Gecko Med
ReferenceAll Years (1st-Final)All UniversitiesGlaucoma

Glaucoma: Notes, PPT and PYQs for MBBS

Glaucoma is a group of progressive optic neuropathies with characteristic cupping of the optic disc and visual field loss, in which raised intraocular pressure (IOP) is the most important modifiable risk factor. Vision lost to glaucoma cannot be recovered, which makes early detection essential. It is a core 3rd Year Ophthalmology topic, with links to Anatomy and Physiology in 1st Year and Pharmacology in 2nd Year.

SME-reviewed. Updated 2026.
Open in GeckoMed for PPT slides and notes.

Quick Summary: What You Need to Know for University Exams

  • Normal IOP is about 10 to 21 mmHg.
  • Main types: primary open-angle (POAG), primary angle-closure (PACG), secondary and congenital (developmental) glaucoma.
  • POAG is painless and often unnoticed until late, earning the name "silent thief of sight".
  • Acute angle-closure is an emergency with sudden pain, red eye, haloes and a mid-dilated fixed pupil.
  • Key investigations: tonometry, gonioscopy, perimetry and optic disc evaluation.
  • Prostaglandin analogues are commonly first-line eye drops for POAG; laser peripheral iridotomy treats angle closure.
  • Trabeculectomy is the standard filtering surgery.

Glaucoma Across MBBS Subjects

MBBS Year

1st Year

Subject

Anatomy

What Is Usually Asked

Angle of the anterior chamber, ciliary body

MBBS Year

1st Year

Subject

Physiology

What Is Usually Asked

Formation and drainage of aqueous humour

MBBS Year

2nd Year

What Is Usually Asked

Antiglaucoma drugs, mechanisms and adverse effects

MBBS Year

3rd Year

What Is Usually Asked

Classification, clinical features, investigations, medical, laser and surgical management

MBBS Year

3rd Year

What Is Usually Asked

Blindness control and screening

Definition and Classification

Definition: Glaucoma is a chronic, progressive optic neuropathy with characteristic structural changes of the optic nerve head and corresponding visual field defects, commonly associated with raised intraocular pressure.

Classification

Type

Primary open-angle glaucoma (POAG)

Examples

Includes normal-tension glaucoma

Type

Primary angle-closure disease

Examples

Primary angle-closure suspect, primary angle closure, primary angle-closure glaucoma; acute angle-closure attack

Type

Secondary glaucoma

Examples

Lens-induced (phacomorphic, phacolytic), steroid-induced, neovascular, uveitic, traumatic (angle recession), pseudoexfoliative, pigmentary

Type

Congenital and developmental

Examples

Primary congenital glaucoma (buphthalmos); glaucoma with other developmental anomalies

Type

Ocular hypertension

Examples

Raised IOP without optic disc damage or field loss

POAG Versus Acute Angle-Closure

Feature

Onset

POAG

Slow, painless

Acute Angle-Closure

Sudden, painful

Feature

Angle on gonioscopy

POAG

Open

Acute Angle-Closure

Closed

Feature

Red eye

POAG

No

Acute Angle-Closure

Yes, with ciliary congestion

Feature

Vision

POAG

Gradual peripheral field loss

Acute Angle-Closure

Sudden blurring with coloured haloes

Feature

Pupil

POAG

Normal

Acute Angle-Closure

Mid-dilated, vertically oval, sluggish or fixed

Feature

Cornea

POAG

Clear

Acute Angle-Closure

Oedematous

Feature

IOP

POAG

Moderately raised or normal

Acute Angle-Closure

Very high

Feature

Main treatment

POAG

Eye drops, laser, surgery

Acute Angle-Closure

Emergency IOP reduction, then laser peripheral iridotomy

Aetiology (Risk Factors)

POAG

Increasing age

Primary Angle-Closure

Increasing age

POAG

Family history

Primary Angle-Closure

Hypermetropia (short eye, shallow anterior chamber)

POAG

Raised IOP

Primary Angle-Closure

Female sex

POAG

Myopia

Primary Angle-Closure

East and South Asian ethnicity

POAG

Thin central cornea

Primary Angle-Closure

Thick or anteriorly placed lens

POAG

Long-term corticosteroid use

Primary Angle-Closure

Pupil dilation in dim light or with certain drugs

Pathophysiology

Aqueous Humour Dynamics

  1. Aqueous humour is produced by the ciliary processes (non-pigmented ciliary epithelium)
  2. It flows from the posterior chamber through the pupil into the anterior chamber
  3. Most drains through the trabecular meshwork into Schlemm's canal (conventional pathway)
  4. The rest drains through the uveoscleral (unconventional) pathway
  5. IOP depends on the balance between production and drainage

Mechanism of Damage (Flowchart)

  1. Resistance to outflow rises (open angle) or the angle is blocked (angle closure)
  2. IOP increases
  3. Mechanical stress on the lamina cribrosa and reduced blood flow to the optic nerve head
  4. Retinal ganglion cell axons are progressively lost
  5. The optic cup enlarges and the neuroretinal rim thins
  6. Characteristic visual field defects develop and progress to tunnel vision and blindness if untreated

Angle closure mechanism: In predisposed eyes, the iris is pushed forward against the trabecular meshwork, often because of pupillary block, cutting off drainage and raising IOP sharply.

(Examiner may ask you to draw the aqueous humour pathway and the angle of the anterior chamber.)


Clinical Features

Primary Open-Angle Glaucoma

  • Usually no symptoms until advanced
  • Frequent change of reading glasses in some patients
  • Difficulty with dark adaptation
  • Gradual loss of peripheral vision, then tunnel vision

Optic Disc Changes

Sign

Increased cup-disc ratio

Description

Enlarged cup, especially vertically

Sign

Cup asymmetry

Description

Difference in cup size between the two eyes

Sign

Neuroretinal rim thinning

Description

Violation of the ISNT rule (normal rim is thickest Inferiorly, then Superiorly, Nasally, Temporally)

Sign

Notching

Description

Focal loss of the rim, often inferior or superior

Sign

Vessel changes

Description

Nasal shift of vessels, bayoneting

Sign

Splinter haemorrhage

Description

Small haemorrhage at the disc margin

Sign

Laminar dot sign

Description

Visible pores of the lamina cribrosa

Visual Field Defects (Typical Progression)

  1. Paracentral scotoma
  2. Arcuate (Bjerrum) scotoma
  3. Nasal step (Roenne)
  4. Ring scotoma
  5. Tubular vision with a temporal island
  6. Complete loss of vision

Acute Angle-Closure Attack

  • Sudden, severe eye pain and headache
  • Blurred vision with coloured haloes around lights
  • Nausea and vomiting
  • Red eye with ciliary congestion
  • Hazy, oedematous cornea
  • Shallow anterior chamber
  • Vertically oval, mid-dilated, non-reactive pupil
  • Stony hard eye on palpation

Congenital Glaucoma (Buphthalmos)

  • Classic triad: photophobia, epiphora (watering) and blepharospasm
  • Enlarged, hazy cornea
  • Breaks in Descemet's membrane (Haab's striae)

Diagnosis

Investigation

Tonometry

Purpose

Measures IOP; Goldmann applanation tonometry is the standard; Schiotz (indentation) and non-contact tonometers are also used

Investigation

Gonioscopy

Purpose

Examines the angle of the anterior chamber to classify open or closed angle

Investigation

Perimetry

Purpose

Detects and monitors visual field defects (automated perimetry)

Investigation

Optic disc examination

Purpose

Fundoscopy or slit-lamp biomicroscopy to assess cupping and the rim

Investigation

Optical coherence tomography (OCT)

Purpose

Measures retinal nerve fibre layer thickness

Investigation

Pachymetry

Purpose

Measures central corneal thickness, which affects IOP readings

Investigation

Van Herick test

Purpose

Slit-lamp estimate of anterior chamber depth

Management

Principles

  1. Lower IOP to a target level that prevents further damage
  2. Preserve remaining vision and quality of life
  3. Monitor regularly with IOP, disc and field examinations
  4. Treat the cause in secondary glaucoma

Antiglaucoma Drugs

Drug Class

Prostaglandin analogues

Examples

Latanoprost, bimatoprost, travoprost

Mechanism

Increase uveoscleral outflow

Key Adverse Effects

Iris pigmentation, lash growth, conjunctival redness

Drug Class

Beta-blockers

Examples

Timolol

Mechanism

Reduce aqueous production

Key Adverse Effects

Bronchospasm, bradycardia; avoid in asthma and heart block

Drug Class

Alpha-2 agonists

Examples

Brimonidine

Mechanism

Reduce production and increase uveoscleral outflow

Key Adverse Effects

Allergy, fatigue; avoided in infants

Drug Class

Carbonic anhydrase inhibitors

Examples

Dorzolamide, brinzolamide (topical); acetazolamide (oral or intravenous)

Mechanism

Reduce aqueous production

Key Adverse Effects

Systemic: paraesthesia, electrolyte disturbance, kidney stones

Drug Class

Miotics

Examples

Pilocarpine

Mechanism

Increase trabecular outflow; pulls the iris away from the angle

Key Adverse Effects

Brow ache, reduced night vision

Drug Class

Hyperosmotic agents

Examples

Mannitol (intravenous), glycerol (oral)

Mechanism

Draw fluid out of the vitreous

Key Adverse Effects

Used short term in acute attacks

Laser Treatment

Procedure

Laser peripheral iridotomy (Nd:YAG)

Use

Angle-closure disease; also done prophylactically in the fellow eye

Procedure

Selective or argon laser trabeculoplasty

Use

Open-angle glaucoma, to improve trabecular outflow

Procedure

Cyclophotocoagulation

Use

Refractory glaucoma, to reduce aqueous production

Surgery

Procedure

Trabeculectomy

Use

Most commonly performed filtering surgery; creates a new drainage route under a scleral flap; antimetabolites (mitomycin C, 5-fluorouracil) reduce scarring

Procedure

Glaucoma drainage devices

Use

Refractory glaucoma

Procedure

Goniotomy or trabeculotomy

Use

Congenital glaucoma

Procedure

Cataract extraction

Use

Lens-induced glaucoma and some angle-closure cases

Emergency Management of Acute Angle-Closure (MBBS Level)

  1. Lower IOP quickly: intravenous acetazolamide and hyperosmotic agents (such as intravenous mannitol)
  2. Topical beta-blocker and alpha agonist
  3. Topical corticosteroid to reduce inflammation
  4. Pilocarpine once IOP starts to fall
  5. Definitive treatment with laser peripheral iridotomy, and prophylactic iridotomy in the other eye

Complications

  • Irreversible visual field loss and blindness
  • Absolute glaucoma: a painful, blind eye
  • Corneal decompensation in chronic high IOP
  • Complications of surgery: infection of the filtering bleb, hypotony, cataract

Prevention and Screening (Community Medicine Angle)

  • Glaucoma is a leading cause of irreversible blindness worldwide.
  • Opportunistic screening of people above 40 years, especially those with a family history, diabetes, myopia or long-term steroid use, helps early detection.
  • India's National Programme for Control of Blindness and Visual Impairment (NPCBVI) supports eye care services, including glaucoma detection and management.

Prognosis

Damage already done cannot be reversed, but good IOP control and regular follow-up usually slow or stop further loss. Outcomes are poorest when glaucoma is diagnosed late or when patients stop treatment.


Quick Viva Questions

Q: What is the normal intraocular pressure? A: About 10 to 21 mmHg.

Q: What is the gold-standard instrument for measuring IOP? A: The Goldmann applanation tonometer.

Q: Why is timolol avoided in asthma? A: It is a non-selective beta-blocker and can be absorbed systemically, causing bronchospasm.

Q: What is the classic triad of congenital glaucoma? A: Photophobia, epiphora and blepharospasm.

Q: Why is iridotomy done in the fellow eye after an acute attack? A: The other eye usually has the same narrow-angle anatomy and a high risk of an attack.


How Glaucoma Appears in MBBS University Exams

Typical question styles (not attributed to specific papers or years):

  1. "Classify glaucoma. Describe the clinical features and management of primary open-angle glaucoma." (Long essay)
  2. "Describe the clinical features and management of acute angle-closure glaucoma." (Long essay)
  3. "Write a short note on antiglaucoma drugs." (Short note, Ophthalmology or Pharmacology)
  4. "Write a short note on congenital glaucoma." (Short note)
  5. "Write a short note on trabeculectomy." (Short note)
  6. "Describe the formation and drainage of aqueous humour." (Physiology)

Frequently Asked Questions

What is the difference between open-angle and angle-closure glaucoma?

In open-angle glaucoma the drainage angle is open but outflow is reduced, causing slow, painless damage. In angle-closure glaucoma the iris blocks the angle; an acute attack causes sudden pain, red eye and very high IOP.

Can glaucoma be cured?

Lost vision cannot be restored, but lowering IOP with drops, laser or surgery can slow or stop further damage.

Can I download the glaucoma PPT for my presentation?

Yes. Use the Download PPT button at the top of this page. The GeckoMed app also gives offline access to the slides and notes.

Try Gecko Med

Practice smarter with the app behind these resources.

Revise high-yield topics, solve previous year questions, and keep your MBBS prep moving in one place.