Glaucoma is a group of eye diseases characterized by optic nerve damage, often due to elevated intraocular pressure, and is a leading cause of blindness globally. It is classified into primary forms such as open-angle and closed-angle glaucoma, as well as secondary types stemming from various causes like trauma or other ocular diseases. Treatment options focus on preserving visual function through medications, laser therapy, and surgery, with various classes of drugs available to either decrease aqueous humor production or increase its outflow.

2. Glaucoma
 It is a heterogenous group of diseases in which
damage optic nerve (optic neuropathy).
 is usually caused by raised ocular pressure (normal
IOP is 15.5 mmHg) acting on the nerve head.
 characterized by:
 optic nerve damage cupping of the optic disc
and subsequent loss of retinal nerve fibre.

3. EPIDEMIOLOGY :
 In the world, glaucoma is the third
leading cause of blindness.
 an estimated 13.5 million people may
have glaucoma and 5.2 million of those
may be blind.

4. Classification of glaucoma
Primary glaucoma:
Open angle glaucoma
Closed (narrow) angle glaucoma
Secondary glaucoma :
•Traumatic glaucoma
•Pigmentory depression glaucoma
• glaucoma associated with other ocular diseases (uveitis)
•Raised episcleral venous pressure
•Steroid induced glaucoma
•Neovascular glaucoma
•Psedoexfoliation glaucoma
•Congenital glaucoma

5. open angle glaucoma
it also called chronic simple or wide angle glaucoma
It is the most common type of glaucoma.
• It affects approximately 1 in 200 of
population over the age of 40 years.

6. cause and mechanism of open angle:
it occurs as a complication of chronic obstruction in
the trabeculare meshwork.
-It causes slow damage to the optic nerve.
Symptoms:
- most time is symptomless
characterized by:
-Cupped optic disc
-Gradual loss of peripheral vision
-Tunnel vision in the advanced stage

7. Close angle glaucoma
-also called acute or narrow angle glaucoma.
-occurs in small eyes (as in hyperopoia) with
shallow anterior chambers.
Cause and mechanism :
iris dilation the lens sticks to the back of the iris
prevent fluid flow from posterior to anterior
chambers
Fluid accumulati0n preventing drainage
rapid IOP

8. Symptoms :
1-eye redness and painful.
2-Blurred vision.
3-Patient may notice haloes (circles of light) around
light.

9. Secondary glaucoma :
 Pigmentory depression glaucoma:
 Pseudoexfoliative glaucoma:
 neovascular glaucoma:
 Steroid induced glaucoma:
 trauma
 uveitis

10. Congenital glaucoma
 It present at birth.
 due to the abnormal development of the anterior
chamber angle before birth.
 this causes decrease in aqueous outflow IOP
loss of vision..
Symptoms
 Tearing  Bupthalmus
 Light sensitivity  Cloudy cornea

11. Risk factors for glaucoma
*Age *Diabetes
*Family history *Thin cornea
*Previous eye injury *Vasospasm
*Systemic HTN *myopia

12. Risk factors for glaucoma
*Age * Family history
*Previous eye injury *myopia *
*Diabetes *Thin cornea
*Systemic HTN *Vasospasm

13. The goal of glaucoma treatment
 preserve the visual field .
 prevent the loss of visual function .
achieved by :
Medication
Laser therapy
Conventional surgery

14. Strategies of treatment
1-Decreasing Production of Aqueous
Humor.
2-Increasing Outflow of Aqueous
Humor.

15. pharmacologicaal treatment:
we have 5 classes of drugs :
1- Beta blockers
2-alpha agonist (alpha-2 agonist and non specific agonist)
3-carbonic anhydrase inhibitors
4- Parasympathomimetics.
5- prostaglandin analogs

16. Also it can be classified as:
1-drugs that decrease aqueous humor production:
Beta blockers.
alpha2 –agonists.
carbonic anhydrase inhibitors
2- drugs that increase aqueous humor outflow:
prostaglandin analoges
non specific adrenergic agonists
cholenergics (Parasympathomimetics)

17. Site of action of anti glaucoma drugs :
1-miotic 2-=miotic 3-Beta blocker 4-prostaglandine adrenaline 5-adrenaline

18. Drug used for open angle
beta blockers
alpha agonists
drug used for close angle

19. 1- Beta blockers:
first choice for initial and maintenance treatment of open-angle.
for ocular HTN.
They block Beta receptor in iris and ciliary body
aqueous humor production IOP.
Classify in to:
 elective B1-blockers . Betaxolol, atenolol and metoprolol
non-selective B-blockers timolol , nadolol, befunolol, carteolol,
penbutolol, labetalol, nipradilol.

20. Side effects:
low BP. cardiac arrhythmias
cardiac insufficency reduced pulse rate
Contraindications
Cardiogenic shock
Over cardiac failure
Sinus bradycardia
history of COPD
Second and third degree AV block

21. 2-alpha agonists
A_ Alpha-2 Adrenergic Agonists :(apraclonidine, brimonidine)
MOA
IOP by reducing production of aqueous humour.
Side effects:
HTN
tachycardia
allergic conjunctivitis
local irritation
head ache
dose:
Apraclonidine : 1-2 drops tid.
brimonidine: : 1 drop every 8 hr.

22. contraindications of Alpha-2 Adrenergic
•Breast-feeding
• Closed-angle glaucoma
• Heart disease
• Liver disease
•Eye infection or damage
•Kidney disease
•Pregnant or trying to get pregnant

23. B_non specific adrenergic agonists
(epinephrine, dipivefrin)
Epinephrine
MOA:
aqueous humor formation
trabecular outflow. (stimulate alpha-2)
Onset : 1 hr
dose: twice daily.
side effects : -HTN
- - allergic lid reactions
- browache, -conjunctival hyperemia

24. Dipivefrine
• is the prodrug of epinephrine.
• better tolerated than epinephrine.
side effects: follicular conjunctivitis.
Contraindications of epinephrine and dipivrfrine
• not be used in patients with narrow angles since any
dilation of the pupil may predispose the patient to an attack
of angle-closure glaucoma

25. 3-carbonic anhydrase inhibitors:
(acetazolamide, methazolamide, dichlorphenamide,
brinzolamide , dorzolamide )
MOA
reduce HCO3 &H2O content of aqeous humor
by secretion of them from the eye.
Administration:
o Orally (Rx. open angle glaucoma )
o IV or IM ( preoperatively for closed angle glaucoma
(acetazolamide))
o Topically

26. Side Effects
-aplastic anemia
-allergic reaction
-electrolyte disorder
-renal or hepatic insuffecency
Contraindications/Precautions:
◊ hepatic disease (may precipitate hepatic coma)
◊ renal or adrenocortical insufficiency
◊ hyponatremia
◊ hypokalemia
◊ hyperchloremic acidosis or electrolyte imbalance.

27. 4-Parasympathomimetics
[pilocarpine, carbachol, echothiophate]
→In the past, miotics were DOC
but currently due to their high side-effects, their use has
declined.
Mechanism:
pupil size drainage of intraocular fluid -increasing
the flow of intraocular fluid from the eye…
or
by contraction of ciliary body muscle Increases
drainage of intraocular fluid.
Administration:
Topical drops and gel.

28. Pilocarpine :
→is the principal alkaloid .
the miotic action of the drug relieves the pupillary block
and also pulls the iris away from the anterior chamber angle
→ It increases the trabecular outflow due to cilliary body contraction.
Its onset of action is rapid, peak effect occurs between 30-60
minutes and lasts for 4-8 hours
Side Effects of this class
* Headache * induced miopia.
* Many people complain of dim vision, especially at night or in
darkened areas such as movie theaters. This is due to constriction
of the pupil.
Dose: 1-2 drops up to 6 time/ day to control intraocular pressure

29. 5- prostaglandin analogs:
(latanoprost, bimatoprost, unoprostone, travoprost)
MOA :
increase the uveoscleral outflow.
Side Effects:
-Iris pigmentation
- local irritation
-increased growth of eyelashes
Latanoprost:
→Its maximum effet is achieved at 12 hrs
→the best time for using it is at 9 pm,because the maximum
IOP lowering effect is after 12 hrs. i.e. at 9 am(and thats also
the time when IOP is at its peak)

30. Unoprostone :
› it is the first docosanoid derivative for glaucoma therapy.
› It acts by enhancing uveoscleral outflow without
affecting aqueous humour production
› It is available as 0.12% ophthalmic solution
Dose: requires twice a day instillation
side effects of this class :
•iritits
• ncrease iris pigmentation
•conjunctival pigmentation
•cytosoid macular edema

31. Combination:
Combigan®
is a combination of beta blocker and alpha agonist
(Brimonidine &Timolol )
Cosopt®
is a combination of beta blocker and carbonic anhydrase
inhibitor(dorzolomide & timolol ).
Mechanism; Decreases production of intraocular fluid
Side Effects:
Side effects of Combigan® include the symptoms of beta blockers and
alpha agonists
Side effects of Cosopt® include burning and/or stinging of the eyes and changes in
sense of taste.

32. Category MOA Drugs Side effect
Β-adrenergic Decrease Timolol systemic effect (bronchospasm,
blockers aqueous Levobunolol bradycardia, heart block,
formation Metrapranolol hypotension..)
Cholinergic Increase Pilocarpine Miosis, decrease night vision,
stimulation aqueous Carbachol headache, increase GI motility,
outflow decreased heart rate
Adrenergic Both Epinephrine HCl Contact allergy, hypotension in
stimulating Dipivitrin children
Brimonidine
Carbonic Decrease Oral acetazolamide Renal calculi, nausea, vomiting,
anhydrase aqueous Topical dorzolamide diarrhea, weight loss, aplastic
inhibitor formation anemia, BM suppression
S/E generally absent with topical
preparation
Prostaglandin Improve Latanoprost Iris color change, lash growth,
agonists uveoscleral trichiasis
outflow

33. The end slide
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