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After being produced by the ciliary body, the aqueous humor enters the
posterior chamber (the space between the iris and the zonules) before
passing through the pupil to enter the anterior chamber (between the iris
and the cornea).
From that site it drains into
veins by way of the trabecular meshwork and Schlemm’s canal.
A delicate balance between the
production and drainage of the aqueous humor maintains transocular
pressure within its physiological range (10-20 mm Hg).
In certain pathologic
states aqueous humor accumulates within the eye, and the intraocular
pressure, which is measured by determining the force required to indent or
flatten the cornea, becomes elevated , producing temporary or permanent
impairment of vision and damage to the optic nerve.
When this occurs, usually when
the intraocular pressure is above 20 mm Hg, the term glaucoma is applied.
Vision becomes impaired
because of degenerative changes in the retina and optic nerve head (a
result of ocular hypertension and resultant ischemia), and because of
corneal edema and opacification.
Effects of Elevated
Intraocular Pressure:
Individuals vary in their ability to
tolerate an elevated intraocular pressure. Some do not develop a visual
field loss or optic atrophy after having an intraocular pressure of three
standard deviations above the mean (24 mm Hg) for many years.
Prolonged ocular hypertension has several
effects on the eye:
1.
In
adults it leads to a characteristic cupped excavation of the optic disc (glaumatous
cupping), accompanied by a nasal displacement of the retinal blood
vessels. In infants cupping of the optic disc tend to be less prominent.
2.
The
cornea or sclera bulges at weak points, such as sites of scars in the
outer coat of the eye.
3.
Optic atrophy, with a loss of axons, gliosis, and thickening of the pial
septa, follows the retinal degeneration and damage to the nerve fibers at
the optic disc.
4.
The
ganglion cell layer of the retina degenerates, thereby impairing vision.
The outer retina, which derives its nutrition from the underlying
choroids, remains intact.
5.
When the intraocular pressure becomes elevated before the age of 3 years,
the pliable eye sometimes enlarges extensively and may resemble an ox eye
(buphthalmos). After the first few years of life, a rigid sclera prevents
glaumatous eyes from enlarging under the elevated pressure.
Visit:
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Normal histology and diseases of the retina : click
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New perspectives in aqueous humor secretion and in glaucoma: The
ciliary body as a multifunctional neuroendocrine gland.Prog
Retin Eye Res. 2007 Jan 17;
The discovery in
the human ocular ciliary body of glaucoma-associated genes (i.e., MYOC,
CYP1B1), neuroendocrine-processing enzymes, neuroendocrine peptides,
steroid-converting enzymes, glutamate transporters,
glutamate-metabolizing enzymes, and anti-angiogenic factors requires a
reevaluation of its function on aqueous humor secretion, intraocular
pressure and its role in glaucoma. The ciliary body should be
considered as a multifunctional and interactive tissue. The intrinsic
hypotensive and/or hypertensive biological activities of many of the
endocrine peptides released by the ciliary epithelium are best
explained within the context of a neuroendocrine system, linking the
inflow and the outflow of aqueous humor. This interpretation is
consistent with physiological and genetic studies indicating that
changes altering the inflow affects intraocular pressure. In the
proposed endocrine system, regulatory peptides secreted by the ciliary
epithelium may subserve multiple functions in the following: inflow
and outflow pathways of aqueous humor, ciliary blood flow, the immune
privilege status of the anterior segment and the diurnal circadian
rhythms of aqueous humor secretion and intraocular pressure. These
previously unsuspected and challenging functions of the ciliary
epithelium should be considered when assessing the multifactorial
events which lead to the pathophysiology of glaucoma affecting the
outflow pathways of aqueous humor. This review highlights published,
and ongoing studies on authors' labs supporting neuroendocrine,
steroidogenic and glutamatergic features of the ciliary epithelium and
the endocrine communication between the inflow and outflow pathways of
aqueous humor. We also discuss how glaucoma-associated genes expressed
in the ciliary body and their mutant proteins could influence
intraocular pressure, contributing to the development of glaucoma.
Influence of
prostaglandins on aqueous humour dynamics and intraocular pressure.Klin
Monatsbl Augenheilkd. 2005
Oct;222(10):802-6.
In the
glaucoma disease the disturbed trabecular outflow results not only in
an increase in the intraocular pressure (IOP) level, but also in an
increase in the intraocular pressure fluctuations in the majority of
patients. This induces a biomechanical stress that may damage the
optic nerve head over time and may result in the typical glaucomatous
excavation. Prostaglandin analogues show positive effects on both risk
factors. They enhance the uveoscleral outflow of the aqueous humour,
improve the trabecular outflow facility and probably the regulatory
capacity of the trabecular meshwork itself. This dual mechanism might
explain the strong IOP-lowering efficacy of the prostaglandins and
their additional property to reduce IOP fluctuations leading to a
general improvement of the aqueous humour dynamics. Therefore, it
makes sense pharmacologically to combine prostaglandins with those
medications that also reduce aqueous humour production.
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