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OHADM2 > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

Glaucomatous damage

A

Retinal Nerve Fibre Layer, parapapillary changes, Neuroretinal Rim, Baring of circumlinear blood vessels, Bayonetting, Laminar dot sign, Disc haemorrhage

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2
Q

Ocular Hypertension pathogenesis

A

IOP >21mmHg without detectable glaucomatous damage

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3
Q

Ocular Hypertension risk factors

A

Old age, high vertical c/d ratio, high IOP, parapapillary changes, thin corneal thickness, family history, high myopia

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4
Q

Ocular Hypertension Managements of High risk

A

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]

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5
Q

Ocular Hypertension Managements of Moderate risk

A

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]

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6
Q

Ocular Hypertension Managements of Low risk

A

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]

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7
Q

Primary Open Angle Glaucoma signs

A

adult onset, open angle, VF loss, glaucomatous optic nerve head changes, IOP >21mmHg

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8
Q

Primary Open Angle Glaucoma Risk factors

A

old age, race(more blacks than white), reduced perfusion pressure, myopia, positive family history, retinal diseases, diabetes

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9
Q

Primary Open Angle Glaucoma Pathogenesis

A

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.

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10
Q

Primary Open Angle Glaucoma Diagnosis

A

raised IOP, optic disc changes, glaucomatous VF loss, VHA/gonioscopy shows open angle, diurnal fluctuations more than 5mmHg

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11
Q

Primary Open Angle Glaucoma Management

A 
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.
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12
Q

Normal tension glaucoma Signs

A

IOP <21mmHg, open angle, VF loss, glaucomatous optic nerve head damages, absence of secondary causes of glaucoma

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13
Q

Normal tension glaucoma risk factors

A

age, gender(female>male), race(japan>europe/NA), family history

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14
Q

Normal tension glaucoma diagnosis

A

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

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15
Q

Normal tension glaucoma Management

A

Refer to ophthalmologist for

  • monitoring of progression
  • topical anti-glaucoma therapy
  • laser trabeculotoplasty
  • surgery
  • monitoring of systemic blood pressure
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16
Q

Primary close angle glaucoma Risk factors

A

old age, gender(female>male), race(SEA, chinese, eskimos), positive family history

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17
Q

Primary close angle glaucoma Mechanism - Pupillary Block

A

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

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18
Q

Angle Closure Suspect Signs and Symptoms

A 
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
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19
Q

Angle Closure suspect management

A

refer to ophthalmologist for prophylactic peripheral laser iridotomy if one eye has acute/subacute angle closure or if both eyes have occludable angle

20
Q

Intermittent Angle Closure pathogenesis

A
  • rapid closure of angle results in spike of IOP

- pupillary block spontaneously relieved and IOP goes back to normal

21
Q

Intermittent Angle Closure Signs and Symptoms

A

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.

22
Q

Intermittent Angle Closure management

A

refer for prophylactic peripheral iridotomy

23
Q

Acute Angle Closure Presentation

A

unilateral vision loss w/ periocular pain maybe associated with nausea and vomitting

24
Q

Acute Angle Closure Signs

A
  • 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
25
Q

Acute Angle Closure Management

A

refer to emergency department for medical treatment and peripheral laser iridotomy

26
Q

Pseudoexfoliation Syndrome Pathogenesis

A

white-grey, pseudoexfoliative material produced by abnormal basement membrane of aging epithelial cells in various structures and deposited on anterior segment structures.

27
Q

Pseudoexfoliative Syndrome SIGNS

A
  • 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
28
Q

Pseudoexfoliative Glaucoma Pathogenesis

A

trabecular obstruction by clogging of PXF material and/or pigment released by iris

29
Q

Pseudoexfoliative Glaucoma Presentation

A

7th decade

30
Q

Pseudoexfoliative Glaucoma Signs

A

PXF with chronic open angle glaucoma is unilateral but IOP may rise despite open angle

31
Q

Pseudoexfoliative Glacuoma Management

A 
Same as POAG
Refer to ophthalmologist for
-confirmation of diagnosis
-topical anti-glaucoma therapy
-laser trabeculoplasty
-trabeculotomy
32
Q

Pigment Dispersion Syndrome Pathogenesis

A

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.

33
Q

Pigment Dispersion Syndrome Signs

A
  • 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
34
Q

Pigment Dispersion Glaucoma Pathogenesis

A

trabecular blockage by pigment and damage to trabecular secondary to sclerosis and collapse.

35
Q

Pigment Dispersion Glaucoma Risk factors and presentation

A

RF:1/3 will develop high IOP
Presentation: PDS with chronic glaucoma

36
Q

Pigment Dispersion glaucoma Management

A 
same as POAG
Refer to ophthalmologist for
-confirmation of diagnosis
-topical anti-glaucoma therapy
-laser trabeculoplasty
-trabeculotomy
37
Q

Neovascular Glaucoma pathogenesis

A
  • 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
38
Q

Neovascular Glaucoma Causes

A

ischemic CRVO, PDR

39
Q

Neovascular Glaucoma Classification

A
  • Rubeosis Iridis
  • Secondary open angle glaucoma (blockage by fibrovascular membrane)
  • secondary synechial angle closure glaucoma (contraction of fibrovascular membrane)
40
Q

Phacolytic glaucoma Pathogenesis

A

trabecular obstruction due to high molecular weight proteins leaked by hypermature cataract

41
Q

Phacolytic Glaucoma Signs

A
  • hypermature cataract, corneal oedema, deep anterior chamber
  • aqueous may manifest floating white particles
42
Q

Phacolytic Glaucoma Management

A

refer for cataract removal and anti- glaucoma therapy

43
Q

Phacomorphic Glaucoma Pathogenesis

A

acute secondary angle closure as a result of a swollen cataract

44
Q

Phacomorphic Glaucoma Signs

A

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
45
Q

Phacomorphic Glaucoma Management

A
  • peripheral laser iridotomy

- subsequent removal of cataract when eye is quiet

46
Q

Inflammatory Glaucoma pathogenesis

A

elevation of IOP secondary to an intraocular inflammation causing glaucoma

47
Q

Inflammatory Glaucoma Classification

A

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

OHADM2 (9 decks)

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