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Related Concept Videos

Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
Ophthalmic Drug Delivery Systems01:23

Ophthalmic Drug Delivery Systems

Ophthalmic drug delivery faces major limitations due to poor absorption across the corneal membrane. This process is primarily driven by diffusion and is influenced by two main factors: the physicochemical properties of the drug and tear drainage. Most ophthalmic drugs, such as pilocarpine, epinephrine, atropine, and local anesthetics, are weak bases. They are typically formulated at an acidic pH to enhance chemical stability. However, this leads to high ionization, reducing their ability to...
Pharmacokinetics in Geriatric Patients: Effect of Age on Drug Absorption01:22

Pharmacokinetics in Geriatric Patients: Effect of Age on Drug Absorption

As individuals age, their body's physiology evolves, affecting drug pharmacokinetics. The most apparent changes occur in the gastrointestinal tract, where an increase in gastric pH, a delay in gastric emptying, and a reduction in gastrointestinal motility are observed. Remarkably, these changes do not substantially modify the absorption of orally administered drugs, particularly those absorbed via passive diffusion.Transdermal drug delivery emerges as a highly viable method for older adults due...
Hypertension III: Clinical Manifestations and Diagnostic Studies01:30

Hypertension III: Clinical Manifestations and Diagnostic Studies

Hypertension is asymptomatic and also referred to as the "silent killer" until it progresses to a severe stage or causes target organ disease. Patients may experience symptoms stemming from the strain on blood vessels and tissues in various organs or the heart's increased workload.Physical exams might show no abnormalities other than high blood pressure. Signs of vascular damage, when present, correspond to the organs supplied by the affected vessels, leading to target organ damage. For...

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Related Experiment Video

Updated: Jun 18, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Basic sciences in clinical glaucoma: steroids, ocular hypertension, and glaucoma.

A F Clark1

  • 1Alcon Laboratories, Inc., Fort Worth, Texas, U.S.A.

Journal of Glaucoma
|November 19, 2009
PubMed
Summary
This summary is machine-generated.

Glucocorticoids can elevate intraocular pressure by altering trabecular meshwork function, potentially contributing to glaucoma. Further research is needed to clarify the causal link and therapeutic steroid options.

More Related Videos

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Published on: June 3, 2018

Related Experiment Videos

Last Updated: Jun 18, 2026

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis
13:47

Laser Capture Microdissection of Highly Pure Trabecular Meshwork from Mouse Eyes for Gene Expression Analysis

Published on: June 3, 2018

Area of Science:

  • Ophthalmology
  • Endocrinology
  • Cell Biology

Background:

  • Glucocorticoids (GC) influence aqueous humor outflow and are linked to primary open-angle glaucoma (POAG).
  • GC administration can elevate intraocular pressure (IOP) by increasing outflow resistance through trabecular meshwork (TM) changes.

Purpose of the Study:

  • To review the effects of glucocorticoids on the trabecular meshwork and their role in ocular hypertension and glaucoma.
  • To discuss the potential causal relationship between glucocorticoids and POAG, and the therapeutic use of steroids in glaucoma management.

Main Methods:

  • Review of existing literature on glucocorticoid effects on the eye, specifically the trabecular meshwork.
  • Analysis of studies investigating ocular hypertension and glaucoma in relation to glucocorticoid exposure and endogenous levels.

Main Results:

  • Glucocorticoids induce morphological and biochemical changes in TM cells, affecting protein expression, cytoskeleton, and extracellular matrix.
  • Glucocorticoid-induced ocular hypertension is observed across species and depends on individual responsiveness, GC potency, and administration route.
  • While altered cortisol metabolism is reported in POAG patients, a direct causal role for glucocorticoids in POAG pathogenesis remains unproven.

Conclusions:

  • Glucocorticoids significantly impact TM function, contributing to elevated IOP and potentially glaucoma.
  • Further research is crucial to elucidate the molecular mechanisms of GC-induced ocular hypertension and POAG, and to evaluate anti-glaucoma steroid therapies.