Glaucoma pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:  Rohan Bir Singh, M.B.B.S.[2]

## Overview[edit | edit source]

The underlying pathogenesis of glaucoma is attributed to retinal ganglion cell death due to elevated level of intraocular pressure. The intraocular pressure is determined by the balance between secretion of aqueous humor by the ciliary body and its drainage through the two pathways i.e. the trabecular meshwork and uveoscleral outflow pathway.

## Pathophysiology[edit | edit source]

### Anatomy[edit | edit source]

Brief overview of the anatomy of the eye may be helpful in understanding the causes of this disease:

* The front part of the eye is filled with a clear fluid called aqueous humor.
* This fluid is always being made in the back of the eye. It leaves the eye through channels in the front of the eye in an area called the anterior chamber angle, or simply the angle.
* Anything that slows or blocks the flow of this fluid out of the eye will cause pressure to build up in the eye.
* This pressure is called intraocular pressure (IOP). In most cases of glaucoma, this pressure is high and causes damage to the major nerve in the eye, called the optic nerve.

### Pathogenesis[edit | edit source]

* The underlying pathogenesis of glaucoma is attributed to retinal ganglion cell death due to elevated level of intraocular pressure.
* The intraocular pressure is determined by the balance between secretion of aqueous humor by the ciliary body and its drainage through the two pathways i.e. the trabecular meshwork and uveoscleral outflow pathway.

Anatomy of the Eye, according to Galen as the Arabs transferred to the West

### Primary Open Angle Glaucoma[edit | edit source]

* An elevated IOP can lead to damage the optic nerve head via induced mechanical changes at the lamina cribrosa, or via vascular dysfunction and resultant ischemia.[1]
* Multiple underlying mechanisms can result in elevated IOP, usually as a consequence of reduced aqueous outflow. These structural changes include:
* Outflow reduction due to obstruction of the trabecular meshwork by a foreign material such as glycosaminoglycans, red blood cells.
* Trabecular beams fusing due to endothelial cell loss.
* Phagocytic activity leading to endothelial cell loss.
* Loss of giant vacuoles from Schlemm’s canal endothelium.
* Reduction of Schlemm’s canal pore size.

### Angle Closure Glaucoma[edit | edit source]

* The angle-closure glaucoma occurs as a result of an obstruction in access to the drainage pathways.
* Typically, apposition or adhesion of the peripheral iris to the trabecular meshwork causes such an obstruction.
* The portion of the anterior chamber angle affected by such apposition is “closed,” and drainage of aqueous humor through the angle is prohibited.[2]
* The angle closure due to peripheral iris can either be appositional (transient obstruction) or synechial (permanent obstruction).
* The consequence of either form of angle closure leads reduced aqueous outflow through the trabecular meshwork. The mechanisms of angle closure can be categorized into:
* Mechanisms that push the iris forward from behind.
* Mechanisms that pull

the iris forward into contact with the trabecular meshwork.

## References[edit | edit source]

1. ↑ Weinreb RN, Aung T, Medeiros FA (2014). "The pathophysiology and treatment of glaucoma: a review". JAMA. 311 (18): 1901–11. doi:10.1001/jama.2014.3192. PMC 4523637. PMID 24825645.CS1 maint: Multiple names: authors list (link)
2. ↑ Agarwal R, Gupta SK, Agarwal P, Saxena R, Agrawal SS (2009). "Current concepts in the pathophysiology of glaucoma". Indian J Ophthalmol. 57 (4): 257–66. doi:10.4103/0301-4738.53049. PMC 2712693. PMID 19574692.CS1 maint: Multiple names: authors list (link)

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