W2 Cat + Glare

Question 1

Lens anatomy:

Answer 1

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)

Question 2

Metabolic activity in lens:

Answer 2

Cuboidal epithelia undergo equatorial mitosis/differentiation/elongation > nuclei/organelle loss > crystallin lens fiber gain (a/b/y)

Question 3

RI / Transparency factors of lens:

Answer 3

Suture (pole to pole), high RI fiber crystallin orientation/conc.

Question 4

General Cataract patho:

Answer 4

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

Question 4

Mechanisms of cataract formation:

Answer 4

Cell proliferation/differentiation disruption (Growth factors)
Metabolic disturbance/osmotic regulation (Na/Ca)
Calpains
Post-translational modification (lens proteins)
Oxidative damage
Loss of defense mechanisms

Question 5

Disturbed cell proliferation in cataracts:

Answer 5

Fibroblast growth factor (FGF) stimulates proliferation/differentiation of epithelia (^FGF at equator)
Change in homeostasis of GFs / cytokine-mediated inhibition of production > opaque PSC

Question 6

Growth factors in lens mitosis:

Answer 6

Fibroblast (FGF)
Epidermal (EGF)
Insulin-like (IGF)
Platelet-derived (PDGF)
Transforming (TGF-beta)

Question 7

Metabolic disturbance in cataracts:

Answer 7

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

Question 8

Calpains in cataracts:

Answer 8

Ca activated intracellular cysteine proteases
Decreased calpains > increased damaged protein levels
^Ca > excess activation > proteolysis of crystallin < precipitation of proteins < disorganization of refractive components

Question 9

Post-translational modification (PTMs) in cataracts:

Answer 9

Additive / Subtractive / Neutral PTMs
Crystallin modifications > change in weight/conformation > thiol group exposure > oxidation > disulphide bond formation > aggregation

Question 10

Additive PTMs in cataracts:

Answer 10

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

Question 11

Subtractive PTMs

Answer 11

Proteolysis/cleavage of crystallins > protein precipitate build up
Cleavage of membrane proteins (channel) > ion/glutathione transport dysregulation > vacuole formation/oxidative damage

Question 12

Neutral PTMs

Answer 12

Isomeration/deamidation > conformation change
Alpha-crystallin (chaperone) isomeration (time related) > loss of b/y crystallin regulation, and aggregation

Question 13

Oxidative damage in cataracts:

Answer 13

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)

Question 14

Loss of defence mechanisms in cataracts:

Answer 14

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

Question 15

Causes of cataracts:

Answer 15

Age
Trauma
Systemic disorders
Ocular disease
Toxic
Congenital/juvinile

Question 16

Age-related cataract causes:

Answer 16

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)

Question 17

Traumatic cataract:

Answer 17

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

Question 18

Systemic disorders in cataracts:

Answer 18

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

Question 19

Ocular disease in cataracts:

Answer 19

Inflammation (uveitis) > PSC
Corticosteroid use > cataracts
Vitrectomy > ascorbate loss > oxidative stress

Question 20

Toxic cataracts:

Answer 20

Direct modulation of Na/K ATPase pumps
Cause crystallin modification
Disruption of Ca homeostasis

Question 21

Congenital cataracts:

Answer 21

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

Question 22

Nuclear cataracts:

Answer 22

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)

Question 23

PSC:

Answer 23

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)

Question 24

HT for visual effect of cataracts:

Answer 24

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

Question 25

Required HT for cataracts:

Answer 25

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

Question 26

Cortical cataracts:

Answer 26

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)

Question 26

Visual assessment in cataracts:

Answer 26

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)

Question 26

Assessing comorbidities of cataracts:

Answer 26

36% comorbidity incidence:
AMD
Glaucoma
Diabetic retinopathy
Fuch’s endothelial dyst.
Ensure visual loss is due to cat and not from comorbid.

Question 27

Education on cataracts:

Answer 27

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

Question 28

Cataracts surgery:

Answer 28

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

Question 29

Contrast definition:

Answer 29

Difference of luminance from target and background relative to average luminance
Contrast = (target luminance - background luminance) / (target luminance + background luminance)

Question 29

Complications of cat. Sx:

Answer 29

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

Question 30

Contrast sensitivity:

Answer 30

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

Question 31

Contrast sensitivity function:

Answer 31

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)

Question 32

Causes of contrast sensitivity loss:

Answer 32

Age* > loss of retina-brain processing / light scatter through ocular components (lens/cornea)
Conditions damaging visual pathway (Optic neuritis)

Question 33

Photopic vs scotopic conditions on contrast sensitivity:

Answer 33

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)

Question 34

Measuring contrast sensitivity:

Answer 34

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

Question 35

Pelli-Robson contrast sensitivity chart:

Answer 35

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)

Question 35

Benefits of pelli robson CS chart test:

Answer 35

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)

Question 36

Glare:

Answer 36

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

Question 37

Causes of disability glare:

Answer 37

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

Question 38

Causes of discomfort glare:

Answer 38

Uveitis
Cone-rod dystrophy
Retinitis pigmentosa
Physiological glare
Ocular albanism

Question 39

Measuring glare loss:

Answer 39

Pelli robson CS loss of 0.35 is expected from light source introduction

Question 40

uwu

Answer 40

uwu