STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (7)
Translation Draft
I will be "expeditive" and punctual in the content of this post, because I have many forms of manifestation to present (probably the same in the next post)...
Macular degeneration is a major cause of bilateral, gradual, painless loss of central vision in the elderly. The old term "senile macular degeneration," misinterpreted by many patients as an offensive term, has been replaced by "age-related macular degeneration."
There is a nonexudative (dry) form and an exudative (wet) form. The nonexudative process begins with the accumulation of extracellular deposits, called hyalini bodies, under the retinal pigment epithelium. In ophthalmoscopy, they have pleiomorphic appearance, but generally appear as small, discrete yellow lesions, grouped in the macula. Over time they become larger, more numerous and confluenced. The retinal pigment epithelium detaches itself in places and atrophies, causing vision loss by interfering with the function of photoreceptors. There is currently no method to prevent the occurrence of age-related macular degeneration.
Various mixtures of vitamins (A, C and E) and minerals (zinc, copper, selenium) have been marketed, which have not been shown to be useful in delaying the macular degeneration process. Exudative macular degeneration, which occurs only in a small number of patients, occurs when the neoformation vessels in the choroid proliferate through gaps in the Bruch membrane, penetrating into the virtual space below the retinal pigment epithelium.
Hemorrhages in these vessels cause the retina and pigment epithelium to rise, with distortion (metamorphopsia) and blurred vision. Although the onset of these symptoms is usually gradual, hemorrhages in the subretinal choroidal neovascular membranes sometimes cause acute loss of vision.
Neovascular membranes can be difficult to visualize when examination of the bottom of the eye, as they are located below the retina. Fluorescein angiography is extremely useful for detecting them. In some patients, prompt laser ablation of choroidal neovascular membranes observed in fluorescein angiography may stop the exudative process.
However, neovascular membranes frequently relapse, requiring constant surveillance and repeated photocoagulation. Massive or repeated subretinal haemorrhage in neovascular membranes leads to fibrosis, with the production of a round macular scar (in the form of a disc) and permanent loss of central vision. In most patients with age-related macular degeneration, attempts to surgically remove subretinal membranes did not improve vision. However, the results were encouraging in patients with choroidal neovascular membranes due to ocular histoplasmosis syndrome.
Serous central chorioretinopathy mainly affects men between the ages of 20 and 50. The extraction of serous fluid from the choroid produces small and localized detachments of the retinal pigment epithelium and neurosensory retina.
When the macola is affected, these detachments produce acute or chronic symptoms of metamorphosis and blurred vision. They are difficult to visualize by direct ophthalmoscopy because the detached retina is transparent and only moderately elevated.
Diagnosis of serous central chorioretinopathy is easily established by fluorescein angiography, which highlights the penetration of the contrast substance into the subretinal space. The cause of serous central chorioretinopathy is unknown. Symptoms may spontaneously resolve if the retina re-settles, but recurrent postings are common. Some patients in this situation benefit from laser photocoagulation.
Diabetic retinopathy was a rare condition until 1921 when insulin appeared, which attracted a spectacular increase in life expectancy in patients with diabetes. Currently, diabetic retinopathy is a major cause of cetate. Diabetic retinopathy develops over the years, but eventually it appears in almost all cases.
Regular surveillance of the dilated eye butt is crucial for any patient with diabetes. In advanced diabetic retinopathy, the proliferation of neoformation vessels leads to blindness through hemorrhages in the vitreous body, retinal detachment and glaucoma. These complications can be avoided in most patients by panretinal laser photocoagulation, practiced at the appropriate time in the course of the disease.
Retinitis pigmentosa is a generic term for a disparate group of dystrophies of cells with canes and cones, characterized by progressive nocturnal blindness (nictalopia), visual field constriction with ring scotom, loss of acuity and abnormal electroretinogram (ERG).
Occurs sporadically or autosomal recessively, dominantly or X-bound. The asymmetrical deposits of black color, made up of agglomeration of pigments in the periphery of the retina, called bone spicules due to their similarity to the spicules of the spongy bone, give the name of this disease. This term is actually inappropriate because retinitis pigmentosa is not an inflammatory process.
Most cases are due to a mutation in the rhodopin gene, photopigment of cane cells or periferin gene, a glycoprotein located in the external segments of photoreceptors. There is no effective treatment for retinitis pigmentosa. Vitamin A is slightly delaying the deterioration of ERG, but has no beneficial effects on visual acuity or visual fields.
Some forms of retinitis pigmentosa occur in association with rare hereditary systemic diseases (such as olivopotocerebereberebelous degeneration, Bassen-Kornzweig disease, Kearns-Sayre syndrome or Refsum disease). Chronic treatment with chloroquine, hydroxychloroquinone and phenothiazine (especially thioridazine) may cause vision loss through toxic retinopathy similar to retinitis pigmentation.
The epiretinal membrane refers to a fibrocellular tissue that proliferates along the inner surface of the retina, producing metamorphosis and reducing visual acuity following macular deformation. With the help of the ophthalmoscope, a wrinkled, cellophane-like membrane can be observed on the retina. epireretinal membrane is very common in patients over 50 years of age and is usually one-sided.
Most cases are idiopathic, but some occur as a result of hypertensive retinopathy, diabetes, retinal detachment or trauma. If the visual acuity is reduced to a level of about 6/24, vitrectomy and surgical curing of the membrane is recommended in order to resolve the folds of the macula. The contraction of an epiretinal membrane sometimes gives rise to a macular orifice.
Most macular orifices, however, are produced by local traction exerted by the vitreous body at the fovea level. Visual acuity is usually low to a level of 6/30 or more. Vitrectomy may improve visual acuity in some patients with macular orifice. Fortunately, less than 10% of patients with macular orifice develop a macular orifice in the other eye.
The melanoma of the choroid is the most common primary tumor of the eyeball. Causes photopsy, extended scotom and vision loss. A small melanoma is often difficult to differentiate from benign choroidal nebula. Serial examinations carried out carefully are necessary to determine the malignancy of proliferation. Treatment of melanoma is controversial.
Options include enuclearea, local resection and irradiation. Metastatic tumors of the eyeball are more numerous than primary tumours originating in the uve. Breast and lung carcinoma have a special predilection for dissemination to the choroid or iris. Leukemias and lymphomas also routinely invade eye tissues. Sometimes, their only sign when examining the eye is the presentation of a cellular detritus in the vitreous cop, which can mimic a chronic posterior uveitis.
Retrobulbar tumors of the optic nerve (meningiomas, gliomas) or chiasmatic tumors (pituitary adenomas, meningiomas) cause gradual loss of vision, with little objective data on examination, except for the pallor of the optic disc. Rarely, the sudden expansion of a pituitary adenoma due to infarction and bleeding (pituitary apoplexy) causes acute retrobulbar loss of vision, with headache, nausea and paralysis of motor eye nerves. In any patient with visual field defects or optic atrophy, where careful background examination and thorough clinical examination of the eye have not identified the cause, CT and MRI examinations should be considered.
I'm going to start my exophthalmia presentations now. Exophthalmia is the abnormal protrusion to the anterior of an eyeball or both. Measure with a Hertel exophthalmeter, a manual instrument that records the position of the anterior surface of the cornea from the lateral edge of the orbit. if such an instrument is not available, the relative position of the eyeball can be assessed by bending the patient's head forward and looking down at the orbit. This can detect an exophthalmia of only 2 mm of an eyeball. The appearance of exophthalmia implies the existence of a space-replacement lesion in the orbit. CT or MRI examinations should be performed in any patient with exophthalmia, unless there is a safe diagnosis of Graves ophthalmopathy.
Graves ophthalmopathy is the major cause of exophthalmia in adults. Inflammation of the orbit and damage to extrinsic eye muscles, especially the medial right and the lower right, are responsible for the protrusion of the eyeball. Corneal exposure, palpebral retraceration, conjunctival congestion, eye limitation, diplopia and loss of vision following compression of the optic nerve are cardinal signs. Compression of the optic nerve should be resolved promptly by radiotherapy or decompression of the orbit to prevent permanent loss of vision.
Orbital pseudotumora is an inflammatory, idiopathic syndrome of the orbit, commonly confused with Graves ophthalmopathy. symptoms include pain, limitation of eye movements, exophthalmia and congestion. Tests for sarcoidosis, Wegener granulomatosis and other types of orbital vasculitis or vascular collagen diseases are negative. Imaging examinations often reveal stupefied eye muscles (orbital myositis) with enlarged tendons.
In contrast, in Graves' ophthalmopathy, the tendons of the eye muscles are usually spared. Tolosa-Hunt syndrome can be considered an extension of orbital pseudotumor, through the upper orbital fissure, in the cavernous sinus. Establishing the diagnosis of orbital pseudotumor is difficult. Orbital biopsy frequently provides non-specific data highlighting the infiltration of adipose tissue with lymphocytes, plasma cells and eosinophils. A spectacular response to the systemic glucocorticoid therapeutic test indirectly provides the best confirmation of diagnosis.
We'll continue... tomorrow...
I will be "expeditive" and punctual in the content of this post, because I have many forms of manifestation to present (probably the same in the next post)...
Macular degeneration is a major cause of bilateral, gradual, painless loss of central vision in the elderly. The old term "senile macular degeneration," misinterpreted by many patients as an offensive term, has been replaced by "age-related macular degeneration."
There is a nonexudative (dry) form and an exudative (wet) form. The nonexudative process begins with the accumulation of extracellular deposits, called hyalini bodies, under the retinal pigment epithelium. In ophthalmoscopy, they have pleiomorphic appearance, but generally appear as small, discrete yellow lesions, grouped in the macula. Over time they become larger, more numerous and confluenced. The retinal pigment epithelium detaches itself in places and atrophies, causing vision loss by interfering with the function of photoreceptors. There is currently no method to prevent the occurrence of age-related macular degeneration.
Various mixtures of vitamins (A, C and E) and minerals (zinc, copper, selenium) have been marketed, which have not been shown to be useful in delaying the macular degeneration process. Exudative macular degeneration, which occurs only in a small number of patients, occurs when the neoformation vessels in the choroid proliferate through gaps in the Bruch membrane, penetrating into the virtual space below the retinal pigment epithelium.
Hemorrhages in these vessels cause the retina and pigment epithelium to rise, with distortion (metamorphopsia) and blurred vision. Although the onset of these symptoms is usually gradual, hemorrhages in the subretinal choroidal neovascular membranes sometimes cause acute loss of vision.
Neovascular membranes can be difficult to visualize when examination of the bottom of the eye, as they are located below the retina. Fluorescein angiography is extremely useful for detecting them. In some patients, prompt laser ablation of choroidal neovascular membranes observed in fluorescein angiography may stop the exudative process.
However, neovascular membranes frequently relapse, requiring constant surveillance and repeated photocoagulation. Massive or repeated subretinal haemorrhage in neovascular membranes leads to fibrosis, with the production of a round macular scar (in the form of a disc) and permanent loss of central vision. In most patients with age-related macular degeneration, attempts to surgically remove subretinal membranes did not improve vision. However, the results were encouraging in patients with choroidal neovascular membranes due to ocular histoplasmosis syndrome.
Serous central chorioretinopathy mainly affects men between the ages of 20 and 50. The extraction of serous fluid from the choroid produces small and localized detachments of the retinal pigment epithelium and neurosensory retina.
When the macola is affected, these detachments produce acute or chronic symptoms of metamorphosis and blurred vision. They are difficult to visualize by direct ophthalmoscopy because the detached retina is transparent and only moderately elevated.
Diagnosis of serous central chorioretinopathy is easily established by fluorescein angiography, which highlights the penetration of the contrast substance into the subretinal space. The cause of serous central chorioretinopathy is unknown. Symptoms may spontaneously resolve if the retina re-settles, but recurrent postings are common. Some patients in this situation benefit from laser photocoagulation.
Diabetic retinopathy was a rare condition until 1921 when insulin appeared, which attracted a spectacular increase in life expectancy in patients with diabetes. Currently, diabetic retinopathy is a major cause of cetate. Diabetic retinopathy develops over the years, but eventually it appears in almost all cases.
Regular surveillance of the dilated eye butt is crucial for any patient with diabetes. In advanced diabetic retinopathy, the proliferation of neoformation vessels leads to blindness through hemorrhages in the vitreous body, retinal detachment and glaucoma. These complications can be avoided in most patients by panretinal laser photocoagulation, practiced at the appropriate time in the course of the disease.
Retinitis pigmentosa is a generic term for a disparate group of dystrophies of cells with canes and cones, characterized by progressive nocturnal blindness (nictalopia), visual field constriction with ring scotom, loss of acuity and abnormal electroretinogram (ERG).
Occurs sporadically or autosomal recessively, dominantly or X-bound. The asymmetrical deposits of black color, made up of agglomeration of pigments in the periphery of the retina, called bone spicules due to their similarity to the spicules of the spongy bone, give the name of this disease. This term is actually inappropriate because retinitis pigmentosa is not an inflammatory process.
Most cases are due to a mutation in the rhodopin gene, photopigment of cane cells or periferin gene, a glycoprotein located in the external segments of photoreceptors. There is no effective treatment for retinitis pigmentosa. Vitamin A is slightly delaying the deterioration of ERG, but has no beneficial effects on visual acuity or visual fields.
Some forms of retinitis pigmentosa occur in association with rare hereditary systemic diseases (such as olivopotocerebereberebelous degeneration, Bassen-Kornzweig disease, Kearns-Sayre syndrome or Refsum disease). Chronic treatment with chloroquine, hydroxychloroquinone and phenothiazine (especially thioridazine) may cause vision loss through toxic retinopathy similar to retinitis pigmentation.
The epiretinal membrane refers to a fibrocellular tissue that proliferates along the inner surface of the retina, producing metamorphosis and reducing visual acuity following macular deformation. With the help of the ophthalmoscope, a wrinkled, cellophane-like membrane can be observed on the retina. epireretinal membrane is very common in patients over 50 years of age and is usually one-sided.
Most cases are idiopathic, but some occur as a result of hypertensive retinopathy, diabetes, retinal detachment or trauma. If the visual acuity is reduced to a level of about 6/24, vitrectomy and surgical curing of the membrane is recommended in order to resolve the folds of the macula. The contraction of an epiretinal membrane sometimes gives rise to a macular orifice.
Most macular orifices, however, are produced by local traction exerted by the vitreous body at the fovea level. Visual acuity is usually low to a level of 6/30 or more. Vitrectomy may improve visual acuity in some patients with macular orifice. Fortunately, less than 10% of patients with macular orifice develop a macular orifice in the other eye.
The melanoma of the choroid is the most common primary tumor of the eyeball. Causes photopsy, extended scotom and vision loss. A small melanoma is often difficult to differentiate from benign choroidal nebula. Serial examinations carried out carefully are necessary to determine the malignancy of proliferation. Treatment of melanoma is controversial.
Options include enuclearea, local resection and irradiation. Metastatic tumors of the eyeball are more numerous than primary tumours originating in the uve. Breast and lung carcinoma have a special predilection for dissemination to the choroid or iris. Leukemias and lymphomas also routinely invade eye tissues. Sometimes, their only sign when examining the eye is the presentation of a cellular detritus in the vitreous cop, which can mimic a chronic posterior uveitis.
Retrobulbar tumors of the optic nerve (meningiomas, gliomas) or chiasmatic tumors (pituitary adenomas, meningiomas) cause gradual loss of vision, with little objective data on examination, except for the pallor of the optic disc. Rarely, the sudden expansion of a pituitary adenoma due to infarction and bleeding (pituitary apoplexy) causes acute retrobulbar loss of vision, with headache, nausea and paralysis of motor eye nerves. In any patient with visual field defects or optic atrophy, where careful background examination and thorough clinical examination of the eye have not identified the cause, CT and MRI examinations should be considered.
I'm going to start my exophthalmia presentations now. Exophthalmia is the abnormal protrusion to the anterior of an eyeball or both. Measure with a Hertel exophthalmeter, a manual instrument that records the position of the anterior surface of the cornea from the lateral edge of the orbit. if such an instrument is not available, the relative position of the eyeball can be assessed by bending the patient's head forward and looking down at the orbit. This can detect an exophthalmia of only 2 mm of an eyeball. The appearance of exophthalmia implies the existence of a space-replacement lesion in the orbit. CT or MRI examinations should be performed in any patient with exophthalmia, unless there is a safe diagnosis of Graves ophthalmopathy.
Graves ophthalmopathy is the major cause of exophthalmia in adults. Inflammation of the orbit and damage to extrinsic eye muscles, especially the medial right and the lower right, are responsible for the protrusion of the eyeball. Corneal exposure, palpebral retraceration, conjunctival congestion, eye limitation, diplopia and loss of vision following compression of the optic nerve are cardinal signs. Compression of the optic nerve should be resolved promptly by radiotherapy or decompression of the orbit to prevent permanent loss of vision.
Orbital pseudotumora is an inflammatory, idiopathic syndrome of the orbit, commonly confused with Graves ophthalmopathy. symptoms include pain, limitation of eye movements, exophthalmia and congestion. Tests for sarcoidosis, Wegener granulomatosis and other types of orbital vasculitis or vascular collagen diseases are negative. Imaging examinations often reveal stupefied eye muscles (orbital myositis) with enlarged tendons.
In contrast, in Graves' ophthalmopathy, the tendons of the eye muscles are usually spared. Tolosa-Hunt syndrome can be considered an extension of orbital pseudotumor, through the upper orbital fissure, in the cavernous sinus. Establishing the diagnosis of orbital pseudotumor is difficult. Orbital biopsy frequently provides non-specific data highlighting the infiltration of adipose tissue with lymphocytes, plasma cells and eosinophils. A spectacular response to the systemic glucocorticoid therapeutic test indirectly provides the best confirmation of diagnosis.
We'll continue... tomorrow...
Have a good day and find
yourself anywhere and in any "Izvor of Healing".
Dorin, Merticaru