2-27,28 - Cataracts Flashcards

1
Q

Treatment of cataracts

A

Surgically remove + replace w/ IOL
- Intracapsular cataract extraction (ICCE) = Remove lens + capsule, add AC-IOL attached to iris or ciliary sulcus
- Extracapsular cataract extraction (ECCE) = REmove lens substance only (post. capsule remains), add PC-IOL using post. capsule as base.
- Phacoemulsification = Vibrations emulsify lens, suck out lens, continue w/ ECCE

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2
Q

Anterior-subcapsular Cataracts
- General information
- General mechanism

A
  • Opacities beneath ant. lens capsule
  • Associated lens epithelium fibrous metaplasia (to myofibroblast) (triggered by injury)
  • Leads to ASC fibrous plaques -> contraction wrinkles lens capsule + disrupt tissue order
  • 5% of cataracts are ASC, not age-related
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3
Q

Cortical cataracts
- General information
- Mechanism

A
  • Anywhere within cortex, usually starts infero-nasal
  • Due to ionic imbalance -> localised lens fibre swelling (disrupt organized packing)
  • Starts as clefts + vacuoles between fibres (pools of fluid displaces fibres causing degen)
    -> then becomes typical cuneiform (wedge) or radial (spoke-like) opacities
    -> then becomes Morgagnian globules (protein leak) -> then cortical liquefaction
  • Nucleus can appear sunken
  • Due to age + DM
  • Most common, least visually significant (unless at visual axis)

Mechanism:
Cannot regulate volume
E.g. Na/K pump inactive or membrane permeability increase
Leads to:
- Imbalance of H2O inward vs outward
- Localised H2O accumulation
- Fibre cell swell -> membrane damage -> clefts -> vacuoles
- Cuneiform + wedge-shaped opacities

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4
Q

Nuclear cataract
- General information
- Mechanism

A
  • At centre of lens
  • Biochemical but not structural changes (unlike cortical)
  • Modifications to crystallin proteins w/ age -> diff. n value
  • Yellowish hue due to urochrome pigment deposition (dark brown if advanced)
  • Risk factors = age, UV, smoking
  • Associated w/ myopic shift

Mechanism:
- Protein absorbs light -> make ROS e.g. H2O2, O2.-, .OH
- ROS scavenger system e.g. Glutathione (GSH) not working
- Lots of ROS (especially at nucleus where furthest from ambient levels in AH) -> lens crystallin protein cross-link -> protein aggregation -> refractive index mismatch -> opacities

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5
Q

Posterior subcapsular cataracts
- General information
- General mechanism

A
  • Just in front of post. lens capsule
  • Due to lens epithelial cells migrating along post. capsule (swelling as they move)
  • Forms grainy/plaque-like PSC depositions (solitary plaques = “wedl” or “bladder” cells)
  • Risk factors of DM and corticosteroid use
  • Severely affects vision
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6
Q

LOCS III grading method

A
  • Mainly for study purposes
  • Uses 0.1 increments between grades
  • Doesn’t have ant. subcapsular due to rarity
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7
Q

WHO grading: Nuclear cataract

A

NUC-0 = No cortical cataract
NUC-1 = Cortical transparency > Centre
NUC-2 = Equal opacification
NUC-3 = Nuclear more opaque than peripheral cortex

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8
Q

WHO grading: Cortical cataract

A

After dilation, you
- Divide lens into 8 sections
- Add up circumference of involved cortical cataract
Grade:
- Trace cortical = <1/8
- COR-1 = 1/8 to ¼
- COR-2 = ¼ to ½
- COR-3 = >½
if reach central 3mm, add “+ CEN”

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9
Q

WHO grading: Posterior-subcapsular cataract

A

Using retro,
- Find largest central opacity
- Measure vertical height (adjust slit beam height to match it)
Grade:
- Trace = <1mm
- PSC-1 = 1mm
- PSC-2 = 2mm
- PSC-3 = 3mm

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10
Q

Maturity classification of Cataracts

A

Only applicable when cataracts is white which is severe end-stage cortical (unlikely to happen in NZ)
Either:
- Mature Completely white opaque lens
- Hypermature (cells burst from swelling, gives wrinkly lens appearance)
- Morgagnian (Liquefaction of cortical fibres so intact brown nucleus sinks down)
Note: Nucleus likely brown from concurrent nuclear cataract.

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11
Q

Senile cataracts

A
  • Age-related (noticed around 50-60yrs, exponential incidence after that)
  • Nuclear (most common) + cortical + PSC
  • Arbitrary amount of opacity used to classify
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12
Q

Penetrating vs blunt trauma cataract

A

Penetrating:
- Sharp obj. E.g. metalic FB
- Focal nonprogressive opacities
Blunt:
- Days or years to develop
- Transient, static, or progressive possible
- Rosette ASC/PSC most common (“sunflower” cataract)
- Vossius ring possible (iris imprint on lens)

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13
Q

Electric shock cataract

A
  • Diffuse milky-white opacity
  • Snowflake-like opacities, sometimes in star-like distribution
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14
Q

Infrared radiation cataracts

A
  • Chronic exposure to IR from heating glass or molten metal
  • “Glassblower’s cataract”
  • Any layer of lens affected
  • Can cause true exfoliation of ant. lens capsule
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15
Q

Ionizing radiation cataracts

A
  • Exposed to stuff like X-rays, CT scans (often medical workers)
  • PSC opacities, sometimes cortical
  • Months to years to manifest
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16
Q

3 Toxic causes of cataracts

A

Corticosteroids:
- Synthetic steroids = potent anti-inflamm
- PSC opacities
- IV/oral > topical
Phenothiazines
- Anti-psychotic medications e.g. schizo
- e.g. Chlorpromazine, thioridazine, fluphenazine
- ASC deposits in stellate config
Amiodarone
- Anti-arrhythmic treating atrial fibrilation
- Punctacte, yellow-whiteish opacities (like phenothizines w/o stellate configuration)

17
Q

Diabetic cataracts
- General information

A
  • Cortical/PSC opacities +/- age-related nuclear cataract at earlier age
  • Children have “snowflake” cortical opacities (“true” DM cataract as there’s no ARN cataract present at that age)
  • Hard to assess retina (often fast-tracked to surgery)
18
Q

Diabetic cataracts
- Mechanism

A
  • Due to high glucose levels, polyol pathway is also used to convert glucose to ATP (normal hexokinase pathway is saturated)
  • Polyol pathway = Glucose –(AR)–> Sorbitol –(SDH)–> Fructose
  • Since Aldose Reductase (AR) section is quicker, sorbitol builds up -> osmostic stress -> fibre volume regulation broke -> lens swell -> depolarise -> sustained Ca2+ influx -> protelytic enzyme activate -> Advanced Glycation Ends (AGE) protein modification + aggregation = cataract.

AR blockers to lower sorbitol levels but doesn’t work well.
- Polyol pathway initiation causes NADPH -> NADP when AR works.
- Lower NADPH means less GSSG -> GSH
- Less GSH (an anti-oxidant at lens) -> oxidative stress -> cataract
- Also, during Sorbitol –(SDH)–> Fructose reaction, NAD –> NADH, NADH –(NADH oxidase)–> ROS -> oxidative stress…

19
Q

Myotonic dystrophy cataracts

A
  • Systemic inability of muscle relaxation -> wasting
  • AD inheritance of too many Trinucleotide Repeats (TNRs) causing unstable DNA
  • Almost all get bilateral cataracts
  • 3rd decade, “christmas tree” cataract where fine iridescent cortical opacities (colourful, sparkly)
  • 5th decade, Cortical + PSC opacities, star-like
  • Eventually, indistinguishable from typical cortical.
20
Q

Atopic Dermatitis cataracts

A
  • Chronic eczematous dermatitis due to type 1 HS
  • 38% get cataract in 2nd to 4th decade
  • Bilateral, quick maturation
  • Shield-like, ASC plaque, wrinkles ant. capsule
  • PSC opacities common (even w/o corticosteroid use)
    Note: Most ppl w/ ASC are likely caused by atopic dermatitis due to ASC rarity
21
Q

3 types of secondary cataracts

A

Chronic ant. uveitis
- ASC or PSC opacities
- More likely if post. synechiae
- Associated w/ corticosteroid Tx

Acute congestive angle closure (Necrotic lens epithelium form small ant. deposits called Glaucomflecken)

Hereditary fundus dystropies

22
Q

Congenital cataracts
- General information
- Management

A
  • Present from birth, can be diagnosed later in life
  • Usually AD inheritance, usually bilateral, underlying reason 50% findable
  • Chromosomal abnorm, metabolic disorder, or intrauterine infections (infect at womb as fetus)
  • If unilateral sporadic, usually general healthy.

Management:
- Investigate cause, refer if need
- Determine visual significance
- Surgically remove early if sight threatening due to critical period for fixation reflex (lead to strabismus) + visual processing (derivational amblyopia)
For long term Tx,
- Aggressive amblyopia Tx
- High powered specs/CLs
- IOL at older age (when visual system stops changing as much)

23
Q

Posterior capsular opacification

A

Common late surgical complication
- Lens epithelium prolif and re-colonise empty spaces of ant. capsule and post. capsule
- Can’t be caused by ICCE since all lens removed

Either:
- Vacuolated (Elschnig pearls)
- Fibrosis-type (fibroplastic metaplasia of epithelium + contractility)
- Soemmering ring (white, annular donut shaped prolif of epithelium)