Diabetic Retinopathy

Also, on the retina is the optic disk. There are no photoreceptors in this area, so any light that falls on this part of the retina is unseen and creates what is called the blind spot. (Hugh

Age related macular degeneration (AMD) is the leading cause of blindness in people over the age of 50. Every ten years after the age of 50 the prevalence of this disease increases exponentially. Many different factors contribute to the development of AMD including genetic, environment, and metabolic functions. Aside from smoking, abnormal blood pressure, and an unhealthy diet low in fruits and vegetables, many more studies are concluding that similar inflammatory and oxidative processes seen in other age related diseases are also playing a key role in the development of AMD. This disease affects the central areas of the retina and choroid. In return central vision is impaired while peripheral vision is usually not lost. AMD is seen in two different forms, the earlier nonneovascular (dry) type and the more advanced neovascular (wet) type. Each form has its own specific pathology and unique characteristics that set them apart. Fatty, protein deposits called drusens may be the key risk factor in understanding dry AMD pathology, progression, and treatment. Once the more advanced wet AMD is diagnosed, pathology and treatment are targeted around the formation and destruction of abnormal blood vessels, characteristic of the wet AMD eye. The increasing prevalence of AMD has influenced more investigation into what factors can be modulated to prevent the onset or to stop the progression of AMD. This text will discuss the pathology of drusens and the role of inflammation and

1. Red – retinal arterioles, hemorrhaging, neovascularization, vascular anomalies, vascular tumors, retinal breaks, holes in retinoschisis, cilioretinal artery, and inner portion of thin areas of retina

This article discussed the eye disease, Glaucoma. There are two types of Glaucoma; open-angle and closed-angle. Open-angle Glaucoma there are no visual abnormalities, but there is a mechanical obstruction interfering with the drainage pathway. While closed-angle Glaucoma is a physical obstruction. Signs and symptoms of Glaucoma are; headache, nausea, vomiting, blurred vision, halo vision, and eye pain. Glaucoma progresses slowly and is asymptomatic at first. As the disease progresses symptoms appear, if symptoms are present then there is already irreversible damage to the eye. There is no cure for Glaucoma, treatment is aimed at slowing the progression of the disease. Diagnostic tests done to detect Glaucoma are; measuring IOP, evaluation of

The most frequent ocular complications reported for all the AVM groups, are: vascular occlusions, aneurysm formation, intraretinal haemorrhage, exudation and cystoid macular oedema. Furthermore, neovascular glaucoma and open angle glaucoma have been described as a result of a retinal central vein occlusion [1].

In the normal eye, the aqueous humor is the fluid circulation within and that also flows out via a drainage canal. When the outward flow is inhibited, there is a buildup of ocular pressure inside that causes damage, and this is called glaucoma. This condition can be traumatic for the patient as it has no cure. There are two categories that will be discussed in this paper and they are open angle glaucoma and closed angle glaucoma (The glaucoma you may be missing, 2013).

The lower pressure in the vitreous cavity also allows the choroidal expansion. Normally, the pressure within the eye drives the fluid from the extravascular choroid outside via the sclera. However, under hypotonous conditions this pressure head is reduced thereby prolonging the time taken for the fluid to disappear.16 The choroidal detachment may also prolongs the

Glaucoma is the name given to a group of eye diseases that causes damage to the optic nerve fibers and can lead to progressive vision loss or blindness if left untreated. The damage is primarily a result of the buildup of intraocular pressure, which results when an imbalance occurs in the production and drainage of aqueous humour. However, some glaucoma is not distinguished by high intraocular pressure, but as optic nerve damage. In the human eye the ciliary body constantly creates aqueous humour to provide sustenance for surrounding tissues. To maintain a healthy balance as new fluid is produced, older fluid must leave the eye through the meshwork drainage system along the periphery of the iris. If too much aqueous humour is produced or the drainage system is not working properly, consequently intraocular pressure builds, causing optic nerve fiber damage and deterioration of vision.

The surgery requires a small instrument that is inserted into eye which cuts the vitreous gel sack and sections out the gel. From here any further treatment can be carried out, whether it's to treat the retina with a laser or repair a

85% of the AMD cases are classified as the dry from, yet wet AMD accounts for 90% of the total cases of legal blindness in AMD. In wet AMD, abnormal neovascular tissue, which was originated from the choriocapillaris, grow underneath the RPE monolayer or into the subretinal space. The newly immature blood vessels can leak fluid into the retina and cause degeneration of the RPE and retinal cells. If left untreated, the degenerated area will continue to enlarge. The end stage of wet AMD is marked by the formation of fibrotic disciform scars on the fovea, which will lead to a permanent central vision loss [3]. Identification of RPE-derived fibrotic cells in surgically excised fibrotic disciform scars from wet AMD patients[4] suggests that RPE cells undergo proliferation and an epithelium-to-mesenchymal transition (EMT) as a part of the wound healing response. Currently the use of anti-vascular endothelial growth factor (VEGF) therapy can ameliorate the condition; however, this treatment can not prevent the formation of scar tissues and can not restore the loss of RPE

Diabetic retinopathy (DR) is a common microvascular complication of diabetes. With increasing global prevalence of diabetes, DR is a major cause of vision impairment, which accounts for 5% of all blindness, affecting approximately 5 million people worldwide, and is characterized by the progressive occlusion of capillaries, leading to retinal nonperfusion.

Treatment of open-angle glaucoma usually begins with prescription eyedrops. These eyedrops lower pressure inside the eyeball, either by causing the eye to produce less fluid or by helping fluid to drain more. As an alternative to medication or when medication does not control glaucoma, laser surgery can be done. This surgery, also called laser trabeculoplasty, uses a laser to make the openings in the eye's drainage network larger. If medication and laser surgery are unsuccessful, conventional eye surgery may be necessary to make a new opening for fluid to leave the eye.

The optic nerve has to enter the confines of the eye somewhere in order to innervate the retina. Where it enters has no rods and cones (the very nerve endings of the optic nerve which allow us to see). Therefore, this is a "blind spot."

The retina is a very delicate and thin layer in the back eye that helps with vision. It is light sensitive and “...acts like the film in a camera. Images come through the eye’s lens and are focused on the retina” (Retina: MedlinePlus Medical Encyclopedia, n.d). Like many parts of the

Two types of photoreceptors can be found in the retina, the rods and cones. Rods are mainly responsible for scoptic vision thus mostly reactive in dim lighting. Cones are responsible for photopicvision, which provides color under bright light conditions. When it is dark out, only the rods are active so you see monochromatic vision. There are three types of cones S, M and L that respond to different wavelengths. Each rod and cone contains two parts the