Glaucoma It is a heterogenous group of diseases in whichdamage optic nerve (optic neuropathy). is usually caused by raised ocular pressure (normalIOP 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.
EPIDEMIOLOGY : In the world, glaucoma is the thirdleading cause of blindness. an estimated 13.5 million people mayhave glaucoma and 5.2 million of thosemay be blind.
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.
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
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
Symptoms :1-eye redness and painful.2-Blurred vision.3-Patient may notice haloes (circles of light) aroundlight.
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
Risk factors for glaucoma*Age *Diabetes*Family history *Thin cornea*Previous eye injury *Vasospasm*Systemic HTN *myopia
Risk factors for glaucoma*Age * Family history*Previous eye injury *myopia **Diabetes *Thin cornea*Systemic HTN *Vasospasm
The goal of glaucoma treatment preserve the visual field . prevent the loss of visual function . achieved by : Medication Laser therapy Conventional surgery
Strategies of treatment 1-Decreasing Production of Aqueous Humor. 2-Increasing Outflow of Aqueous Humor.
pharmacologicaal treatment: we have 5 classes of drugs : 1- Beta blockers2-alpha agonist (alpha-2 agonist and non specific agonist) 3-carbonic anhydrase inhibitors 4- Parasympathomimetics. 5- prostaglandin analogs
Also it can be classified as:1-drugs that decrease aqueous humor production: Beta blockers. alpha2 –agonists. carbonic anhydrase inhibitors2- drugs that increase aqueous humor outflow: prostaglandin analoges non specific adrenergic agonists cholenergics (Parasympathomimetics)
Site of action of anti glaucoma drugs :1-miotic 2-=miotic 3-Beta blocker 4-prostaglandine adrenaline 5-adrenaline
Drug used for open anglebeta blockersalpha agonistsdrug used for close angle
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 metoprololnon-selective B-blockers timolol , nadolol, befunolol, carteolol, penbutolol, labetalol, nipradilol.
Side effects:low BP. cardiac arrhythmiascardiac insufficency reduced pulse rate ContraindicationsCardiogenic shockOver cardiac failure Sinus bradycardia history of COPD Second and third degree AV block
2-alpha agonistsA_ Alpha-2 Adrenergic Agonists :(apraclonidine, brimonidine) MOA IOP by reducing production of aqueous humour.Side effects:HTNtachycardiaallergic conjunctivitislocal irritationhead ache dose: Apraclonidine : 1-2 drops tid. brimonidine: : 1 drop every 8 hr.
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
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
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
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.
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.
Pilocarpine :→is the principal alkaloid .the miotic action of the drug relieves the pupillary blockand 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 30-60minutes and lasts for 4-8 hoursSide Effects of this class* Headache * induced miopia.* Many people complain of dim vision, especially at night or indarkened areas such as movie theaters. This is due to constrictionof the pupil. Dose: 1-2 drops up to 6 time/ day to control intraocular pressure
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)
Unoprostone :› it is the first docosanoid derivative for glaucoma therapy.› It acts by enhancing uveoscleral outflow withoutaffecting aqueous humour production › It is available as 0.12% ophthalmic solutionDose: requires twice a day instillationside effects of this class : •iritits • ncrease iris pigmentation •conjunctival pigmentation •cytosoid macular edema
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 andalpha agonistsSide effects of Cosopt® include burning and/or stinging of the eyes and changes insense of taste.
Category MOA Drugs Side effectΒ-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 rateAdrenergic Both Epinephrine HCl Contact allergy, hypotension instimulating Dipivitrin children BrimonidineCarbonic Decrease Oral acetazolamide Renal calculi, nausea, vomiting,anhydrase aqueous Topical dorzolamide diarrhea, weight loss, aplasticinhibitor formation anemia, BM suppression S/E generally absent with topical preparationProstaglandin Improve Latanoprost Iris color change, lash growth,agonists uveoscleral trichiasis outflow