Download MBBS Ophthalmology PPT 47 Primary Open Angle Glaucoma Lecture Notes

Primary open angle glaucoma

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Acknowledgement

? Kanski's Clinical Ophthalmology (8th Edition).

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? Becker- Schaffer's Diagnosis and therapy of The

Glaucomas (8th Edition).

? Comprehensive Ophthalmology (A.K.Khurana)

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(7th Edition).

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Learning Objectives

? At the end of this class the students shall be able to :
? Define primary open angle glaucoma(POAG).

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? Comprehend the pathophysiology and
risk factors of POAG.
? Understand the clinical features of POAG.
? Understand the fundamentals of managing
primary open angle glaucoma

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4
Question

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Glaucoma is defined as:
? a. a group of diseases that have in common a

characteristic optic neuropathy associated with increased

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intraocular pressure.

? b. a group of diseases that have in common a

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characteristic optic neuropathy with associated visual

function loss.

? c. a group of diseases that have in common high

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intraocular pressure with or without optic neuropathy.

? d. a group of diseases that have in common a

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characteristic optic neuropathy with poor visual acuity.

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Definition of POAG

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? Chronic, progressive optic neuropathy

characterised by morphological changes at the

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optic disc and retinal nerve fibre layer leading to

characteristic visual field changes, in the absence

of other ocular diseases or congenital anomalies

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(with or without a raised IOP).

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Etiopathogenesis

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? Multifactorial aetiology
? Risk factors include:

? Elevated Intra Ocular Pressure(IOP)

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(More than 21 mm Hg)

? Optic disc cupping

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? Increasing Age : More common in 5th to 7th decades

? Race: More common and severe in Black population

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Etiopathogenesis

? Heredity/ Family History: Risk of about 10% in

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siblings; 4% in off springs

? Diabetes

? Systemic Hypertension

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? Myopia

? Thin central corneas

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? Steroid usage

? ?Migraine, Cigarette smoking

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Pathophysiology of POAG

? Decrease in aqueous outflow facility due to

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increased resistance to outflow leads to rise in IOP

? Two theories of axonal loss in optic disc
? 1. Mechanical: Distortion of lamina cribrosa

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leading to impaired axoplasmic flow

2. Vascular: Optic disc ischaemia with
defective autoregulation of blood vessels

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FORMATION OF AQUEOUS HUMOR

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CILIARY PROCESSES

-approx. 70-80 radial folds in the pars plicata which form

the site of aqueous production.

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-Zonular fibers attach primarily in the valleys of the ciliary

processes and also along the pars plana

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DIFFUSION

SECRETION
(80-90%)

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ULTRA-
FILTRATION

FORMATION PROCESSES 11

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Formation of aqueous humor

? Diffusion and ultrafiltration are both

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passive mechanisms so no active cellular

participation occurs.

? Active secretion is an active process.

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? Rate of formation of aqueous humor in a

healthy human eye is-

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2 - 3 microlitres/minute

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Table 1. Constituents of Human Aqueous Humor*

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Constituent (?mol/mL) Anterior Chamber

Aqueous

Plasma

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Ascorbate

1.06

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0.04

Bicarbonate

22.0

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26.0

Calcium

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2.5

4.9

Chloride

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131.0

107.0

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Glucose

2.8

5.9

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Lactate

4.5

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1.9

Magnesium

1.2

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1.2

Phosphate

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0.6

1.1

Potassium

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22.0

26.0

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Sodium

152.0

148.0

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Urea

6.1

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7.3

Protein (gm/dL)

0.024

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7.0

pH

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7.21

7.4

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Differences between

aqueous humor & plasma

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AQUEOUS PLASMA

-Marked deficit of

0.024 7.0

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proteins

gm/dl gm/dl

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-Marked excess of

1.06 0.04

Ascorbate

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micromol/ml micromol/ml

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-Excess of Lactate

4.5 1.9

micromol/ml micromol/ml

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-Excess of Chloride &

certain amino acids

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Functions of aqueous humor

*Maintaining IOP :
-important for early ocular development &

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maintaining global integrity throughout life.
*Serves as a vascular system for the avascular
structures of the eye: cornea, lens & TM.
- by providing substrates & nutrients & removing
metabolites.

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Functions of aqueous humor

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*Delivering high concentration of Ascorbate:

- scavenges free radicals & protects against UV

rays & other radiations.

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*Local paracrine signaling & immune responses.

*Colourless & transparent medium as part of eye's

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optical system.

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Aqueous humor outflow

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Video of aqueous humor outflow

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Major amount of aqueous humor leaves the

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eye by


BULK FLUID FLOW

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i.e. fluid flows along normal pressure

gradient through non-energy dependent

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process

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Ciliary processes

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Aqueous Humor in PC

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through pupil

Anterior Chamber

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Trabeculo-canalicular outflow

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*It is the main outlet for aqueous from the AC

*70-90% of total aqueous is drained by this route

TRABECULAR MESHWORK

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-A sponge work of
connective tissue
beams arranged as
super-imposed

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perforated sheets.
- Extracellular spaces
contain hydrophilic

glycosaminoglycans &

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collagen.

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JUXTACANALICULAR

(ENDOTHELIAL) MESHWORK

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- Outermost portion of

TM which mainly

offers the normal

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resistance to

aqueous outflow

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- Connects the

corneoscleral

meshwork with

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schlemm's canal

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? Veins from the anterior part of ciliary body form the

Ciliary venous plexus

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Anterior ciliary veins & Episcleral veins

communicate with Schlemm's canal

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Schlemm's Canal

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20-30 Collector channels Aqueous Vein

Intra-scleral venous plexus

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Episcleral venous plexus
& Anterior Ciliary vein

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UNCONVENTIONAL

OUTFLOW

*responsible for 10-25% of total aqueous outflow

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UVEO-SCLERAL OUTFLOW

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Trans-corneal outflow

- Aqueous humor from anterior chamber

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goes into tear film through cornea.

- Very little aqueous passes through this

pathway.

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- Total volume of fluid transferred is limited

by high hydraulic resistance of the cornea.

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Clinical features of POAG

Symptoms
? Usually asymptomatic in early cases

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? Mild headache and eye ache
? Frequent changes in presbyopic glasses
? Delayed dark adaptation
? Loss of peripheral vision
? Loss of central vision(late cases)

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Signs of POAG

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? Normal anterior segment
? Pupil reaction to light may be sluggish(in

advanced cases only)

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? Elevated IOP(More than 21 mm Hg) with

diurnal variation more than 5-8 mmHg

? Optic disc changes (Progressive,

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asymmetric)

? Visual field defects

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Optic disc changes in glaucoma

? Early changes
o Retinal nerve fibre layer atrophy

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o Vertically oval cup

o Asymmetry of the cups(More than 0.2

difference)

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o Large cup(CD more than 0.6)

o Splinter haemorrhages

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Advanced glaucomatous disc changes

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? Marked cupping (More than 0.7)
? Thinning of NRR (Neuroretinal rim)
? Lamellar dot sign
? Vascular alterations
o Nasal shifting of retinal vessels

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o Bayonetting sign(convoluted path due to NRR

loss)

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o Baring of circumlinear vessels and overpass

vessels

? Glaucomatous optic atrophy

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Normal Optic Disc

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Glaucomatous optic disc

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Is this a normal or

Glaucomatous optic disc

glaucomatous disc ?

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Recording and documenting disc changes

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? Serial drawings (10 square grid) after

seeing fundus by ophthalmoscopy/slit

lamp with +90D/+78D lens

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? Disc photography
? HRT(Heidelberg retinal tomography)
? OCT (Optical coherence tomography)
? NFA(Nerve fibre analyser)

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View of optic disc by 90D lens examination

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Field of vision

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Visual field defects in glaucoma

? Arcuate nerve fibres in the superior and

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inferior temporal portions of the optic disc:

Most sensitive to damage
? Macular fibres : Most resistant to damage

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CENTRAL VISION IS PRESERVED TILL

THE LAST IN GLAUCOMA

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Progression of field defects

? Isopter contraction: Generalised field

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constriction

? Baring of blind spot : Non specific
(Exclusion of blind spot from central field)
? Paracentral scotoma: Wing shaped and

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occurs above or below the blind spot in the

Bjerrum's area(10-25 degrees from

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fixation)

Is the earliest clinically significant defect

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Progression of field defects

? Seidel's scotoma: sickle shaped
Due to joining of blind spot and
paracentral scotoma

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? Bjerrum's/Arcuate scotoma:
Extension of Seidel's scotoma to reach the
horizontal line.
? Double arcuate/ring scotoma

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Progression of field defects

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? Roenne's central nasal step:
Sharp right angled defect at the horizontal
meridian when arcuate scotomas run in
different arcs
? Peripheral field defects

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? Advanced defects
Residual Tubular vision
Temporal island of vision

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Quantification of visual field defects

? Visual field analyzer

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Kinetic perimeter
Static perimeter (automated)

Testing more than once is required before
final interpretation

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Enlarged blind spot

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Superior arcuate scotoma

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Bjerrum's scotoma

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Roenne's nasal step

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Double arcuate

10-2- Advanced VFD , macular split

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Advanced glaucoma

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Diagnostic work up/Investigations

? Tonometry

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? Goniscopy: Open angles
? Perimetry: To detect visual field defects
? Slit lamp examination: To rule out causes

of secondary open angle glaucoma

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? Fundus examination to document optic

disc changes

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? Diurnal variation testing
? Provocative testing: Water drinking test 50
Diagnosis

? POAG: Raised IOP(More than 21 mm Hg),

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glaucomatous optic disc cupping, visual
field changes.
? Ocular hypertension/glaucoma suspect:
Raised IOP
? NTG(Normal tension glaucoma):

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Glaucomatous optic disc cupping with or
without visual field changes with normal IOP


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Management of POAG

? Therapeutic choices

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q Medical therapy

q Argon/Diode Laser Trabeculoplasty

q Filtration surgery

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Basic principles of therapy

? Make a correct diagnosis

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? Set a target IOP
? Start with a single drug to lower IOP
? Switch to another group of drugs if needed
? Control IOP on minimal medications
? Monitor therapy and reset target IOP

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whenever needed

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Topical drugs used for POAG therapy

? Prostaglandin/Prostamides
Latanoprost, Bimatoprost, Travoprost
? Beta blockers

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Timolol maleate, Betaxolol
? Carbonic anhydrase inhibitors
Dorzolamide, Brinzolamide
? Sympathomimetics
Brimonidine, Apraclonidine

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? Parasympathomimetics
Pilocarpine

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Systemic drugs used for POAG therapy

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? Used rarely, for short term control of IOP
? Oral carbonic anhydrase inhibitors
Acetazolamide, Methazolamide

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Laser treatment

? Indications

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Target IOP not achieved with medical
therapy
Non compliance of medical therapy

Argon/ Diode Laser Trabeculoplasty (ALT)

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Selective Laser Trabeculoplasty (SLT)

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Surgical therapy

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? Indications
v Target IOP not achieved with maximal
tolerated medical therapy and laser
trabeculoplasty
v Non compliance of medical therapy

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v Non availability of laser therapy
v Advanced glaucoma

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Surgical therapy

? Filtration surgery : Trabeculectomy

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? Modified trabeculectomy :
Use of antifibrotic agents
Mitomycin/5FU
? Aqueous drainage devices:
Ahmed glaucoma valve

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In cases with no/poor visual potential:
Cycloablative therapy with laser/cryotherapy

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Conclusion

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? Primary open angle glaucoma is a

progressive optic neuropathy with

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characteristic optic disc and visual field

changes.

? Increased resistance to aqueous outflow

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leads to rise in IOP.

? Aim of management is to reduce IOP to

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minimize damage to optic disc and

resultant visual field defects.

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Question

Which of the fol owing is not a risk factor

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for the development of primary open

angle glaucoma?
a. positive family history.
b. advanced age.

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c. increased IOP.
d. increased corneal thickness.

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Question

You have been referred a case of open

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angle glaucoma. Which of the fol owing

would be an important point in

diagnosing the case?

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a. Shallow anterior chamber
b. Optic disc cupping
c. Narrow angle
d. Visual acuity and refractive error

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THANK YOU

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