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Duke Elder Exam Prep COPY > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What is the ciliary body made from?

A

Pars plicata anteriorly

Pars plana posteriorly

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2
Q

How is the aqueous humour formed?

A

Formed by the ciliary proves in the pars plicata - there are three mechanisms of secretion:

1) diffusion
2) ultrafiltration
3) active - this is 80% of the secretion mediated by transmembrane aquaporin and activated by the Na+/K+ ATPase enzyme

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3
Q

What is the function of aqueous humour?

A

To supply essential nutrients to the cornea and lens

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4
Q

What is the composition of aqueous humour?

A 
Fills the anterior chamber and posterior chamber
Composition:
Water
protein & glucose (plasma)
Sodium (same as plasma)
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5
Q

What direaction does aqueous humour flow?

A

Posterior to anterior

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6
Q

What are the two routes the aqueous humour can travel?

A

Trabecular outflow - through the trabecular meshwork and into Schlemm’s’ canal
Uveoscleral outflow - passes through the ciliary muscle into the suprachoroidal space and eventually drains via the choroidal veins of the sclera and ciliary body.

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7
Q

What are the three parts of the trabecular meshwork?

A

Uveal meshwork
Corneoscleral meshwork
Juxtacanalicular meshwork

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8
Q

What is Schlemm’s canal?

A

This is an endothelial lined canal situated circumferentially in the scleral sulcus which contains holes for collector channels which then terminate in the episcleral veins.

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9
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
Normal - 0.3
Some patients may have physiological cupping with a ratio of 0.6/0.7 and no glaucomatous changes

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10
Q

Define the neuroretinal rim:

A

this is the area of the optic disc which is between the margins of the central cup and the disc, containing retinal neuronal cells.

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11
Q

Where does thinning occur first in glaucomatous changes?

A

The neuroretinal rim

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12
Q

What are the thickest to thinnest areas of the neuroretina rim?

A 
Inferiorly
Superiorly
Nasally
Temporally 
(ISNT rule)
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13
Q

What is a trabeculotomy and when might it be used?

A

Its an IOP lowering surgery so can be used in raised IOP

Involves the creation of a fistula for aqueous outflow from the anterior chamber to the sup-Tenon space creating a bleb

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14
Q

What adjunctive antimetabolites can be used alongside a trabeculotomy to prevent bleb failure?

A

5-fluorouracil - a pyrimidine analogue which inhibits fibroblasts by blocking DNA synthesis
Mitomycin - an alkylating agent which also inhibits fibroblasts

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15
Q

Define ocular hypertension:

A

This is a raised IOP >21mmHg without any glaucomatous damage.

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16
Q

What is a risk associated with untreated ocular hypertension:

A

open angle glaucoma

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17
Q

What are some of the risk factors for ocular hypertension converting to open angle glaucoma?

A

Older age
higher IOP
Large cup/disc ratio
A thinner CCT (<555um CCT is 3.4x more likely to convert)
(Less significant risks African American, male, heart disease PMH)

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18
Q

When is medical management indicated in raised IOP?

A

When the IOP is >30mmHg or if patient’s are high risk

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19
Q

What gene mutations are linked with primary open angle glaucoma?

A

MYOC and OPTN

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20
Q

What is primary open angle glaucoma?

A

This is a chronic condition characterised by glaucomatous visual field defects due to optic nerve damage

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21
Q

What are the main features of primary open angle glaucoma?

A

open anterior chamber angle
high cup disc ratio with thinning of the neuroretinal rim
IOP raised >21mmHg
Glaucomatous VF defects (e.g. nasal step, temporal wedge etc defects)

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22
Q

How is primary open angle glaucoma investigated?

A

Visual field test
fundoscopy - optic disc cupping (cup/disc ratio increased)
Gonioscopy - decides if angle open or closed
pachymetry - measures the CCT (thicker can give higher iop than is accurate)

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23
Q

How is primary open angle glaucoma managed?

A

Topical IOP lower agents e.g. beta blockers or prostaglandin analogues
Laser trabeculoplasty
Trabeculotomy (if all else fails)

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24
Q

What is normal tension glaucoma?

A

This is a type of primary open angle glaucoma where the IOP remains <21mmHg however the investigations and management are relatively the same is primary open angle, as studies have shown lowering the IOP further (by 30%) will reduce the risk of progression.

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25
Q

What are some risk factors for developing normal tension glaucoma?

A

Older age (than primary open angle)
Race - East Asian
CCT - lower
Systemic disease e.g. Raynaud, migraines, hypotension

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26
Q

What features of tension glaucoma are different to primary open angle?

A

Optic nerve head is larger in patients with normal tension

Flame shaped haemorrhages on optic nerve are more common in NTG

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27
Q

In primary angle-closure glaucoma, what does angle closure mean?

A

this is when the trabecular meshwork becomes occluded and aqueous flow is obstructed, causing a rise in IOP and optic nerve damage

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28
Q

What is PACS?

A

This is primary angle closure suspects - it is a narrow angle in the peripheral iris almost toughing the trabecular meshwork but there is no peripheral anterior synechiae in the anterior chamber

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29
Q

What is peripheral anterior synechiae?

A

This is when the peripheral iris adheres to the anterior chamber’s angle

30
Q

What is the difference between primary angle closure and primary angle closure glaucoma?

A

The primary angle closure = raised IOP with peripheral anterior synechiae but no glaucomatous changes or visual field defects, if there was changes and defects, it would then be a fully fledged primary closed angle glaucoma

31
Q

What are some risk factors for developing a primary closed angle glaucoma?

A 
Age
Race - east Asian
Hypermetropia
Family history
Short axial length of eye
32
Q

What is the main cause of primary closed angle glaucoma?

A

Relative pupillary block. this is failure of the normal aqueous flow through the pupil, leading to an increase in the pressure differences in anterior and posterior chambers, resulting in the anterior bowing of the iris leading to angle closure

33
Q

Apart from relative pupillary block, what else can cause primary closed angle glaucoma?

A

Plateau iris configuration: an important pathophysiological mechanism relative to eastern Asian descent. Th iris is flat, with a normal anterior chamber depth and anteriorly positioned ciliary processes. This displaces the iris base, leading a narrow and potentially close angle

34
Q

What are the clinical features of a primary angle closure glaucoma?

A 
Sudden onset on pain, headache, vomiting, haloes nd blurring or transient vision loss
Fixed mid dilated pupil
Corneal oedema
conjunctival hyperaemia
Highly raised IOP
35
Q

How is primary angle closure glaucoma managed

A

Acutely - supine position, systemic acetazolamide, topical beta blocker +/- alpha-2-agonists and topical prednisolone
Bilateral peripheral Nd:YAG laser iridotomies to be performed after resolution of an acute attack
Cataract extraction has shown to be effective in lowering your IOP in both acute and chronic stages

36
Q

Define neovascular glaucoma:

A

This is a secondary cause of either open or closed angle glaucoma which occurs when here is proliferation of the fibrovascular tissue in the anterior angle which leads to rubeosis iridis.

37
Q

Give some causes of neovascular glaucoma:

A 
Ischaemic central retinal vein occlusion
Central retinal artery occlusion
Diabetes mellites
Ocular ischaemic syndrome
Retinal detachment
38
Q

What is the pathophysiology of neovascular glaucoma?

A

Retinal ischemia which leads t hypoxia of the retinal cells causes a release in angiogenic factors such as VEGF and IL-6
This results in the neovascularisation of the anterior segment and subsequent overlying fibrovascular membrane formation

39
Q

What are some features of neovascular glaucoma?

A

New radially orientated vessels on the iris surface and pupillary margins
PAS and posterior synechiae may form
Corneal oedema
Raised IOP with open angle which may progress

40
Q

How is neovascular glaucoma investigated?

A

Establish the cause of retinal ischaemia

41
Q

How is neovascular glaucoma treated?

A

Panretinal photocoagulation (PRP)
+/- anti-VEGF injections
Avoid mitotic agents as they can worsen the synechial angle closure
Use prostaglandin analogues carefully because they may exacerbate ocular inflammation
Osmotic agents can be used for corneal oedema
Surgery
- if there is good visual prognosis - drain glaucoma
- if there is bad visual prognosis - cyclodiode laser
Trabeculotomy can often result in bleb failure due to scarring

42
Q

What is an autosomal dominant condition than can cause secondary open angle glaucoma and is characterised by excessive shedding of pigment material of the iris throughout the anterior segment?

A

pigment dispersion syndrome

43
Q

What group of patients is pigment dispersion syndrome commonly seen in?

A

Myopic males

44
Q

What are some features of pigment dispersion syndrome?

A

Blurred vision and haloes on exertion
Raised IOP and glaucomatous damage
TM pigmentation
concave peripheral iris
Sampaolesi line
Vertical oval shaped pigments on the corneal endothelium
Mid peripheral, spoke like defects, of the iris seen on transillumination

45
Q

How is pigment dispersion syndrome managed?

A

Avoid extraneous exercise
Medical treatment similar to POAG (prostaglandin analogues preferred)
Pilocarpine - prophylaxis for exercise induced raised IOP
Laser trabeculoplasty
Trabeculotomy

46
Q

Why should pilocarpine be used cautiously in pigment dispersion syndrome?

A

Miotics in general can lead to myopia induction which increases the risk of retinal detachment

47
Q

What secondary cause of open angle glaucoma causes grey-white fibrillar deposits that block the anterior chamber?

A

Pseudoexfoliation syndrome

48
Q

What gene mutation is commonly associated with Pseudoexfoliation syndrome?

A

LOXL1

49
Q

What patient demographic are more likely to suffer from Pseudoexfoliation syndrome?

A

Scandinavian
Female
>50y/o

50
Q

What are some associations with Pseudoexfoliation syndrome?

A

Hearing loss
Alzheimer’s
High plasma homocysteine levels
Low folate intake

51
Q

What are some features of Pseudoexfoliation syndrome?

A

Increased IOP
Flaky white deposits on the anterior lens capsule
Sampaolesi lines
peripapillary defect on transillumination with a slit lamp

52
Q

What is the name of a rare disorder which is characterised by recurrent unilateral attacks of IOP elevation, and is a secondary cause of open angle glaucoma?

A

Posner-Schlossman syndrome

53
Q

What other things is Posner-Schlossman syndrome associated with besides elevated IOP?

A

HLA-BW5
Helicobacter pylori infections
CMV

54
Q

What are some features of Posner-Schlossman syndrome ?

A

Discomfort haloes and blurred vision
Anterior chamber inflammation
Mydriasis

55
Q

How is Posner-Schlossman syndrome managed?

A

Topical steroids and IOP lowering agents

56
Q

Define phacolytic glaucoma?

A

Secondary open angle glaucoma caused by trabecular obstruction due to leakage of lens proteins from a hypermature cataract

57
Q

What are some features of phacolytic glaucoma?

A

Painful red eye with photophobia and decreased vision
Corneal oedema
Mature cataract
White particles in the anterior chamber due to inflammatory response against the lens protein

58
Q

How is a phacolytic glaucoma managed?

A

Topical or systemic IOP lowering agents

Cataract extraction is definitive

59
Q

What is a secondary cause of angle closure glaucoma following the swelling of a cataractous lens, leading to pupillary block?

A

Phacomorphic glaucoma

60
Q

How is Phacomorphic glaucoma managed?

A

IOP reduction

Cataract extraction

61
Q

Define red cell glaucoma:

A

This is the formation of a hyphema (collection of blood in the anterior chamber) which leads to blockage of the tm, causing raised IOP and secondary open angle glaucoma

62
Q

What can cause a hyphema to form?

A

Blunt force trauma usually

63
Q

This is a type of secondary open angle glaucoma which occurs 2-4 weeks after vitreous haemorrhage, due to TM obstruction with red blood cells

A

Ghost cell glaucoma

64
Q

A congenital, neuro-oculocutaneous disorder which can cause secondary open-angle glaucoma:

A

Sturge-Weber syndrome

65
Q

What is the pathophysiology behind glaucoma formation in Sturge-Weber syndrome?

A

Anterior chamber angle malformation leading to early onset glaucoma during first year of life
OR
Increased episcleral venous pressure causing later life onset glaucoma

66
Q

What are some features of Sturge-Weber syndrome:

A

Port wine stain, typically along CNV1 or CNV2
Neurological; seizures and learning disability
Ocular - choroidal haemangiomas, glaucoma ipsilateral to the cutaneous lesion

67
Q

How is Sturge-Weber syndrome managed

A

Early onset glaucoma: goniotomy or trabeculotomy

Late onset: medical therapy first, then trabeculotomy

68
Q

This is a rare bilateral condition causing glaucoma, which is due to the malformation of the anterior chamber angle, occurring in the first year of life:

A

Primary congenital glaucoma

69
Q

What is the epidemiology of Primary congenital glaucoma?

A

Boys>girls
Sporadic but can be AR
Higher in patients with the CYP1B1 gene

70
Q

How is Primary congenital glaucoma managed?

A

Surgery - goniotomy if cornea clear, trabeculotomy is cornea is cloudy

71
Q

What are the appropriate investigations for Primary congenital glaucoma?

A

IOP measurement
Optic disc evaluation
Corneal diameter measurement

72
Q

What are some features of Primary congenital glaucoma?

A

Photophobia
Epiphora
Blepharospasm
Corneal oedema, large corneal diameter, haab straie, and buphthalmos (large eyes due to >IOP)

Duke Elder Exam Prep COPY (18 decks)

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