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OPTO3003 > W2 Cat + Glare > Flashcards

W2 Cat + Glare Flashcards

1
Q

Lens anatomy:

A

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)

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2
Q

Metabolic activity in lens:

A

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

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3
Q

RI / Transparency factors of lens:

A

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

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4
Q

General Cataract patho:

A

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

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4
Q

Mechanisms of cataract formation:

A

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

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5
Q

Disturbed cell proliferation in cataracts:

A

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

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6
Q

Growth factors in lens mitosis:

A

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

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7
Q

Metabolic disturbance in cataracts:

A

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

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8
Q

Calpains in cataracts:

A

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

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9
Q

Post-translational modification (PTMs) in cataracts:

A

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

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10
Q

Additive PTMs in cataracts:

A

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

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11
Q

Subtractive PTMs

A

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

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12
Q

Neutral PTMs

A

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

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13
Q

Oxidative damage in cataracts:

A

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)

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14
Q

Loss of defence mechanisms in cataracts:

A

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

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15
Q

Causes of cataracts:

A

Age
Trauma
Systemic disorders
Ocular disease
Toxic
Congenital/juvinile

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16
Q

Age-related cataract causes:

A

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)

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17
Q

Traumatic cataract:

A

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

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18
Q

Systemic disorders in cataracts:

A

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

19
Q

Ocular disease in cataracts:

A

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

20
Q

Toxic cataracts:

A

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

21
Q

Congenital cataracts:

A

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

22
Q

Nuclear cataracts:

A

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)

23
Q

PSC:

A

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)

24
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
25
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
26
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)
26
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)
26
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.
27
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
28
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
29
Contrast definition:
Difference of luminance from target and background relative to average luminance Contrast = (target luminance - background luminance) / (target luminance + background luminance)
29
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
30
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
31
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)
32
Causes of contrast sensitivity loss:
Age* > loss of retina-brain processing / light scatter through ocular components (lens/cornea) Conditions damaging visual pathway (Optic neuritis)
33
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)
34
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
35
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)
35
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)
36
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
37
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
38
Causes of discomfort glare:
Uveitis Cone-rod dystrophy Retinitis pigmentosa Physiological glare Ocular albanism
39
Measuring glare loss:
Pelli robson CS loss of 0.35 is expected from light source introduction
40
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OPTO3003 (18 decks)

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