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Ophthalmology > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What are the two structures which comprise the ciliary body?

A 
Pars plicata (anteriorly)
Para plana (posteriorly)
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2
Q

What produces aqueous humour?

A

Formed by the ciliary processes in the pars plicata

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3
Q

What three mechanisms control the secretion of aqueous humour?

A

Diffusion - concentration gradient

Ultrafiltration - pressure gradient between oncotic and hydrostatic pressures (capillary and IOP)

Active (approx. 80%) - Mediated by transmembrane aquaporin activated by Na+/K+ ATPase enzyme and carbonic anhydrase enzyme

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4
Q

Describe the neural control of aqueous humour production

A

Sympathetic (adrenergic innervation) system

B2 receptor stimulation increases secretion
A2 receptor stimulation inhibits secretion

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5
Q

What is the function of aqueous humour?

A

Supplies essential nutrients to the cornea and the lens

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6
Q

What spaces does aqueous humour occupy?

A

0.25ml in the anterior chamber and less in the posterior chamber

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7
Q

What changes occur to the anterior chamber with age?

A

Becomes shallower

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8
Q

What refraction disorder is also associated with a shallow anterior chamber?

A

Hypermetropia (far-sightedness)

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9
Q

Describe the electrolyte composition of aqueous humour

5

A

Water = >99%

Lower concentrations of protein and glucose than plasma

High concentrations of ascorbic acid and lactate

Similar concentrations of sodium

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10
Q

The aqueous humour can take what routes for outflow?

A 
Trabecular outflow (approx. 70%) 
Uveoscleral outflow
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11
Q

Describe the trabecular outflow of aqueous humour

A

Conventional route - moving through the trabecular meshwork and Schlemm’s canal to the episcleral veins

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12
Q

Describe the uveoscleral outflow of aqueous humour

A

Passes through the ciliary muscle to the suprachoroidal space and eventually drained by choroidal veins, emissary canals of the sclera (vortex veins) or veins of the ciliary body

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13
Q

What is Schlemm’s canal?

A

An endothelial lined oval canal situated circumferentially in the scleral sulcus

It contains holes for collector channels which terminate in episcleral veins

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14
Q

What are two important metrics when assessing the optic disc?

A

Neuroretinal rim

Cup to disc ratio (C/D ratio)

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15
Q

What is the neuroretinal rim?

A

Refers to the area of the optic disc, between the margins of the central cup and the disc containing retinal neuronal cells

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16
Q

Describe the thickness of the neuroretinal rim in the four quadrants

A

ISNT Rule

Thickest is inferior, then superioir, nasal and finally temporal

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17
Q

What changes to the neuroretinal rim can be seen in glaucoma?

A

Thinning

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18
Q

What is the cup to disc ratio?

A

Defined as the vertical diameter of the optic cup divided by the vertical diameter of the optic disc

Remember teacup sits on the plate

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19
Q

What is the normal C/D ratio in most people?

A

0.3 but some individuals may have physiological cupping of 0.6-0.7 without glaucomatous changes

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20
Q

What is trabeculectomy?

A

An IOP-lowering surgical technique which involves the creation of a fistula for aqueous outflow from the anterior chamber to the sub-Tenon space, creating a bleb

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21
Q

What is the sub-Tenon space?

A

A potential space superficial to Tenon’s capsule and deep to the sclera

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22
Q

Outline the use of adjuncts to a trabeculectomy?

A

Antimetabolites such as 5-fluorouracil (5-FU) or Mitomycin C both inhibit fibroblasts and prevent bleb failure

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23
Q

What is ocular hypertension?

A

Defined as raised IOP >21mmHg without glaucomatous damage

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24
Q

What is the risk of conversion from ocular hypertension to open-angle glaucoma?

A

Approx. 9.5%

This can be halved with a 20% reduction of IOP

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25
Q

List some risk factors for conversion of OHTS to POAG

A

Older age
Higher IOP
Large cup/disc ratio
A thinner CCT (central corneal thickness)

Others: African American origin, males, heart disease

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26
Q

How should ocular hypertension be managed?

A

Regular monitoring

Medical treatment in high-risk patients or patients with over 30mmHg IOP

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27
Q

What is Primary Open-Angle Glaucoma?

A

A chronic disorder characterised by glaucomatous visual field defects due to optic nerve damage

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28
Q

What gene mutations are implicated in POAG?

A

MYOC and OPTN gene mutations

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29
Q

List some features of POAG?

A

Open anterior chamber angle (39.5+/- 5.7 degrees)

Glaucomatous VF defects

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30
Q

List some investigations indicated in the case of POAG?

A

Fundoscopy: Evaluate optic disc
Gonioscopy: Assessment of angle
Pachymetry: Measure CCT
Perimetry: Visual field assessment

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31
Q

List some treatment options for POAG

A

Topical IOP-lowering agents
Laser trabeculoplasty
Trabeculectomy if failure of other treatment

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32
Q

What is normal-tension glaucoma (NTG)?

A

A condition considered to be a form of POAG with a persistently normal IOP (<21mmHg)

Investigation and management are similar to POAG

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33
Q

What is the risk of progression of NTG to POAG?

A

35% in a five-year follow-up.

Reducing IOP by 30% in NTG reduces the risk of progression to POAG to 12% over the same period

34
Q

What is gonioscopy?

A

In addition to a slit-lamp examination with the use of a goniolens to observe the iridocorneal angle

35
Q

List risk factors for developing NTG

A

Age: commonly older than patients with POAG
Race: East Asians (e.g. Japanese)
CCT: Commonly lower than POAG patients
Systemic vascular disease: E.g. Raynauds, migraines and systemic hypotension

36
Q

What is primary angle-closure glaucoma?

A

Refers to occlusion of the TM, causing obstruction of aqueous outflow and potential damage of the optic nerve from raised IOP

37
Q

What are the three components of the trabecular meshwork?

A

Uveal meshwork (innermost) - contains large holes

Corneoscleral meshwork - contains smaller holes accounting for greater resistance

Juxtacanalicular meshwork (outermost) - connects the TM with the Schlemm canals (contains narrow intercellular spaces and supplies the major part of the outflow resistance)

38
Q

PACS versus PAC versus PACG

A

PACS (primary angle-closure suspect): a narrow-angle with the peripheral iris almost touching the TM. No peripheral anterior synechiae (PAS) present

Primary angle-closure (PAC): PAS +elevated IOP. However, there are no glaucomatous changes to VFs

Primary angle-closure glaucoma: PAS +raised IOP + VF changes

39
Q

What is PAS (peripheral anterior synechiae?

A

Refers to the adherence of the peripheral iris anteriorly to the anterior chamber

40
Q

What risk factors increase the risk of developing PACG?

A 
Increasing age
East Asian race
Hypermetropia 
Family history 
Short axial length of eye
41
Q

What are the two pathophysiologies in the development of PACG?

A

Relative pupillary block (the majority of cases) - failure of normal aqueous flow causing a pressure differential in the anterior and posterior chambers leading to bowing of peripheral iris and closure of the angle (most common in the mid-dilated pupil)

Plateau iris configuration (commonly in East Asian race) due to flat iris and anteriorly positioned ciliary body

42
Q

OUtline the features of PACG

A

Sudden onset headache, vomiting, haloes and blurring or transient visual loss (symptoms exacerbated by watching TV in a dark room, pharmacological mydriasis or reading

Fixed mid-dilated pupil, corneal oedema, conjunctival hyperaemia and highly raised IOP

Resolved acute attack: Descemet membrane folds, Low IOP and glaukomflecken

43
Q

What are the five layers of the cornea?

A 
Epithelium
Bowmanns layer 
Stroma
Descemet's membrane
Endothelium
44
Q

What are glaukomflecken?

A

Glaukomflecken are grey-white epithelial and anterior cortical lens opacities that occur following an episode of markedly elevated IOP

45
Q

What is the acute management of PACG?

A

Supine position

Systemic acetazolamide

Topical beta-blockers (+/- alpha-2 agonists +/- topical prednisolone

46
Q

Following the resolution of an acute attack of PACG, what treatment options are there?

A

YAG laser iridotomies

Cataract extraction has been shown to be effective in lowering IOP in both acute and chronic

47
Q

What is NVG?

A

Neovascular glaucoma - a cause of either open or closed angle secondary glaucoma

48
Q

What is the pathophysiology of NVG?

A

Proliferation of fibrovascular tissue in the anterior angle and results from rubeosis iridis

49
Q

List the potential causes of NVG

A 
Ischaemic CRVO ('100 day glaucoma'
CRAO
DM
Ocular ischaemic syndrome
Retinal detachment
50
Q

How does ischaemia lead to NVG?

A

Hypoxia in retinal cells causes release of VEGF and IL-6 causing neovasculaisation in the anterior chamber

51
Q

What are the clinical features of NVG?

A

New radially orientated vessels on iris surface and pupillary margins

Peripheral anterior synechaie and posterior synechiae form

Corneal oedema and elevated IOP

52
Q

How is NVG managed?

A

PRP and IV anti-VEGF

Medical treatment same as POAG (avoid miotics, osmotic agents for corneal oedema)

53
Q

Outline surgical treatment options and their indications in NVG

A

If good visual prognosis - glaucoma drainage device (tube)

If bad visual prognosis - cyclodiode laser to destroy ciliary epithelium

Trabeculectomy often results in bleb failure due to scarring

54
Q

What is pigment dispersion syndrome?

A

An AD-inherited cause of secondary OAG characterised by excessive shedding of pigmented material of the iris and deposited throughout the anterior segment

55
Q

What demographic is pigment dispersion syndrome most commonly seen in?

A

Myopic males

56
Q

What are the features of pigment dispersion syndrome?

A

Blurred vision and haloes on exertion

Mid-peripheral spoke-like defects of the iris on transillumination

Increased IOP and glaucomatous change

Vertical, oval-shaped pigments on corneal endothelium (Krunkenberg spindles)

Concave peripheral iris

Sampaolesi line may be present

57
Q

What is a Sampaolesi line?

A

A band of pigment anterior to the Schwalbe line on gionioscopy

58
Q

How is pigment dispersion syndrome treated?

A

Avoid exercise

Medical treatment similar to POAG (prostaglandin analogues)

Pilocarpine is prophylactic

Laser trabeculoplasty or trabeculectomy

59
Q

What is pseudoexfoliation syndrome?

A

A cause of secondary OAG in which grey-white fibrillar deposits block the anterior chamber angle

60
Q

What mutation is associated with pseudo exfoliation syndrome?

A

LOXL1 (enzyme contributing to elastin formation)

61
Q

What associations are there with pseudo exfoliation syndrome?

A

Hearing loss

Alzheimer’s disease

High plasma homocysteine

Low folate intake

62
Q

What demographic is most likely to present with pseudo exfoliation syndrome?

A

Scandinavians, females, age >50

63
Q

What is Posner-Scholssman Syndrome?

A

A rare disorder characterised by unilateral acute attacks of IOP elevation and may cause secondary OAG

64
Q

What associations are there with Posner-Schlossman Syndrome?

A

CMV, H. pylori and HLA-BW5

65
Q

What are the features of Posner-Schlossman Syndrome?

A

Discomfort, haloes and blurred vision

Anterior chamber inflammation

Mydriasis

66
Q

What is the treatment for Posner-Schlossman Syndrome?

A

Topical steroids and IOP-lowering agents

67
Q

What is phacolytic glaucoma?

A

A secondary OAG caused by trabecularr obstruction due to leakage of the lens protein from a hyper mature cataract

68
Q

What are the features of phacolytic glaucoma?

A

Painful red eye with photophobia and decreased vision

Corneal oedema, mature cataract and white particles in the anterior chamber

69
Q

What is phacomorphic glaucoma?

A

An acute secondary angle closure glaucoma due to swelling of a cataractous lens potentiating a pupillary block

70
Q

What is red cell glaucoma?

A

A hyphema can cause blockage of the TM leading to raised IOP and 2ary OAG

Beware of rebleed 3-7d post-initial injury

71
Q

What is ghost cell glaucoma?

A

A type of 2ary OAG occurring 2-4w after a vitreous haemorrhage due to TM obstruction with red blood cells

72
Q

What is angle recession glaucoma?

A

A cause of chronic 2ary OAG due to ciliary body rupture caused by blunt trauma

73
Q

What findings are seen in angle recession glaucoma?

A

Gionioscopy shows irregular widening of the ciliary body face

74
Q

What is the risk of angle recession glaucoma after traumatic incident?

A

10% after 10 years

75
Q

What is Sturge-Weber Syndrome?

A

A congenital neuro-oculocutaneous disorder that can cause secondary OAG

76
Q

What is the pathophysiology of Sturge-Weber Glaucoma?

A

AC angle malformation (causing glaucoma in first year of life) or increased episcleral venous pressure (causes later onset of glaucoma)

77
Q

What is the treatment of Sturge-Weber Syndrome?

A

Early-onset: goniotomy and trabeculectomy or combined trabeculectomy/trabeculotomy

Late-onset: medical treatment followed by trabeculectomy

78
Q

What is primary congenital glaucoma?

A

A rare, bilateral condition due to malformation of the AC chamber angle that occurs in the first year of life

79
Q

Outline the epidemiology of PCG

A

More common in boys

Mostly sporadic but can be AR

Prevalence higher in patients with CYP1B1 gene

80
Q

What are the features of PCG?

A

Photophobia, epiphora and blepharospasm
Corneal oedema
Large corneal diameter
Buphthalmos (large eyes due to elevated IOP)
Haab striae (healed breaks in the Descement membrane due to oedema, best seen on retroillumination)

81
Q

What are the investigations of PCG?

A

IOP measurement (normal newborn between 10-12mmHg)

Optic disc evaluation for cupping (look for asymmetry or ration >0.3)

82
Q

What is the management of PCG?

A

Angle surgery:

Goniotomy if the cornea is clear

Trabeculotomy if cloudy cornea

Ophthalmology (7 decks)

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