2 Cataracts Flashcards
Lens nucleus and lens cortex definition:
Nucleus: formed before birth (compacts after birth)
Cortex: formed after birth (mostly before 3rd year)
Physiological Lens changes with age for cataracts:
Proteins modify non-enzymatically via post-translation
Fluorescent chromophores accumulate = oxidation / cross-linking = scatter
Glutathione transport blocked
Lens changes with age:
Increased light scatter > 40yo
Decreasing elasticity of nucleus (proteins and lens size changes)
Protein changes
Lens protein changes with age
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
Chromophores:
Milliard products
Cross-links with crystallin’s leading to brown colouration
Cortical cataract formation:
Membrane permeability and enzyme fluxuation.
Shear-stress between peripheral cones C3-C2 as lens hardens
Cortical cataract opacities:
Dot-like / radial / circular shades: dots in far periphery
Spoke opacities: Common wedge
Lens retrodots: Spiral, seen in retrolight
How lens transparency is maintained
Avascular
Lack of organelles
Regular protein/cell organisation
Nuclear cataract causes
Altered protein levels Abnormal proliferation Ion imbalance Protein oxidation Decreased antioxidants
Cataract cause risks:
Altered protein levels Abnormal proliferation Ion imbalance Protein oxidation Decreased antioxidants
Cataract cause risks:
Diabetes Vascular disease Corticosteroid intake UV radiation Genetics
Effect of opacities on vision
Daylight: 3mm pupil = wedge / spoke opacities
Night: 8mm = all opacities
Opacities may cause astigmatism from localised RI change
Formation of nuclear cataracts:
Loss of reduced glutathione (GSH) and age related changes form aggregates, protein insolubility, PSSPs and disulphides leading to opacity and chromophores.
Formation of cortical cataracts:
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.
Nuclear cataract on vision
Myopic shift, increased RI
Decreased VE
Tritan color defect, blue light blocked by yellow fibers.
Cortical cataract on vision
Loss of contrast
Astigmatism (localized RI change)
Nocturnal VA loss
Most common age related
PSC pathophysiology
Defective epithelium fiber production > defective cell migration to C1 > opacity formation
Age related PSC irreversible
Hypoglycaemia / corticosteroid induced PSC reversible
PSC on vision
Rapid development, vacuoles appear and disappear
VA loss
Contrast loss
Cataract management
Surgery IOL implant: (intra/extra capsular)
Extra: lens capsule retained for internal barrier.
Phacoemulsification: lens removed by ultrasound
Post op care for cataracts:
Topical corticosteroid and antibiotic
Types of IOLs
Flexible: easy surgery Rigid: PMMA Aspheric Toric Accommodating Multifocal
Cataract surgery complications
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
Refractive error with cataracts:
Myopic shift with nuclear and PSC proportional to severity
Astigmatic change with cortical cataract
