IT CONTAINS ADEQUATE INFORMATION TO UNDERSTAND GLAUCOMA.

1. Presentation on
PRESENTATION ON
GLAUCOMA
PRESENTED BY:
AYESHA RUQSAR

2. CONTENTS:
INTRODUCTION.
ETIOLOGY.
PATHOPHYSIOLOGY.
GLAUCOMA CLASSIFICATION.
CLINICAL MANIFESTATION.
DIAGNOSIS.
TREATMENT.
REFERENCES

3. 
•Glaucoma refers to a group of
ophthalmic disorders characterized
by neuropathy of the optic nerve and
progressive loss of retinal ganglion
cells,
VISUAL
FIELD
LOSS
OPTIC
NERVE
DAMAGE
GLAUCO
MA
INCREASE
IOP
•Which leads to
permanent
deterioration of the
visual field eventually
lead to blindness.

4. ETIOLOGY
• All types of glaucoma – progressive optic neuropathy due to
the death of retinal ganglion cells(RGCs)
• RGCs death is initiated by block in transport of neurotrophins
from brain to RGCs
damaging cascade activation
Apoptosis of RGCs
• RGCs death – loss of retinal fibers – optic neuropathy & visual
field defects

5. • Mechanical theory :
↑IOP – mechanical stretch of lamina cribtosa –
axonal deformation & altered capillary blood
flow -- ↓neurotrophins to reach RGC`s
(normal IOP pressure is 5-22mm/Hg)
• Pressure independent factors :
- Failure of autoregulation
- Vasospasm
- Systemic hypotension
- Blood / fluid loss
• Excitotoxicity theory:
glutamate , oxygen free radicals, nitric oxide.

6. Intraocular pressure is a function of
production of liquid aqueous humour by
the ciliary processes of the eye, and its
drainage through the trabecular
meshwork. Aqueous humor flows from
the ciliary processes into the posterior
chamber, bounded posteriorly by
the lens and the zonules of Zinn, and
anteriorly by the iris. It then flows
through the pupil of the iris into
the anterior chamber, bounded posteriorly
by the iris and anteriorly by the cornea.
From here, the trabecular meshwork
drains aqueous humor via the scleral
venous sinus (Schlemm's canal)
into scleral plexuses and general blood
circulation.
MECHANISM OF PRODUCTION OF AQUEOUS
HUMOUR AND ITS OUFLOW

8. PATHOPHYSIOLOGY
A- POAG :
• Increased IOP causes retinal ganglion cell axons
to undergo mechanical stress, alters axonal
protein transport, and decreases blood supply to
the retina and the optic nerve leading to tissue
ischemia.
• The level of IOP is related to the death of retinal
ganglion cell and optic nerve fibers.

9. B- PACG :
Involves Two major mechanisms of
Mechanical obstruction of trabecular
meshwork by the peripheral iris include
1- Pupillary block (more common)
2- Iris plateau.
• Both of these mechanisms result in the
occlusion of aqueous humor outflow
causing IOP elevation at extreme levels
that can lead to vision loss in hrs to days.

10. GLAUCOMA CLASSIFICATION

11. CLINICAL MANIFESTATION
 A- POAG: General
• POAG is usually bilateral with asymmetric disease
progression
Symptoms:
1. Loss of peripheral vision.
2. Presence of scotomata (blind spots) in vision field.
Signs:
Ophthalmoscopic examination may reveal
1.Optic nerve head (optic disc) cupping.
2.Large cup-to-disc ratio.
3.Notching of the optic nerve head rim.
4.Splinter hemorrhages (using a slit-lamp biomicroscope)

12. B- PACG: General
(Medical emergency due to high risk of vision loss)
• Unilateral in presentation , the other eye is at risk.
Symptoms
1. Ocular pain.
2. Red eye.
3. Blurry vision.
4. Halos around lights.
• Nausea/vomiting.
• Headache / Diaphoresis.
Signs
1. Cloudy cornea
2. Conjunctival hyperemia.
3. Pupil semidilated and fixed to light
4. Eye will be harder on palpation.a

13. DIAGNOSIS
Eye pressure test (intraocular
pressure).
Anterior chamber angle exam.
Optic angle exam.
Visual field test.

14. TREATMENT :
1. NON PHARMACOLOGICAL
TREATMENT.
2. PHARMACOLOGICAL
TREATMENT.

15. Non
pharmacol
-ogical
treatment
1. Eat
healthy
diet
2. Maintain
good
health
3. Avoid
stress
4. Go for
aromatothe
rapy,
acupunctur
e.
5. Avoid
caffeine,
alcohol,
watching tv
etc.,.
6. Avoid
allergic
foods.
NON PHARMACOLOGICAL
TREATMENTS

16. PHARMACOLOGICAL TREATMENT
 Ophthalmic Drugs for Glaucoma Lowering IOP by
1-REDUCING PRODUCTION OF AQUEOUS
HUMOR:
β-Blockers. α2Adrenergic Agonists
Carbonic Anhydrase Inhibitors.
2-DECREASING THE RESISTANCE TO OUTFLOW
OF AQUEOUS HUMOR THROUGH TRABECULAR
MESHWORK:
cholinergics and cholinesterase inhibitors.
3-IMPROVING THE OUTFLOW OF AQUEOUS
HUMOR:
prostaglandins (uveoscleral outflow)
sympathomimetics (trabecular meshwork and
the uveoscleral outflow).

17. A.TOPICAL Β-ADRENERGIC BLOCKING
DRUGS
Includes:
1. Non-selective: Timolol, Levobunolol, Metipranolol &
Carteolol.
2. β1-Selective: Betaxolol.
-Dosing: 1 drop BID
-Side effects:
1- Bronchospasm.
2- Bradycardia.
3- Hypotension.
4- CHF exacerbation.
5- Mask hypoglycemia.
6- Tachyphylaxis (20% to 50% of pts)
. -Nasolacrimal occlusion is a technique to decrease amount of
drug absorbed systemically and decrease the incidence of side
effects and improve medication effectiveness.
Contraindications
1- Asthma
2- COPD
3- Sinus bradycardia
4- 2nd or 3rd degree heart failure 16
Betanolol can be used

18. B. A2-ADRENERGIC AGONISTS
-Includes: Brimonidine(more selective) & Apraclonidine.
-Brimonidine: (Effective long-term monotherapy / adjunctive
therapy)
- Apraclonidine (Short-term use only due to high rate of
tachyphylaxis)
Used for prevention & ttt of postsurgical IOP elevations.
-Dosing: 1 drop BID to TID.
-Side effects:
1-Blepharoconjunctivitis.
2-Foreign body sensation.
3-Papillary mydrasis (Apraclonidine).
4-Eyelid retraction(Apraclonidine).
5-Mild systemic hypotension and lethargy.
( Brimonidine pass BBB ).
Contraindications
1. hypersensitivity.
2. Patients receiving
MOA inhibior therapy.

19. C. CARBONIC ANHYDRASE INHIBITORS
1- Topical agents :
-Includes: Dorzolamide and Brinzolamide.
-Dosing: 1 drop BID with beta blockers or TID alone.
-Combination of Timolol+Dorzolamide is commonly
used
-Side effects:
1-Burning.
2-Stinging.
3-Itching.
4-Dry eyes.
5-Conjunctivitis
Contraindications
patients with history of
hypersensitivity to
sulphonamides.

20. 2- Orally-administered CAIs:
-Includes: Acetazolamide , Dichlorphenamide,
and Methazolamide.
-Dosing: 250-1000mg daily , given in divided
doses for amount over 250mg.
-Side effects:
1-Paresthesia of hands and feet.
2-Hypokalemia and hyponatremia.
3-Nephrolethiasis and renal failure.
4-Hepatic insufficiency.
5-Blooddyscrasias from bone marrow
suppression
Contraindications:
1-Hypokalemia.
2-Hyponatremia

21. D. CHOLINERGICS AND CHOLINESTERASE
INHIBITORS
1- CHOLINERGICS:
-Includes: Pilocarpine and Carbachol.
-Dosing:1–2 drops TID or QID.
-Used with caution for closed angle
-Side effects:(due to miosis)
1-Brow ache and headache.
2-Affect night vision.
3-Bradycardia at high conc.
4-Retinal detachment.
5-Lacrimation, myopia, blurred vision.
Contraindications:
1. Severe myopia to avoid
detachment.
2. pregnancy

22. 2- CHOLINESTERASE INHIBITORS:
Includes: Echothiophate iodide &Demecarium
bromide.
-Irreversible AchE inhibitors e’ long durations of
action.
-Stop at least 1 week before general surgical
procedure.
Dosing: 1 drop BID.
Side effects:
1- Depletion of systemic cholinesterase and
pseudocholinesterase.
2- Cataracts: occur in 30–50% of elderly patients
using these drugs for at least 6 months.

23. E. PROSTAGLANDINS
Includes: Latanoprost, Bimatoprost, Travoprost.
-First-line alternatives to topical β-blockers.
-Patients required to lower IOP by greater than 25%.
-Lower IOP by 25% to 35% (Lower nocturnal IOP).
Dosing: 1 drop once a day at bedtime
Side effects:
1- Conjunctival hyperemia.
2- Stinging on instillation.3- Inc. in iris pigmentation.
4- Hypertrichosis.
5- Eyelashes darkening.

24. F. SYMPATHOMIMETICS
Includes: DIPIVEFRIN HCL , EPINEPHRINE.
-IOP is reduced by 20–25%.
-Last line agents due to their systemic S.E. Profile
Dosing:1 drop BID.
Intolerance to ocular adverse effects leads to
discontinuation of epinephrine in 80% of patients.
Side effects:
1-Burning, tearing.
2-Reactive conjunctival hyperemia.
3-Allergic blepharoconjunctivitis.
4-Mydriasis → Blurring of vision.

25. THANK YOU