Glaucoma Diska

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    GLAUCOMA

    Diska Astarini

    I11109083

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    Glaucoma is an optic neuropathy characterized by

    cupping of the optic disc and the loss of visual

    field.

    Associated to intraocular pressure (IOP) visual field sensitivity and eventually leads to

    blindness in the affected eye

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    Worldwide, glaucoma is the leading cause of

    irreversible blindness

    Almost 60 millions people have Glaucoma.In fact, as many as 6 millions individuals are

    blind in both eyes from this disease

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    Pathophysiologyincreased intraocular pressure(usually > 24 mmHg)

    Overproduction of HA with normal

    Drainage

    block of fluid flow from posterior to

    anterior chamber

    reduced flow through the trabecular

    meshwork

    Ischemic of Optical

    nerve

    Push Optical Nerve

    Diffuse ganglional cell

    atrophy

    Effect to the Vision

    http://en.wikipedia.org/wiki/Ocular_hypertensionhttp://en.wikipedia.org/wiki/Ocular_hypertension
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    Risk Factors

    Age

    Family History

    Drug consumption (steroid)

    Trauma

    Severe Hypermethrophya

    Other systemic disease (ex ; DM, Hypertension)

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    Sign and symptom

    Symptoms may include:

    Blurred vision

    Severe eye pain

    Headache

    Rainbow haloes around lights

    Nausea and vomiting

    Elevated intraocular pressure

    Visual field loss

    Optic disk changes

    Enlargement of the eye.

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    Diagnosis

    Measuring intra ocular pressure (tonometry);

    Inspecting the drainage angle of your eye (gonioscopy);

    Evaluating any optic nerve damage (ophthalmoscopy);

    Testing the visual field of each eye (perimetry).

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    Classification

    1. Open Angle Glaucoma

    2. Angle closure glaucoma

    3. Congenital Glaucoma

    4. Secondary glaucoma

    Glaucoma can be divided roughly into two maincategories, "open angle" and "closed angleglaucoma.

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    Types of glaukcoma

    Types Cause Symptoms Comment

    Chronic Open Angle

    Glaucoma

    Gradual blockage of

    drainage channel

    Pressure builds slowly

    Gradual loss of side

    vision

    Affects side vision first

    This type of glaucoma

    progresses very slowly

    andis a lifelong condition.

    Acute Closed

    Angle Glaucoma

    Total blockage of

    drainage channel

    Sudden increase

    in pressureNausea

    Blurred vision

    Severe pain

    Halos around lights

    This condition

    constitutes a

    medical emergency, as

    permanent blindnessoccurs rapidly without

    immediate treatment.

    Secondary Glaucoma Injury, infection, tumors,

    drugs, or inflammation

    cause scar tissue which

    blocks the drainage

    channel

    Gradual loss of side

    vision

    Affects side vision first

    This form of glaucoma

    may progress slowly, as

    in cases of chronic

    glaucoma.

    Congenital

    Glaucoma

    Fluid drainage system

    abnormal at birth

    Enlarged eyes

    Cloudy cornea

    Light sensitivity

    Excessive tearing

    This condition must be

    treated soon after birth if

    vision is to be saved.

    A aGrafix materials call 770-641-7310 - Atlanta GA USA

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    Examination Methods

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    Oblique Illumination of the Anterior Chamber

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    Slit-Lamp Examination

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    Gonioscopy Gonioscopy can differentiate the following conditions:

    Open angle: open angle glaucoma.

    Occluded angle: angle closure glaucoma.

    Angle access is narrowed: configuration with imminent risk

    angle of an acute closure glaucoma.

    Angle is occluded: secondary angle closure glaucoma, for

    example due to neovascularization in rubeosis iridis.

    Angle open but with inflammatory cellular deposits,

    erythrocytes, or pigment in the trabecular meshwork: secondary

    open angle glaucoma.

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    Measuring Intraocular Pressure

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    Applanation Tonometry

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    Visual Field Testing

    visual field testing can be grouped into several

    important categories:

    Confrontational

    Amsler grid

    Static perimetry

    Kinetic perimetry Frequency doubling analysis

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    Treatment

    Principe: reducing IOP by decreasing aqueous

    production or increasing aqueous outflow

    Currently, the effectiveness of a medication in

    the treatment of glaucoma is measured by its

    ability to lower IOP

    Medical, surgical or laser

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    Medical Treatment Suppression of Aqueous Production

    Topical beta-adrenergic blocking agents, Apraclonidine,Brimonidine, Dorzolamide hydrochloride and brinzolamide,Carbonic anhydrase inhibitorsacetazolamide

    Facilitation of Aqueous OutflowThe prostaglandin analogsbimatoprost 0.003%, latanoprost0.005%, and travoprost 0.004% solutions,Parasympathomimetic agents Pilocarpine, Epinephrine,Dipivefrin

    Reduction of Vitreous VolumeHyperosmotic agents, Oral glycerin (glycerol)

    Miotics, Mydriatics, and Cycloplegics

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    Surgical and laser treatment

    Peripheral Iridotomy, Iridectomy, andIridoplasty

    Laser Trabeculoplasty

    Glaucoma Drainage Surgery Trabeculectomy

    Viscocanalostomy and deep sclerectomy with

    collagen implant Goniotomy

    Cyclodestructive Procedures

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    OPEN ANGLE GLAUKOMA

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    OPEN ANGLE GLAUCOMA

    Primary open-angle glaucoma (POAG), the mostcommon form of glaucoma, accounts for 6070% of all glaucomas and 9095% of primaryglaucomas.

    POAG is a bilateral,chronic progressive conditionthat typically appears in

    individuals over 60years of age

    PRIMARY OPEN ANGLE GLAUCOMA

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    Groups at risk

    Age : from the 40-49 age group into those

    aged over 80.

    ocular hypertension

    myopia

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    Signs

    the optic disc changes.

    The cup to disc ratio

    increases. Asymmetry

    of disc cupping

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    Diagnostic considerations

    Measurement of intraocular pressure

    Elevated intraocular pressure is an alarming

    sign

    Twenty-four-hour pressure curve

    Fluctuations in intraocular pressure of over 5

    6 mmHgmay occurover a 24-hour period.

    Gonioscopy

    Ophthalmoscopy

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    treatment

    The goal is to maintain IOP less than 21 mmHg

    and continued visual field loss should be minimal.

    Various treatment modalities include medical

    treatment, laser therapy,and surgery.

    Patients will initially start with topical ocular drug

    therapy

    Prognosis : If discovered early and treatedadequately, the prognosis for POAG is excellent

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    ACUTE ANGLE CLOSURE

    GLAUCOMA

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    Acute angle closure glaucoma

    History

    The attack comes on quite quickly

    the intraocular pressure rises rapidly

    Red eye

    There is pain in one eye, can be extremely severe

    impaired vision and haloes around lights

    may have had similar attacks in the past may be systemically unwell, with severe

    headache, nausea, and vomiting

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    Risk factors

    increasing age

    female gender

    family history of glaucoma

    South-East Asian, Chinese, or Inuit ethnic

    background.

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    Examination

    The eye is inflamed and tender

    The cornea is hazy and the pupil is semidilated

    and fixed. Vision is impaired according to the

    state of the cornea

    On gentle palpation the eye feels harder than

    the other eye.

    The anterior chamber seems shallower than

    usual, with the iris being close to the cornea

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    Aqueous Humor flow after iridectomy

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    Congenital Glaucoma

    Primary congenital glaucoma

    Together with other anomaly

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    Primary Congenital Glaucoma

    Present at birth; however, but its manifestationsmay not be recognized until infancy or earlychildhood

    Pathophysiology : Primary congenital glaucoma isrestricted to a developmental abnormality thataffects the trabecular meshwork

    Estimated to affect fewer than 0.05% of

    ophthalmic patients The disease is bilateral in approximately 75% of

    cases.

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    Primary congenital glaucoma usually is diagnosed

    at birth or shortly thereafter, and most cases are

    diagnosed in the first year of life.

    Most cases oare sporadic in occurrence may betransmitted through an autosomal recessive

    pattern

    Male patients are found to have a higherincidence of the disease, comprising

    approximately 65% of cases.

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    Clinical

    History

    Triad of manifestations :

    Epiphora

    Photophobia

    Blepharospasm

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    Secondary glaucoma Inflammatory glaucoma

    Uveitis of all types

    Fuchs heterochromic iridocyclitis

    Phacogenic glaucoma

    Angle-closure glaucoma with mature

    cataract

    Phacoanaphylactic glaucoma secondary to

    rupture of lens capsule

    Phacolytic glaucoma due to phacotoxic

    meshwork blockage

    Subluxation of lens

    Glaucoma secondary to intraocular

    hemorrhage Hyphema

    Hemolytic glaucoma, also known as

    erythroclastic glaucoma

    Neovascular glaucoma

    Traumatic glaucoma

    Angle recession glaucoma: Traumaticrecession on anterior chamber angle

    Postsurgical glaucoma

    Aphakic pupillary block

    Ciliary block glaucoma

    Drug-induced glaucoma

    Corticosteroid induced glaucoma

    Alpha-chymotrypsin glaucoma.

    Postoperative ocular hypertension from

    use 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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