glaucoma
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Questions and Answers

What are the primary mechanisms that can lead to the forward shift of the iris in acute angle-closure glaucoma?

The primary mechanisms include pupillary block, ciliary body swelling, aqueous misdirection, posterior segment tumors, and effects from scleral buckling procedures.

Describe the symptoms of acute angle-closure glaucoma and explain why they occur.

Symptoms include ocular pain, headache, blurred vision, rainbow-colored halos around lights, nausea, vomiting, bradycardia, and sweating, primarily due to the elevated intraocular pressure and corneal edema.

What findings are crucial for the definitive diagnosis of acute angle-closure glaucoma?

Definitive diagnosis is based on gonioscopic findings, which reveal angle closure and other ocular changes.

Explain the role of the sphincter pupillae in the pupillary changes observed in acute angle-closure glaucoma.

<p>The sphincter pupillae paralysis, due to reduced blood supply from elevated IOP, leads to a mid-dilated, sluggish pupil with poor constriction.</p> Signup and view all the answers

Discuss the implications of fellow eye involvement in patients diagnosed with primary angle-closure glaucoma.

<p>Fellow eyes have a 40%-80% chance of experiencing an acute angle-closure attack within 5-10 years, indicating the necessity for monitoring and preventative measures.</p> Signup and view all the answers

What role does aerobic exercise play in intraocular pressure (IOP) management?

<p>Aerobic exercise is associated with a decrease in intraocular pressure.</p> Signup and view all the answers

Identify two factors that may increase intraocular pressure and explain their impact.

<p>Elevated episcleral venous pressure and the Valsalva maneuver can increase IOP by obstructing venous outflow.</p> Signup and view all the answers

How do hormonal influences during pregnancy affect intraocular pressure?

<p>Hormonal influences during pregnancy can lead to a decrease in intraocular pressure.</p> Signup and view all the answers

Explain how metabolic acidosis affects intraocular pressure.

<p>Metabolic acidosis decreases aqueous humor production, leading to a reduction in intraocular pressure.</p> Signup and view all the answers

What is the initial optical consequence of glaucoma, and why does it occur?

<p>Glaucoma initially causes peripheral vision loss due to damage to peripheral ganglion cells with longer axons.</p> Signup and view all the answers

What are two typical visual field defects associated with primary open angle glaucoma (POAG)?

<p>Paracentral scotoma and arcuate (Bjerrum) scotoma.</p> Signup and view all the answers

What is a characteristic ophthalmoscopic sign that indicates glaucoma progression?

<p>Progressive enlargement of the optic cup.</p> Signup and view all the answers

Describe how beta-blockers reduce intraocular pressure (IOP) in glaucoma treatment.

<p>Beta-blockers inhibit cAMP production in the ciliary epithelium, reducing aqueous humor secretion.</p> Signup and view all the answers

What ocular hypotensive agents can increase aqueous outflow for the management of glaucoma?

<p>Parasympathomimetic agents, like pilocarpine and carbachol.</p> Signup and view all the answers

What defines the treatment threshold for primary open angle glaucoma?

<p>Treatment is initiated when there is optic nerve damage or elevated IOP likely to cause further damage.</p> Signup and view all the answers

What is a common surgical approach when medical therapy for glaucoma is insufficient?

<p>Surgical therapy is undertaken when medical therapy is not effective or tolerated.</p> Signup and view all the answers

Name a less specific sign observed in glaucoma that may indicate structural changes in the eye.

<p>Exposed lamina cribrosa.</p> Signup and view all the answers

What can be a consequence of untreated elevated intraocular pressure in glaucoma patients?

<p>Progressive pathologic cupping of the optic nerve.</p> Signup and view all the answers

What structures comprise the anterior chamber angle?

<p>Schwalbe's line, trabecular meshwork, Schlemm's canal, scleral spur, anterior border of ciliary body, and iris.</p> Signup and view all the answers

Describe Schwalbe's line and its significance in gonioscopy.

<p>Schwalbe's line is the termination of Descemet's membrane and appears white in gonioscopy, important for measuring the iridocorneal angle.</p> Signup and view all the answers

What are the three processes involved in aqueous humor formation?

<p>Active secretion by ciliary epithelium, ultrafiltration, and simple diffusion.</p> Signup and view all the answers

Explain the difference between trabecular outflow and uveoscleral outflow.

<p>Trabecular outflow is pressure-dependent, mainly through the trabecular meshwork, while uveoscleral outflow is pressure-independent and involves drainage through the ciliary muscle.</p> Signup and view all the answers

What factors can increase uveoscleral outflow?

<p>Cycloplegia, adrenergic agents, prostaglandin analogues, and certain surgical procedures.</p> Signup and view all the answers

What role does the juxtacanalicular meshwork play in aqueous outflow?

<p>It is thought to be the major site of outflow resistance in the trabecular pathway.</p> Signup and view all the answers

How does age influence the uveoscleral outflow percentage?

<p>The uveoscleral outflow can range from 15-45%, with variations influenced by age.</p> Signup and view all the answers

What accessory drainage pathways exist for aqueous humor aside from the trabecular route?

<p>Uveoscleral pathways, diffusion into the iris, cornea, and posterior segment.</p> Signup and view all the answers

What is the primary mechanism by which both direct and indirect acting agents reduce intraocular pressure (IOP)?

<p>They cause contraction of the ciliary muscle, tightening the trabecular meshwork and increasing aqueous humor outflow.</p> Signup and view all the answers

How do prostaglandin analogues, such as Latanoprost, affect intraocular pressure compared to other agents?

<p>Prostaglandin analogues increase uveoscleral aqueous outflow and can reduce IOP by 25-30%, which is greater than many other agents.</p> Signup and view all the answers

What is the role of carbonic anhydrase inhibitors in managing intraocular pressure, and what is their expected reduction in IOP?

<p>Carbonic anhydrase inhibitors decrease aqueous humor formation and reduce IOP by 15-20%.</p> Signup and view all the answers

Describe the dual action of α2 adrenergic agents like brimonidine in reducing IOP.

<p>They decrease aqueous production and increase uveoscleral outflow, leading to an IOP reduction of 20-30%.</p> Signup and view all the answers

What complications can arise from the use of hyperosmotic agents like oral glycerin in glaucoma patients?

<p>Hyperglycemia or ketoacidosis can occur in diabetic patients, making glycerin contraindicated in diabetes mellitus.</p> Signup and view all the answers

Explain the mechanical hypothesis regarding optic nerve damage in glaucoma.

<p>The mechanical hypothesis suggests that RGC compression reduces axonal transport of trophic factors essential for RGC survival, leading to cell death.</p> Signup and view all the answers

What is the vascular hypothesis in the context of glaucomatous optic neuropathy?

<p>The vascular hypothesis posits that chronic hypoxia or ischemia contributes to optic nerve damage in glaucoma.</p> Signup and view all the answers

Identify two factors associated with elevated IOP and briefly explain their impact on glaucoma.

<p>Factors include postural change and use of general anesthesia; both can temporarily increase IOP and exacerbate glaucoma damage.</p> Signup and view all the answers

What structure forms the anterior border of the ciliary body in the anterior chamber?

<p>The iris forms the anterior border of the ciliary body.</p> Signup and view all the answers

What is the average rate of aqueous humor production in the eye?

<p>Aqueous humor is produced at an average rate of 2 µL/min.</p> Signup and view all the answers

Where does the majority of aqueous humor exit the eye?

<p>Most aqueous humor exits the eye through the trabecular meshwork and Schlemm's canal.</p> Signup and view all the answers

How does uveoscleral outflow differ from trabecular outflow?

<p>Uveoscleral outflow is pressure-independent, while trabecular outflow is pressure-dependent.</p> Signup and view all the answers

What is the significance of Schwalbe’s line in gonioscopy?

<p>Schwalbe's line indicates the termination of Descemet's membrane and helps measure the anterior chamber angle.</p> Signup and view all the answers

What effect do adrenergic agents have on uveoscleral outflow?

<p>Adrenergic agents increase uveoscleral outflow.</p> Signup and view all the answers

What anatomical feature acts as a major site of outflow resistance in the eye?

<p>The juxtacanalicular meshwork acts as a major site of outflow resistance.</p> Signup and view all the answers

Which structures comprise the anterior chamber angle?

<p>The anterior chamber angle consists of Schwalbe's line, trabecular meshwork, Schlemm's canal, scleral spur, anterior border of the ciliary body, and iris.</p> Signup and view all the answers

What are two mechanisms that can cause acute angle-closure glaucoma without pupillary block?

<p>Ciliary body swelling and aqueous misdirection are two mechanisms that can cause acute angle-closure glaucoma without pupillary block.</p> Signup and view all the answers

How does the mid-dilated pupil contribute to pupillary block in acute angle-closure glaucoma?

<p>A mid-dilated pupil relaxes the peripheral iris, causing it to bow forward and appose the trabecular meshwork, leading to pupillary block.</p> Signup and view all the answers

What are the key clinical signs of acute angle-closure glaucoma?

<p>Key clinical signs include corneal epithelial edema, shallow anterior chamber, and a mid-dilated sluggish pupil.</p> Signup and view all the answers

Why is acute angle-closure glaucoma considered a bilateral disease?

<p>Acute angle-closure glaucoma is bilateral because the fellow eye has a 40%-80% chance of developing an acute attack within the next 5-10 years.</p> Signup and view all the answers

What role does corneal epithelial edema play in acute angle-closure glaucoma?

<p>Corneal epithelial edema results from the rise in intraocular pressure, causing visual symptoms such as blurred vision.</p> Signup and view all the answers

What is a characteristic visual field defect associated with primary open angle glaucoma (POAG)?

<p>Paracentral scotoma.</p> Signup and view all the answers

What is a general ophthalmoscopic sign indicating glaucoma progression?

<p>Progressive enlargement of the optic cup.</p> Signup and view all the answers

What is the primary treatment for mild attacks of angle closure glaucoma?

<p>Cholinergic agents like pilocarpine, which induce miosis, are the primary treatment.</p> Signup and view all the answers

How do beta-blockers help in reducing intraocular pressure (IOP) in glaucoma treatment?

<p>By inhibiting cAMP production in ciliary epithelium, reducing aqueous humor secretion.</p> Signup and view all the answers

What triggers the initiation of treatment for primary open angle glaucoma?

<p>Demonstrable optic nerve damage or significantly elevated IOP.</p> Signup and view all the answers

What should be administered when intraocular pressure (IOP) is elevated above 40-50 mmHg?

<p>A combination of topical β2 blockers, carbonic anhydrase inhibitors, and hyperosmotic agents should be administered.</p> Signup and view all the answers

Name a medical agent that increases aqueous outflow for glaucoma management.

<p>Prostaglandin analogues.</p> Signup and view all the answers

What is the treatment of choice for angle closure glaucoma secondary to pupillary block?

<p>Laser iridotomy with YAG laser is the treatment of choice.</p> Signup and view all the answers

What is one focal ophthalmoscopic sign of glaucoma?

<p>Narrowing of the rim.</p> Signup and view all the answers

What is phacolytic glaucoma and its primary treatment?

<p>Phacolytic glaucoma occurs due to lens material leakage from a hypermature cataract, treated with cataract extraction.</p> Signup and view all the answers

Describe the primary goal of glaucoma therapy.

<p>To preserve visual function by lowering IOP.</p> Signup and view all the answers

Describe phacomorphic glaucoma and how it can be treated.

<p>Phacomorphic glaucoma results from lens swelling causing pupillary block, and the treatment is cataract extraction.</p> Signup and view all the answers

What causes phacoanaphylactic glaucoma?

<p>It is caused by an autoimmune reaction to lens proteins due to a traumatic rupture of the anterior capsule.</p> Signup and view all the answers

What is the effect of parasympathomimetic agents in glaucoma treatment?

<p>They increase aqueous outflow.</p> Signup and view all the answers

What role do hyperosmotic agents play in treating elevated IOP?

<p>Hyperosmotic agents, like oral glycerol or intravenous mannitol, help reduce IOP by drawing fluid out of the eye.</p> Signup and view all the answers

Explain the importance of preventing excessive intraocular pressure in glaucoma management.

<p>Preventing excessive intraocular pressure is crucial to avoid optic nerve damage and preserve vision.</p> Signup and view all the answers

What characterizes neovascular glaucoma (NVG) and its common causes?

<p>NVG is characterized by iris neovascularization due to severe retinal ischaemia, commonly caused by central retinal vein occlusion or proliferative diabetic retinopathy.</p> Signup and view all the answers

How does primary open angle glaucoma (POAG) typically present?

<p>POAG is usually insidious, painless, and progresses slowly, often without noticeable symptoms until advanced stages.</p> Signup and view all the answers

What role does elevated intraocular pressure (IOP) play in primary open angle glaucoma?

<p>Elevated IOP is a major risk factor for POAG, contributing to optic nerve damage and visual field loss.</p> Signup and view all the answers

What demographic factors influence the prevalence of primary open angle glaucoma?

<p>The prevalence of POAG is higher among older adults and particularly among individuals of African descent.</p> Signup and view all the answers

Which are the critical assessments used in diagnosing primary open angle glaucoma?

<p>Diagnosis involves evaluating intraocular pressure levels, optic disc appearance, and patterns of visual field loss.</p> Signup and view all the answers

What microscopic changes occur in the optic nerve head in primary open angle glaucoma?

<p>In POAG, there is atrophy and cupping of the optic nerve head due to retinal ganglion cell loss.</p> Signup and view all the answers

Explain the importance of family history in the risk factors for primary open angle glaucoma.

<p>Family history is a significant risk factor, indicating a genetic predisposition to developing POAG.</p> Signup and view all the answers

What are two common treatments for managing intraocular pressure in glaucoma patients?

<p>Common treatments include medication to lower IOP and surgical options like trabeculectomy when medical therapy fails.</p> Signup and view all the answers

Study Notes

Anterior Chamber

  • The anterior chamber is located between the cornea and the iris.
  • The anterior chamber angle is found at the junction of the cornea and iris.
  • The anterior chamber angle consists of the following structures:
    • Schwalbe’s line
    • Trabecular meshwork and Schlemm’s canal
    • Scleral spur
    • Anterior border of ciliary body
    • Iris
  • Schwalbe’s line is the termination of Descemet’s membrane.
  • Schlemm’s canal is a large channel lined by endothelium and thin connective tissue.

Aqueous Humor

  • Aqueous humor is produced by the ciliary epithelium at an average rate of 2 µL/min.
  • Aqueous humor is produced by:
    • Active secretion
    • Ultrafiltration
    • Simple diffusion
  • Aqueous humor outflow occurs through two major mechanisms:
    • Trabecular outflow: Trabecular meshwork - Schlemm's canal - venous system
    • Uveoscleral outflow: Anterior chamber - ciliary muscle - supraciliary and suprachoroidal space
  • Uveoscleral outflow accounts for 15-45% of total outflow.
  • Various factors, including age, can impact the proportion of uveoscleral outflow.

Angle Closure Glaucoma (ACG)

  • ACG is caused by closure of the anterior chamber angle, blocking aqueous humor outflow.
  • There are two main mechanisms that contribute to ACG:
    • Mechanisms that push the iris forward from behind (with or without pupillary block)
    • Mechanisms that pull the iris forward (without pupillary block)
  • Pupillary block occurs when the iris is pushed forward and blocks the flow of aqueous humor from the posterior chamber.
  • Mid-dilated pupils can relax the peripheral iris, allowing the iris to bend forward and backward causing apposition of the iris with the trabecular meshwork and the lens, resulting in pupillary block.
  • Secluded pupils with 360° posterior synechiae can also lead to pupillary block.
  • Other factors, including ciliary body swelling, aqueous misdirection, posterior segment tumors, and surgical procedures (e.g., scleral buckling), can cause ACG without pupillary block.

Clinical Features of Acute ACG

  • Symptoms:
    • Ocular pain
    • Headache
    • Blurred vision
    • Rainbow-colored halos around light
    • Nausea
    • Vomiting
    • Bradycardia
    • Sweating
  • Signs:
    • Corneal epithelial edema
    • Congested episcleral and conjunctival blood vessels
    • Mild aqueous flare and cells
    • Mid-dilated, sluggish, and irregular pupil
    • Shallow anterior chamber
    • High IOP
  • Gonioscopy is crucial for definitive diagnosis.
  • The pupillary change is thought to result from paralysis of the sphincter pupillae caused by reduced blood supply due to elevated IOP and possibly degeneration of the ciliary ganglion.

Primary Open Angle Glaucoma (POAG)

  • POAG is an asymptomatic disease until late stages when visual field constriction occurs.
  • Typical glaucomatous defects in perimetry include:
    • Paracentral scotoma
    • Arcuate or Bjerrum scotoma
    • Nasal step
    • Altitudinal defect
    • Temporal wedge

Ophthalmoscopic Signs of Glaucoma

  • Generalized Signs:
    • Large optic cup
    • Asymmetry of the cups
    • Progressive enlargement of the cup
  • Focal Signs:
    • Narrowing of the rim
    • Vertical elongation of the cup
    • Cupping to the rim
    • Regional pallor
    • Splinter hemorrhage
    • Nerve fiber layer loss
  • Less Specific Signs:
    • Exposed lamina cribrosa
    • Nasal displacement of vessels
    • Baring of circumlinear vessels
    • Prepapillary crescent

Treatment of POAG

  • POAG is treated when optic nerve damage is evident through progressive cupping and/or visual field loss, or when IOP is elevated to a level likely to cause nerve damage.
  • The goal of glaucoma therapy is to preserve visual function by lowering IOP to a safe level.
  • Initial treatment typically involves medical therapy.
  • Surgical therapy is considered when medical therapy is ineffective, not tolerated, or not utilized by the patient, and glaucoma remains uncontrolled.

IOP-Lowering Agents

  • β Blockers
    • Examples: Timolol, Betaxolol
    • Mechanism of action: Inhibit cAMP production in ciliary epithelium, reducing aqueous humor secretion.
    • Reduce IOP by 20-30%.
  • Parasympathomimetic Agents
    • Examples: Pilocarpine, Carbachol
    • Mechanism of action: Cause contraction of the ciliary muscle, tightening the trabecular meshwork.
    • Reduce IOP by 10-20%.
  • Prostaglandin Analogs
    • Examples: Latanoprost
    • Mechanism of action: Increase uveoscleral outflow
    • Reduce IOP by 25-30%
  • Carbonic Anhydrase Inhibitors
    • Examples: Acetazolamide, Dorzolamide
    • Mechanism of action: Decrease aqueous humor formation by inhibiting carbonic anhydrase.
    • Reduce IOP by 15-20%.
  • Adrenergic Agonists
    • Examples: Epinephrine, Dipivefrin
    • Mechanism of action: Increase outflow of aqueous humor
  • α2 Adrenergic Agents
    • Examples: Apraclonidine, Brimonidine
    • Mechanism of action: Reduce aqueous production, increase uveoscleral outflow, and decrease episcleral venous pressure
    • Reduce IOP by 20-30%.
  • Hyperosmotic Agents
    • Examples: IV mannitol, oral glycerin
    • Mechanism of action: Dehydrate the vitreous
    • Potential complications: Subdural and subarachnoid hemorrhage
    • Contraindicated in patients with diabetes due to hyperglycemia and ketoacidosis risk.

Other Treatment Options

  • Argon Laser Trabeculoplasty
  • Filtering Surgery
    • With or without glaucoma tube shunt (e.g., Ahmed valve)

Optic Neuropathy in Glaucoma

  • Mechanical Hypothesis:
    • Trophic factors, like brain-derived neurotrophic factor (BDNF), are essential for retinal ganglion cell (RGC) survival.
    • RGC compression reduces axonal transport of trophic factors, leading to RGC death due to trophic insufficiency.
  • Vascular Hypothesis:
    • Chronic hypoxia or ischemia can contribute to glaucomatous optic neuropathy.

Factors Affecting IOP

  • Factors that may increase IOP:
    • Elevated episcleral venous pressure
    • Valsalva maneuver
    • Breath holding
    • Playing a wind instrument
    • Wearing a tight collar or necktie
    • Bending over or being in a supine position
    • Elevated central venous pressure
    • Orbital venous outflow obstruction
    • Intubation
    • Blepharospasm
    • Squeezing and crying
    • Elevated body temperature
    • Hypothyroidism
    • Thyroid ophthalmitis
    • Lysergic acid diethylamide (LSD)
    • Topiramate (Topamax)
    • Corticosteroids
    • Anticholinergics
    • Anesthetic drugs (Ketamine, succinylcholine)
  • Factors that may decrease IOP:
    • Aerobic exercise
    • Anaesthesia
    • Metabolic or respiratory acidosis
    • Hormonal influences (pregnancy)
    • Alcohol consumption
    • Heroin
    • Marijuana (cannabis)

Peripheral Ganglion Cell Vulnerability

  • Peripheral ganglion cells have longer axons, making them more susceptible to glaucoma-induced damage.
  • Glaucoma initially affects peripheral vision due to the involvement of peripheral ganglion cells.

Anterior Chamber

  • Bordered anteriorly by the cornea
  • Bordered posteriorly by the iris diaphragm and pupil
  • Anterior chamber angle lies at the junction of the cornea and iris
    • Schwalbe's line is the termination of Descemet's membrane and is white in gonioscopy
    • Trabecular meshwork and Schlemm's canal
    • Scleral spur
    • Anterior border of ciliary body
    • Iris
  • Schlemm’s canal is a large channel resembling a lymphatic vessel formed by a continuous monolayer of nonfenestrated endothelium and a thin connective tissue wall

Aqueous Humor Formation

  • Produced by the non-pigmented ciliary epithelium at a rate of 2 µL/min
  • Consists of three processes at an average rate of 2 µL/min
    • Active secretion by the double-layered non-pigmented ciliary epithelium
    • Ultrafiltration
    • Simple diffusion

Aqueous Humor Outflow

  • Occurs by two major mechanisms
    • Trabecular outflow (pressure-dependent): Most of the aqueous humor leaves through the trabecular meshwork, Schlemm's canal, and then the venous system. The juxtacanalicular meshwork is thought to be the major site of outflow.
    • Uveoscleral Outflow (Pressure independent): Any non-trabecular outflow is considered uveoscleral outflow. Aqueous humor moves from the anterior chamber into the ciliary muscle, and then into the supraciliary and suprachoroidal space.
      • Accounts for 15-45% of total outflow
      • This outflow is increased by cycloplegia, adrenergic agents, prostaglandin analogues, and surgical procedures
      • This outflow is decreased by miotics

Angle Closure Glaucoma (ACG)

  • Mechanism:
    • Forward shift of the iris either because of mechanisms that push the iris forward or mechanisms that pull the iris forward
  • ACG is most frequently caused by pupillary block, but can also occur without pupillary block, such as with:
    • Ciliary body swelling
    • Aqueous misdirection
    • Posterior segment tumors
    • Scleral buckling procedures

Clinical Features of Acute ACG

  • Symptoms:
    • Ocular pain, headache, blurred vision, rainbow-coloured halos around lights, nausea, vomiting, bradycardia, sweating
  • Signs:
    • Corneal epithelial edema, congested episcleral and conjunctival blood vessels, a mild amount of aqueous flare and cells, mid-dilated sluggish and often irregular pupil (no or poor constriction to light reflex), shallow anterior chamber, high IOP
  • Gonioscopic findings are the definitive diagnosis

Treatment of Acute ACG

  • Mild attacks may be treated with cholinergic agents
  • Topical β2 blockers, oral, topical, or IV carbonic anhydrase inhibitors, and hyperosmotic agents may be used to lower IOP
  • Topical steroids or glycerin may treat corneal inflammation and edema

Laser Iridotomy

  • Treatment of choice for ACG secondary to pupillary block
  • Prophylactic iridotomy should be performed in the fellow eye (because it is a bilateral disease)
  • Surgical iridectomy is indicated if laser iridotomy cannot be accomplished

Secondary Glaucoma

  • Lens-induced glaucoma
    • Phacolytic glaucoma: Hypermature cataract leads to leakage of lens material into the anterior chamber through an intact capsule, causing trabecular obstruction
    • Phacomorphic (Intumescent) glaucoma: Swelling of the lens leads to pupillary block, causing secondary acute ACG
    • Phacoanaphylactic (phacoantigenic) glaucoma: Immune reaction to lens proteins in an eye with a ruptured anterior capsule Lens particle glaucoma: Lens particles from trauma or surgery will physically block the trabecular meshwork
  • Neovascular glaucoma (NVG): Caused by iris neovascularization (Rubeosis iridis) due to severe chronic retinal ischemia - Central retinal vein occlusion (CRVO, commonest cause)
    - Branch retinal vein occlusion (BRVO)
    - Proliferative diabetic retinopathy (PDR)
    - Central retinal artery occlusion (CRAO)
    - Carotid obstructive disease (Ocular ischemic syndrome, OIS)
    - Intraocular tumours
    - Long standing retinal detachment
    - Chronic intraocular inflammation
  • Inflammatory (uveitic) glaucomas: Uveitis

Primary Open Angle Glaucoma (POAG)

  • A chronic, slowly progressive optic neuropathy characterized by atrophy and cupping of the optic nerve head and associated with characteristic patterns of visual field loss
  • Increase IOP is an important risk factor
  • It is usually insidious in onset, slowly progressive, and painless.
  • Bilateral, but can be quite asymmetric
  • Central visual acuity is relatively unaffected until late in the disease
  • Diagnosed by assessing IOP, optic disc appearance, and visual field loss
  • Prevalence shows racial disparity (black population is 3-4 times higher than white population)
  • Prevalence increases with age
  • Risk factors:
    • Increased IOP
    • Race (black population)
    • Age
    • Family history
    • Association with myopia
    • Diabetes
    • Decreased corneal thickness (central thickness 0.52 mm, paracentral zone 0.52 mm inferior, 0.57 superior)
  • Typical glaucomatous defects seen in perimetry:
    • Paracentral scotoma
    • Arcuate or Bjerrum scotoma
    • Nasal step
    • Altitudinal defect
    • Temporal wedge

Ophthalmoscopic Signs of POAG

  • Generalized:
    • Large optic cup
    • Asymmetry of the cups
    • Progressive enlargement of the cup
  • Focal:
    • Narrowing of the rim
    • Vertical elongation of the cup
    • Cupping to the rim
    • Regional pallor
    • Splinter hemorrhage
    • Nerve fiber layer loss
  • Less specific:
    • Exposed lamina cribrosa
    • Nasal displacement of vessels
    • Baring of circumlinear vessels
    • Prepapillary crescent

Treatment of POAG

  • Treatment is required when damage to the optic nerve has been demonstrated
  • Goal of treatment is to preserve visual function by lowering IOP
  • Medical therapy is the initial approach
    • β blockers: Reduce aqueous humor secretion
    • Parasympathomimetic agents: Increase outflow through the trabecular meshwork, decrease outflow resistance, miotics
    • α2-agonists: Decreases aqueous production
    • Carbonic anhydrase inhibitors: Inhibits aqueous humor formation
    • Prostaglandin analogues: Increase uveoscleral outflow
  • Surgical therapy is undertaken if medical therapy is not an option or is ineffective
    • Trabeculectomy
    • Various implants

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Description

Test your knowledge on the anterior chamber and aqueous humor. This quiz covers the anatomy and functions of structures such as Schwalbe’s line and Schlemm’s canal, as well as the mechanisms of aqueous humor production and outflow. Challenge yourself with questions that highlight important concepts in eye physiology.

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