Glaucoma (Ocular Hypertension) – group of ocular disorders that result in optic nerve damage, (damage to nerve

fiber bundle containing axons from both inferonasal and inferotemporal retina
resulted to arcuate defect)
- often associated with increased fluid pressure in the eye (IOP) of above
21 mmHg or 2.8 kPa
- "silent thief of sight” due to loss of vision often occurs gradually over a long
period of time, and symptoms only occur when the disease is quite advanced
- second cause of blindness next to cataract (#1 cause of blindness)

Scotoma – interruption/break in the visual field (blind) surrounded by a remaining normal visual field
 PAPILLOMACULAR AREA
SN – Sup. Nasal ST – Sup. Temporal
IN – Inf. Nasal IT – Inf. Temporal
Arcuate areas
Divided into two main categories:
1. "Open-angle" (chronic/simple angle glaucoma, wide angle glaucoma, compensated glaucoma)
- painless, tends to develop slowly over time and often has no symptoms until the disease has progressed
significantly and is treated medically
a. Primary open angle glaucoma (POAG) – increased pressure is caused by trabecular blockage
Etiology: idiopathic
S/Sx:
a. imperceptible very gradual vision loss
b. loss of peripheral vision
c. cupping of optic disc
Treatment: anti-glaucoma agents

1) Juvenile open angle glaucoma – rare, autosomal dominant subset of glaucoma diagnosed
- seen in more than 3–40 y/o tends to be rapidly progressive with more severely elevated IOP
Treatment: Trabeculectomy (less responsive to medications)
b. Secondary open angle glaucoma
Etiologies:
1. Pigment Dispersion Syndrome (PDS) → phenylephrine & epinephrine
Pigment dispersion syndrome – melanin pigments from back of iris rubs off by zonular fibers.
2. hyphema – blood at aqueous chambers
3. medications – corticosteroids (Dexamethasone and Betamethasone)→ accumulation of glucosaminoglycans →
blocks the trabecula and canal
4. rupture Morgagnian cataract → hypermature cataract (liquified)
 Crystalline Lens

Open Angle Glaucoma

Peripheral Loss of Vision
NORMAL OPTIC NERVE ATROPHY
PDS
Hyphema
Morgagnian Cataract (brownish nucleus)
2. "Closed-angle" (acute congestive angle glaucoma, narrow angle glaucoma, uncompensated glaucoma or emergency glaucoma)
– sudden eye pain, redness, nausea and vomiting and is treated by surgical intervention
a. Primary close angle glaucoma (PCAG) – caused by contact between the iris and trabecular meshwork, which in turn
obstructs outflow of the aqueous humor from the eye.
Etiology: idiopathic
S/Sx:
1. blurred vision
2. halos around bright lights (iridescent vision)
3. pupils are mid-dilated non-responsive to direct light → Marcus Gunn pupil
4. edematous, cloudy cornea
5. ciliary injection
6. ocular pain
7. headache and vomiting
Treatment: surgery
1. peripheral laser iridotomy using YAG or Argon laser

b. Secondary close angle glaucoma

Etiologies:
1. Morgagnian cataract → swelling
2. anterior uveitis

3. Low tension or normal tension glaucoma – optic nerve damage and associated visual field loss but normal or low IOP
Etiology: idiopathic
Close Angle Glaucoma
Iridescent Vision
Ciliary Injection with Hazy Cornea – Acute Glaucoma
 Pathophysiology
of
Optic Nerve Atrophy
Posterior Scleral Foramina
Lamina Cribrosa
The nerve fibers forming the optic nerve exit the eye posteriorly through a hole in the sclera that is occupied by a
mesh-like structure called the lamina cribrosa. It is formed by a multilayered network of collagen fibers that insert
into the scleral canal wall. It is the weakest part of the sclera.
Glaucoma causing Cupping (optic nerve atrophy)
 Drugs for Glaucoma
I. Miotic Agents (Cholinergic/Parasympathomimetic agent) → Green
A. Direct-acting Cholinergic Agents – interact with M3- receptor (sphincter pupillae → miosis) → enhance AH outflow
1. Pilocarpine – lipid soluble P/P: Oph sol’n and Pilo20/40 CL
uses:
> angle closure → miosis → widen the angle → enhance AH outflow
> open angle → contract Bruck’s muscles → open trabecula → enhance AH outflow
2. Carbachol – more potent, lipid insoluble + BAK (wetting agent)
B. Indirect-acting Cholinergic Agents
1. Acetylcholinesterase (AchE) inhibitors – S/E: iris cyst, cataract
a. Physostigmine
b. Echothiophate
c. Diisoprophylfluorophosphate (DFP)
d. Demecarium
II. Adrenergic Agents/Sympathomimetic Agents
A. Selective Alpha 2 Adrenergic Agents
1. Apraclonidine → partially selective at A (A1, A2)
2. Brimonidine → very selective A2
A2 → inhibitory ciliary process → decrease AH secretion → lower IOP
B. Non-selective Adrenergic Agents
1. Epinephrine
2. Dipivefrin → Epinephrine
III. Adrenergic Blocker or Sympatholytic agent
A. Beta Blockers → inhibiting B2 → decrease AH secretion → lower IOP
1. Non-selective beta blocker → B2 block → bronchial smooth muscles → contract → bronchoconstriction → C/I: COPD/COLD
B2 bronchial smooth muscles → stimulate → relax → bronchodilation
B2 blockers → decrease AH secretion
a. Timolol – safe any types of glaucoma
b. Levobunolol
c. Metipranolol
d. Carteolol
2. Cardio (B1)-selective (β-2) beta blocker
a. Betaxolol → safer for COPD
IV. Carbonic Anhydrase Inhibitors – usually given orally
- produce synergistic effect w/ miotic agent to lower IOP
MOA: reduces HCO3 transport and Na+ thus decrease AH secretion
Uses:
1. Open angle and angle closure glaucoma
S/E:
1. parasthesia – most common, characterized by numbness and tingling sensation at mouth & extremities
2. induce diuresis because HCO3 and Na+ are excreted by kidneys
3. diarrhea
*Carbonic anhydrase – enzyme which increase the availability of H+ & HCO3
- HCO3 enhances Na+ transport and secretion into the posterior aqueous chamber
- present in:
a. eyes – uvea (ciliary process), lens, vitreous, retina
b kidneys
Preparations:
A. Oral
1. Acetazolamide 250 mg every 4 hours
S/E:
a. nephrolithiasis – kidney stone
b. K+ loss due to diuretic effect
c. myopia – due to shallowing of anterior chamber secondary to ciliary body swelling
2. Methazolamide
3. Ethoxyzolamide
4. Dichlorphenamide
B. Ophthalmic
1. 1% Brinzolamide
2. 2% Dorzolamide – combine w/ timolol
3. Lodoxamide
V. Prostaglandin analog
MOA: increase uveo-scleral outflow → lower IOP
1. 0.005% Latanoprost
2. 0.004% Travaprost
3. 0.03% Bimatoprost
4. 0.0015% Tafluprost

S/E of Prostaglandin analogs:

a. blurred vision
b. eye redness/discomfort/itching
c. dry eyes
d. tearing
e. eyelid crusting
f. increase in eyelash number/length/thickness
g. darkening of the eyelashes and eyelids
h. increased sensitivity to light may occur
i. brown discoloration of iris persists months or years (heterochromia iridis)
HETEROCHROMIA
EYELASHES
VI. Osmotherapeutic Agents – usually given systemically
MOA: enhance reabsorption of aqueous in uveal vasculature by creating osmotic gradient
Uses:
a. angle closure glaucoma
b. preoperative agent to lower IOP prior to surgery
c. cerebral edema – mannitol
d. corneal edema – glycerol, ascorbate, isosorbide, sucrose
e. deepens anterior chamber and contract vitreous away from corneal endothelium by dehydrating the vitreous

1. Glycerol/Glycerine – oral, cause transient rise in blood glucose (C/I in DM)

2. Isosorbide – oral, safe for DM
3. Urea – IV given only, C/I in renal disease
4. Mannitol – IV only, safe in renal disease
- most commonly use because it has large molecular weight thus remains in the blood circulation
5. Ethanol – inhibit ADH thus inducing diuresis
6. Ascorbate – has low molecular weight thus can pass blood-ocular barrier
7. Sucrose
Surgical Management:
A. Laser surgery
1. Argon Laser Trabeculoplasty (ALT) → for open-angle glaucoma
2. Selective Laser Trabeculoplasty (SLT) → for open-angle glaucoma
3. Micropulse Laser Trabeculoplasty (MLT) → for open-angle glaucoma
4. Laser Peripheral Iridotomy (LPI)→ for angle closure glaucoma
*Creates small hole in the iris connecting the posterior to anterior aqueous chambers.
5. Laser Cyclophotocoagulation (Cycloablation) → for open angle glaucoma
Trans-scleral cyclophotocoagulation uses a laser to direct energy through the outer sclera of the eye to reach and destroy
portions of the ciliary processes, without causing damage to the overlying tissues.
ALT and SLT
Micropulse Laser Trabeculoplasty
Laser Peripheral Iridotomy
Laser Cyclophotocoagulation
Trans-scleral Cyclophotocoagulation
B. Conventional Surgery Filtering Microsurgery – tiny drainage hole is made in the sclera in trabeculectomy or sclerostomy
1. Trabeculectomy – most commonly used for both open and angle closure glaucoma
2. Drainage Implant Surgery – a small silicone tube that extends into the anterior chamber of the eye. The tube is connected
to one or more plates, which are sutured to the surface of the eye, usually not visible. Fluid is
collected on the plate and then absorbed by the tissues in the eye.

C. Promising Surgery
1. ExPress mini-glaucoma shunt – stainless steel device that is inserted into the anterior chamber of the eye and placed under
a scleral flap. It lowers IOP by diverting aqueous humor from the anterior chamber.
2. Canaloplasty – compared to an ocular version of angioplasty, in which the physician uses an extremely fine catheter to clear
the drainage canal.
3. Trabectome – new probe-like device inserted into anterior chamber and make tiny incision and delivers thermal energy to
the trabecula
Trabeculectomy
Drainage Implant Surgery
ExPress mini-glaucoma shunt
Canaloplasty Trabectome