Lecture 30+31 Glaucoma, Cataracts, AMD, Diabetic retinopathy Flashcards
What is the fxn of the macula, layers?
responsible for central vision that allows us to see fine details clearly - helps you perform tasks such as reading, driving, recognizing faces
this area has highest density of cones in retina - cones responsible for detecting colour and visual acuity
this also contains a pigment that helps with clarity and contrast
Layers: Photoreceptors - detects light and converts into electrical signals
Retinal Pigment Epithelium (RPE) - plays role in health fxn including absorbing excess light, transporting nutrients and removing waste
Bruch’s Membrane - located between the RPE and capillaries, provides structural support and maintains health
Choroid and Capillaries - provides blood supply
What are age-related macular degeneration, risk fx, early sx, sx?
is a progressive chronic disease that affects the macula of an aging eye, cause unknown
Risk Fx: age (strongest factor), smoking or heavy alcohol use, poor diet, sunlight exposure, CV diseases, FHx
Early Sx: visual distortions (straight lines seem bent), need for brighter light when reading/working, trouble adapting to low light (such as when entering dim room), blurriness of printed words, reduced intensity/brightness of colours, difficulty recognizing faces
Sx: metamorphopsia, decreased vision
What are classifications of age-related macular degeneration?
four main stages,,, 1. Mild Dry AMD: small accumulation of drusen (waste product and proteins), may be no sx or mild vision changes
Moderate Dry AMD: accumulation of larger drusen, may be some noticeable vision changes such as blurriness or difficulty seeing in low light
Severe Dry AMD: geographic atrophy (scarring) of retinal pigment epithelium, significant vision loss including difficulty in reading, recognizing faces and performing daily activities
Wet AMD: neovascularization (abnormal blood vessel growth) leading to bleeding, significant vision loss and if left untreated, can lead to blindness
What is the management of dry AMDs?
cannot cure mild/moderate/severe, can only slow down progression
Mild: manage modifiable risk fx - smoking cessation, CV risk fx
Moderate-Severe: manage modifiable risk fx, consider AREDS supplementation to delay progression, Macumira - requires larger sample size in study but shows promising results
AREDS: contains antioxidant vitamins and minerals (ex. Vitalux or PreserVision), MOA unclear, evidence suggests benefit in moderate-severe and wet
if person is a smoker ⇒ avoid any supplementation that has beta-carotene as it increases risk of developing lung cancer (newest Vitalux do not have it), beware of ocular multivitamins as no evidence of benefit ⇒ stick with AREDS or ADREDS2
What is the management of wet AMDs?
treated by preventing more growth of abnormal blood vessels and reducing any accumulated blood/fluid
management generally handled by ophthalmologist as these are more severe cases
Options: manage modifiable risk fx, AREDS supplementation, anti-vascular endothelial growth factor (anti-VEGF) antibody intravitreal injections
ophthalmologists will be involved for these injections when disease progresses to a certain point
Anti Vascular Endothelial Growth Factor (Anti-VEGF): ranibizumab (Lucentis) - covered, bevacizumab (Avastin) - not covered ⇒ MOA: inhibits human vascular endothelial growth factor A, prevents angiogenesis by reducing 1. endothelial cell proliferation, 2. vascular leakage, 3. new vessel formation
What is glaucoma, classifications, anatomy of anterior chamber?
Def: irreversible, progressive damage to optic nerve resulting in loss of peripheral vision, unknown direct cause
Class: PRIMARY - Mechanical Theory: compression of axons due to increased intraocular pressure (IOP)
Vascular Theory: reduced blood flow to optic nerve leads to damage
could be combo of mechanical and vascular theories
Genetics: some people more susceptible
SECONDARY - Trauma: certain injuries
Meds: various meds can increase risk such as corticosteroids
Med Conditions: DM, HTN, hypothyroidism may increase risk
Anatomy: OPEN ANGLE- slow and progressive, no sx until late stages, needs to be monitored regularly if found by optometrist
CLOSED ANGLE - always acute and pt has extremely high intraocular pressure (IOP), Sx: painful red eye, blurry vision, H/A, N/V
med emergency, needs to see optometrist immediately
What is tx for open angle glaucoma (all meds, principle)?
is chronic and tx is lifelong, optometrist and ophthalmologist will re-evaluate tx, surgery required if poor compliance to meds or poor control with meds alone
Tx: 1. prostaglandins, 2. BBs, 3. alpha agonists, 4. carbonic anhydrase inhibitors, 5. miotic,
surgery is option if its not controlled sufficiently, could involve adding a stent to create a new drainage pathway
Prostaglandins for tx of open angle glaucoma (drugs, MOA, dose, AE)
Drugs: Latanoprost (Xalatan/Monoprost), bimatoprost (Lumigan), Travoprost (Travatan), Latanoprostene bunod (Vyzulta)
MOA: increases uveoscleral outflow
Dose: generally 1 drop into affected eyes QHS
AE: foreign body sensation or stinging/burning of eyes, change colour of eye, lengthen eyelashes, orbital darkening
generally first line due to ease of admin frequency and less systemic AEs
BBs for tx of open angle glaucoma (drugs, MOA, dose, AE)
Drugs: timolol, betaxolol (Betoptic S),, MOA: decrease aqueous production
Dose: generally 1 drop into affected eyes QHS but can be given BID based on control of condition,, AE: burning or stinging of eyes,,, can be prescribed first line based on pt fx
Alpha agonists for tx of open angle glaucoma (drugs, MOA, dose, AE)
Drugs: ex. brimonidine
MOA: reduces aqueous production and increases uveoscleral outflow
Dose: generally 1 drop into affected eyes BID
AE: burning of eyes, visual disturbances
generally second line
Carbonic anhydrase inhibitors for tx of open angle glaucoma (drugs, MOA, dose, AE)
Drugs: ex. brinzolamide (Cosopt), dorzolamide (Trusopt)
MOA: reduces aqueous secretion
Dose: generally 1 drop into affected eye TID
AE: dysgeusia (altered taste) or blurred vision
generally second line
Miotics for tx of open angle glaucoma (drugs, MOA, dose, AE)
Drugs: ex. pilocarpine
MOA: reduces resistance of aqueous outflow
Dose: 1 drop into affected eyes up to QID based on severity
AE: burning sensation or blurry vision due to constriction of pupils
generally third line
What are some common open angle glaucoma tx combination eye drops offered?
Travoprost (Travatan, PGE)/timolol (BB) (Duotrav) - QD
Latanoprost (PGE)/timolol (BB) (Xalacom) - QD
Brimonidine (AA)/timolol (BB) (Combigan) - BID
Brinzolamide (carbonic anhydrase inhibitor)/brimonidine (AA) (Simbrinza) - TID
What are storage considerations for specific open angle glaucoma treatments?
Latanoprost/timolol: prior to opening kept in fridge 2-8C, after open can store up to 25C for 10 weeks, protect from light
Latanoprost: fridge before opening 2-8C, after opened can be up to 25C for 6 weeks, protect from light
Travatan: stored at 2-25C
Brinzolamide/brimonidine (Simbrinza): stored at 2-25C
Brimonidine/timolol (Combigan): stored at 15-25C, protect from light
What is tx for closed angle glaucoma (all meds, principle)
generally acute and tx generally short-term
ophthalmologist will re-evaluate tx and determine whether surgery is needed
Tx: 1. BBs, 2. AAs, 3. carbonic anhydrase inhibitors (CAIs)
What are cataracts, causes and risk fx, S&S?
refers to opacification of the ocular lens which results in visual changes, different types of these depending on what caused it and location of it
Causes/Risk Fx: typically due to aging, may be exacerbated/accelerated by: UV radiation, meds (ex. long term corticosteroids), systemic disorders (ex. DM, HTN, autoimmunes), smoking, alcohol, eye trauma
S&S: painless loss of vision in one or both eyes, blurry vision, difficulty reading, increased glare, troubles with night driving
What does tx of cataracts entail?
surgery is the only tx,, procedure is called phacoemulsification and is done by an ophthalmologist - involves removing the cloudy lens and replacing it with a new clear lens
pt waits around 9-16 months for surgery, one eye has surgery at a time and takes about 20 min, second eye usually is done two weeks after if needed
also entails eye drops used pre and post-op which may include: antibiotics, corticosteroids, NSAIDs, artificial tears
For eye drops used pre and post-op for cataract surgery, what meds are they, when are they given, what do they do?
A: Antibiotics - ex. Vigamox (moxifloxacin), Zymar (gatifloxacin), always given, they prevent infection
they are started one day before surgery and continue after surgery for a week
B: Corticosteroids - ex. Loteprednol acetate (Lotemax), fluorometholone (FML), Prednisolone acetate (Pred-Forte), always given, they manage inflammation related to the surgery
they are started on the day of the surgery and continue for 3 weeks after, they are usually tapered during the second week after surgery
C: NSAIDs - ex. Ketorolac (Acular), nepafenac (Nevanac), diclofenac (Voltaren), not always given - some surgeons will use it following surgery but some will wait for a follow-up,, it manages edema of the macula
D: Artificial Tears - ex. Refresh tears, Systane Ultra, Hylo,, always given, helps with dryness, discomfort, irritation,, used for first 3 days post-op and then PRN for irritation
What is diabetic retinopathy, what does it involve, S&S?
characterized as damage to the blood vessels of the retina, can lead to bleeding into layers of retina or into vitreous
unmanaged this can lead to vascular endothelial dysfxn, inflammation, and oxidative stress, this leads to vascular permeability leading to macular edema and retinal neovascularization
S&S: if without macular edema ⇒ no sx,, if with macular edema ⇒ decreased vision in center
if has retinal detachments ⇒ flashes of light, blurry vision in certain area, dark curtains/missing parts of vision, increase in floaters
What is pharmacologic tx for diabetic retinopathy?
ophthalmologists will be involved for intravitreal injections when disease progresses to certain point
Anti-Vascular Endothelial Growth Factor (Anti-VGEF): ranibizumab (Lucentis) - covered, bevacizumab (Avastin) - not covered
MOA: inhibits this, prevents angiogenesis by reducing 1. endothelial cell proliferation, 2. vascular leakage, 3. new vessel formation
Other: laser photocoagulation - laser used to create microscopic burn to stop abnormal vessel formation or seal leaking vessel
vitrectomy - due to excessive blood leakage into vitreous this removes vitreous gel in eye and replaces it with saline, a gas bubble or silicone oil to maintain eye shape
What are cases where vision therapy may be considered?
Strabismus (Eye Turns): train both eyes to work together and improve vision in this condition,, Convergence Insufficiency: training eyes that have trouble working together to see close objects
Concussions: pt may have issues with connections between eye and brain
Sports Vision Training: help athletes improve visual skills like hand-eye and rxn time
