Endocrine pathology and eye changes

With insufficient activity of the parathyroid glands as a result of hypocalcemia, cataracts develop along with convulsions, tachycardia, and respiratory disorders. Clouding of the lens with tetany can occur within a few hours. With biomicroscopy, point and streaky gray opacities are visible in the cortex of the lens, under the anterior and posterior capsules, alternating with vacuoles and water gaps, then the cataract progresses. It is removed surgically. Treatment of hypocalcemia consists of prescribing parathyroid gland preparations and calcium salts.

In patients with acromegaly, retinal angiopathy develops due to pituitary dysfunction, a symptom of congestive disk appears, central vision and color perception decrease, and visual fields fall out bitemporally. The disease can end in atrophy of the optic nerves and complete blindness. Most often, the cause of the disease is eosinophilic adenoma of the pituitary gland.

In case of hyperfunction of the adrenal cortex and medulla, developing hypertension causes changes in the retina typical of secondary arterial hypertension. In case of hypofunction (Addison's disease), electrolyte and carbohydrate metabolism is disrupted. The patient has no appetite, general weakness develops, body weight decreases, hypothermia, arterial hypotension and skin pigmentation are observed, including the skin of the eyelids and conjunctiva. In case of a long-term course of the disease, the color of the iris and fundus becomes darker. Treatment is carried out by an endocrinologist.

Dysfunction of the thyroid gland causes changes in the orbital tissue and external eye muscles, which leads to the development of endocrine exophthalmos.

Diabetes mellitus develops in representatives of all human races. According to world statistics, diabetes affects 1 to 15% of the world's population, and the incidence is constantly increasing. The focus of modern diabetologists is the problem of vascular complications of diabetes mellitus, on which the prognosis of the disease, the ability to work and the life expectancy of the patient depend. With diabetes, the vessels of the retina, kidneys, lower limbs, brain and heart are intensively affected. An ophthalmologist can be the first to detect changes in the fundus characteristic of diabetes mellitus when patients come with complaints of decreased vision, seeing black dots and spots, unaware of the presence of diabetes mellitus. In addition to retinopathy, diabetes causes cataracts, secondary neovascular glaucoma, corneal damage in the form of punctate keratopathies, recurrent erosions, trophic ulcers, endothelial dystrophy, blepharitis, blepharoconjunctivitis, styes, iridocyclitis, and sometimes the oculomotor nerves are affected.

The first signs of changes in the fundus are dilation of the retinal veins, venous stasis, and venous hyperemia. As the process progresses, the retinal veins acquire a spindle-shaped form, become tortuous, and stretched - this is the stage of diabetic angiopathy. Then the walls of the veins thicken, and parietal thrombi and foci of periphlebitis appear. The most characteristic sign is saccular aneurysmal dilations of small veins scattered throughout the fundus, located paramacularly. During ophthalmoscopy, they look like a cluster of individual red spots (they are confused with hemorrhage), then the aneurysms turn into white foci containing lipids. The pathological process passes into the stage of diabetic retinopathy, which is characterized by the appearance of hemorrhages, from small-point to large, covering the entire fundus. They most often occur in the area of the macula and around the optic disc. Hemorrhages occur not only in the retina but also in the vitreous body. Preretinal hemorrhages are often precursors to proliferative changes.

The second characteristic sign of diabetic retinopathy is deep waxy and cottony whitish foci of exudation with blurred borders. They are more common when diabetic retinopathy is combined with hypertension or nephropathy. Waxy exudates have the form of droplets with a whitish tint.

Retinal edema and focal changes are often localized in the macular area, which leads to decreased visual acuity and the appearance of relative or absolute scotomas in the visual field. Damage to the macula area in diabetes mellitus is called diabetic maculopathy, which can occur at any stage of the disease and manifests itself in exudative, edematous and ischemic (the worst prognosis for vision) forms.

Fluorescent angiography helps to establish the correct diagnosis and decide on laser coagulation of the affected vessels. This is the most informative method that allows you to determine the initial damage to the vessel wall, their diameter, permeability, microaneurysms, capillary thrombosis, ischemic zones and blood circulation rate.

The next stage of development of pathological changes is proliferative diabetic retinopathy, in which proliferative changes in the retina and vitreous body join the changes that appeared in the stage of angiopathy and simple diabetic retinopathy. At this stage, new formation of capillaries is noted, the loops of which appear on the surface of the retina, the optic nerve disc and along the course of the vessels.

As the process progresses, capillaries grow into the vitreous body with detachment of the hyaloid membrane. In parallel with neovascularization, fibrous growths appear, localized preretinal and growing into the vitreous body and retina. During ophthalmoscopy, proliferates appear as grayish-white stripes, foci of various shapes covering the retina.

Fibrovascular tissue penetrating the posterior hyaloid membrane of the vitreous body gradually thickens and contracts, causing retinal detachment. The proliferative form of diabetic retinopathy is particularly severe, progresses rapidly, has a poor prognosis, and usually occurs in young people.

The picture of the fundus changes in diabetes mellitus if it is combined with hypertension, atherosclerosis, nephropathy. Pathological changes in these cases increase faster.

Diabetic retinoangiopathy is considered benign if it progresses in stages over 15-20 years.

Treatment is pathogenetic, i.e. regulation of carbohydrate, fat and protein metabolism, and symptomatic - elimination and prevention of manifestations and complications of diabetes mellitus.

Enzyme preparations are effective for resorption of hemorrhages in the vitreous body: lidase, chymotrypsin, iodine in small doses. ATP is prescribed to improve oxidation-reduction processes.

The most effective method of treating diabetic retinopathy is laser coagulation of retinal vessels, aimed at suppressing neovascularization, closing and limiting vessels with increased permeability, and preventing tractional retinal detachment. Special laser treatment methods are used for different types of diabetic pathology.

In case of diabetic cataract, surgical treatment is indicated. After cataract extraction, complications often arise: hemorrhages in the anterior chamber of the eye, detachment of the vascular membrane, etc.

In the presence of hemorrhages in the vitreous body with a significant decrease in visual acuity, tractional retinal detachment, and fibrovascular proliferation, the altered vitreous body (vitrectomy) is removed with simultaneous endolaser coagulation of the retina. In recent years, thanks to new technical equipment, vitreoretinal surgery has achieved great success. It has become possible to excise preretinal adhesions covering the area of the macula. Such operations restore vision to patients who were previously considered incurable.

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