Final Flashcards
I cant see up close HX:
Any other problems?
How far do you read?
How well can you walk/steps?
Problems with bright light?
Itchy burny eyes Hx:
When did it start?
Vision affected?
Contacts?
Affect your tasks?
Discharge?
Family with same condition?
Hayfever/GH?
Glaucoma/DM?
How do you manage a patient with idiopathic macular oedema:
VA/pinhole
VF/Amsler > confrontation
IOP > DFE/OCT
Document and compare
Reffer for FFA
anti-VEGF treatment if symptomatic
How do you manage a patient with confluent drusen in one eye:
Regular monitoring > amsler recheck
Documentation > OCT/photography
Lifestyle > smoking cessation
Supplements > AREDS
Education > return if worsening
Low vision referral
Dry AMD:
Age/oxidation > dysfunctional metabolism of rod OS (^at macula) > ^metabolic by-products:
Basal laminar deposit (RPE/basement): collagen (cell stress)
Basal linear deposit (inner portion of bruchs): lipid/lippofuscin/complement (soft drusen; pro-inflammatory)
Progression > soft drusen (>67um) > ^size/confluent > thickening/inflammation > calcification/degeneration of elastin/collagen layers of bruchs > hydrophobic barrier to fluid/nut. > loss between outer retina/choroid
Nutrient loss / Drusen reabsorbtion > RPE ischemia / lipofuscin tox > ^dysfunction > apoptosis (seen as hypo/hyperpigmentation)
Wet AMD:
RPE loss > PR/CC dysfunction > largening chorioretinal geographic atrophy
RPE-produced trophic factor (VEGF) loss > CC atrophy > altered perfusion of choroidal vessels
Choroidal BV stenosis / Drusen inflammation > CC toxicity/death > CC perfusion loss > adjacent RPE hypoxia > angiogenic compound production (VEGF) > BV growth stimulation in CC > neovascular membrane (CNV) breaking bruchs > BRB loss > serum leak > PR loss
Aquired cataract patho:
PSC from corticosteriods > dysfunctional epithelial differentiation
CC from inflammation/injury > altered cellular metabolism
Blunt trauma > mechanical water influx (rosette)
RP patho:
Mutations > altered rhodopsin/RPE/PR-structure/PTD/Visual cycle > Rod PR/RPE dysfunction
Rod apoptosis > RPE dysfunction > retinal remodelling > altered signalling to cone PRs > apoptosis > central vision loss
RP remodelling patho:
PR loss > RPE dysfunction >
RPE hyperplasia / inward migration (bony spicules)
Glial cell migration/proliferation (ON pallor)
PR loss > O2 consumption loss > BV attenuation
RPE degen. > BRB loss > intraretinal fluid leakage > macula edema
Lost vision in one eye DDX:
CRAO/CRVO > Are you hypertensive/diabetic
MS/TED/GCA > autoimmune disorders
Wet AMD > history of AMD causing a vit haemorrhage
Explain to Px they have bacterial keratitis:
You have a bacterial infection in the front portion of your eye
Causing pain and blur
Medical emergency > need intensive treatment to preserve eye health
Ciprofloxacin 0.3% ointment every 10min for an hour, then every hour for 24, ill see you after 24h to ensure effect
We continue for a day > taper to QID, or perform a culture
Explain Wet AMD refferal:
Noticed progression of AMD
Choroidal neovascular membrane formation > new BV formation in eye
This can lead to permenant blindness, you’ll need Anti-VEGF injections to prevent this
Tests to asses cataract Px:
VA w/pinhole
Colour vision test
Slit lamp w/retroillumination
Contrast sensitivity
Refraction (RI change) compare BCVA
Manage epithelial HSK/HSV keratitis:
Live virus (dendritic/geographic):
Topical aciclovir 3% 5/d for 10d
Assisted with topical lubricants
AC reaction can be assisted with cycloplegics
If corneal toxicity at risk > oral acyclovir 400mg 5/d for 10d w/specialist refferal
Metaherpetic / neuroprophic:
Topical lubricants per hour
Manage bacterial conjuntivitis:
Acute bacterial: Self limiting 2w, Clorsig 0.5% QID 1w to lessen lifespan
Patho of MG:
Loss of self tolerance > autoantibody production against the ACHR of striated muscle > autoantibodies blocking receptors > loss of ACH reception > muscle fatigue
Patho of graves opthalmopathy:
Autoantibodies against the THSR also target tissue in the orbit that have similar antigen presentation
Antibody binding initiates Tcell response and influx of immune cells leading to fibroblast activation and GAG production
Fibroblasts proliferate and GAGs bring water in leading to swelling
Leading to proptosis / Exposure / ON compression
Tests to assess afferent pupil pathway
Direct light response > poor response
Direct / consensual / swinging
GPC cause:
Antigens coat CLs > constant contact with tarsal conj.
Mechanical trauma > TH2 response > IL-8 expression with dendritic cell recruitment > increased number of antigen presenting cells
Induces type IV/I hypersensitivity
AMD pauls notes
Age > poor RPE metabolism of photoreceptor OS > Lipofuscin deposits in RPE (undegradable):
> ROS production (light/O2 presence) > Antioxidant loss (age) > mitochondrial damage > Ischemia
Age > Loss of ubiquitin pathway > Decreased protein degradation by ubiquitin> buildup of protein
lipid/lipofuscin/complement deposit near bruch’s membrane
Drusen develops at macula
Bruchs membrane deposit > local activation of complement > inflammatory influx > Drusen build-up > Bruch’s degeneration > barrier to nutrient influx > ischemia > RPE apoptosis
DDX acute red eye:
Visual effect: AACG, Keratitis, corneal abrasion
Painless: Sub. Conj. Haem.
Discharge
Pain type
