By Erni D. F. Simbolon

8/14/2019 By Erni D. F. Simbolon

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Definition

Glaucoma is a disease caused byincreased intraocular pressure (IOP)resulting either from a malformation

or malfunction of the eyes drainagestructures.

Left untreated, an elevated IOP causesirreversible damage the optic nerveand retinal fibers resulting in aprogressive, permanent loss of vision.

However, early detection and treatment

can slow, or even halt the progressionof the disease.


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Glaucoma is often called "the sneakthief of sight." This is because, asalready mentioned, in most cases, theintraocular pressure can build up anddestroy sight without causing obvioussymptoms.

Thus, awareness and early detection ofglaucoma are extremely important

because this disease can besuccessfully treated when diagnosedearly.

While everyone is at risk for glaucoma,certain people are at a much higher

risk and need to be checked more


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Pathophysiology

The major risk factor for most glaucomas andfocus of treatment is increased intraocularpressure.

Intraocular pressure is a function of production of

liquid aqueous humor by the ciliary processesof the eye and its drainage through thetrabecular meshwork.

Aqueous humor flows from the ciliary processesinto the posterior chamber, boundedposteriorly by the lens and the zonules of Zinnand anteriorly by the iris.

It then flows through the pupil of the iris into theanterior chamber, bounded posteriorly by theiris and anteriorly by the cornea.

From here the trabecular meshwork drains

aqueous humor via Schlemm's canal intoscleral plexuses and general blood circulation.


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The pathophysiology ofglaucoma lies on theoverproduction of theaqueous humor, the clearfluid that fills the anterior

chamber (the spacebetween the cornea andiris) or a drainage problem.

Any imbalance between theproduction and drainage ofthe aqueous will lead to anincrease in intraocular

pressure.Normal IOPs of most people

falls between 8 and 21mmHg.

Some eyes can tolerate higherpressures than others.


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In most people, the filtering angles arewide open, although in someindividuals, they can be narrow. For

example, the usual filtering angle isabout 45 degrees, whereas a narrowangle is about 25 degrees or less.

After exiting through the trabecular

meshwork in the filtering angle, theaqueous fluid then drains into tinyblood vessels (capillaries) into themain bloodstream. The aqueoushumor should not be confused withtears, which are produced by a gland


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Also, if the sink's faucet is on toohigh, the water may overflow.Again, if this sink were a closed

system, the pressure within the sinkwould increase. Likewise, if too much fluid is being

produced within the eye, the

intraocular pressure may becometoo high. In either event, since theeye is a closed system, if it cannotremove the increased fluid, the

pressure builds up and nerve


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In open angle glaucoma there isreduced flow through the trabecularmeshwor

In angle closure glaucoma, the iris ispushed forward against thetrabecular meshwork, blocking fluid

from escaping.


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A. The drainage angleformed between thecornea and the iris iswide open to about 40.Aqueous fluid flows freely

to the trabecularmeshwork and out of theeye.

B. The drainage angle isclosed. The iris and thecornea are in contact (*)and block the flow ofaqueous fluid to thetrabecular meshwork.

The fluid is trapped in theeye causing intraocularpressure to rise.


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Causes

Ocular hypertension (increased pressurewithin the eye) is the largest riskfactor in most glaucomas, but in somepopulations only 50% of patients withprimary open angle glaucoma actuallyhave elevated ocular pressure.

Those of African descent are three timesmore likely to develop primary open

angle glaucoma. People who are older,have thinner corneal thickness, andmyopia also are at higher risk forprimary open angle glaucoma. Peoplewith a family history of glaucoma have

about a six percent chance ofdevelo in laucoma.


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Many East Asian groups are prone todeveloping angle closure glaucomadue to their shallower anterior

chamber depth, with the majority ofcases of glaucoma in this populationconsisting of some form of angleclosure.

Inuit also have a twenty to forty timeshigher risk than Caucasians ofdeveloping primary angle closureglaucoma. Women are three timesmore likely than men to develop acuteangle-closure glaucoma due to their


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There is increasing evidence that ocularblood flow is involved in thepathogenesis of glaucoma. Current dataindicate that fluctuations in blood floware more harmful in glaucomatous opticneuropathy than steady reductions.Unstable blood pressure and dips arelinked to optic nerve head damage and

correlate with visual field deterioration. A number of studies also suggest a

possible correlation betweenhypertension and the development ofglaucoma. In normal tension glaucoma,nocturnal hypotension may play a


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There is no clear evidence that vitamindeficiencies cause glaucoma in humans. Itfollows then that oral vitamin supplementationis probably not useful in glaucoma treatment.

Various rare congenital/genetic eyemalformations are associated with glaucoma.Occasionally, failure of the normal thirdtrimester gestational atrophy of the hyaloidcanal and the tunica vasculosa lentis isassociated with other anomalies. Angle closure

induced ocular hypertension andglaucomatous optic neuropathy may alsooccur with these anomalies and modelled inmice.

Those at risk for glaucoma are advised to have adilated eye examination at least once a year.


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Classification of glaucoma

1. Primary glaucoma and its variants(H40.1-H40.2) Primary angle-closure glaucoma, also known

as primary closed-angle glaucoma,narrow-angle glaucoma, pupil-blockglaucoma, acute congestive glaucoma

Acute angle-closure glaucoma Chronic angle-closure glaucoma Intermittent angle-closure glaucoma Superimposed on chronic open-angle

closure glaucoma ("combinedmechanism" - uncommon)


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Primary open-angle glaucoma, alsoknown as chronic open-angleglaucoma, chronic simple glaucoma,

glaucoma simplex High-tension glaucoma Low-tension glaucoma

Variants of primary glaucoma Pigmentary glaucoma Exfoliation glaucoma, also known as

pseudoexfoliative glaucoma orglaucoma capsulare


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2. Developmental glaucoma(Q15.0)

Developmental glaucoma Primary congenital glaucoma Infantile glaucoma Glaucoma associated with hereditary

of familial diseases


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Drug-induced glaucoma Corticosteroid induced glaucoma Alpha-chymotrypsin glaucoma.

Postoperative ocular hypertension fromuse of alpha chymotrypsin.

Glaucoma of miscellaneous origin Associated with intraocular tumors Associated with retinal detachments Secondary to severe chemical burns of the

eye Associated with essential iris atrophy Toxic Glaucoma


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-rim a ry a n g le clo su reg la u co m a This is caused by contact between the iris

and trabecular meshwork, which in turnobstructs outflow of the aqueous humorfrom the eye.

This contact between iris and trabecularmeshwork (TM) may gradually damagethe function of the meshwork until it failsto keep pace with aqueous production,and the pressure rises.

In over half of all cases, prolonged contactbetween iris and TM causes theformation of synechiae (effectively"scars").

These cause permanent obstruction ofaqueous outflow.


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Diagnosis is made from physical signsand symptoms: pupils mid-dilated andunresponsive to light, corneaedematous (cloudy), reduced vision,redness, pain.

However, the majority of cases areasymptomatic.

Prior to very severe loss of vision, these

cases can only be identified byexamination, generally by an eye careprofessional.

Once any symptoms have beencontrolled, the first line (and oftendefinitive) treatment is laser iridotomy.


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The goal of treatment is to reverse,and prevent, contact between irisand trabecular meshwork.

In early to moderately advancedcases, iridotomy is successful inopening the angle in around 75% of

cases. In the other 25% laser iridoplasty,

medication (pilocarpine) orincisional surgery may be required.


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-rim a ry o p e n a n g leg la u co m a Optic nerve damage resulting in

progressive visual field loss. This is associated with increased

pressure in the eye. Not all people with primary open-

angle glaucoma have eye pressure

that is elevated beyond normal, butdecreasing the eye pressure furtherhas been shown to stop progressioneven in these cases.


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The increased pressure is caused bytrabecular blockage which is wherethe aqueous humor in the eye

drains out. Because the microscopic passage

ways are blocked, the pressure

builds up in the eye and causesimperceptible very gradual visionloss.

Peripheral vision is affected first buteventually the entire vision will be


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Diagnosis is made by looking for cupping of theoptic nerve.

Prostoglandin agonists work by openinguveoscleral passageways.

Beta blockers such as timolol, work bydecreasing aqueous formation. Carbonic anhydrase inhibitors decrease

bicarbonate formation from ciliary processes inthe eye, thus decreasing formation of Aqueoushumor.

Parasympathetic analogs are drugs that work onthe trabecular outflow by opening up thepassageway and constricting the pupil.

Alpha 2 agonists (brimonidine, apraclonidine)both decrease fluid production (via. inhibition

of AC) and increase drainage.


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eo vascu lar g lau co m a Neovascular glaucoma is an uncommon

type of glaucoma that is difficult ornearly impossible to treat.

This condition is often caused byproliferative diabetic retinopathy(PDR) or central retinal vein occlusion(CRVO).

It may also be triggered by otherconditions that result in ischemia ofthe retina or ciliary body.

Individuals with poor blood flow to the

eye are highly at risk for thiscondition.


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Neovascular glaucoma results whennew, abnormal vessels begindeveloping in the angle of the eye

that begin blocking the drainage. Patients with such condition begin to

rapidly lose their eyesight.

Sometimes, the disease appears veryrapidly, specially after cataractsurgery procedure.


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In neovascularglaucoma, the iris isoften covered by

new vessels(arrow).These vessels can

grow

and eventuallyblock the drainageof fluid through thetrabecularmeshwork.


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A new treatment for this disease, asfirst reported by Kahook andcolleagues, involves use of a novel

group of medications known as Anti-VEGF agents.

These injectable medications can

lead to a dramatic decrease in newvessel formation and, if injectedearly enough in the diseaseprocess, may lead to normalization

of intraocular pressure.


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Toxic glaucoma

Toxic glaucoma is open angleglaucoma with an unexplainedsignificant rise of intraocular

pressure following unknownpathogenesis.

Intraocular pressure can sometimes

reach 80 mmHg (11 kPa). It characteristically manifests as

ciliary body inflammation andmassive trabecular oedema that

sometimes extends to Schlemm's


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This condition is differentiated frommalignant glaucoma by thepresence of a deep and clear

anterior chamber and a lack ofaqueous misdirection.

Also, the corneal appearance is not as

hazy. A reduction in visual acuity can occur

followed neuroretinal breakdown.


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Associated factors include inflammation,drugs, trauma and intraocular surgery,including cataract surgery and

vitrectomy procedures. Gede Pardianto (2005) reports on fourpatients who had toxic glaucoma. Oneof them underwentphaecoemulsification with smallparticle nucleus drops. Some casescan be resolved with somemedication, vitrectomy procedures ortrabeculectomy. Valving procedures

can give some relief but further


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The major risk factors include:

Age over 45 years Family history of glaucoma Black racial ancestry Diabetes

History of elevated intraocular pressure Nearsightedness (high degree of myopia), which is

the inability to see distant objects clearly History of injury to the eye Use of cortisone (steroids), either in the eye or

systemically (orally or injected) Farsightedness (hyperopia), which is seeing distant

objects better than close ones (Farsighted peoplemay have narrow filtering angles, which predisposethem to acute (sudden) attacks of closed-angleglaucoma.)

Ri k F C S


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Risk Factor Category Score

Age younger than 50 years50-64 years65-74 yearsolder than 75 years

0123

Race Caucasian/other African American

02

Family History of Glaucoma Negative or positive in non-first degreerelativePositive for parentsPositive for siblings

012

Last Complete Eye Exam Within last two years2-5 years agomore than 5 years ago

012

Level of Glaucoma Risk (Total Score)

High 4 or greater

Moderate 3

Low 2 or less


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SYMPTOMS


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Diagnosis

Because glaucoma does not causesymptoms in most cases, those whoare 40 or older should have an annual

examination including a measurementof the intraocular pressure. Thosewho are glaucoma suspects may needadditional testing.

Screening for glaucoma is usuallyperformed as part of a standard eyeexamination performed byophthalmologists and optometrists.


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The doctor evaluates the optic nerveand grades its health by noting thecup to disc ratio. This is simply a

comparison of the cup (thedepressed area in the center of thenerve) to the entire diameter of theoptic nerve.

As glaucoma progresses, the area ofcupping, or depression, increases.

Therefore, a patient with a higher

ratio has more damage.


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The above photos show progressiveoptic nerve damage (indicated bythe cup to disc ratio) caused by

glaucoma. Notice the paleappearance of the nerve with the0.9 cup as compared to the nervewith the 0.3 cup.


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The progression of glaucoma is monitoredwith a visual field test. This test mapsthe peripheral vision, allowing the doctorto determine the extent of vision loss

from glaucoma and a measure of theeffectiveness of the treatment. Thevisual field test is periodically repeated toverify that the intraocular pressure is

being adequately controlled. The structures in the front of the eye arenormally difficult to see without the helpof a special gonioscopy lens. This specialmirrored contact lens allows the doctor to

examine the anterior chamber and the


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Owing to the sensitivity of all methods oftonometry to corneal thickness, methodssuch as Goldmann tonometry should beaugmented with pachymetry to measure

central corneal thickness (CCT). A thicker-than-average cornea can result in

a pressure reading higher than the 'true'pressure, whereas a thinner-than-

average cornea can produce a pressurereading lower than the 'true' pressure. Because pressure measurement error can

be caused by more than just CCT (i.e,corneal hydration, elastic properties,etc.), it is impossible to 'adjust' pressure


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At St. Lukes, another test called theArden Screening Test is used toconfirm the diagnosis of glaucoma.

This color test may show vision

changes that occur before problemsappear on the visual field test. The Frequency Doubling Illusion can also

be used to detect glaucoma with the

use of a Frequency DoublingTechnology (FDT) perimeter. Examination for glaucoma also could be

assessed with more attention given tosex, race, history of drugs use,

refraction, inheritance and family


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M a n a g e m e n t

The modern goals of glaucoma management are toavoid glaucomatous damage, nerve damage,preserve visual field and total quality of life forpatients with minimal side effects.

This requires appropriate diagnostic techniques and

follow up examinations and judicious selection oftreatments for the individual patient. Although intraocular pressure is only one of the major

risk factors for glaucoma, lowering it via variouspharmaceuticals and/or surgical techniques iscurrently the mainstay of glaucoma treatment.

Vascular flow and neurodegenerative theories ofglaucomatous optic neuropathy have promptedstudies on various neuroprotective therapeuticstrategies including nutritional compounds some ofwhich may be regarded by clinicians as safe for usenow, while others are on trial.


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M e d ication

Intraocular pressure can be lowered withmedication, usually eye drops. There areseveral different classes of medicationsto treat glaucoma with several different

medications in each class. Each of these medicines may have local

and systemic side effects. Adherence tomedication protocol can be confusing

and expensive; if side effects occur, thepatient must be willing either to toleratethese, or to communicate with thetreating physician to improve the drugregimen. Initially, glaucoma drops may

reasonably be started in either one or in


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Poor compliance with medications andfollow-up visits is a major reason forvision loss in glaucoma patients. A2003 study of patients in an HMO

found that half failed to fill theirprescription the first time and one infour failed to refill their prescriptions asecond time.

Patient education and communicationmust be ongoing to sustain successfultreatment plans for this lifelongdisease with no early symptoms.

The possible neuroprotective effects of

various topical and systemic


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C om m o n ly u sed m ed ication s

Prostaglandin analogs like latanoprost(Xalatan), bimatoprost (Lumigan) andtravoprost (Travatan) increaseuveoscleral outflow of aqueous humor.

Bimatoprost also increases trabecularoutflow

Topical beta-adrenergic receptorantagonists such as timolol, levobunolol

(Betagan), and betaxolol decreaseaqueous humor production by the ciliarybody.

Alpha2-adrenergic agonists such asbrimonidine (Alphagan) work by a dualmechanism, decreasing aqueous


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Less-selective sympathomimetics likeepinephrine and dipivefrin (Propine)increase outflow of aqueous humorthrough trabecular meshwork and

possibly through uveoscleral outflowpathway, probably by a beta2-agonistaction.

Miotic agents (parasympathomimetics)like pilocarpine work by contraction ofthe ciliary muscle, tightening thetrabecular meshwork and allowingincreased outflow of the aqueoushumour. Ecothiopate is used in chronic

glaucoma.


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Carbonic anhydrase inhibitors likedorzolamide (Trusopt), brinzolamide(Azopt), acetazolamide (Diamox)

lower secretion of aqueous humorby inhibiting carbonic anhydrase inthe ciliary body.

Physostigmine is also used to treatglaucoma and delayed gastricemptying


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Surgery

Conventional surgery to treat glaucomamakes a new opening in themeshwork. This new opening helpsfluid to leave the eye and lowersintraocular pressure.

Both laser and conventional surgeriesare performed to treat glaucoma.

Surgery is the primary therapy for thosewith congenital glaucoma. Generally, these operations are a

temporary solution, as there is not yet

a cure for glaucoma


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Canaloplasty

Canaloplasty is a nonpenetrating procedure utilizingmicrocatheter technology.

To perform a canaloplasty, an incision is made intothe eye to gain access to Schlemm's canal in asimilar fashion to a viscocanalostomy.

A microcatheter will circumnavigate the canal aroundthe iris, enlarging the main drainage channel andits smaller collector channels through the injectionof a sterile, gel-like material called viscoelastic.

The catheter is then removed and a suture is placedwithin the canal and tightened.

By opening the canal, the pressure inside the eyemay be relieved, although the reason is unclearsince the canal (of Schlemm) does not have anysignificant fluid resistance in glaucoma or healthyeyes. Long-term results are not available.


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Laser surgery

Laser trabeculoplasty may be used to treat open angleglaucoma.

It is a temporary solution, not a cure. A 50 m argon laser spot is aimed at the trabecular

meshwork to stimulate opening of the mesh to allow

more outflow of aqueous fluid. Usually, half of the angle is treated at a time. Traditional laser trabeculoplasty utilizes a thermal argon

laser. The procedure is called Argon LaserTrabeculoplasty or ALT.

A newer type of laser trabeculoplasty exists that uses a

"cold" (non-thermal) laser to stimulate drainage in thetrabecular meshwork. This newer procedure which uses a 532 nm frequency-

doubled, Q-switched Nd:YAG laser which selectivelytargets melanin pigment in the trabecular meshworkcells, called Selective Laser Trabeculoplasty or SLT.

Studies show that SLT is as effective as ALT at lowering eyepressure.


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Trabeculectomy

The most common conventional surgeryperformed for glaucoma is the trabeculectomy.

Here, a partial thickness flap is made in thescleral wall of the eye, and a window openingmade under the flap to remove a portion of thetrabecular meshwork.

The scleral flap is then sutured loosely back inplace.

This allows fluid to flow out of the eye throughthis opening, resulting in lowered intraocular

pressure and the formation of a bleb or fluidbubble on the surface of the eye. Scarring can occur around or over the flap

opening, causing it to become less effective orlose effectiveness altogether.

One person can have multiple surgicalrocedures of the same or different t es.


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Glaucoma drainageimplants There are also several different glaucoma drainage

implants. These include the original Molteno implant (1966), the

Baerveldt tube shunt, or the valved implants, such as theAhmed glaucoma valve implant or the ExPress MiniShunt and the later generation pressure ridge Molteno

implants. These are indicated for glaucoma patients not responding

to maximal medical therapy, with previous failedguarded filtering surgery (trabeculectomy).

The flow tube is inserted into the anterior chamber of theeye and the plate is implanted underneath the

conjunctiva to allow flow of aqueous fluid out of the eyeinto a chamber called a bleb. The first-generation Molteno and other non-valved implants

sometimes require the ligation of the tube until the blebformed is mildly fibrosed and water-tight

This is done to reduce postoperative hypotonysuddendrops in postoperative intraocular pressure (IOP).


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Valved implants such as the Ahmedglaucoma valve attempt to controlpostoperative hypotony by using amechanical valve.

The ongoing scarring over the conjunctivaldissipation segment of the shunt maybecome too thick for the aqueous humorto filter through. This may require

preventive measures using anti-fibroticmedication like 5-fluorouracil (5-FU) ormitomycin-C (during the procedure), oradditional surgery. And for Glaucomatouspainful Blind Eye and some cases of

Glaucoma, Cyclocryotherapy for ciliary


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THANKZ!!!!

By Erni D. F. Simbolon

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