Glaucoma Medications Mechanism of Action
Glaucoma is a group of diseases affecting the optic nerve and involving loss of retinal ganglion cells. Glaucoma results in optic neuropathy. Elevated intraocular pressure (i.e., eye pressure) is a significant risk factor for developing glaucoma; however, there is no set threshold for intraocular pressure that causes glaucoma. One person may develop nerve damage at a relatively low pressure, while another person may have high eye pressures for years and yet never develop damage. Untreated glaucoma leads to permanent damage of the optic nerve and resultant visual field loss, which can progress to blindness.
Glaucoma is the second leading cause of blindness in the United States and is the leading cause of blindess in African-Americans. Approximately 2.3 million people in the United States have glaucoma with 66.8 million worldwide.
Glaucoma is treated with medications and with surgery. We are currently working on a book directed for patients and non-ophthalmologists. Please return to read the book as chapters are published.
The table below lists the general classes of glaucoma medications and their mechanism of action.
| Medication Class | Aqueous Production | Trabecular Outflow | Uveoscleral Outflow |
| cholinergic agonists | no affect | increase | decrease |
| nonselective adrenergic agonists | slight Decrease | increase | minor increase |
| α2-adrenergic agonists | decrease | no affect | minor increase with brimonidine (Alphagan®) |
| β-adrenergic antagonists | decrease | no affect | no affect |
| carbonic anydrase inhibitors | decrease | no affect | no affect |
| prostaglandin analogues | no affect | no affect | increase |
Reference
Alward, Wallace L.M. Glaucoma The Requisites in Ophthalmology. Mosby. 2000.


0 Comments:
Post a Comment
Links to this post:
Create a Link
<< Home