Glaucoma Flashcards
Glaucomatous damage
Retinal Nerve Fibre Layer, parapapillary changes, Neuroretinal Rim, Baring of circumlinear blood vessels, Bayonetting, Laminar dot sign, Disc haemorrhage
Ocular Hypertension pathogenesis
IOP >21mmHg without detectable glaucomatous damage
Ocular Hypertension risk factors
Old age, high vertical c/d ratio, high IOP, parapapillary changes, thin corneal thickness, family history, high myopia
Ocular Hypertension Managements of High risk
RNFL defects, parapapillary changes, IOP 30mmHg or more, IOP 26mmHg or more with central corneal thickness <555um, vertical C/D ratio 0.4 or more with central corneal thickness <555um
[refer to ophthalmologist for diagnosis, monitoring and treatment]
Ocular Hypertension Managements of Moderate risk
IOP 24-29mmHg w/o RNFL defects, IOP 22-25mmHg w/ central corneal thickness <555um, vertical C/D ratio 0.4 or more with central corneal thickness 555-558um, positive family history and high myopia.
[refer to ophthalmologist if incapable of monitoring VF or if suspecting glaucomatous changes]
Ocular Hypertension Managements of Low risk
IOP 22-23mmHg w/ central corneal thickness >558um
vertical C/D ratio of 0.4 or less with central corneal thickness >558
[monitor patient annually for changes in IOP and C/D ratio, refer if glaucomatous changes arises]
Primary Open Angle Glaucoma signs
adult onset, open angle, VF loss, glaucomatous optic nerve head changes, IOP >21mmHg
Primary Open Angle Glaucoma Risk factors
old age, race(more blacks than white), reduced perfusion pressure, myopia, positive family history, retinal diseases, diabetes
Primary Open Angle Glaucoma Pathogenesis
elevation of IOP due to increased resistance of aqueous outflow at trabecular meshwork.
retinal ganglion cells death through apoptosis.
factors influencing cell death:
-ischemic theory: compromise microvasculature results in ischemic of optic nerve head
-direct mechanical theory: raised IOP directly injures the retinal nerve fibres as it passes through the lamina cribosa.
Primary Open Angle Glaucoma Diagnosis
raised IOP, optic disc changes, glaucomatous VF loss, VHA/gonioscopy shows open angle, diurnal fluctuations more than 5mmHg
Primary Open Angle Glaucoma Management
Refer to ophthalmologist for -confirmation of diagnosis -topical anti-glaucoma therapy -laser trabeculoplasty -trabeculotomy Primary aim is to prevent functional impairment of vision by slowing the rate of ganglion cells death, best way is to lower IOP.
Normal tension glaucoma Signs
IOP <21mmHg, open angle, VF loss, glaucomatous optic nerve head damages, absence of secondary causes of glaucoma
Normal tension glaucoma risk factors
age, gender(female>male), race(japan>europe/NA), family history
Normal tension glaucoma diagnosis
IOP <21mmHg
Optic disc changes
- cupping and parapapillary changes
-splinter shaped hemorrhages and acquired optic disc pits
Glaucomatous VF loss
Others
-reduced blood flow due to emotional stress or cold
-nocturnal systemic hypertension
-migraine
-reduced blood flow velocity in ophthalmic and posterior ciliary arteries
Normal tension glaucoma Management
Refer to ophthalmologist for
- monitoring of progression
- topical anti-glaucoma therapy
- laser trabeculotoplasty
- surgery
- monitoring of systemic blood pressure
Primary close angle glaucoma Risk factors
old age, gender(female>male), race(SEA, chinese, eskimos), positive family history
Primary close angle glaucoma Mechanism - Pupillary Block
1) failure of aqueous outflow through the pupil
2) difference in pressure between anterior and posterior chamber.
3) results in anterior bowing of the iris (iris bombe) and iridotrabecular contact
Angle Closure Suspect Signs and Symptoms
symptoms: absent signs: -less than normal axial anterior chamber depth w/ convex len- iris diaphragm -close proximity of iris to cornea -VHA/goniocopy shows occludable angle
Angle Closure suspect management
refer to ophthalmologist for prophylactic peripheral laser iridotomy if one eye has acute/subacute angle closure or if both eyes have occludable angle
Intermittent Angle Closure pathogenesis
- rapid closure of angle results in spike of IOP
- pupillary block spontaneously relieved and IOP goes back to normal
Intermittent Angle Closure Signs and Symptoms
symptoms: transient blurring of vision associated with haloes around light
signs:
-during an attack, eye is white and corneal is oedematous
-between attacks, eye is normal but angle is narrow.
Intermittent Angle Closure management
refer for prophylactic peripheral iridotomy
Acute Angle Closure Presentation
unilateral vision loss w/ periocular pain maybe associated with nausea and vomitting
Acute Angle Closure Signs
- ciliary flush and corneal oedema
- IOP 50-100mmHg
- shallow anterior chamber w/ cells and flares
- VHA/gonioscopy shows complete irdiocorneal contact
- semi-dilated fixed pupil
Acute Angle Closure Management
refer to emergency department for medical treatment and peripheral laser iridotomy
Pseudoexfoliation Syndrome Pathogenesis
white-grey, pseudoexfoliative material produced by abnormal basement membrane of aging epithelial cells in various structures and deposited on anterior segment structures.
Pseudoexfoliative Syndrome SIGNS
- Cornea shows PXF on endothelium as well as pigment deposition
- Iris shows PXF on pupillary margin and sphincter atropy results in transillumination defects
- Gonioscopy shows hyperpigmentation of trabecular and PXF deposits
Pseudoexfoliative Glaucoma Pathogenesis
trabecular obstruction by clogging of PXF material and/or pigment released by iris
Pseudoexfoliative Glaucoma Presentation
7th decade
Pseudoexfoliative Glaucoma Signs
PXF with chronic open angle glaucoma is unilateral but IOP may rise despite open angle
Pseudoexfoliative Glacuoma Management
Same as POAG Refer to ophthalmologist for -confirmation of diagnosis -topical anti-glaucoma therapy -laser trabeculoplasty -trabeculotomy
Pigment Dispersion Syndrome Pathogenesis
pigment shedding due to the rubbing of the posterior pigment layer of the iris against packets of lens zonules due to the excessive posterior bowing of the mid peripheral portion of iris.
Pigment Dispersion Syndrome Signs
- cornea may show pigment deposition in a vertical spindle shaped distribution
- anterior chamber is very deep and melanin granules can be seen floating in aqueous
- fine surface deposit maybe seen on iris that may extend on to the lens
- mid peripheral radial slit-like retroillumination defects
- gonioscopy/VHA shows wide open angle
Pigment Dispersion Glaucoma Pathogenesis
trabecular blockage by pigment and damage to trabecular secondary to sclerosis and collapse.
Pigment Dispersion Glaucoma Risk factors and presentation
RF:1/3 will develop high IOP
Presentation: PDS with chronic glaucoma
Pigment Dispersion glaucoma Management
same as POAG Refer to ophthalmologist for -confirmation of diagnosis -topical anti-glaucoma therapy -laser trabeculoplasty -trabeculotomy
Neovascular Glaucoma pathogenesis
- neovascular glaucoma is cause by iris neovascularization
- common cause is severe, diffuse and chronic retinal ischemia
- hypoxic retinal tissues produces VEGF, which induces retinal neovascularization
- VEGF diffuses and anterior segment causing rubeosis iridis and neovascularization of anterior chamber angle
- NVA will impair aqueous outflow in an open angle, as it contracts it causes secondary close angle glaucoma
Neovascular Glaucoma Causes
ischemic CRVO, PDR
Neovascular Glaucoma Classification
- Rubeosis Iridis
- Secondary open angle glaucoma (blockage by fibrovascular membrane)
- secondary synechial angle closure glaucoma (contraction of fibrovascular membrane)
Phacolytic glaucoma Pathogenesis
trabecular obstruction due to high molecular weight proteins leaked by hypermature cataract
Phacolytic Glaucoma Signs
- hypermature cataract, corneal oedema, deep anterior chamber
- aqueous may manifest floating white particles
Phacolytic Glaucoma Management
refer for cataract removal and anti- glaucoma therapy
Phacomorphic Glaucoma Pathogenesis
acute secondary angle closure as a result of a swollen cataract
Phacomorphic Glaucoma Signs
Same as PACG
- ciliary flush and corneal oedema
- IOP 50-100mmHg
- shallow anterior chamber w/ cells and flares
- semi-dilated fixed pupil
- VHA/goniocopy shows complete iridocorneal contact
Phacomorphic Glaucoma Management
- peripheral laser iridotomy
- subsequent removal of cataract when eye is quiet
Inflammatory Glaucoma pathogenesis
elevation of IOP secondary to an intraocular inflammation causing glaucoma
Inflammatory Glaucoma Classification
open angle glaucoma:
(trabecular obstruction by inflammatory cells and debris)
-acute anterior uveitis
-chronic anterior uveitis
- acute/ chronic trabeculitis: reduction of aq outflow
Possner-Schlossman syndrome
-recurrent attacks of unilateral, acute secondary open angle glaucoma w/ mild anterior uveitis and trabeculitis
