what is eye disease?

Detecting Eye Disease

Some of the other research we are currently doing at Betham Eye Institute involves us looking at the retina with extremely interesting and state-of-the-art imaging technology.There are ways we can never do this before and there are several different ways we do this. We look at extremely broad field images. Retina photos that take up a much wider area than we did before. To give you some perspective, when people started talking about how to classify diabetic retinopathy in the late 1960s, the ability to move photos of the retina to the periphery of the retina and montage them together for twelve hours and now with a single image About 82 percent of the retina is retrieved and it takes less than a quarter of a second to retrieve.

So it’s a big improvement and Dr. Paulo Silva and Dr. Lloyd Ailo and I and our team are starting to see changes in the ultra wide-field images and now we can see farther than the edge of the retina. This is done before changing the way predictive progressions of diabetic eye complications can be made, which will help them better understand who can make their eye disease worse. Then there are some very interesting data from the studies done by Dr. Silva. We can suggest that there are diabetic lesions or diabetic changes on the periphery of the retina to help us better predict who will develop eye diseases that will get worse over time. Also, my specialized team looked at the retina of the nerves using a cross-section of the retina to see if diabetes could not only worsen retinopathy but also better predict those with better or worse vision. 

This will become very important over time. Because we now have no good way to predict whether diabetics will regain their sight over time or lose their sight over time. We are evaluating new therapies, and our team in Jocelyn recently published a newspaper report on the use of optical reflection, a specific component of the retina that we can now evaluate on a technology called optical coherence tomography imaging. We have shown that the disorganization of the retina and the inner layers of the retina is very close to looking at the individual retina layers. ci ratios lose vision and gain over time and this is a new biomarking machine and will be evaluated by us in further studies. The ultimate imaging technology we evaluate and use to evaluate the eyes of diabetics is called the Adaptive Optics Scanning Laser Eye Test, which was first proposed in astronomy to correct distortions of incoming light wavelengths for sharper and better images. Using AOSLO technology we can visualize the retina and get the resolution. The largest blood vessels in the eye are about 125 microns in diameter and the diameter of the red blood cells that pass through those blood vessels. 

A resolution of 6 microns to 8 microns in diameter means that we can see single red blood cells flowing through the vessels of the retina. K is a capillary and can make image structures smaller than that diameter, including the central photoreceptor or light sensor cells in the eye, giving us the ability to see the human eye for the first time in a dynamic way during blood flow. Through the vessels of the retina and the changes that those vessels cause in diabetes. Therefore, we are interested in using this technology again to see if new and prognostic signs of diabetes can be explored in the future.

 Thyroid Eye Disease: Diagnosis and Symptoms

Describe the application of balm anatomy to the development of thyroid eye disease to identify the symptoms of thyroid eye disease and to find a clinical approach to the diagnosis and treatment of thyroid eye disease. In the following slide, it will be useful to review orbital anatomy to better illustrate the volume of orbital fat and all external activity, including how it relates to thyroid ocular disease and the appearance that often accompanies it. Muscles, including the nose, can push the contents of the orbit forward by increasing the altitude as well as the orbit of this Saturday, causing the burning sensation that is often seen with this disease. Let’s look at the pathogenesis we have just mentioned, including loss of vision due to compression of the optic nerve.

Previous slide Autoimmune antibodies directed against antibodies are often thyroid-stimulating hormone antagonists on thyroid cells. are available. Clinical manifestations of thyroid-stimulating hormone receptor inhibiting thyroid-stimulating hormone receptor binding and TSI III associated with thyroid-stimulating hormone inhibiting thyroid-stimulating hormone receptor binding. % Of Affected Patients These thyroid-stimulating hormone antibodies and activated cytokines cause fibroblasts to activate and increase hydrophilic glycosaminoglycan secretion in the extracellular matrix This figure indicates the appearance of normal extraocular muscles. Activation or CT scan of the retrograde orbital swelling is called eye protrusion or exophthalmos swelling. This is because it depends on the anatomy of the orbit rather than the level of swelling. Can produce protrusion or exophthalmos, and retrieval of the previously discussed lid may blur the vision of periorbital edema, burning or tearing of a foreign object. Tears can be burning and blurry because the lid is retrievable and cannot be trusted properly because it is dry. 

The tear-producing glands automatically affect the immune system, preventing them from functioning properly, or preventing the four eyelids from completely covering the eyelids, or preventing retinal detachment or pain due to swelling and swelling restriction. It can lead to diplopia or duplicate color vision saturation or dyschromia, which is an early sign of high SIA optic neuropathy and can lead to further vision loss, but how can a doctor or an unstable medical student diagnose thyroid disease? The disease is clinically diagnosed by a combination of the described ocular abnormalities in the pre-slide and hyperthyroid laboratories, which we often think of as low TSH and high 3T4 and T3, all of which may be normal in an affected patient, but progressive prophylaxis of typhoid fever Testing for receptor antibodies should be encouraged. In general, it is important to rule out specific signs of thyroid hormone access, regardless of the pathogenesis of the thyroid stimulatory immune subtype mentioned earlier, and to delay calf trauma temporary flare-ups and lid closures. 

Highlights are helpful in the differential diagnosis but are more often used to assess retinal detachment. Another example for. This An objective measure of the disease is usually assessed by seven findings that can be assessed in patients for the first time using clinical activity scores, and subsequent assessments and more than three-thirds of the additional scores of three or more or similar subsequent assessments for first-time patients Up to four out of ten are linked to the likelihood of responding to functional diseases and immunosuppressive therapies such as corticosteroids and now we have a method to diagnose thyroid eye disease and discuss the severity of the disease activity and therapeutic treatment. Treatment for active inflammatory eye disease stage and treatment for the permanent post-inflammatory stage The active period can last up to two to three years and requires careful monitoring. During this time Intel Stable Therapeutic should focus on protecting the site and the integrity of Konya. Dual vision therapy interferes with daily activities and in many cases becomes a troublesome treatment during the indefinite relaxation phase.

 Correction of unacceptable permanent changes that exist after the stabilization of the eye conditions during the active phase This figure shows the severity of the symptoms that may occur during the active phase. I now look closely at the components of the active phase treatment, such as the appearance of a stable phase with liver prolapse or perhaps mild protrusion. The most important step is to reverse hyperthyroidism. Be careful as none of these hyperthyroid reversal methods can directly improve thyroid gland fluid retention and worsen the course of the disease. Therefore it is very important to monitor the activity of the thyroid gland.

 It is very important to advise your patients in smoking cessation studies. By involving the optic nerve, it increases the likelihood of photophobia and response to anti-inflammatory therapies that may be associated with the use of artificial tears and sunglasses to increase sensitivity to wind or cold air, as far as the eye can use to reduce eye irritation. Although retro ocular pressure or pain can be managed with corticosteroids to treat inflammation and swelling of the periorbital tissues during sleep and should be used with caution by physicians, steroids are usually prescribed because the side effects are often worse than the symptoms. As a temporary measure for patients with compression optic neuropathy, the orbit is removed until surgical dissection of the orbit, or orbital dissection surgery is found on the lateral wall or wall of the roof. Temporary therapeutic diplopia or double vision often occurs as a form of an eye patch or scotch tape over the patient ‘Surgery directly on one side of the glass or directly into the lens of the prison glass that remains stuck after the disease has stabilized To wrap. 

All of the treatment options available during the permanent remission phase are surgery for patients with proptosis. The removal of the lateral or medial walls of the orbital roof by orbital dissection surgery as mentioned in the previous slide is free of enlarged retro ocular tissue. One problem with this surgery, out of their limited limitations, is that in some patients the district avoids double vision. This brings us to our next treatment option, strabismus surgery. Strabismus surgery is the reconstruction of the eyes relative to each other. This is primarily done by weakening or relaxing the outer muscles of the eye. Basically, the recession is done by technology. It separates the eye muscles from the surface of the eye and reconnects. Later eye surgery may be performed to correct post-traumatic or peripheral edema. This is the last time strabismus surgery can change the position of the eye, so to conclude our discussion of thyroid eye disease, we will discuss the volume of orbital fat and autoimmune ocular antibodies, as well as thyroid-stimulating anticoagulant antibodies as well as cytokines We found symptoms of thyroid ocular disease in which the hydrophilic glycosaminoglycan refuses to secrete. 

We found that post-traumatic imperial edema and, ultimately, clinical activity scores, as well as treatment options and non-invasive local measurements, ranging from systemic actions to surgery, are not limited to proptosis.

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