Glaucoma pathophysiology: Difference between revisions
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{{Glaucoma}} | {{Glaucoma}} | ||
{{CMG}} {{AE}} {{RBS}} | |||
== Overview == | |||
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== | ==Pathophysiology== | ||
=== Anatomy === | |||
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 === | ||
The [[ | * 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. | |||
[[File:Screen Shot 2017-08-14 at 13.01.49.png|thumb|Anatomy of the Eye, according to Galen as the Arabs transferred to the West|link=https://www.wikidoc.org/index.php/File:Screen_Shot_2017-08-14_at_13.01.49.png|center]] | |||
The consequence of | ===Primary Open Angle Glaucoma=== | ||
* An elevated [[Intraocular pressure|IOP]] can lead to damage the [[optic nerve]] head via induced mechanical changes at the [[Lamina cribrosa sclerae|lamina cribrosa]], or via vascular dysfunction and resultant [[ischemia]].<ref name="pmid24825645">{{cite journal| author=Weinreb RN, Aung T, Medeiros FA| title=The pathophysiology and treatment of glaucoma: a review. | journal=JAMA | year= 2014 | volume= 311 | issue= 18 | pages= 1901-11 | pmid=24825645 | doi=10.1001/jama.2014.3192 | pmc=4523637 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24825645 }}</ref> | |||
* Multiple underlying mechanisms can result in elevated [[Intraocular pressure|IOP]], usually as a consequence of reduced [[Aqueous humour|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|endothelial cell loss]]. | |||
** Loss of giant vacuoles from Schlemm’s canal [[endothelium]]. | |||
** Reduction of Schlemm’s canal pore size. | |||
===Angle Closure Glaucoma=== | |||
* 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 of eyeball|anterior chambe]]<nowiki/>r angle affected by such apposition is “closed,” and drainage of [[aqueous humor]] through the angle is prohibited.<ref name="pmid19574692">{{cite journal| author=Agarwal R, Gupta SK, Agarwal P, Saxena R, Agrawal SS| title=Current concepts in the pathophysiology of glaucoma. | journal=Indian J Ophthalmol | year= 2009 | volume= 57 | issue= 4 | pages= 257-66 | pmid=19574692 | doi=10.4103/0301-4738.53049 | pmc=2712693 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19574692 }}</ref> | |||
* 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 glaucoma|angle closure]] leads reduced [[Aqueous humour|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== | ==References== | ||
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[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
[[Category:Mature chapter]] | [[Category:Mature chapter]] | ||
[[Category:Needs overview]] | [[Category:Needs overview]] | ||
Latest revision as of 21:53, 29 July 2020
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Glaucoma pathophysiology On the Web |
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Risk calculators and risk factors for Glaucoma pathophysiology |
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
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
Anatomy
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
- 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.
Primary Open Angle Glaucoma
- 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
- 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
- ↑ 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.
- ↑ 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.