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Glaucoma


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Definition

acquired chronic optic neuropathy characterized byoptic 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


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Starts from

Sodioum ions are actively transported between theepithelial cells, pulling chloride and bicarbonate ionsto sustain electrical neutrality.

Hence, causing water osmosis from the bloodcapillaries into the same epithelial spaces.

The resulting solution flows into the anterior chamberof the eye.

Other substances: amino acids, ascorbic acid, and glucoseare also actively transported, or through facilitateddiffusion.


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Aqueous Humor Dynamics

extraocular veins

TM minute openings: 2-3 micrometers

as the pressure rises,the flows of fluid into the canal is

increased.

At approximately 15 mmHg, outflow fluid

through the canal of Schlemm is about 2.5

microliters

per minute, = inflow of aqueous humorfrom the ciliary body.

The average: 15 mmHg, a range from 12

to 20 mmHg


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Defense mechanism

phagocytic cells on the surface of TM

outside the canal of Schlemm is a layer ofinterstitial 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 smallparticles.


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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, extremely high loss of vision in days oreven hours

High pressure compressed optic nerve at the optic disc. blockage of the axonal flow to the optic fibers leading tothe brain inadequate nutrition and consequently deathof fibers.

Another cause the retinal artery might be compressed precipitate the neuronal damage.


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Triad

Tonometry

Gonioscopy Optic Disc Examination

How to Diagnose


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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


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pen-light


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Schwalbes line or a small portion of the trabecular meshwork is seen means that the angle is

narrow;

full trabecular meshwork, scleral spur, and the iris processes are seen means the angle is open;

unable to seeSchwalbes

line means that the angle is closed

Gonoscopy


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Optic Disk Examination

normal range: 0.2 to 0.5


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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


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Classification

primary angle-closure glaucoma

Acute PACG: two different mechanisms. papillary block mechanism, where the apposition of the iris to the lens blocks

aqueous flows to the anterior chamber. Therefore, causing a buildup pressurebehind the iris, anterior bowing of the peripheral iris, and angle closure.

The second mechanism is plateu iris mechanism where the peripheral iris

bunches up and block the TM directily. Sign and symptoms are severe pain, redness, and blurring of vision.

Subacute PACG incomplete closure of the angle episodes ofincreased IOP that spontaneously resolves blurred vision, halos, andred eye.

Chronic PACG synechial closure, an asymptomatic or repeated episodes of acute or subacute

angle closure

a POAG-like mechanism, where there is a trabecular dysfunction in narrow,but clinically open angles.


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POAGPOAG Treatment

Algorithm


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Pharmaco Treatment

Suppression of Aqueous Production

Facilitation of Aqueous Outflow

Reduction of Vitreous Volume Miotics, Mydriatics, and Cycloplegics


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Pharmaco Treatment


Beta-blockers topically

It blocks beta2 receptors on the ciliary body

decreasing the production of aqueous humor

timolol maleate, betaxolol hydrochloride,

carteolol hydrochloride, levobunolol

hydrochloride, metipranolol.


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Pharmaco Treatment



systemic >> local

decreased heart rate, reduced blood pressure,conduction defects, CNS effects, alteration ofserum lipids, and may block the symptoms of

hypoglycemia. These effects are not elicited by B1 specific

agents.


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Pharmaco Treatment



caution in patients with pulmonary diseases, sinusbradycardia, second or third degree heart block,

congestive heart failure, atherosclerosis, diabetes, andmyasthenia gravis, and also in patients receiving oralbeta-blockers.

To avoid systemic effects, use ofnasolacrimalocclusion technique during administration may bedone. It can also optimize the response.

Beta-blockers are usually well tolerated in mostpatients.


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Pharmaco Treatment


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.


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Pharmaco Treatment


Carbonic anhidydrase inhibitors

systemically

it helps to converse carbon dioxide and water tocarbonic acid (bicarbonate).

The production of aqueous humor depends on theactive transport of bicarbonate and Na+ ions.

reducing the activity of carbonic anhydrase

decrease of aqueous humor production. acetazolamide, or dichlorpheamide, or dorzolamide.


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Pharmaco Treatment


Prostaglandin analogs, such as bimatoprost 0.003%,latanoprost 0.005%, and travoprost 0.004% solutions (eachonce daily at night), and unoprostone 0.15% solution (twicedaily)

increasing the uveoscleral and to a lesser extent, trabecularoutflow of aqueous humor decrease IOP

It is well tolerated and produce fewer systemic adverseeffects than timolol.

Prostaglandin can be used in combination with otheragents for additional IOP control. It can be used as first-linetherapy for primary open-angle glaucoma (POAG).


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Pharmaco Treatment


Parasympathomimetic agents

contracting cilliary muscle opening the trabecularmeshwork reducing resistance to outflow

increasing aqueous humor trabecular outflowreduce IOP

However it may reduce uveoscleral outflow.

Their use as a primary or adjunctive agent in glaucoma

treatment has decreased, due to its ocular side effectsand/or frequent dosing requirements.


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Pharmaco Treatment


Epinephrine

mechanism is not fully know,

beta-2 receptor-mediated increase in outflow facility through thetrabecular meshwork and the uveoscleral route appears to be its

mechanism, althought its activity to reduce IOP is less compared tobeta-blockers or miotics.

Epinephrine 0,25 to 2 % instilled once or twice daily is infrequentlyused today, due to advances in better tolerated and more

efficacious agent.

Prodrug of epinephrine is dipivefrin, these drugs cannot be used ineyes with narrow anterior chamber angles.


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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 vitreousand causing it to shrink. Moreover, it also

decrease aqueous production. This agent is

important in the treatment of acute angle closureglaucoma and in secondary angle-closure

glaucoma.


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Pharmaco Treatment

Miotics, Mydriatics, and Cycloplegics

The use ofMiotics is usefull to activate muscarinicreceptors on the iris and ciliary body, causing pupilconstriction and ciliary muscle contraction, thus improvingthe uveoscleral outflow.

Carbachol and pilocarpine may assist the drainage ofaqueous humor.

side effect: permanent accommodative spasm blurredvision and headache.

These occur in all patients, but wears off in older patients.To minimize these effects, the use ofslow-releaseformulation of miotics may be optional.


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References

1. Vaughan. Vaughan & Asburys: General ophthalmology. 17th ed. Lange; 2007.

2. Schlote T, Rohrbach J, Grueb M, Mielke J. Pocket atlas of ophthalmology. Thieme;2006.

3. Guyton AC, Hall JE. Textbook of medical physiology. 11th ed. Elsevier; 2006.

4. Kumar V, Abbas AK, Fausto N, Aster JC. Robbins & cotran: pathologic basis ofdisease. 8th ed.Saunders; 2010.

5. Tsai JC, Denniston AKO, Murray PI, et al. Oxford American handbook ofophthalmology. NY: Oxford University Press, Inc; 2011.

6. McKay D, ODjay J, Swann P. Glaucoma vascular and nerve fibre layer signs:glaucomatous optic neuropathy signs. Available from:URL:http://www.opticianonline.net/assets/getAsset.aspx?ItemID=2265

7. Page CP, Curtis MJ, Sutter MC, et al. Integrated pharmacology. London: Mosby.

8. Dipiro JT, Talbert RL, Yee GC. Pharmacotherapy: a pathophysiologic approach.7

th

ed. USA: The McGraw-Hill Companies, Inc.

9. Garg A, Melamed S, Mortense JN, et al. Mastering the techniques of glaucomadiagnosis & management. India: Jaypee Brothers Medical Publishers Ltd; 2006.
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