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Eye > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What is the definition of glaucoma?

A

Glaucoma is an optic neuropathy, with characteristic optic nerve head changes (i.e. increased cup to disc ratio (C/D ratio)) (structural lesion) and a corresponding visual field defect (functional problem), which may or may not be associated with raised IOP.

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2
Q

what is the definition of oculohypertension?

A

IOP > 21 mmHg, without detectable glaucomatous damag

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3
Q

how does one screen for glaucoma?

A
  • Gonioscopy – visualize the anterior chamber
  • Dilated ophthalmoscopy – dilated eye, examining fundus and optic nerve head
  • Automated perimetry – visual field testing, e.g. Humphrey (static perimetry)
  • Tonometry – to check IOP (can be affected if corneal thickness differs from norm, see Imbert Fick Law, or can be increased when eye is dilated)
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4
Q

who are the high risks groups who should be screened for glaucoma?

A
  • Older individuals: Risk increases once you are above 50 years old
  • Age > 40 + history of POAG in a close family member (strong FHx of glaucoma)
  • PMHx of raised IOP
  • FHx of POAG
  • Asians are at a higher risk of angle-closure glaucoma, as compared to Caucasians
  • High myopia (increased risk of POAG), high hypermetropia (increased risk of PACG)
  • Other risk factors, e.g. smoking
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5
Q

what is the main surgery for POAG?

A

Trabeculectomy

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6
Q

what are the types of visual field defects that can occur with POAG?

A
  • paracentral sctomas
  • Nasal step
  • temporal wedge
  • arcuate scotoma ( beginning as downward/upward extensions of the blind spot)
  • ring scotoma (when superior and inferior arcuate scotomas become continuous)
  • end stage (small island of central vision + temporal island)
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7
Q

what are the risk factors for normal tension glaucoma?

A
  • Family history of glaucoma
  • History of major blood loss or blood transfusion
  • History of migraine
  • History of Raynaud’s phenomenon- spasm of blood vessels leading to discolouration of fingers and toes.
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8
Q

Definition of primary angle closure suspect (PACS)?

A
  • Gonioscopy shows posterior meshwork iridotrabecular contact in 3 or more quadrants, but no peripheral anterior synechiae (PAS).
  • Normal IOP, optic disc, and visual field.
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9
Q

Definition of primary angle closure (PAC)?

A
  • Gonioscopy shows 3 or more quadrants of iridotrabecular contact, with raised IOP and/or PAS.
  • Normal optic disc and field.
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10
Q

Definition of primary angle closure glaucoma (PACG)?

A
  • ITC in 3 or more quadrants, with glaucomatous optic neuropathy.
  • Optic nerve damage from an episode of severe IOP elevation, such as acute angle closure, may not appear as typical glaucomatous cupping.
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11
Q

What are the mechanisms of angle closure

A
  • Relative pupillary block
  • non pupillary blcok (associated with deeper anterior chamber)
  • lens induced angle closure (usually rapid progression of lens intumescence [phacomorphic glaucoma] or anterior lens subluxation)
  • retrolenticular
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12
Q

what are the risk factors for PACG?

A
  • Age: elderly 🡪 more relative pupillary block
  • Gender: F > M
  • Race: Asian
  • FHx: angle closure (anatomical predisposition)
  • Refraction: eyes with pure pupillary block are typically hypermetropic
  • Axial length: short eyes tend to have shallow AC
  • Cataracts
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13
Q

what is the presentation of a patients with PACG?

A
  • Intermittent, mild symptoms of blurring (“smoke-filled room”) and haloes (“rainbow around lights”) due to corneal epithelial oedema, OR
  • Acutely with markedly decreased vision, redness and ocular/periocular pain and headache
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14
Q

what are the signs of chronic PACG?

A
  • VA is normal unless damage is advanced

- AC is usually shallower in relative pupillary block than non-pupillary block

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15
Q

what are the signs of acute PACG?

A
  • VA is usually 6/60 to HM
  • IOP is usually very high (50-100 mmHg)
  • Conjunctival hyperaemia, with violaceous circum corneal injection
  • Corneal epithelial oedema
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16
Q

what is the management of primary angle closure suspect?

A

Laser iridotomy

17
Q

what is the management for acute primary angle closure?

A

Initial management (aim to break the attack – medical)

  • Pt to assume supine position to encourage lens to shift posteriorly under the influence of gravity
  • IV acetazolamide 500 mg (lowers IOP)
  • Single dose apraclonidine 0.5% or 1% (lowers IOP), timolol 0.5% (lowers IOP), and prednisolone 1% or dexamethasone 0.1% (reduces inflammation) to affected eye, leaving 5 minutes between each
  • Pilocarpine 2-4% (miotic) one drop to BOTH eyes (in fellow eye for prophylaxis), repeated after 30 minutes

Subsequent management – surgical (after attack is broken, i.e. clear cornea, normalised IOP)
- Subsequent management – surgical (after attack is broken, i.e. clear cornea, normalised IOP)

  • Consider cataract surgery (because of possible lens involvement or contribution)
18
Q

what is the pathophysiology of acute angle closure glaucoma?

A
  • Contact between pupil margin and anterior lens surface (in pre-existing narrow angle) -> resistance to aqueous outflow from post to ant chamber -> pressure differential builds up -> peripheral iris bows forward -> angle block -> aqueous outflow obstructed -> acute increase in IOP
  • Pupillary block is 1’ cause of IOP, not the angle block
19
Q

what are the symptoms of acute angle closure glaucoma?

A
  • sudden onset, usually unilateral, painful red eye, LOV, BOV
  • A/w one-sided headache, N/V
  • Pt may see coloured halos/rainbows around light
  • Usually presents at night due to pupil dilation (radial muscles of the iris contract)
20
Q

what are the signs of acute angle closure glaucoma?

A
  • Eye feels firm on palpation
  • Conjunctival injection
  • Hazy cornea (corneal oedema)
  • Shallow AC (anterior chamber)
  • High IOP
  • ***Fixed, mid-dilated pupil that is unresponsive to light
21
Q

what is the pathogenesis of neovascular glaucoma?

A
  • NVG occurs as a result of aggressive iris neovascularisation (rubeosis iridis). The most common aetiological cause is severe, diffuse, and chronic retinal ischaemia
  • hypoxic retinal tissue produces angiogenic factors in an attempt to revascularize hypoxic areas; the most important of these is probably VEGF.
  • The mediators induce both retinal and anterior segment neovascularisation, the latter initially impairing aqueous outflow in the presence of an open angle, with subsequent progression to typically severe and relentless secondary synechial angle closure glaucoma (when new blood vessels develops fibrosis 🡪 then the fibrovascular tissue contracts 🡪 closes the angle).
22
Q

what are the causes of neovascular glaucoma?

A
  • Ischaemic central retinal vein occlusion (CRVO): Glaucoma typically occurs 3 months after the occlusive event (100-day glaucoma)
  • Diabetes mellitus (DM)/diabetic retinopathy: Risk of glaucoma is decreased by panretinal photocoagulation (PRP)
  • Arterial retinal vascular disease, e.g. central retinal arterial occlusion (CRAO)
  • Others: Intraocular tumours, long-standing retinal detachment (RD), chronic intraocular inflammation
23
Q

what is management of neovascular glaucoma?

A

Rubeosis iridis: PRP, intravitreal anti-VEGF, treat underlying cause

Secondary open angle glaucoma

  • Medical: IOP lowering agents, intravitreal anti-VEGF, topical steroids if significant inflammation is present
  • PRP
  • Surgical: cyclodiode (if medical IOP control not possible)

Secondary angle closure glaucoma

  • Medical as above (intravitreal anti-VEGF will not reverse established angle closure)
  • PRP
  • Surgical: cyclodiode, endocyclodiode, drainage surgery (enhanced trabeculectomy or shunt)
24
Q

beta blockers

  • examples
  • mechanism
  • c/i
  • pros
A
  • timolol
  • Decrease pdtn
    (by non-pigmented ciliary epithelium, i.e. ciliary body)
  • Asthma, bradycardia, heart block
  • cheap + efficacious = 1st line
25
Q

carbonic anhydrase inhibitors

  • examples
  • mechanism
  • c/i
  • cons
A

acetazolamide, dorzolamide

Inhibits CA which catalyses rxn that creates osmotic grad for passive flow of aqueous

C/I

  • G6PD deficiency
  • Sulfonamides allergy
  • Sickle cell anaemia
  • Severe renal impairment/ - ESRF – metabolic acidosis

cons

  • PO: LT use limited by S/E of malaise, fatigue, anorexia, depression
  • opical: S/E stinging sensation, cornea endothelium dysfunction
26
Q

prostaglandin analogues

  • examples
  • mechanism
  • pros
  • cons
A

latanoprost, travaprost

increases uvoscleral outflow + relaxes ciliary body muscle and dilates spaces between ciliary body muscle bundles

Pros: efficacious + ON dosing but more ex than BB = 2nd line

Cons (S/E)

  • conjunctival hyperaemia, burning and stinging sensation
  • increased iris + around eye pigmentation
  • eyelash growth (hypertrichosis)
27
Q

a adrenergic agonists

  • examples
  • mechanism
  • c/i
  • cons
A

brimonidine

Increases uvoscleral outflow

Young children, due to potential to cross BBB, and respiratory depression

increased incidence of allergic rxns

28
Q

miotics

  • examples
  • cons
A

physostigmine

Ocular S/E: small pupils, myopia, increased subjective visual disturbance

Eye (39 decks)

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