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Summary Table

Category	Details
Risk Factors	Age > 40 (prevalence increases with age), African descent, family history, elevated intraocular pressure (IOP), myopia, thin central corneal thickness, diabetes mellitus
Etiology	Chronic, progressive optic neuropathy caused by impaired aqueous humor drainage through the trabecular meshwork, leading to elevated IOP and retinal ganglion cell death
Patient Presentation	Insidious, painless, bilateral (often asymmetric) loss of peripheral vision; patient is typically asymptomatic until late stages
Classic Physical Exam	Increased cup-to-disc ratio (> 0.5), asymmetric cupping between eyes, optic disc pallor, loss of neuroretinal rim tissue
Key Diagnostic Results	Elevated IOP on tonometry (> 21 mmHg, though can be normal), visual field defects on perimetry (arcuate scotoma, nasal step), increased cup-to-disc ratio on fundoscopy, open anterior chamber angle on gonioscopy
Management	Topical prostaglandin analogs (latanoprost) as first-line; alternatives include topical beta-blockers (timolol), alpha-agonists (brimonidine), carbonic anhydrase inhibitors (dorzolamide); laser trabeculoplasty or trabeculectomy for refractory cases
Keywords	"Painless vision loss," "tunnel vision," "increased cup-to-disc ratio," "open angle on gonioscopy," "gradual peripheral field loss," "no eye pain or redness"

1. Pathophysiology

The eye continuously produces aqueous humor from the ciliary body in the posterior chamber. This fluid flows through the pupil into the anterior chamber, where it drains primarily through the trabecular meshwork into the canal of Schlemm, and from there into the episcleral venous system. In open angle glaucoma, the anterior chamber angle remains anatomically open, but there is increased resistance to outflow at the level of the trabecular meshwork. This leads to a gradual elevation of intraocular pressure (IOP).

The elevated IOP transmits mechanical stress to the lamina cribrosa, a sieve-like structure at the optic nerve head through which retinal ganglion cell axons pass. Chronic compression and ischemia at this site cause progressive retinal ganglion cell apoptosis. Because the peripheral nerve fibers (which correspond to the arcuate bundle) are affected earliest, patients lose peripheral vision first while central acuity is preserved until late in the disease. This is why patients are unaware of their deficit for years.

The hallmark finding on fundoscopy is optic disc cupping, which represents the loss of neural tissue at the optic nerve head. As ganglion cell axons die, the neuroretinal rim thins and the cup enlarges relative to the disc. A cup-to-disc ratio greater than 0.5, or asymmetry of more than 0.2 between the two eyes, should raise concern.

It is critical to understand that IOP can be within the statistically normal range (< 21 mmHg) and the patient can still have glaucoma. This entity is called normal-tension glaucoma and represents a subset where the optic nerve is susceptible to damage at lower pressures. The diagnosis of open angle glaucoma is therefore made based on the combination of optic nerve changes and visual field loss, not on IOP alone.

2. Classification and Clinical Manifestation

Type	Mechanism	IOP	Key Features
Primary Open Angle Glaucoma (POAG)	Idiopathic increased trabecular outflow resistance	Usually elevated (> 21 mmHg)	Most common form; painless, bilateral, chronic course; open angle on gonioscopy
Normal-Tension Glaucoma	Optic nerve susceptibility at normal IOP levels	Normal (< 21 mmHg)	Same optic disc and visual field changes as POAG; more common in Japanese descent; may have vascular dysregulation
Secondary Open Angle Glaucoma	Obstruction of trabecular meshwork by debris	Variable	Caused by pigment dispersion syndrome, pseudoexfoliation syndrome, steroid use, trauma, or uveitic debris
Steroid-Induced Glaucoma	Increased trabecular meshwork resistance from corticosteroid use	Elevated	Occurs with prolonged topical, periocular, or systemic corticosteroids; reversible if caught early

Classification by Stage

Stage	Symptoms	Visual Field	Cup-to-Disc Ratio
Early	Asymptomatic	Small paracentral scotomas, nasal step	0.5 to 0.6
Moderate	Subtle peripheral vision difficulty (e.g., bumping into objects)	Arcuate scotoma, enlarging nasal defect	0.7 to 0.8
Advanced	Noticeable tunnel vision	Dense arcuate defects, only central island remaining	> 0.8 to 0.9
End-Stage	Severe visual impairment or blindness	Complete or near-complete field loss	1.0 (total cupping)

3. Diagnostic Workup

Test	Role	Key Findings
Tonometry	Best initial screening test	IOP > 21 mmHg (but can be normal)
Fundoscopy / Ophthalmoscopy	Assess optic nerve head	Increased cup-to-disc ratio (> 0.5), disc hemorrhage, neuroretinal rim thinning, nerve fiber layer defects
Visual Field Testing (Perimetry)	Detect and monitor functional damage	Arcuate scotoma, nasal step, paracentral scotomas; assessed via Humphrey automated perimetry
Gonioscopy	Confirm angle status	Open anterior chamber angle (distinguishes from angle-closure glaucoma)
Pachymetry	Measure central corneal thickness	Thin corneas underestimate true IOP; thick corneas overestimate
Optical Coherence Tomography (OCT)	Structural assessment of retinal nerve fiber layer	Thinning of the retinal nerve fiber layer (RNFL); can detect damage before visual field loss appears

Tonometry is the best initial test and the standard screening tool. It measures intraocular pressure. However, a single normal reading does not exclude glaucoma, because IOP fluctuates throughout the day and normal-tension glaucoma exists. If screening reveals elevated IOP, further workup is warranted.

Fundoscopic examination is where the diagnosis becomes apparent. The examiner evaluates the optic disc for cupping. An increased cup-to-disc ratio, especially if asymmetric between the two eyes, is the cardinal structural sign. Disc hemorrhages (Drance hemorrhages) are an ominous sign indicating active damage.

Visual field testing (perimetry) is the functional correlate. The classic pattern is an arcuate scotoma that follows the distribution of the arcuate nerve fiber bundle. A nasal step (asymmetric sensitivity across the horizontal midline in the nasal field) is another early finding. Perimetry is used both for diagnosis and for monitoring disease progression over time.

Gonioscopy is essential to confirm that the angle is open. This step distinguishes primary open angle glaucoma from angle-closure glaucoma, which has a fundamentally different mechanism and treatment. If gonioscopy is not performed, the diagnosis is incomplete.

OCT of the retinal nerve fiber layer has become a key tool because it can detect structural thinning before the patient develops measurable visual field loss. This makes it valuable for early detection and for following patients with ocular hypertension (elevated IOP without optic nerve damage yet).

The overall diagnostic logic: tonometry screens, fundoscopy and OCT identify structural damage, perimetry confirms functional loss, and gonioscopy classifies the type of glaucoma.

4. Management and Treatment

Treatment	Class	Mechanism	Key Notes
Latanoprost (0.005%)	Prostaglandin analog	Increases uveoscleral outflow	First-line; once daily at bedtime; side effects include iris darkening, eyelash growth, periorbital fat atrophy
Timolol (0.25-0.5%)	Non-selective beta-blocker	Decreases aqueous humor production	Twice daily; avoid in asthma, COPD, bradycardia, heart block
Brimonidine (0.1-0.2%)	Alpha-2 agonist	Decreases production and increases uveoscleral outflow	Avoid in children under 2 (risk of CNS depression); can cause allergic conjunctivitis
Dorzolamide (2%)	Topical carbonic anhydrase inhibitor	Decreases aqueous humor production	Can be used as adjunct; avoid in sulfa allergy
Acetazolamide	Oral carbonic anhydrase inhibitor	Decreases aqueous humor production	Used for acute IOP spikes; causes metabolic acidosis, hypokalemia, paresthesias; avoid in sickle cell disease
Pilocarpine	Cholinergic (miotic)	Increases trabecular outflow via ciliary muscle contraction	Rarely first-line for open angle; more important in angle-closure; causes miosis and brow ache
Laser Trabeculoplasty (SLT/ALT)	Laser procedure	Improves trabecular outflow	Can be used as initial therapy or as adjunct when medications are insufficient
Trabeculectomy	Surgical	Creates a new drainage pathway (filtering bleb)	Reserved for medically refractory cases; risk of infection, hypotony, bleb leak

First-line therapy is a topical prostaglandin analog, most commonly latanoprost, administered once nightly. Prostaglandin analogs reduce IOP by 25-30% and have the best efficacy-to-side-effect profile. The test-relevant side effects are iris color darkening (increased melanin in the iris stroma, permanent in some cases), eyelash lengthening, and periorbital fat atrophy (causing a sunken appearance around the eye).

If a prostaglandin analog alone is insufficient, topical timolol is typically added. Timolol reduces aqueous production and lowers IOP by roughly 20-25%. The contraindications to timolol are high-yield: it is a non-selective beta-blocker, so it must be avoided in patients with asthma, COPD, decompensated heart failure, second or third-degree heart block, and symptomatic bradycardia. Even topical application can produce systemic beta-blockade.

Brimonidine and dorzolamide serve as second or third-line adjuncts. Brimonidine is contraindicated in infants and young children due to the risk of crossing the blood-brain barrier and causing respiratory depression and apnea.

For patients who fail medical therapy, selective laser trabeculoplasty (SLT) can be offered. It is non-destructive and repeatable. If laser therapy also fails, trabeculectomy (a surgical filtering procedure) is the definitive intervention. The target in all cases is to lower IOP to a level that halts optic nerve damage, often defined as a target IOP reduction of at least 20-30% from baseline or an absolute target tailored to the severity of damage.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Looks Similar	Key Discriminator
Acute Angle-Closure Glaucoma	Also involves elevated IOP and risk of vision loss	Presents acutely with severe eye pain, red eye, nausea/vomiting, mid-dilated fixed pupil, and a shallow/closed angle on gonioscopy; open angle glaucoma is painless and chronic
Optic Neuritis	Can cause visual field defects and optic disc changes	Painful eye movement, central scotoma (not peripheral), afferent pupillary defect, associated with multiple sclerosis; disc may be swollen acutely rather than cupped
Anterior Ischemic Optic Neuropathy (AION)	Causes sudden visual field loss and optic disc abnormalities	Sudden painless monocular vision loss (usually altitudinal defect, not arcuate); disc edema acutely (not cupping); associated with giant cell arteritis (arteritic type) or vascular risk factors (non-arteritic)
Chronic Open Angle Closure (Plateau Iris)	Elevated IOP and chronic course	Angle appears narrow or intermittently closed on gonioscopy; different anatomy and treatment approach
Ocular Hypertension	Elevated IOP on screening	No optic disc damage and no visual field loss; IOP is elevated but there is no glaucomatous neuropathy yet; these patients are monitored and may be treated prophylactically
Retinitis Pigmentosa	Progressive peripheral vision loss, tunnel vision	Night blindness (nyctalopia) as the earliest symptom; bone-spicule pigmentation on fundoscopy; no elevated IOP or optic disc cupping
Papilledema	Optic disc swelling	Bilateral disc edema from elevated intracranial pressure; disc is swollen, not cupped; associated with headache, nausea, transient visual obscurations

6. Traps and High-Yield Pearls

The single most common trap with open angle glaucoma is confusing it with acute angle-closure glaucoma. If the vignette describes a patient with sudden, severe eye pain, a red eye, nausea, vomiting, and a mid-dilated non-reactive pupil, that is angle-closure. Open angle glaucoma is the opposite: the patient is asymptomatic, has no pain, no redness, and the vision loss is discovered incidentally or on screening. The moment you see "painless" and "gradual peripheral vision loss," think open angle.

A second trap involves normal-tension glaucoma. Students often dismiss glaucoma if the IOP is within normal range. If a vignette describes a patient with progressive cupping and arcuate visual field defects but a normal IOP, the answer is still glaucoma.

A third frequently tested concept is the contraindication of timolol in asthmatics. A vignette may present a patient with glaucoma and a history of asthma, then ask for the best medication. Timolol is the wrong answer; latanoprost or brimonidine would be appropriate.

Finally, understand that steroid use can cause or worsen open angle glaucoma. Any patient on chronic corticosteroids (topical ophthalmic, inhaled, or systemic) who develops elevated IOP should be evaluated for steroid-induced glaucoma. This is reversible if the steroid is discontinued early.

The core competency being tested is the ability to recognize a slowly progressive, painless optic neuropathy, to differentiate it from acute angle-closure and other causes of visual field loss, and to select appropriate pharmacotherapy while respecting contraindications.

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