Steroid induced glaucoma causes

The first isolation and structure identifications of prednisone and prednisolone were done in 1950 by Arthur Nobile . [23] [24] [25] The first commercially feasible synthesis of prednisone was carried out in 1955 in the laboratories of Schering Corporation, which later became Schering-Plough Corporation , by Arthur Nobile and coworkers. [26] They discovered that cortisone could be microbiologically oxidized to prednisone by the bacterium Corynebacterium simplex. The same process was used to prepare prednisolone from hydrocortisone . [27]

After the plate is attached to the globe, the tube is laid across the cornea and cut with a sharp scissors to create a beveled edge with the opening toward the cornea. The tube should extend approximately to 3 mm into the anterior chamber to minimize the risk of tube-cornea touch or retraction out of the anterior chamber. A 23-gauge needle is used to create a track through which the tube is inserted into the anterior chamber just anterior and parallel to the iris. The tube may be secured to the sclera a few millimeters anterior to the plate with 7- 0 or 8-0 Vicryl suture. This suture helps to stabilize the tube and should not be tight; otherwise, it will restrict flow in valved devices.

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandrosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Q: Please, explain the use of calcium channel blockers in glaucoma treatment. Do they replace other medications such as beta-blockers or are they used in conjunction with other glaucoma medication? Is it more dangerous to the patient to use calcium channel blockers when the patient is being treated for other health problems such as heart disease?
A: Calcium channel blockers represent an entirely new approach to the treatment of glaucoma. Hopefully, the advent of these drugs marks only the beginning of a trend in finding new approaches to the treatment of glaucoma over the coming years.
  Previously, the only form of treatment of glaucoma has involved lowering intraocular pressure (IOP), even when IOP is normal to begin with. Although the evidence is not all in yet, calcium channel blockers have been reported to increase blood flow to the eye and to stabilize the visual field. Thus, instead of lowering IOP (although they appear to do this also), calcium channel blockers increase the resistance of the eye to glaucomatous damage. Because they represent an entirely new approach to the treatment of glaucoma, they do not replace other medications that are used in conjunction with them.
  There are different types of calcium channel blockers. Some primarily affect the strength with which the heart contracts, while others affect peripheral blood vessels, making them dilate so that more blood can pass through. The calcium channel blockers used in the treatment of glaucoma ideally would be those which increase blood flow to the brain, since the eye and the brain share a common blood supply.
  It remains to be determined just which patients will be helped and which will not be helped, or even perhaps harmed, by calcium channel blockers. Calcium channel blockers can also lower blood pressure, and a low blood pressure predisposes to glaucomatous damage. Therefore, we do not use these drugs at the present time in patients who have low blood pressure, but only in those with normal or high blood pressure. The patient's internist or family physician should be consulted with regard to the treatment plan.

Steroid induced glaucoma causes

steroid induced glaucoma causes

Q: Please, explain the use of calcium channel blockers in glaucoma treatment. Do they replace other medications such as beta-blockers or are they used in conjunction with other glaucoma medication? Is it more dangerous to the patient to use calcium channel blockers when the patient is being treated for other health problems such as heart disease?
A: Calcium channel blockers represent an entirely new approach to the treatment of glaucoma. Hopefully, the advent of these drugs marks only the beginning of a trend in finding new approaches to the treatment of glaucoma over the coming years.
  Previously, the only form of treatment of glaucoma has involved lowering intraocular pressure (IOP), even when IOP is normal to begin with. Although the evidence is not all in yet, calcium channel blockers have been reported to increase blood flow to the eye and to stabilize the visual field. Thus, instead of lowering IOP (although they appear to do this also), calcium channel blockers increase the resistance of the eye to glaucomatous damage. Because they represent an entirely new approach to the treatment of glaucoma, they do not replace other medications that are used in conjunction with them.
  There are different types of calcium channel blockers. Some primarily affect the strength with which the heart contracts, while others affect peripheral blood vessels, making them dilate so that more blood can pass through. The calcium channel blockers used in the treatment of glaucoma ideally would be those which increase blood flow to the brain, since the eye and the brain share a common blood supply.
  It remains to be determined just which patients will be helped and which will not be helped, or even perhaps harmed, by calcium channel blockers. Calcium channel blockers can also lower blood pressure, and a low blood pressure predisposes to glaucomatous damage. Therefore, we do not use these drugs at the present time in patients who have low blood pressure, but only in those with normal or high blood pressure. The patient's internist or family physician should be consulted with regard to the treatment plan.

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