W2 Cat + Glare Flashcards
Lens anatomy:
Capsule: elastic membrane, molds lens
Epithelium: single layer cuboidal, equatorial mitosis, nutrient transport, secretes capsule
Fibers: formed from epithelia, contains crystallins a/b/y (soluble proteins with RI)
Metabolic activity in lens:
Cuboidal epithelia undergo equatorial mitosis/differentiation/elongation > nuclei/organelle loss > crystallin lens fiber gain (a/b/y)
RI / Transparency factors of lens:
Suture (pole to pole), high RI fiber crystallin orientation/conc.
General Cataract patho:
Genetic/metabolic/nut./environmental changes disrupt organization/homeostasis of lens components > changes in spatial density / absorption/scatter of light
Light scatter via protein aggregation/seperation from water influx
Mechanisms of cataract formation:
Cell proliferation/differentiation disruption (Growth factors)
Metabolic disturbance/osmotic regulation (Na/Ca)
Calpains
Post-translational modification (lens proteins)
Oxidative damage
Loss of defense mechanisms
Disturbed cell proliferation in cataracts:
Fibroblast growth factor (FGF) stimulates proliferation/differentiation of epithelia (^FGF at equator)
Change in homeostasis of GFs / cytokine-mediated inhibition of production > opaque PSC
Growth factors in lens mitosis:
Fibroblast (FGF)
Epidermal (EGF)
Insulin-like (IGF)
Platelet-derived (PDGF)
Transforming (TGF-beta)
Metabolic disturbance in cataracts:
Altered gene expression > enzyme/GF/membrane protein dysregulation > ATP/ion transport/Ca metabolism/antioxidant dysregulation
Na/K ATPase pump loss > Na influx > water influx (^with membrane protein alteration) > swelling
Altered membrane protein > Ca influx (from ^aqueous conc.) > Ca oxylate crystals/ Ca-protein bonds/ calpain activation/ epithelia differentiation alteration
Calpains in cataracts:
Ca activated intracellular cysteine proteases
Decreased calpains > increased damaged protein levels
^Ca > excess activation > proteolysis of crystallin < precipitation of proteins < disorganization of refractive components
Post-translational modification (PTMs) in cataracts:
Additive / Subtractive / Neutral PTMs
Crystallin modifications > change in weight/conformation > thiol group exposure > oxidation > disulphide bond formation > aggregation
Additive PTMs in cataracts:
Disease: diabetes (glucose/ascorbate)/renal loss (cyanate)/aging (photo-oxidation products)/steroids (ketoimines) > methylation/acetylation/carbamylation/glycation > molecules added to lens proteins > alteration > aggregation
Polymerization > protein susceptible to photo-oxidation (UV) > modification of protein-bound tryptophan (or glycation) > presence of fluorescent chromophores > brown coloration
Subtractive PTMs
Proteolysis/cleavage of crystallins > protein precipitate build up
Cleavage of membrane proteins (channel) > ion/glutathione transport dysregulation > vacuole formation/oxidative damage
Neutral PTMs
Isomeration/deamidation > conformation change
Alpha-crystallin (chaperone) isomeration (time related) > loss of b/y crystallin regulation, and aggregation
Oxidative damage in cataracts:
Cortex mitochondria must keep O2 conc. Low in nucleus, crystallin oxidation > high weight aggregate formation > ^RI/scatter/hardening (nuclear sclerosis)
Age* > mitochondrial function loss > ^ROS presence > ^O2/ROS in nucleus
UV filter breakdown/photosensitizer breakdown > ^ROS
Antioxidant loss > decreased O2 consumption > ^O2 exposure of proteins > ^crystallin oxidation
Age > nucleus-cortex antioxidant barrier > glutathione loss > ^nucleus generated oxidative components (H2O2)
Loss of defence mechanisms in cataracts:
Glutathione/ascorbate (from vit.)/tocopheroles/carotenoids/antioxidant enzymes keep proteins from oxidation.
Age > nucleus-cortex glutathione barrier
Vitreous degeneration (age) / vitrectomy > ascorbate loss > nuclear cat
Causes of cataracts:
Age
Trauma
Systemic disorders
Ocular disease
Toxic
Congenital/juvinile
Age-related cataract causes:
Altered enzyme/GF/protein levels
Abnormal proliferation/differentiation
Na/Ca transport dysregulation > osmotic imbalance > vacuole/high weight aggregates
Altered calpain conc.
PTMs
Oxidative damage
Loss of defence mechanisms (cortex barrier/antioxidant loss)
Traumatic cataract:
Blunt (without capsule rupture) > ant./PS cataract from rapid water influx > opacity (rosette cat)
Opacity will subside if capsule is not ruptured
Heat > IR exposure > glass blowers cat
Systemic disorders in cataracts:
Diabetes > ^glucose > conversion to sorbitol by aldose reductase in lens > water influx > lens fiber swelling/rupture > PSC/Cortical opacity
Glycation PTM > aggregation
Sorbitol reduction > antioxidant loss > ^oxidative stress
Diabetes > snowflake cataracts
Ocular disease in cataracts:
Inflammation (uveitis) > PSC
Corticosteroid use > cataracts
Vitrectomy > ascorbate loss > oxidative stress
Toxic cataracts:
Direct modulation of Na/K ATPase pumps
Cause crystallin modification
Disruption of Ca homeostasis
Congenital cataracts:
Systemic disorders resulting in cataracts in early years of life (trisomy 21)
Christmas tree (myotonic dystrophy)
Blue-dot
Lamellar
Sutural
Pos./ant. polar
Oil-droplet
Nuclear cataracts:
Most common
Accumulation of high weight aggregates > hardening (sclerosis)/^RI > scattering > VA/contrast loss/myopic shift
^fluorescent chromophores > nuclear brunescence > blue-yellow color defect (Tritan)
PSC:
Age/Stress/UV/H2O2/cytokines > dysplastic epithelia migrate to pos. pole > collate with adjacent fibers > balloon cell formation > dysfunctional Na/K ATPase > swelling > intercellular/interfiber vacuoles and extracellular granular material formation > disruption of regular lens organization > light scatter
Vacuoles in flux
Near/light VA worse than far/dark (miosis)
HT for visual effect of cataracts:
Open ended question about commonly affected tasks:
Reading/distance
Facial recognition
TV watching
Bright/dark
Glare
Day/night driving
Moving in unfamiliar places
Using steps
Employment/housework
Hobbies
Required HT for cataracts:
Onset of vision change: sudden (trauma), range from 4 weeks (PSC), gradual (nuc.)
Ocular hist. (refractive/disease/amblyopia/surj./trauma)
Systemic health: (coronary art./cerebrovascular disease / hypertension / diabetes m. / dementia/arrhythmias/ chronic obstructive pulmonary disease) *conditions on supine position difficulty
Medications: a-antagonists (tamsulosin hydrochloride) lead to surj. Complications (floppy iris syndrome)
Allergies: anaesthetics/anti-inflammatories/antibiotics
Cortical cataracts:
Hydration of cortex > subcapsular vacuoles > ray like transparent liquid spaces > decrease in soluble proteins/^insoluble proteins > opacification of rays > cuneiform opacities originating from periphery
Localized RI change > astigmatism
Glare in night (greatest glare)
Visual assessment in cataracts:
VA dist/near
Contrast sensitivity
Contrast sensitivity under glare (^loss of 0.35 logCS units is significant)
Colour vision (^3.0 LOCS III causes tritan)
Assessing comorbidities of cataracts:
36% comorbidity incidence:
AMD
Glaucoma
Diabetic retinopathy
Fuch’s endothelial dyst.
Ensure visual loss is due to cat and not from comorbid.
Education on cataracts:
Sx. Improves QoL
Cat will progress
Nothing is lost from defferal
Specs needed after (6 weeks)
Opthal initial and 2 follow-up appt.
Sx. Needs 2 operations on 2 days
Anti inflammatory/microbial drops
Public is free (1-2years)
20min surgery under local anasthesia (blurred)
Unlikely complications
Cataracts surgery:
Phacoemulsification: Common, tunnel incision > ultrasound probe emulsifies nuc. > cortex removed via irrigation/aspiration cannula/suction pump > IOL implant via scleral tunnel
Minimal small incision: lesser VA, hydro dissection and irrigating lens loop with aspiration
Femtosecond laser: new (unknown effects) corneal incision > capsulorexis > lens fragmentation
Contrast definition:
Difference of luminance from target and background relative to average luminance
Contrast = (target luminance - background luminance) / (target luminance + background luminance)
Complications of cat. Sx:
1/200 VA loss
50% PSO by 3y
Dislocated IOL
Rupture of capsule
Dislocation of capsule (weak zonules)
Suprachoroidal hemorrhage
^IOP
Cystoid macular oedema (^prostaglandins > vessel leak)
Retinal detachment (^with myopia)
Endophthalmitis (+/- infectious) > blindness 0.04-0.4% by 6w
Contrast sensitivity:
Minimum contrast where an image can be resolved
* Expressed by contrast sensitivity function CSF
Increases with spatial frequency until 3 cycles per degree (6/60), then decreases to minimum by 30 cycles per degree (6/6) due to receptive fields
Contrast sensitivity function:
Y-axis: Log contrast sensitivity
X-axis: spatial frequency (cycles per degree)
CSF is plotted as multiplication of the modulation transfer function by the retinal testing function
MTF (transfer of image through optical components)
RTF (retina-brain processing / enhancement)
Causes of contrast sensitivity loss:
Age* > loss of retina-brain processing / light scatter through ocular components (lens/cornea)
Conditions damaging visual pathway (Optic neuritis)
Photopic vs scotopic conditions on contrast sensitivity:
Peak of CSF decreased from 4cpd (photopic) to 1-2(scotopic)
Due to decreased retinal illumination (contrast equation)
Decrease in cone sensitivity (small receptive fields) > activation of rod photoreceptors (large receptive fields)
Measuring contrast sensitivity:
Pelli robson CS chart detects CS only at a given spatial frequency, 1m (0.5cpd) or 3m (1.5cpd)
Vistech CS detects spatial frequency at given contrast
Pelli-Robson contrast sensitivity chart:
Most common contrast test:
16 letter triplets (4.9cm high) in decreasing contrast by 0.15 Log CS units (first triplet of 0 Log CS)
0.05 Log CS score for each letter after first triplet
Px 20-50y should have 1.80 Log CS with each eye, older Px should have min 1.65 Log CS (Binocular score should be 0.15 greater)
Benefits of pelli robson CS chart test:
Reliable/repeatable, moreso than sine-wave charts (vistech/FACT)
No ceiling effect
Not greatly affected by refractive error
Whole CSF function determined via VA comparison
Ideal for screening contrast loss of low spatial frequency (optic neuritis/MS/Lesions) at 1m, detects cat/corneal oedema effect at high spatial frequency 3m
Increased exposure time will let Px see more (variable end-point)
Glare:
Contrast lowering effect of scattered light
Discomfort glare: brightness flux > pupil dilation/constriction > rod/cone confusion > poor adaptation
Veiling/disability glare: misdirected light > reduced contrast > poor VA/starburst
Causes of disability glare:
Age^ 45y: scatter from opacity / lens fluroescence (UV converted to visible blue) / senile miosis
Refractive error / keratoconus
Refractive Sx
Corneal opacity/dystrophy
Cataracts/PSO
Corneal oedema
Macular oedema
Causes of discomfort glare:
Uveitis
Cone-rod dystrophy
Retinitis pigmentosa
Physiological glare
Ocular albanism
Measuring glare loss:
Pelli robson CS loss of 0.35 is expected from light source introduction
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