Diabetic Retinopathy: Symptoms, Progression and Pathogenesis

This article discusses the symptoms, progression and pathogenesis of Diabetic Retinopathy. It explains the complications of Type 2 Diabetes Mellitus and its impact on the eye. The article also highlights the role of VGEF in the growth of abnormal blood vessels in the eye.

Running head: DIABETIC RETINOPATHY
DIABETIC RETINOPATHY
Name of the Student:
Name of the University:
Author note:

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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

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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

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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).

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References
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Al-Jarrah, M.A. and Shatnawi, H., 2017. Non-proliferative diabetic retinopathy symptoms
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