to macromolecules.

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Interstitial sclerosis and mesangial expansion follows leading to progression of disease and glomerular sclerosis. The macrovascular problems of diabetes come from hyperglycemia, insulin resistance, and excess free fatty acid. These cause amplified oxidative stress, protein kinase initiation and triggering of RAGE or the receptor for advanced glycation end products. These elements act on the endothelium. It does this by first decreasing nitric oxide, increasing endothelin, and increasing angiotensin II, which causes vasoconstriction that generates hypertension as well as cell growth of vascular smooth muscle.

Second, is a decrease in nitric oxide, activation of nuclear factor-KB or NFKB, and an increase in angiotensin II. Furthermore, there is activation of triggered protein-1 that causes increased inflammation, resulting in the release of cytokines, chemokines, and expression of "cellular adhesion molecules." Last, are decreased levels of nitric oxide, increased levels of tissue factor, increased plasminogen activator inhibitor-1, as well as decreased prostacyclin; resulting in thrombosis, platelet activation, hyper-coagulation, and decreased fibrinolysis. Each pathway can ultimately lead to atherosclerosis. Atherosclerosis is the main cause of the macrovascular problems found in diabetes patients.

Current Research

Current research offers some practical approaches to diabetes self-management. Internet-based programs may provide positive potential for inexpensive, practical, continuing disease self-management programs. Glasgow et al., reported 12-month results derived from an online-based diabetes self-management program, optional additional support, paralleled to improved typical care within a 3-arm applied randomized trial. 463 patients were randomized and only 77.3% accomplished 12-month follow-up. Main outcomes were vicissitudes in the health behaviors of physical activity, healthy eating, and medication taking. Ancillary results were hemoglobin A1C, lipids, body mass index, psychosocial factors, and blood pressure. The results were positive. "Internet conditions improved health behaviors significantly vs. usual care over the 12-month period (d for effect size = .09 -- .16). All….....

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