Glaucoma pathophysiology

Glaucoma Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Glaucoma from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic study of choice
History and Symptoms
Physical Examination
Laboratory Findings
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Glaucoma pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Glaucoma pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Glaucoma pathophysiology
CDC on Glaucoma pathophysiology
Glaucoma pathophysiology in the news
Blogs on Glaucoma pathophysiology
Directions to Hospitals Treating Glaucoma
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

• 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

• 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.
• 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.
• 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