Ophthalmology - Gradual Vision Loss (Open Angle Glaucoma, ARMD and Cataracts) Flashcards
What is the pathophysiology of Open Angle Glaucoma (AOG)?
-Gradual increase in resistant through trabecular meshwork - more difficult for aqueous humour to exit the eye.
What are risk factors for OAG?
- Increase age
- Family Hx (screen from age 40 if have 1st degree affected relative)
- Black ethnic origin
- Nearsightedness (myopia)
What is the PC (sx) of OAG?
- Usually diagnosed at routine optometry screening
- Peripheral vision affected first, gradually turns into tunnel vision
- Visual acuity is maintained until late stages
- Gradual onset of fluctuating pain, headaches, blurred vision and halos around light (night time)
What investigations should you perform on a patient with suspected OAG?
Measure intraocular pressure
- Non-contact tonometry: ‘puff of air’ blown at cornea (less accurate)
- Goldman applanation tonometry: gold standard, applies different pressures to cornea to measure IOP (must have been calibrated for corneal thickness)
Other
- Corneal thickness measurement
- Fundoscopy: check for optic disc cupping (>0.5 of optic disc is bad)
- Visual field assessment: peripheral vision loss
How do you manage OAG?
-Treat a IOP of 24mmHg and above
Medication
- 1st line: Prostaglandin analogue (latonoprost) increases uveoscleral flow (increases drainage from ant chamber to iridocorneal angle) but SEs are eyelash growth, eyelid pigmentation and iris pigmentation
- Beta Blockers: timolol reduces production of aqueous humour
- Carbonic anhydrase inhibitors: dorzolamide reduces production of aqueous humour
- Sympathomimetics: bromonidine reduces production of aqueous humour and increases uveoscleral flow
How do you manage OAG if medications are not effective?
-Trabeculectomy: creation of new canal from anterior chamber, through sclera to location under conjunctiva, where aqueous humour drained and is then reabsorbed into general circulation
What is age-related macular degeneration (ARMD)?
- Degeneration of the macula that causes progressive deterioration in vision
- Dry: 90% of cases, Drusen (yellow deposits of proteins and lipids) appear between the retinal pigment epithelium and Bruch’s membrane (common to both wet and dry) + degeneration of macula
- Wet: 10% of cases and worst prognosis, neovascularisation growing from choroid layer into the retina. These vessels leak fluid/blood and cause oedema (more rapid loss of vision)
Common features
- Atrophy of retinal pigment epithelium
- Degeneration of photoreceptors
What are some risk factors for ARMD?
-Age -Smoking -White/Chinese origin -FHX -CVS disease
How will a patient with ARMD present?
-Gradually worsening central visual field loss (bilateral usually)
-Reduced visual acuity (esp near field objects)
-Crooked or wave appearance of straight lines
-Fluctutations in visual disturbance which vary significantly from day to day
*Wet ARMD will present more acutely and often progresses to full loss of vision over 2-3 years.
What type of ARMD is this?
What type of ARMD is this?
What investigations will you perform on someone with suspected ARMD?
- Snellen chart: reduced visual acuity
- Fields of vision: scotoma
- Amsler grid test: distortion of straight lines
- Fundoscopy: Drusen visible
- Optical coherence tomography (1st line for wet ARMD) - shows cross sectional view of layers of retinal
- Fluorescein angiography (2nd line if OCT doesn’t confirm wet ARMD) - looks at blood supply to retina and will show any oedema and neovascularisation
How to you manage dry ARMD?
- No specific treatment for dry ARMD
- Management is focused on lifestyle: no smoking, controlled BP, vitamins supplementation
How to you manage wet ARMD?
- Anti VEGF medications injected into vitreous chamber every month
- Eg: ranibizumab, bevacizumab - slow and even reverse progression of disease
- Must be started within 3 months to be beneficial
What are cataracts? Name some causes of congenital catarcts
- Lens of the eye becomes cloudy and opaque - reduces visual acuity by reducing the light that reaches the retina.
- Must cataracts develop with advanced age but you can also have congenital cataracts (idiopathic, rubella, Wilson’s disease/Galactoseamia
