This action might not be possible to undo. Are you sure you want to continue?
• acquired chronic optic neuropathy characterized by optic disk cupping and visual field loss. • characterized by:
– Raised IOP, >21 mmHg – Abnormal optic disc
• • • • • • Cup-disc ratio asymmetry Large cup-disc ratio for disc size Disc hemorrhage Vessel bayoneting/ nasally displaced Peripapillary atropy (B-zone) Thinning of the (inferior – superior – nasal - temporal rule) neuroretinal rim
– Visual field defect
Aqueous Humor Dynamics
Aqueous humor is actively secreted, 2-3 microliters per minute, by the cilliary processes, which are highly folded, making a considerable large area of 6 square cms in each eye.
Starts from… • Sodioum ions are actively transported between the epithelial cells. and glucose are also actively transported. pulling chloride and bicarbonate ions to sustain electrical neutrality. . – Other substances: amino acids. ascorbic acid. • Hence. or through facilitated diffusion. • The resulting solution flows into the anterior chamber of the eye. causing water osmosis from the blood capillaries into the same epithelial spaces.
The average: 15 mmHg. outflow fluid through the canal of Schlemm is about 2. a range from 12 to 20 mmHg .Aqueous Humor Dynamics extraocular veins TM minute openings: 2-3 micrometers as the pressure rises.5 microliters per minute. the flows of fluid into the canal is increased. At approximately 15 mmHg. = inflow of aqueous humor from the ciliary body.
.Defense mechanism • phagocytic cells on the surface of TM • outside the canal of Schlemm is a layer of interstitial gel that contains reticuloendothelial cells • surfaces of the iris and other surfaces behind the iris are covered by an epithelium • capable to phagocytoze proteins and small particles.
Aqueous Humor and Its relation to Glaucoma • 20 to 30 mmHg can cause loss of vision if it is not treated • 60 to 70 mmHg. . blockage of the axonal flow to the optic fibers leading to the brain inadequate nutrition and consequently death of fibers. extremely high loss of vision in days or even hours • High pressure compressed optic nerve at the optic disc. • Another cause the retinal artery might be compressed precipitate the neuronal damage.
How to Diagnose • • • • Triad Tonometry Gonioscopy Optic Disc Examination .
Gonoscopy • open-angle. or angle-closure glaucoma? Narrow? • oblique illumination with pen-light • or by slitlamp observation of the depth of the peripheral anterior chamber • BEST: GONOSCOPY .
scleral spur. unable to see Schwalbe’s line means that the angle is closed .Gonoscopy Schwalbe’s line or a small portion of the trabecular meshwork is seen means that the angle is narrow. and the iris processes are seen means the angle is open. full trabecular meshwork.
Optic Disk Examination normal range: 0.5 .2 to 0.
Classification • open-angle glaucoma • increased resistance to aqueous outflow in open angle high IOP • MYOC gene! • Characteristics of primary open-angle glaucoma: – – – – IOP greater than 21 mmHg An open chamber angle Characteristic disk cupping with visual field defects Absence of a known secondary cause of glaucoma .
redness. and red eye. but clinically open angles. Therefore. • Chronic PACG – synechial closure.Classification • primary angle-closure glaucoma • Acute PACG: two different mechanisms. halos. an asymptomatic or repeated episodes of acute or subacute angle closure – a POAG-like mechanism. . where the apposition of the iris to the lens blocks aqueous flows to the anterior chamber. where there is a trabecular dysfunction in narrow. causing a buildup pressure behind the iris. anterior bowing of the peripheral iris. • Sign and symptoms are severe pain. • Subacute PACG incomplete closure of the angle episodes of increased IOP that spontaneously resolves blurred vision. and angle closure. – The second mechanism is plateu iris mechanism where the peripheral iris bunches up and block the TM directily. – papillary block mechanism. and blurring of vision.
POAG Treatment Algorithm POAG .
and Cycloplegics . Mydriatics.Pharmaco Treatment • • • • Suppression of Aqueous Production Facilitation of Aqueous Outflow Reduction of Vitreous Volume Miotics.
levobunolol hydrochloride. metipranolol. carteolol hydrochloride. . betaxolol hydrochloride.Pharmaco Treatment • Suppression of Aqueous Production • Beta-blockers topically • It blocks beta2 receptors on the ciliary body decreasing the production of aqueous humor • timolol maleate.
• These effects are not elicited by B1 specific agents. CNS effects. conduction defects. alteration of serum lipids. .Pharmaco Treatment • • • • Suppression of Aqueous Production Beta-blockers topically systemic >> local decreased heart rate. reduced blood pressure. and may block the symptoms of hypoglycemia.
atherosclerosis. • To avoid systemic effects. use of nasolacrimal occlusion technique during administration may be done. second or third degree heart block. • Beta-blockers are usually well tolerated in most patients.Pharmaco Treatment • Suppression of Aqueous Production • Beta-blockers topically • caution in patients with pulmonary diseases. and also in patients receiving oral beta-blockers. congestive heart failure. and myasthenia gravis. It can also optimize the response. diabetes. . sinus bradycardia.
.Pharmaco Treatment • Suppression of Aqueous Production • Alpha adrenoreceptor agonis can also reduce the aqueous humor formation. The mechanism is the agonism of alpha-2 receptors on the ciliary body. and/or alpha-1 (vasoconstrictors) receptor in cilliary vessels.
• acetazolamide. • The production of aqueous humor depends on the active transport of bicarbonate and Na+ ions. • reducing the activity of carbonic anhydrase decrease of aqueous humor production. or dichlorpheamide. .Pharmaco Treatment • • • • Suppression of Aqueous Production Carbonic anhidydrase inhibitors systemically it helps to converse carbon dioxide and water to carbonic acid (bicarbonate). or dorzolamide.
005%. and unoprostone 0.004% solutions (each once daily at night). • Prostaglandin can be used in combination with other agents for additional IOP control.003%. trabecular outflow of aqueous humor decrease IOP • It is well tolerated and produce fewer systemic adverse effects than timolol. . latanoprost 0. It can be used as first-line therapy for primary open-angle glaucoma (POAG). such as bimatoprost 0. and travoprost 0.Pharmaco Treatment • Facilitation of Aqueous Outflow • Prostaglandin analogs.15% solution (twice daily) • increasing the uveoscleral and to a lesser extent.
due to its ocular side effects and/or frequent dosing requirements.Pharmaco Treatment • Facilitation of Aqueous Outflow • Parasympathomimetic agents • contracting cilliary muscle opening the trabecular meshwork reducing resistance to outflow increasing aqueous humor trabecular outflow reduce IOP • However it may reduce uveoscleral outflow. • Their use as a primary or adjunctive agent in glaucoma treatment has decreased. .
althought its activity to reduce IOP is less compared to beta-blockers or miotics. due to advances in better tolerated and more efficacious agent.25 to 2 % instilled once or twice daily is infrequently used today. . • Epinephrine 0. these drugs cannot be used in eyes with narrow anterior chamber angles. • Prodrug of epinephrine is dipivefrin.Pharmaco Treatment • • • • Facilitation of Aqueous Outflow Epinephrine mechanism is not fully know. beta-2 receptor-mediated increase in outflow facility through the trabecular meshwork and the uveoscleral route appears to be its mechanism.
it also decrease aqueous production.Pharmaco Treatment • Reduction of Vitreous Volume • Hyperosmotic agents can cause the reduction of vitreous volume by making the blood hypertonic. therefore drawing the water out of the vitreous and causing it to shrink. . Moreover. This agent is important in the treatment of acute angle closure glaucoma and in secondary angle-closure glaucoma.
causing pupil constriction and ciliary muscle contraction. . • Carbachol and pilocarpine may assist the drainage of aqueous humor. Mydriatics. • side effect: permanent accommodative spasm blurred vision and headache. • These occur in all patients. the use of slow-release formulation of miotics may be optional. but wears off in older patients.Pharmaco Treatment • Miotics. and Cycloplegics • The use of Miotics is usefull to activate muscarinic receptors on the iris and ciliary body. thus improving the uveoscleral outflow. To minimize these effects.
and Iridoplasty • Laser Trabeculoplasty • Glaucoma Drainage Surgery • Cyclodestructive Procedures . Iridectomy.Surgical and Laser Treatment • Peripheral Iridotomy.
. Oxford American handbook of ophthalmology. Curtis MJ. Rohrbach J. Swann P. Pocket atlas of ophthalmology.References 1. Guyton AC. McKay D. 11th ed. 2006. USA: The McGraw-Hill Companies. 5. 2007.7th ed. 2006. Tsai JC. London: Mosby. Inc. Available from: URL:http://www. Hall JE. Mastering the techniques of glaucoma diagnosis & management. Talbert RL. Aster JC.Saunders. Grueb M. Robbins & cotran: pathologic basis of disease. India: Jaypee Brothers Medical Publishers Ltd. Page CP. Yee GC. Mielke J.net/assets/getAsset. 2010. Dipiro JT. Vaughan & Asbury’s: General ophthalmology. Lange.opticianonline. Denniston AKO. Inc. Murray PI. Textbook of medical physiology. Vaughan.aspx?ItemID=2265 7. 4. Thieme. Integrated pharmacology. Schlote T. Abbas AK. 8. Kumar V. O’Djay J. 2. 9. 3. Mortense JN. 8th ed. Elsevier. 17th ed. 2006. Garg A. Sutter MC. Glaucoma – vascular and nerve fibre layer signs: glaucomatous optic neuropathy signs. 6. et al. Melamed S. 2011. Pharmacotherapy: a pathophysiologic approach. et al. Fausto N. NY: Oxford University Press. et al.
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.