Clinical CNS Eye Flashcards by Ambra Copping

Is glaucoma just elevated IOP?

No, not always

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What is glaucoma?

An irreversible, progressive disease of the optic nerve associated with characteristic optic nerve head changes and visual field defects, which untreated results in tunnel vision and eventually blindness

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What is the lamina cribosa?

1-2mm in diameter
Supporting structure, holes in this structure allows axons of retinal ganglion cells to exit the eye

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Describe the optic nerve head:

Where the optic nerve exits the eye via the lamina cribs
There are no photoreceptors here
AKA optic disc is the cause for the normal ‘blind spot’
Where BVs enter and exit the eye

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What occurs if there is damage to the optic nerve head?

May relay to an area of retinal ganglion cells, create a visual field defect:
-superior compared to inferior damage
-damage to superior fibre leads to large area of damage so defect on inferior
-progression of disease, an arcuate area e.g inferior which is associated with arcuate superior
Can then join up to form a common arc

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What is visual field analysis?

Computerised automated visual field analysis which is printed out

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What does the optic disc look like normally compared to a person who has glaucoma?

Normal- small pale depression in the middle
Glaucoma- enlarged hole and brighter; the nerve tissue has become damaged and disappeared, increased cup, decreasing rim

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Name the different types of glaucoma:

Congenital vs acquired*
1º* vs 2º(due to another ocular condition)
Open angled vs closed angle

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What is closed angle glaucoma?

Drainage angle between cornea and iris
Usually due to pupil block
Edge of iris rests on lens, causes relative block of flow of aqueous from posterior to anterior chamber so increases pressure in posterior, pushes iris forward so no fluid to exit and increase pressure

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What are the normal values for IOP?

Mean= 16mmHg
SD= 2.5
Range= 11-21
Non gaussian, skewed to high so normal around 11-24

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What is primary angle closure (PAC)?

Irido-corneal angle occlusion

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What are the different classifications of PAC?

PACS (suspect)
PAC (established)
PACG (glaucoma)
Both acute (medical emergency) and chronic

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Who does PAC normally affect?

Small hypermetropic (long sighted) eyes

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What are the types of treatment for PAC?

Laser iridotomy or cataract surgery (small hole in iris so aq released)
Medicine
Glaucoma surgery

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What are the symptoms of acute angle closure (AAC)?

Painful red eye
Blurred vision/ haloes
N&V
Mid-dilated pupil
Cloudy cornea
Shallow anterior chamber
Elevated IOP
Closed angle at gonioscopy
Glaukomflecken (small white pasties on front of lens)
Other eye PAC(s)
Cataracts

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Name topical mydriatic (dilatory) drugs which can cause drug induced angle closure (DAC):

Topicamide
Cylopentolate
Phenylephrine
Atropine

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Name nebulised drugs which can cause drug induced angle closure:

Ipatropium
Salbutamol
Ephedrine

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Name oral/ IV drugs which can cause drug induced angle closure:

TCA (amitriptyline etc), SSRIs (paroxetine, citalopram)
Epinephrine
Anticholinergics (e.g oxybutinin)
Atropine

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Name other drugs (very rare) which can cause drug induced angle closure:

Topiramate
Hydrchlorthiazide
Acetazolamide
Quinine
Tetracycline
Pilocarpine
Botox
OTC flu remedies

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What is POAG?

Primary open angle glaucoma- most common type of glaucoma in UK
-initially asymptomatic
-usually slowly progressive
-often presents late

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Describe the epidemiology of POAG:

67 mill cases worldwide (10% blind)
In caucasian population:
-1% at 50yrs
-4% at 80yrs
-15% at over 80 yrs
For each 1-2 diagnosed another is undiagnosed

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What is the aetiology of POAG?

Poorly understood
Most freq associated with raised IOP
Multifactorial pathogenesis:
-mechanical- movement of laminal cribosa- direct trauma to retinal ganglion
-ischaemic- problems at optic nerve head

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What are the POAG risk factors?

Study These Flashcards

*IOP
Age
Genetics/FH (4x increase)
Myopia (short sighted)
Type of optic nerve head
Vascular/ haematological
Neurogenic

What is the value for high IOP in POAG?

Study These Flashcards

Around more than than 30mmHg

What are the problems with using IOP as a screening device for glaucoma?

Some patients have glaucoma with normal eye pressure (normal tension glaucoma) Some patients have elevated eye pressure but no glaucomatous damage (ocular hypertension)

What is involved in the screening of glaucoma in the community?

Optic nerve head examination/imaging Visual field testing Risk factor assessment: -IOP -central corneal thickness -FH -Other e.g CVD Slit lamp examination and gonioscopy (see corneal angle)

What is a natural product that people may wish to take but has no evidence for glaucoma?

Ginkgo biloba

What is the MOA of topical eye drops for glaucoma?

Decrease production of aq Increase outflow of aq -conventional route -uveo-scleral outflow

Name topical anti-glaucoma therapy:

PG analogues BBs Carbonic anhydrase inhibitors (CAIs) Alpha agonists

How do PG analogues work?

Increase uveoscleral outflow (and smaller effect on conventional outflow) Most potent ocular hypotensives (all OD at night)

Name systemic SEs of PG analogues:

Rare: Brittle asthma worse Can induce possible labour

Name ocular SEs of PG analogues:

Common: Lash growth Iris pigmentation Periocular skin darkening Conjunctival infection (red eye) Orbital fat atrophy Post op cystoid macular oedema

Name examples of PG analogues:

Latanoprost 0.005% Travoprost 0.004% Bimatoprost 0.01% Tafluprost 0.0015%

Describe latanoprost:

Xalatan or non-proprietary/ generic The first PG to be used Monoprost (PF) SDU

Describe travoprost:

Travatan Long term storage unrefrigerated Well tolerated Now PQ1 preserved

Describe bimatoprost:

May act as a prostamide and PG Possibly most potent May work when others fail but less well tolerated Lumigan (P or PF 0.03% SDU) Eyreida (PF 0.03% bottled)

Describe tafluprost:

First PG available PF Very well tolerated Saflutan

How do BBs work for glaucoma?

Decrease aq production (BD or OD) If OD, apply drop in morning to avoid nocturnal hypotensive dips and reduced optic disc perfusion Generally well tolerated Good/moderate efficacy Can get non-selective or cardio selective All P or PF

What are the SEs of topical BBs?

Asthma/ breathlessness Bradycardia Tiredness Depression ED Hypotension Angina

Name examples of topical BBs:

Timolol (0.1,0.25,0.5%) Levobunolol 0.5% Betaxolol (0.25, 0.5%) Carteolol

Describe timolol:

Non-selective Non-proprietary Timoptol (SDU/bottle/gel OD) Nyogel 0.1% gel OD

Describe Levobunolol:

Non-selective Non-proprietary Betagan bottle/SDU

Describe Betaxolol:

Cardio-selective Less efficacious of others Betopic Betopic-S SDU

Describe carteolol:

Non selective Intrinsic sympathomimetic activity, helps with SEs

How do CAIs work?

Decrease production of aq Least potent ocular hypotensives, few SEs TDS (BD if used in combo with other drops)

What are the CI of CAIs?

Sulphonamide sensitivity

Name examples of CAIs:

Dorzolamide 2% Brinzolamide 10mg/ml Acetazolamide- not recommended for long term, not an eye drop

Describe dorzolamide:

Trusopt (solution) or non-proprietary Trusopt (SDU) Eydelto (PF bottled) Stings upon intimation

Describe brinzolamide:

Azopt (suspension) or non-proprietary Oily drop, leaves deposits but doesn't sting

Name examples of alpha agonists:

Brimonidine 0.2% BD Apraclonidine 0.5, 1% BD

What are the interactions with alpha agonists?

Avoid concomitant use of antidepressants (MAOIs and TCA)

Describe brimonidine:

Alphagon SEs: Allergy, taste perversion, CNS effects e.g nightmares

Describe apraclonidine:

Iopidine 0.5% Iopidine SDU 1% Only recommended for short term use e.g laser procedure to prevent post laser spikes

Name different laser surgery for glaucoma:

Selective laser trabeculoplasty Cyclodiode laser therapy

Describe selective laser trabeculoplasty:

Improved aq drainage Better at lowering IOP than topical and better accepted by patients, cost effective

Describe cyclodiode laser therapy:

Decreases aq production More used last resort

Clinical CNS Eye Flashcards

(56 cards)