W1 Refractive error Flashcards by Dyllan Nye

Ocular process on near work:

Near work > focal point behind retina > retinal defocus stimulates Reflex Accommodation Mechanism > ^lens curvature > ^power > light focused on retina

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Level of myopia on visual distance:

-2.5D > 40cm clear (normal working distance)
-10D > 10cm clear
1/F (in meters)

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Astigmatism types:

WTR (flat meridian at 180)
ATR (flat meridian at 90)
Oblique (flat meridian at 45/135)
Irregular (flat meridian not perpendicular)

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Regions around focal points of astigmatism:

Area between focal points (blur zone): Interval of strum
Mid point between focal points > circle of lease confusion

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Presbyopia with age:

AA = 15D at birth
AA = 12D at 10
AA = 3D at 40
AA = 1D by 60

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Emmetropisation:

Coordinated development of lens/cornea/axial length via defocus detection from retina to visual cortex.
Power and focal length change to match axial length.
Accurate accommodation required for correct emmetropisation

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Emmetropisation with age:

3-9 months greatest change
9-18 months small change
Initial 12 months > astigmatic reduction
Refractive error stabilises until 8y (myopia progression)

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Patho of emmetropisation:

Blur detection > release of factors triggering signalling cascades and protein transcription
Changes in collagen content and extracellular matrix (ECM) of sclera
Axial elongation
Reduced retinal blur

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The emmetropisation mechanism:

Hyperopic defocus decreases amplitude of response from retinal cells
Altered signal communication through RPE and choroid to sclera
Gene expression in scleral fibroblast altered
Scleral ECM remodelled, increasing scleral creep rate
Axial elongation > decreased hyperopic defocus

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Genetic input for emmetropisation process:

Genes related to enzymes, growth factors, structural proteins that control:

Scleral fibroblast proliferation
Fibroblast collagen production
Quantity and width of scleral lamellae
Scleral composition (GAGs, integrin mediated cell adhesions)

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Development of refractive error:

Inappropriate input (environment)
Dysfunction of signalling loop (genetic)

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Emmetropisation dysfunction conditions:

Marfan’s / Stickler syndrome:
Poor scleral collagen remodelling
Down’s syndrome / cerebral palsy:
Slight hypermetropia from poor emmetropisaiton
Decreased outdoor work > dysfunction of emmetropisation loop > hyperopic defocus ( school myopia)

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Changes in refractive error with age:

2D at birth
1D at 2
0D at 40
(6% of students are expected to need glasses)

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Myopia visual impairment risks:

Greater risk with high myopia (>6D)
Retinal detachment/hole/tear
Peripapillary atrophy (atrophy near ON)
Lattice degeneration (pigmented retinal thinning)
Tilted insertion of OD
Tigroid fundus (tessellated colouration from RPE thinning)
Lacquer cracks (break in bruchs membrane)
Fuchs’ spot at macula
Pavingstone degeneration (chorioretinal atrophy)
Posterior staphyloma (scleral stretching)
Loss of choroidal circulation > CNV

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Types of myopia:

Simple myopia: progresses 0.5D per year till 20 years
Pathologic myopia: excessive axial elongation > myopic maculopathy/ optic neuropathy
Pseudomyopia: over-reactive accommodation from ciliary spasm
Nocturnal myopia: poor visual cures > tonic accommodation > myopic blur (night driving)

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Myopia eitology:

7% no parents, 30% one parent, 50% of both (risk increased with myopic magnitude)
80% school leavers in asia (15% high myope)
Urbanization, decreased outdoor time, more education.

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Gene prevalence for myopia:

Loci usually on autosomal dominant or X linked (MYP1-13): coding for growth factors/enzymes in outer retina causing cone or ON bipolar cell disfunction affecting blur detection, or scleral collagen/ECM composition.

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Theories for myopia development:

Dopamine theory: Decreased sun > poor activation of dopamine receptors in eye > myopic development
Hyperopic defocus theory: peripheral hyperopic defocus (accom lag from near work) > axial elongation to resolve peripheral blur > foveal blur

Myopia management stats:

4 main options with ~40% myopia slowing
Atropine
OrthoK
MF soft CLs
DIMS/Stellest lenses

Atropine:

Muscarinic antagonist for M4 scleral receptor, thought to be unrelated to relaxation of accomodation

Atropine effect:

ATOM-1 study:
1% atropine > 77% reduction in 2 years / photophobia/accom loss
ATOM-2 and LAMP study:
0.05% has best effect with less rebound (axial elongation following cessation)

OrthoK:

Hard lens forming neg-pressure on cornea overnight > thickens epithelium in mid periphery (vise-versa central epith) > myopic correction at macula / hyperopic correction at periphery
ROMEO / HM-PRO studies > 50% myopic reduction

MF soft CLs on myopia control:

Plus power on periphery corrects hyperopic defocus
Misight lenses have 55% reduction in myopia progression
(greater add power > better reduction / worse vision)

Stellest/DIMS/myosmart:

Lenslets in peripheral lens (<>9mm optical zone) reduces hyperopic defocus
Reduces myopic progression (in dioptres) by 50%
May be combined with atropine if significant progression

Unacceptable myopic control methods:

PALs (progressive add lenses) Undercorrection Part-time wear

Stable Myopia correction:

PRK LASIK LESEK SMILE Clear lens extraction / replacement All flatten central cornea, require >18y and stable refraction

Laser surgeries for myopia:

PRK (used in thin cornea): epithelium / stroma ablated > pain LASIK/LASEK: epithelial flap with stromal ablation (Lasik requires thick cornea) SMILE: least invasive, femtosecond laser through small incision Clear lens extraction: Cataract surgery (risks tears/holes/detachments)

Accommodation process in latent hyperopia:

Blur signal received by visual cortex > bilateral Edinger Westphal nuclei (CN3 oculomotor) in midbrain > preganglionic parasympathetic fibres move with CN3 to ciliary ganglion to synapse to postganglionic neurons > neurons travel with CNV1 (Opth of trigem) ciliary nerves to ciliary muscle and pupillary sphincter muscle > activation of muscarinic receptors by Ach > contraction of ciliary muscle and sphincter muscle

Helmholtz theory of accommodation (what ciliary contraction does)

Contraction > forward movement of muscle, slacking zonules attached to lens > lens bulges naturally > increased curvature/thickness/refractive power > image focus moved forward onto retinal plane.

Convergence process in accommodation:

Blur/disparity activates supraocular motor nuclei > innervating oculomotor nuclei > axons sent to medial longitudinal fasiculus > contraction of medial rectus via CN3 > convergence while accommodating

Pupil constriction process in accommodation :

Detection of blur in visual cortex > activation of bilateral pretectal nuclei > bilateral Edinger Westphal nuclei > preganglionic parasympathetic nerves with CN3 move to ciliary ganglion > post ganglionic fibres with CNV1 to iris sphincter muscle > contraction of IRIS

Hyperopia and aging:

Latent becomes manifest as accommodation decreases. Noted increase in asthenopia (fatigue) Commonly produces esophoria (sometimes tropia) > inward turn

Hyperopia pathophysiology:

Product of poor emmetropisation (commonly 0.5D) Genetic factors/environment > dysfunction of signalling loop

Latent Hyperopia:

Light focused behind retina > retinal defocus > stimulating accommodation mechanism > clear vision (with large accommodative reserves) Noted difficulty during near work (increased accommodative demand)

Consequences of uncorrected hyperopia:

Anisometropia (different refractive error) > poor development of visual pathway > amblyopia Excess accommodation > over convergence > esophoria greater at near > diplopia > amblyopia

Management of hyperopia:

Cyclopentolate > full hyperopia measurement Education for small latent hyperopia Specs for symptomatic (asthenopia/esophoria/strabismus/amblyopia/blur)

Near triad of close work:

Accommodation Convergence Pupil constriction (increase depth of focus and reduce accommodative demand)

Simple patho of near tiad:

Blur detected unilaterally in visual cortex (alternate blur is averaged) > Bilateral supraoculomotor area activation > stimulation of bilateral edinger westphal / oculomotor nuclei > ciliary (and pupil sphincter) muscle contraction / medial rectus contraction

Presbyopia pathophysiology:

^ thickness / loss of Ant. Capsule pliability > capsule failure to mould lens Loss of lens elasticity with constant growth (mitosis) > decreased amplitude of accommodation

Lens and cornea power in emmetropisation

increase in power

IOP on myopia

increase in IOP > constant pressure on sclera > myopic shift

Functional and incipient presbyopia

functional: Px cant read at desired distance Incipient: fine print difficult but can manage without

faculative and absolute hyperopia

Facultative: accomodation overcomes (Latent) Absolute: cannot be overcome