Clinical CNS Eye Flashcards
Is glaucoma just elevated IOP?
No, not always
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
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
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
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
What is visual field analysis?
Computerised automated visual field analysis which is printed out
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
Name the different types of glaucoma:
Congenital vs acquired*
1º* vs 2º(due to another ocular condition)
Open angled vs closed angle
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
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
What is primary angle closure (PAC)?
Irido-corneal angle occlusion
What are the different classifications of PAC?
PACS (suspect)
PAC (established)
PACG (glaucoma)
Both acute (medical emergency) and chronic
Who does PAC normally affect?
Small hypermetropic (long sighted) eyes
What are the types of treatment for PAC?
Laser iridotomy or cataract surgery (small hole in iris so aq released)
Medicine
Glaucoma surgery
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
Name topical mydriatic (dilatory) drugs which can cause drug induced angle closure (DAC):
Topicamide
Cylopentolate
Phenylephrine
Atropine
Name nebulised drugs which can cause drug induced angle closure:
Ipatropium
Salbutamol
Ephedrine
Name oral/ IV drugs which can cause drug induced angle closure:
TCA (amitriptyline etc), SSRIs (paroxetine, citalopram)
Epinephrine
Anticholinergics (e.g oxybutinin)
Atropine
Name other drugs (very rare) which can cause drug induced angle closure:
Topiramate
Hydrchlorthiazide
Acetazolamide
Quinine
Tetracycline
Pilocarpine
Botox
OTC flu remedies
What is POAG?
Primary open angle glaucoma- most common type of glaucoma in UK
-initially asymptomatic
-usually slowly progressive
-often presents late
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
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
What are the POAG risk factors?
*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?
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
