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Duke Elder > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

which part of the ciliary body produces aqueous humour?

A

pars plicata

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2
Q

Which branch of the ANS controls aqueous humour production?

A

sympathetic

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3
Q

Which adrenoceptors increase aqueous secretion?

A

beta 2

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4
Q

Which adrenoceptors decrease aqueous secretion?

A

alpha 2

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5
Q

Is IOP higher in the mornings or evenings?

A

mornings

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6
Q

What is the most common outflow route for aqueous?

A

trabecular outflow through the meshwork and canal of Schlemm to the episcleral veins

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7
Q

What is the less common outflow route for aqueous?

A

uveoscleral outflow through the ciliary muscle to the suprachoroidal space then drained by choroidal veins

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8
Q

How does the conc of glucose, proteins and ascorbate in aqueous compare to the serum?

A

less glucose and proteins

more ascorbate

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9
Q

By what mechanism is most aqueous secreted by the pars plicata?

A

via Na/K transporters

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10
Q

What are the three mechanisms by which aqueous is secreted by the pars plicata?

A

Na/K transporters
ultrafiltration
osmosis

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11
Q

What are the 5 layers of the ciliary body?

A 
lamina
stroma
pigment epithelium
non-pigment epithelium 
endothelium
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12
Q

Which layer of the trabecular meshwork has the highest resistance and is removed to decrease IOP?

A

juxtacircular tissue

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13
Q

Name the structures seen on gonioscopy from ant to post when the iridocorneal angle is open?

A 
Schwalbe's line
non-pigmented epithelium
pigmented epithelium 
scleral spur
ciliary body band 
iris
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14
Q

What term describes the iris adhering to more anterior structures as a result of inflammation?

A

peripheral anterior synechiae

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15
Q

What term describes the iris adhering to the lens as a result of inflammation?

A

posterior synechiae

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16
Q

What is normal intraocular pressure?

A

10-21

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17
Q

What is ocular hypertension?

A

IOP >21 with no glaucomatous changes

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18
Q

What were the findings of the ocular hypertension treatment study?

A

9.5% of patients with OHT converted to open angle glaucoma in 50 years. If you reduce IOP by 20% risk falls to 4.4.%

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19
Q

What are the risk factors for conversion of OHT to open angle glaucoma?

A

older ages
IOP >25.75
large cup to disc ration
thinner CCT

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20
Q

What is primary open angle glaucoma?

A

Visual field defect, open angle and IOP >21

21
Q

What changes are seen on fundoscopy in primary open angle glaucoma?

A

high cup to disc ratio and thinning of neuro retinal rim

22
Q

What investigation measures central corneal thickness?

A

pachymetry

23
Q

What are the two most common initial visual field defects associated with glaucoma?

A

nasal step

temporal wedge

24
Q

What conditions are associated with normal tension glaucoma?

A

Raynauds, migraines and hypotension

25
Q

What is the risk of progression of visual field defects at 5 years if normal tension glaucoma goes untreated?

A

50%

26
Q

What drugs are used in the treatment of normal tension glaucoma?

A

prostaglandin analogues

27
Q

By what mechanism do PGAs lower IOP?

A

increased uveoscleral outflow

28
Q

By what mechanism do beta blockers, carbonic anhydrase inhibitors and alpha agonists lower IOP?

A

decreased aqueous production

29
Q

What are the features of primary angle closure suspects (PACS)?

A

narrow angle, no peripheral anterior synechiae

30
Q

What are the features of primary angle closure (PAC)?

A

peripheral anterior synechiae and elevated IOP but no glaucomatous optic nerve changes

31
Q

What are the features of primary angle closure glaucoma (PACG)?

A

peripheral anterior synechiae, raised IOP, glaucomatous changes and visual field defects

32
Q

Risk factors for primary angle closure glaucoma

A

increasing age
east asian
hyperopia
short axial length

33
Q

Patient has sudden pain and headache while watching TV in a dark room. Describes haloes around lights and has vomited. Patient has fixed mid dilated pupil, raised IOP, corneal oedema and conjunctival hyperaemia

A

primary angle closure glaucoma

34
Q

What is the acute management of primary angle closure glaucoma?

A

supinate patient

give systemic acetazolamide, topical beta blockers

35
Q

What procedure should be carried out once an acute attack of primary angle closure glaucoma has resolved?

A

bilateral YAG laser peripheral iridotomy

36
Q

Patient with Alzheimers presents with secondary open angle galucoma. Flaky white deposits on anterior lens capsule, sampaolesi line and peripupillary defect on slit lamp.

A

pseudoexfoliation syndrome

37
Q

Myopic male presents with secondary open angle glaucoma. Blurred vision and haloes on exertion. There are mid-peripheral spoke-like defects of the iris and Krukenburg spindles in the corneal endothelium. There is pigmentation of the trabecular meshwork. AD condition.

A

pigment dispersion syndrome

38
Q

Patient with proliferative diabetic retinopathy presents with painful eye. Evidence of rubeosis iridis on examination. Corneal oedema and raised IOP.

A

neovascular glaucoma

39
Q

What are the management option for neovascular glaucoma?

A

panretinal photocoagualtion and/or anti-vegf
topical steroids and atropine
iop lowring agents
good visual potential- glaucoma drainage device
bad visual potential- cyclodiode laser

40
Q

what drugs should NOT be used in neovascular glaucoma?

A

pilocarpine and prostaglandin anaogues

41
Q

Recurrent unilateral acute attacks of raised IOP. Anterior chamber inflammation with white keratitic precipitates and mydriasis. Associated wth CMV, H. pylori and HLA BW5

A

Possner-Schlossman syndrome

42
Q

What lens pathology can lead to phacolytic or phacomorphic glaucoma?

A

cataract

43
Q

What is the pathogenesis of red cell glaucoma?

A

blunt trauma causes hyphaema which blocks trabecular meshwork

44
Q

What is the pathogenesis of angle recession glaucoma?

A

rupture of ciliary body following blunt trauma

45
Q

After how many days may a secondary bleed occur in red cell glaucoma?

A

3-7 days

46
Q

What type of glaucoma can be caused by vitreous haemorrhage?

A

ghost cell glaucoma

47
Q

What sort of glaucoma is associated with anterior uveitis?

A

Schwartz-Matsuo syndrome

48
Q

Baby presenting with port wine stain along CNV1/V2, seizure, ipisilateral choroidal hemangiomas and secondary open angle glaucoma.

A

Sturge-Weber syndrome

49
Q

Bilateral glaucoma in boys under 1 year. Epiphora, corneal oedema, photophobia and blepharospasm. Large eyes and increased corneal diameter. Haab striae.

A

primary congenital glaucoma

Duke Elder (8 decks)

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