To understand the pathophysiology of glaucoma, it is important to understand three main principles: 1) aqueous production, 2) aqueous outflow, and 3) intraocular pressure.
Glaucoma comes in many forms with a number of underlying aetiologies, however fundamentally what all forms have in common is progressive optic neuropathy associated with visual field loss, where intraocular pressure IOP is an important modifiable factor.
Aqueous humour, which fills the anterior and posterior chamber, is produced by the non-pigmented epithelium of the pars plicata, producing around 2.5 μl of aqueous humour per minute. There are three main processes that contribute to this process:
1) Diffusion (passive): Solutes, especially lipid soluble substances, diffuse from an area of high concentration to low through the lipid portions of the membranes between the capillaries and the posterior chamber.
2) Ultrafiltration (passive): A passive process where water-soluble substances, limited by size and charge flow across fenestrated ciliary capillary endothelia, resulting in ultrafiltrated plasma within the ciliary body’s stroma. This also produces an almost protein-free liquid, resulting in an optically clear medium for vision.
These two passive process allow plasma ultrafitrate to accumulate in the stroma, behind tight junctions of the non-pigmented epithelium, where the aqueous humour is produced.
3) Active secretion (active) This process is the main contributor to aqueous formation, responsible for approximately 80% to 90% of the total aqueous humour. As the Na+/K+ ATPase actively transports Na+ ions into the posterior chamber, the water collected in the stroma of the ciliary body follows.
This process is under control by the sympathetic (adrenergic) nervous system. β2 receptor stimulation increases aqueous secretion, whilst α2 receptor stimulation has the opposite effect and decreases it.