HLST274 Global Health Care Management

Question: Anne Baptiste Anne Baptiste is a 32 year old Afro-Caribbean woman What is her condition/complication? Anne was diagnosed with type 2 diabetes mellitus (non-insulin dependent) in 2008. In June 2008, following Anne’s diagnosis, she attended an appointment with the diabetic nurse specialist for support with managing her high blood glucose levels and she is struggling to keep them within normal range (she has hyperglycaemia). What is the impact on the Anne and her family? Anne works as a part-time Dental Nurse. She is recently separated from her partner but has a large network of friends which includes members of her local church where she also runs the children’s church group. Anne lives in rented accommodation with her 13 year old daughter Jacinta, who has been identified as having increasing Answer: Diabetes is characterized by faulty metabolism of glucose, either due to the insufficiency or the difficulty of the body to appropriately utilize insulin. Type 1 diabetes mellitus is characterized by the insufficient production of insulin by the pancreatic cells (Atkinson et al. 2014). The second type, known as type 2 or non-insulin dependent diabetes mellitus, is characterized by insulin resistance or a reduced ability of the body to respond to the hormonal functions of insulin, hence leading to hyperglycemia as observed in Anne (Zinman et al. 2015). Certain ethnic groups belonging to South Asia, as well as African-Caribbean groups in the United Kingdom, are highly susceptible to the disease, hence leaving Anne at a greater risk (Meeks et al. 2016). If left untreated for prolonged periods, as observed in the lack of monitoring of Anne’s blood glucose levels, type 2 diabetes mellitus can lead to further complications in the form of diabetic retinopathy. Anne has initially been diagnosed with non-proliferative diabetic retinopathy, and is characterized by abnormal changes in the blood vessels of the eye, occurring at the microscopic level (Al-Jarrah, M.A. and Shatnawi 2017). One of the major symptoms of non-proliferative diabetic retinopathy is microaneurysms, which includes the formation of bulges in the retinal blood vessels, which are filled with blood. Hemorrhages may occur leading to leakage of blood into the retinal space, further forming ‘dotting’ in the form of blood spots (Ahsan, 2015). With further progression of the disease, presence of hard exudates can be observed which results due to the leakage of accumulated fluid content into the retina from the blood vessels. The interplay of such symptoms leads to the occurrence of blurred vision, as evident in Anne. Blurred vision in type 2 diabetes is due to the altered physiology of the blood vessels situated in the retinal area of the eye. Sugar possesses hygroscopic abilities leading to absorption of moisture. Hence excessive blood sugar in retinal blood vessels, leads to endothelium thickening, accumulation of fluid, disruption of blood circulation and often, growth of abnormal blood vessels, further affecting the visual prowess of the eye (Gardner and Davila 2017). While the exact physiology outlining non-proliferative diabetic retinopathy remains unknown, a reduction in the conduction of nerve transmission by peripheral nerves have been associated with an increased susceptibility (Wert et al. 2016). In the following sessions, it was observed that Anne’s condition has progressed to proliferative diabetic retinopathy, which is characterized by the growth of abnormal blood vessels in the eye, known as neovascularisation (de Carlo et al. 2016). Such blood vessels may ultimately burst and cause spillage of its contents in to the retina, leading to loss of vision The abnormal growth of such blood vessels is often associated with the altered physiology of growth factor production, most commonly being VGEF or vascular endothelial growth factor. This growth factor initiates neovascularisation, angiogenesis, increase in permeability of the vascular membrane, abnormal growth of endothelial cells as well as breakage of the blood-retinal barrier (Choudhuri 2015). In the final stage of progression, Anne was observed to be suffering from diabetic maculopathy, which involves a disruption of the circulation to the macula, due to the serious damage inflicted on the macular capillaries. While the exact pathogenesis behind macular retinopathy has not yet been documented, the alterations in physiology occurs primarily in the increased permeation of the retina, caused to the abnormal VGEF actions, followed by malfunctioning of the blood-retinal barrier (Bek and Jørgensen 2016). This leads to increased fluid accumulation or retinal edema, further resulting in malfunctioning of the secondary receptors of the eye. The characteristic loss in capillary function is outlined by the death of endothelial cells, due to the inflammatory processes outlined by the production of advanced glycation end products (AGEs) – a common pathogenic production in advanced diabetes, which also leads to the malfunctioning of the transmembrane proteins forming the blood-retinal barrier (Singh et al. 2014). References Ahsan, H., 2015. Diabetic retinopathy–biomolecules and multiple pathophysiology. Diabetes & Metabolic Syndrome: Clinical Research & Reviews, 9(1), pp.51-54. Al-Jarrah, M.A. and Shatnawi, H., 2017. Non-proliferative diabetic retinopathy symptoms detection and classification using neural network. Journal of medical engineering & technology, 41(6), pp.498-505. Atkinson, M.A., Eisenbarth, G.S. and Michels, A.W., 2014. Type 1 diabetes. The Lancet, 383(9911), pp.69-82. Bek, T. and Jørgensen, C.M., 2016. The systemic blood pressure and oxygen saturation in retinal arterioles predict the effect of intravitreal anti-VEGF treatment on diabetic maculopathy. Investigative ophthalmology & visual science, 57(13), pp.5429-5434. Choudhuri, S., Chowdhury, I.H., Das, S., Dutta, D., Saha, A., Sarkar, R., Mandal, L.K., Mukherjee, S. and Bhattacharya, B., 2015. Role of NF-κB activation and VEGF gene polymorphisms in VEGF up regulation in non-proliferative and proliferative diabetic retinopathy. Molecular and cellular biochemistry, 405(1-2), pp.265-279. de Carlo, T.E., Bonini Filho, M.A., Baumal, C.R., Reichel, E., Rogers, A., Witkin, A.J., Duker, J.S. and Waheed, N.K., 2016. Evaluation of preretinal neovascularization in proliferative diabetic retinopathy using optical coherence tomography angiography. Ophthalmic surgery, lasers and imaging retina, 47(2), pp.115-119. Gardner, T.W. and Davila, J.R., 2017. The neurovascular unit and the pathophysiologic basis of diabetic retinopathy. Graefe’s Archive for Clinical and Experimental Ophthalmology, 255(1), pp.1-6. Meeks, K.A., Freitas-Da-Silva, D., Adeyemo, A., Beune, E.J., Modesti, P.A., Stronks, K., Zafarmand, M.H. and Agyemang, C., 2016. Disparities in type 2 diabetes prevalence among ethnic minority groups resident in Europe: a systematic review and meta-analysis. Internal and emergency medicine, 11(3), pp.327-340. Singh, V.P., Bali, A., Singh, N. and Jaggi, A.S., 2014. Advanced glycation end products and diabetic complications. The Korean Journal of Physiology & Pharmacology, 18(1), pp.1-14. Wert, K.J., Mahajan, V.B., Zhang, L., Yan, Y., Li, Y., Tosi, J., Hsu, C.W., Nagasaki, T., Janisch, K.M., Grant, M.B. and Mahajan, M., 2016. Neuroretinal hypoxic signaling in a new preclinical murine model for proliferative diabetic retinopathy. Signal transduction and targeted therapy, 1, p.16005. Zinman, B., Wanner, C., Lachin, J.M., Fitchett, D., Bluhmki, E., Hantel, S., Mattheus, M., Devins, T., Johansen, O.E., Woerle, H.J. and Broedl, U.C., 2015. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. New England Journal of Medicine, 373(22), pp.2117-2128.

HLST274 Global Health Care Management

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