2 Cataracts

Question 1

Lens nucleus and lens cortex definition:

Answer 1

Nucleus: formed before birth (compacts after birth)
Cortex: formed after birth (mostly before 3rd year)

Question 2

Physiological Lens changes with age for cataracts:

Answer 2

Proteins modify non-enzymatically via post-translation
Fluorescent chromophores accumulate = oxidation / cross-linking = scatter
Glutathione transport blocked

Question 3

Lens changes with age:

Answer 3

Increased light scatter > 40yo
Decreasing elasticity of nucleus (proteins and lens size changes)
Protein changes

Question 4

Lens protein changes with age

Answer 4

Post-translational crystallin: antioxidant decline (GHS enzyme loss) > denaturing > oxidation
Conformational changes: Oxidation > cross-links > aggregates
Loss of chaperone function: leads to loss of antioxidant capacity

Question 5

Chromophores:

Answer 5

Milliard products

Cross-links with crystallin’s leading to brown colouration

Question 6

Cortical cataract formation:

Answer 6

Membrane permeability and enzyme fluxuation.

Shear-stress between peripheral cones C3-C2 as lens hardens

Question 7

Cortical cataract opacities:

Answer 7

Dot-like / radial / circular shades: dots in far periphery
Spoke opacities: Common wedge
Lens retrodots: Spiral, seen in retrolight

Question 8

How lens transparency is maintained

Answer 8

Avascular
Lack of organelles
Regular protein/cell organisation

Question 9

Nuclear cataract causes

Answer 9

Altered protein levels
Abnormal proliferation
Ion imbalance
Protein oxidation
Decreased antioxidants

Question 10

Cataract cause risks:

Answer 10

Altered protein levels
Abnormal proliferation
Ion imbalance
Protein oxidation
Decreased antioxidants

Question 11

Cataract cause risks:

Answer 11

Diabetes
Vascular disease
Corticosteroid intake
UV radiation
Genetics

Question 12

Effect of opacities on vision

Answer 12

Daylight: 3mm pupil = wedge / spoke opacities
Night: 8mm = all opacities
Opacities may cause astigmatism from localised RI change

Question 13

Formation of nuclear cataracts:

Answer 13

Loss of reduced glutathione (GSH) and age related changes form aggregates, protein insolubility, PSSPs and disulphides leading to opacity and chromophores.

Question 14

Formation of cortical cataracts:

Answer 14

Age > membrane permeability > increased Na/Ca ions (also with diabetes) > reduced Na/K ATPase activity > overhydration / protein loss > protein aggregation.
Stress and damage between C layers can instigate.

Question 15

Nuclear cataract on vision

Answer 15

Myopic shift, increased RI
Decreased VE
Tritan color defect, blue light blocked by yellow fibers.

Question 16

Cortical cataract on vision

Answer 16

Loss of contrast
Astigmatism (localized RI change)
Nocturnal VA loss
Most common age related

Question 17

PSC pathophysiology

Answer 17

Defective epithelium fiber production > defective cell migration to C1 > opacity formation
Age related PSC irreversible
Hypoglycaemia / corticosteroid induced PSC reversible

Question 18

PSC on vision

Answer 18

Rapid development, vacuoles appear and disappear
VA loss
Contrast loss

Question 19

Cataract management

Answer 19

Surgery IOL implant: (intra/extra capsular)
Extra: lens capsule retained for internal barrier.
Phacoemulsification: lens removed by ultrasound

Question 20

Post op care for cataracts:

Answer 20

Topical corticosteroid and antibiotic

Question 21

Types of IOLs

Answer 21

Flexible: easy surgery
Rigid: PMMA
Aspheric
Toric
Accommodating
Multifocal

Question 22

Cataract surgery complications

Answer 22

Posterior capsular opacity: 2y post-op 1/2 Px epithelial cells proliferate over IOL, fixed by laser
Dislocated IOL
Rupture: leads to prolapse of vitreous into ant. chamber
IOP increase
Infection: leads to blindness
Cystoid macula oedema

Question 23

Refractive error with cataracts:

Answer 23

Myopic shift with nuclear and PSC proportional to severity

Astigmatic change with cortical cataract