shit to know week 4 (a girl is tired...)

which muscle opens the eye

levator palpebrae

which muscle closes the eye

orbicularis oculi

which muscle of the eyelid may be affected in horner syndrome

superior tarsal muscle which joins the levator palpebrae → ptosis

also iris dilator muscles

which part of the eye contains the meibomian glands

tarsus

ptosis palpebrae

• drooping eyelid, different causes

1. congenital

   • eyelid doesnt move when glancing down

   • underdeveloped affected eyelid

   • usually due to aplasia of oculomotor n (neurogenic) or less commonly underdeveloped levator (myogenic)

2. acquired

   1. paralytic ptosis = neurogenic = oculomotor palsy

      • if its complete palsy then the inner ciliary muscles and sphincter papillae muscles are also affected on top of the levator

   2. sympathetic ptosis = neurogenic, eg. due to Horner syndrome

   3. myotonic ptosis eg. due to myasthenia gravis

   4. traumatic ptosis

unilateral ptosis is usually a sign of x

neurogenic causes

how can you distinguish congenital ptosis palpebrae from acquired

in congenital, the upper eyelid doesnt move when they glance down

there is a risk of x in unilateral congenital ptosis

amblyopia

amblyopia

reduced vision in one eye caused by abnormal visual development early in life

why does amblyopia not occur in bilateral ptosis

because they would typically tilt their head back to see and not only one eye is affected

triad in horner syndrome

ptosis, miosis and anhidrosis

enophthalmos (eye sinking into socket) also occurs

which nerve innervates the levator palpebrae

oculomotor nerve

which nerve innervates the orbicularis oculi

facial nerve

entropion

• inversion of the eyelid margin → skin touches not only the bulbar conjunctiva but also the globe

1. congenital

   • usually asymptomatic

   • seen commonly in asians

   • due to thickening of the skin and orbicularis m near the margin of the eyelid

   • rarely needs treatment

2. senile

   • only affects the lower eyelid

   • eg. due to structures supporting the lower lid becoming lax with age

3. cicatricial entropion

   • usually due to post infectious or traumatic tarsal contracture (also allergic/toxic reactions)

what may occur w/ entropion

blephorospasms due to permanent contact between eyelashes and globe (trichiasis)

there is a risk of x in entropion

corneal epithelial damage w/ superinfection which may become a corneal ulcer

disorders of the eyelid glands

1. hordeolum (stye)

   • = acute bacterial infection of the eyelid glands

   • painful

   • internal = infection of Zeis or Moll glands → more severe reaction → conjunctivitis etc may occur

   • external = infection of Meibomian glands = near the eyelashes

   • often associated with DM, acne and GI disorders

   • treat w/ antibiotics

2. chalazion

   • = formation of a firm nodular bulb within the tarsus (eyelid) due to chronic granulomatous inflammation due to build up of secretion from the meibomian gland

   • not painful, usually asymptomatic

   • surgical excision must be done

parts of the lacrimal system

• lacrimal gland = orbital and palpebral part

• meibomian glands

• inferior and superior punctum lacrimale collect the fluid → enters inferior and superior lacrimal lacrimal canaliculus → into the lacrimal sac → nasolacrimal duct and out

the eye closes progressively from x to x

lateral to medial

allows tear fluid to move towards the medial conthus and then out

tear film

1. layer 1 → oil layer from the meibomiab glands (and sebaceous and sweat glands) → stabilises tear film, stops evaporation

2. layer 2 → serous layer from the lacrimal gland → protects cornea + allows for smooth surface for high quality optical images

3. layer 3 → mucin layer from the conjunctival goblet cells → stabilises tear film + allows for even distribution of the watery layer

also contains lysozymes, beta lysin and IgA

dacryocystitis

• = inflammation of the lacrimal sac

• most common disorder of the lower lacrimal system

• obstruction of the nasolacrimal duct is the most common cause

1. acute

   • usually due to stenosis within the lacrimal sac → retention of fluid → infection from staph etc

   • usually 50-60 y/o

   • painful swelling

   • maybe malaise, fever and involvement of regional lymph nodes

   • diagnosis → radiographic contrast studies

   • start w/ local and systemic antibiotics first, maybe disinfectant compresses

   • drain pus

   • post op treatment is often needed → dacryocystorhinostomy = lower system bypass

   • risk of sepsis and cavernous sinus thrombosis

2. chronic

   • obstruction secondary to chronic inflammation of the connective tissue or nasal mucosa

   • initial characteristic = increased lacrimation

   • pressure causes large amounts of transparent mucoid pus to come out the punctum

   • no signs of inflammation

   • surgical intervention is the only effective treatment in most cases

3. neonatal

   • 6% of newborns have a stenosis of the mouth of the nasolacrimal duct due to a persistent mucosal fold → retention of tear fluid → ideal conditions for growth of miroorganisms

   • might open spontaneously (massaging also helps) so monitor at first, if needed → irrigation or probing

what is the most common disorder of the lower lacrimal system

dacryocystitis

what is the most common cause of dacryocystitis

obstruction of the nasolacrimal duct, usually unilateral

dacryocystorhinostomy

lower lacrimal system bypass

keratoconjunctivitis sicca

• = chronic bilateral desiccation (drying) of conjunctiva and cornea due to too little tear production, wrong composition of tear film/ accelerated tear evaporation

• reduced tear production is associated w/ systemic disorders or due to atrophy of the lacrimal gland

• altered tear film can be due to vitamin a deficiency, medication etc → tear film breaks up too quickly and evaporates

• burning reddened eyes, excessive REFLEX lacrimation from slight environmental causes, foreign body sensation

• tests → schrimer tear testing = less watery component, tear break up time = less mucin = less stability, slit lamp shows dilated conjunctival vessels

• may show corneal lesions

• in severe cases the tear film will contain thick mucus and small filaments from small epithelial lesions, seen with fluorescein dye

• treat with artificial tear solutions

• if it doesnt work → close the puncta

there is reflex … in keratoconjunctivitis sicca

lacrimation

what can happen in keratoconjunctivitis sicca

corneal lesions

how to test for keratoconjunctivitis sicca

1. schrimer tear testing = less watery component

2. tear break up time = decreased = less mucin = less stability

3. rose bengal → dyes dead epithelial cells and mucin

4. impression cytology → tests the density of goblet cells

these top 4 are used to evaluate tear formation in all cases, last 2 are mainly for KS but may also be in general

1. slit lamp shows dilated conjunctival vessels

2. in severe cases the tear film will contain thick mucus and small filaments from small epithelial lesions, seen with fluorescein dye

keratoconjunctivitis sicca occurs more commonly in …

women due to hormonal changes

aqueous humor

• released by the ciliary processes → into posterior chamber → through the first resistance (pupillary resistance) ie bypassing the place where the iris and lens meet → into anterior chamber → drained by the trabecular meshwork (2nd resistance)

• nourishes and protects the eye

is aqueous humour flow pulsatile

yes

production is continuous but due to 1st resistance its pulsatile flow

normal occular p

15

zonule fibres

insert into the lens from the ciliary body

the lens lies in the…

posterior chamber

cataracts

• = decreased opacity of the lens

• 99% are acquired and 90% of the total are senile

• only treatment is surgery

• generalised reduction in visual acuity with starbursts around lights

how does the lens grow

centre out

so older nuclei (embryonic nucleus) is in the centre while the adult nucleus is on the periphery

zonular fibres vs suspensory ligaments

the same thing

uvea

iris + choroid + ciliary muscles

senile cataracts

1. nuclear/sclerotic

   • starts from the centre and spreads

   • slow progression

   • pressure of peripheral lens fibre production causes hardening of lens especially in the lens → nucleus becomes yellow brown ish

   • the refractive power increases due to compaction of older fibres and apposition of new bones → myopia and maybe diplopia

2. cortical

   • due to changes in the ionic composition of the lens cortex and the eventual change in hydration of the lens fibers = increased water content

   • radial patterns of water filled fissures between fibres

   • separation of lamellae by fluid

3. posterior subcapsular

   • special forms of ^

   • due to formation of granular and plaque like opacities in the posterior subcapsular cortex

   • begins in the visual axis

   • leads to early rapid and severe visual acuity but dilating eye drops can help

4. mature cataracts

   • means the lens has undergone complete opacification of the cortex

   • diffusely white lens

   • risk of angle closure glaucoma

     mature cataracts → increase in lens thickness → increase in resistance of pupil → angle closure glaucoma

   • can only see light and dark w/o surgery

5. hypermature/morgagni

   • when mature cataracts reaches the liquefecation stage → dense brown nucleus will subside and move inferiorly

   • fluid leaks out

   • can cause phacolytic glaucoma

how does cataracts affect vision

cloudy lens → increased refractive power → light scatters upon entering (sort of myopia?) → blurry image

mature cataracts has a risk of …

angle closure glaucoma

mature cataracts → increase in lens thickness → increase in resistance of pupil → angle closure glaucoma

how does the refrative power of the lens change with cataracts

increases → myopia and maybe diplopia

due to compaction of older fibres and apposition of new bones

how is congenital cataracts screened for

red reflex

cataracts vs glaucoma vs macular degeneration

• Cataracts cause a generalised reduction in visual acuity with starbursts around lights

• Glaucoma causes a peripheral loss of vision with halos around lights

• Macular degeneration causes a central loss of vision with a crooked or wavy appearance to straight lines

  it would be like a black dot in the middle

congenital cataracts can be either x or x

hereditary or acquired transplacentally from an infection

secondary cataracts

can occur after extracapular catarct extractions bc only the anterior central portion is removed → leftover ells

treat with laser

the blind spot is

the optic cup / disc

part of the retina with highest visual quality

fovea

the fovea is within the…

macula

why does glaucoma change the optic area

glaucoma = increased intraocular pressure and decreased blood flow to the optic n → tissue atrophy and fibre death → increase in optic CUP size (+ pale discolouration)

changes in ophthalmoscopy in glaucoma

• optic cup size increases → ratio to optic disc decreases

• optic cup becomes brighter

• optic disc becomes oval shaped

• blood vessels abruptly plunge into the deep cup

• cup/disc move more nasally / away from the fovea towards the midline

how does the fovea sit in relation to the optic disc

fovea is lateral/temporal to the optic disc

a visual defect in glaucoma is…

the beginning of the end

most common type of glaucoma

primary open angle glaucoma = trabecular meshwork outflow impediment

factors that increase resistance to pupillary outflow = risk of angle closure glaucoma

• increased contact between the margin of the pupil and lens →

  • small eyes

  • large lens

  • miosis (small pupil)

  • posterior synechiae = adhesions between lens and iris

• increased viscosity of the aqeuous humour due to inflammation or bleeding

primary open angle glaucoma

• problem in 2nd physiological resistance

• middle aged and elderly patients

• most common glaucoma

• minimal symptoms that worsen progressively

• many dont experience symptoms at first → can be far advanced before noticed

• maybe non specific symptoms (headache, burning eyes, blurred vision)

• rings of colour around light sources at night are characteristic

• intraocular p > 22

• fluctuations in 24 hr pressure curve → fluctuations >5-6 mm Hg = warning sign

• gonioscopy → normal and open anterior chamber angle

• ophthalmoscopy → glaucomatous cupping

• perimetry → visual field → peripheral loss

x is characteristic in glaucoma

rings of colour around light sources at night

introcular p over x is a warning sign for glaucoma

22

what, other than intraocular p, can be measured in glaucoma

fluctuations in 24 hr pressure curve → fluctuations >5-6 mm Hg = warning sign

gonioscopy shows…

anterior angle chamber

primary angle closure glaucoma

• = problem in 1st physiological resistance =

• associated with a physically obstructed anterior chamber angle

• acute episodic increase in IOP due to sudden blockage

  due to widening of the pupil (eg. darkness or stress) → When the iris dilates, forces pull the iris centripetally and posteriorly causing increasing iris–lens contact, which prevents aqueous from passing between the lens and iris, through the pupil, and into the anterior chamber

• iris kind of looks like 2 hills on top of the lens

• increased IOP also acts on the corneal nerves → pain

  may also affect the other branches of the trigeminal nerve

• irritation of the vagus n may cauase nausea and vomiting

• corneal epithelial oedema → decreased (peripheral) visual acuity and halos

• triad → unilateral red eye w/ conjunctival or ciliary injection + fixed and dilated pupil + hard pupil on dilation

what causes an attack in angle closure glaucoma

When the iris dilates, forces pull the iris centripetally and posteriorly causing increasing iris–lens contact, which prevents aqueous from passing between the lens and iris, through the pupil, and into the anterior chamber

= episodic increase in IOP, due to darkness or emotional stress

angle closure glaucoma triad

unilateral red eye w/ conjunctival or ciliary injection + fixed and dilated pupil + hard pupil on dilation

conjunctivitis

• inflammatory process involving the surface of the eye

• characterised by vascular dilatation, cellular infiltration and exudation

• 2 categories → infectious and not (persistent irritation, allergic, toxic etc)

• reddened eyes, sticky eyelids, swollen eyelids, foreign body sensation, burning sensation, photophobia and lacrimation

• simultaneous presence of blephorospasm means theres corneal involvement = keratoconjunctivitis

what is present in all types of conjunctivitis

injections

if there is blephotospasm in conjunctivitis…

it means theres corneal involvement = keratoconjunctivitis

the limbus is…

the border between the cornea and conjunctiva

pinguecula

• harmless, greyish yellow thickening of the conjuctival epithelium in the palpebral fissue (opening between eyelids)

• usually at the limbus

• due to hyaline degeneration due to ageing and sun/wind/dust exposure

• treatment is not needed

pterygium

• triangular fold of conjunctiva that grows from the medial portion of the palpebral fissure towards the cornea

• only produces symptoms when it reaches the cornea, only then is surgery needed

• tends to recur

what is the most common conjunctival change

pinguecula

in what order does light hit layers of the retina

goes to the very bottom first

1st order neuron = cones and rods

synapse

2nd order neuron = bipolar cells

synapse

3rd order = ganglion cells

synapse

4th = optic nerve

beneath the cones and rods is…

pigment epithelium (stops light from scattering) then choroid and then sclera

visual pathway

!! face foreward ok, the light that comes in from the right side of EACH eye will hit the LEFT side of EACH eye (think of diagonal lines entering through the pupil) and is therefore detected by cells on the opposite side of the light source

now

light that hits the temporal side of the eye (ie light that originally came in medially) will NOT cross at the optic chasm, light that hits the medial side will

0. cones and rods → bipolar cells → ganglion cells →

1. optic nerve

2. optic chiasm (medial cross, lateral not)

3. optic tract → due to ^…

   left optic tract = left temporal fibres + right nasal fibres

   right optic tract = right temporal fibres + left nasal fibres

4. lateral genicular body = where the optic tract ends → synapses w/ 5th neurons, then

5. optic radiation = new pathway = geniculocalanine tracts

   • fibres of the inferior retinal quadrants pass through the temporal lobe

   • superior quadrants through the parietal lobe

6. primary visual area = brodmann area 17

the macula is represented in the most … portion of the occipital lobe

posterior

how many extraocular muscles are there

4 straight

2 oblique

minimum threshold resolution

how far apart 2 objects must be for the eye to perceive them as distinct objects

what is the requirement for the eye to perceive 2 distinct objects as 2 distinct objects

at least one unstimulated cone must lie within 2 stimulated cones of the retina

where are cones concentrated the most

in the centre of the retina

this is where visual acuity is the highest

rods are more x than cones

photosensitive

emmetropia

normal eye sight

ametropia

refractive error due to incorrect ratio of axial length of eye to the refractive power of the cornea and lens

the lens refracts x and the cornea refracts x

cornea refracts more (2/3) than the lens

hyperopia / far sightedness

• light rays that enter the eye meet posterior to the retina

• short eyeball or deficient lens refractive power

• may occur in cortical cataracts

• most newborns exhibit slight hyperopia

• axial hyperopia is typically congenital

• shallow anterior chamber with a thick sclera and well developed ciliary muscles (to compensate)

• risk of angle closure glaucoma due to shallow anterior chamber

• estropia (cross eyes) may also occur because even when looking at far objects they still need to accommodate

• asthenopic symptoms esp. when reading (headaches etc)

• converging lenses needed (biconvex)

which, hyper or myopia, is likely to become presbyopic earlier

hyperopia since they need to accommodate for both far and close objects but accommodation decreases with age

why does estropia occur in hyperopia

because even when looking at far objects they still need to accommodate

latent hyperopia

inability to relax ciliary muscles even after having lenses due to the overuse of the muscles

myopia / near sightedness

• light rays that enter the eye meet anterior to the retina

• long eyeball (its just long or the anterior chamber is deep) or high lens refractive power

• may occur in nuclear cataracts which may also cause diplopia

• most common functional eye disorder other than age related

• ciliary muscles are atrophied since theyre barely used (they can already see things up close, and to see up close the ciliary muscles contract so they dont need it → atrophy)

• risk of retinal detachment and glaucoma

• require ‘hourglass’ lenses

ciliary muscles in hyperopia and myopia

atrophied in myopia due to lack of use

sclera in hyperopia and myopia

well developed in hyperopia

there is a risk of x in myopia

retinal detachment and open angle glaucoma

there is a risk of x in hyperopia

angle closure glaucoma due to shallow anterior chamber

is refractive power of the lens constant

no, it changes to see close vs faraway things

done by accommodation which is due to elasticity of the lens + zonule fibres + ciliary muscles

how does the lens change shape with close vs faraway objects

thinner when things are further away = due to relaxed ciliry muscles (which actually means that the zonule fibres are under tension and taught)

relaxed ciliary muscles

zonule fibres are under tension and taught

lens is thin

faraway objects or at rest

in ametropia, is the problem usually axial or refractive

axial

amisometropia

= a difference in refractive power between the 2 eyes, usually < 4 diopters

if the difference in refractive power between the 2 eyes is > 4 diopters…

the size difference of the 2 retinal images becomes too great for the brain to fuse the 2 images together = aniseikonia

aniseikonia may lead to…

amblyopia

(also called lazy eye) is a type of poor vision that usually happens in just 1 eye but less commonly in both eyes. It develops when there's a breakdown in how the brain and the eye work together, and the brain can't recognize the sight from 1 eye

keratoconus

• Conical, usually bilateral central deformation of the cornea with parenchymal opacification and thinning of the cornea

• cornea thins out → cone in the centre

• progressive, starts around puberty

• causes myopia and astigmastism

• Left untreated, in rare cases keratoconus can cause tears of Descemet’s membrane due to the continuous stretching. The entire cornea can then bulge out at this site = acute keratoconus → sudden loss of visual acuity accompanied by intense pain, photophobia, and increased tearing

• Degeneration of visual acuity can usually be corrected initially with eyeglasses; hard contact lenses will be required as the disorder progresses

keratoglobus

same idea as keratoconus but is present from birth and not progressive (also rarer)

also causes myopia and astigmastism