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Our Glaucoma class of Eye medications are used to treat glaucoma, in which there is a build-up of fluid in the eye, to reduce intraocular pressure that can cause damage to the optic nerve.

Use the search feature to quickly find the product you are looking for, by entering either the active ingredient, e.g. brimonidine or the product name, e.g. Alphagan

What is glaucoma?

Glaucoma is damage to the optic nerve leading out of the back of the eye to the brain that results in loss of vision, starting with peripheral vision and can lead to total blindness if not treated. It is caused by excessive intraocular pressure (IOP). Normal pressure in the eye is maintained by production of a fluid called aqueous humour by the ciliary bodies, by filtration from the capillaries. This fluid normally drains out of the eye through the spongy tissue called the trabecular network between the cornea and the iris at a steady rate. If the drainage is blocked, more fluid is produce than is drained away and causes a gradual increase in IOP.

Although there are different forms of glaucoma, the most common form is chronic open angle glaucoma that progresses slowly, often without symptoms until already well developed.

Increased IOP is a risk factor for glaucoma, although it is possible to have increased IOP without developing nerve damage and this is know as ocular hypertension.

Medications for glaucoma

Several medications are available to treat glaucoma and prevent its progression, thereby reducing the risk of loss of sight. They are administered as eye drops that work by different mechanisms to reduce intraocular pressure (IOP) and restore the balance between the amount of aqueous humour produced and its drainage out of the eye.
These include:
  • Alpha-2 adrenergic agonist like brimonidine, which bind to specific alpha adrenergic receptors on the ciliary bodies of the eye to reduce the amount of aqueous humour produced and also to increase uveoscleral outflow, an alternative drainage route for fluid, back through the ciliary bodies where it is produced.

  • Beta-adrenergic receptor blockers like timolol, which bind to specific beta-adrenergic receptor receptors on the ciliary bodies of the eye and block the stimulation of aqueous humour production, to reduce the amount produced.

  • Prostaglandin analogues like travoprost, an analogue of naturally occurring prostaglandin F2 alpha that increases the uveoscleral outflow of aqueous humour from the eye. Bimatoprost is a synthetic analogue of the naturally occurring prostamide, which is a prostaglandin-like chemical that increases the flow of aqueous humour out of the eye through the trabecular network.

  • Carbonic anhydrase inhibitors like dorzolamide and acetazolamide, which block the action the carbonic anhydrase enzyme in the ciliary bodies of the eye and this reduces formation of bicarbonate ions and secretion of aqueous humour into the eye.
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