Glaucoma pathophysiology: Difference between revisions
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===Primary Open Angle Glaucoma=== | ===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.<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> | * 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 IOP, usually as a consequence of reduced aqueous outflow. These structural changes include: | * 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. | ** 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. | ** Trabecular beams fusing due to endothelial cell loss. | ||
** Phagocytic activity leading to endothelial cell loss. | ** [[Phagocytic]] activity leading to [[Endothelial cell|endothelial cell loss]]. | ||
** Loss of giant vacuoles from Schlemm’s canal endothelium. | ** Loss of giant vacuoles from Schlemm’s canal [[endothelium]]. | ||
** Reduction of Schlemm’s canal pore size. | ** Reduction of Schlemm’s canal pore size. | ||
===Angle Closure Glaucoma=== | ===Angle Closure Glaucoma=== | ||
* The [[angle-closure glaucoma]] occurs as a result of an obstruction in access to the drainage pathways. | * 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. | * Typically, apposition or [[adhesion]] of the peripheral [[iris]] to the trabecular meshwork causes such an obstruction. | ||
* The portion of the anterior | * 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 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: | * 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 push the iris forward from behind. | ||
** Mechanisms that pull | ** Mechanisms that pull [[Category:Needs content]] [[Category:Aging-associated diseases]] [[Category:Blindness]] [[Category:Disease]] [[Category:Ophthalmology]] [[Category:Emergency medicine]] [[Category:Mature chapter]] [[Category:Primary care]] [[Category:Needs overview]] the iris forward into contact with the trabecular meshwork. | ||
==References== | ==References== | ||
Revision as of 14:08, 24 September 2018
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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
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
- 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.