Orbit And Eye Flashcards

1
Q

Descirb the anatomy of the orbit

A

Ss, spr

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2
Q

Which bones make up the orbit

A

Sup

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3
Q

What is the main arterial supply to the orbit

A

• Main arterial supply is ophthalmic artery and its
branches
Central retina artery pierces the (smh) nerve?

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4
Q

Descirb the Opthalmic veins

A

Ophthalmic veins (superior and inferior) drain
venous blood into cavernous sinus, pterygoid plexus
and facial vein
Sup orb fiss ->
Inf -> pterygoid venous plexus

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5
Q

What are the anatomical relation of the orbit

A

• Important anatomical relations include
– Paranasal air sinuses (maxillary and ethmoid) - sinusitis can move into orbit, particularly ethmoid, due to thin walls.
– Nasal cavity
– Anterior cranial fossa
• Implications for
Coronal Section
• Orbital trauma
• Spread of infection
Medial wall and floor of the orbit are the weakest parts of the orbital cavity

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6
Q

What is an orbital blow out fracture

A
Sudden increase in intra-orbital pressure (e.g. from retropulsion of eye ball [globe] by fist or ball) fractures floor of orbit [maxilla]
• Orbital contents can prolapse and
bleed into maxillary sinus,
• Fracture site can ‘trap’ structures
e.g. soft tissue, extra ocular muscle
located near orbital floor
• Prevents upward gaze on the
affected side- Orbital contents tethered from below
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7
Q

Describe and explain teh clinical presentation of orbital blowout fractures

A

• History of trauma to the eye/orbit
• Periorbital swelling, painful
• Double vision (worse on vertical
Looking straight ahead gaze)
• Double vision
• Anaesthesia over affected cheek (upper teeth and gums) on affected side
Eye appears sunken because floor of orbit has given way, contents have shifted down. When asked to oo up, affected eye struggles because orbital contents are tethered
Losss of feeling over cheek, upper teeth and gums, - infraorbital nerve which is one of the branches of Vb, runs though floor of orbit though infraorbial foramen - innervates skin of lower eyelid, cheek upper teeth, gums

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8
Q

Describe teh structure of the eyelid

A

• Consist of skin, subcutaneous tissue, tarsal plate, muscles
– Orbicularis oculi (Palpebral part)
– Levator palpebrae superioris
Tarsal plate is a connective tissue stature which gives structure to the eyelid

• And glands
– Meibomian glands - Glands within the tarsal plate secrete an oily (lipid-rich) substance onto edges of lid; help prevent evaporation of tear film and tear spillage: can block causing a Meibomian cyst
Eyelash follicles can also block (infection-staph) causing styes

– Sebaceous glands associated
with lash follicle
Sebaceous glands help nourish the hair folllicle
Glands secrete on lid margin - substances form part of tear film

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9
Q

Whar are diseases of the glands of the eyelid and the eyelid

A

Glands within the tarsal plate secrete an oily (lipid-rich) substance onto edges of lid; help prevent evaporation of tear film and tear spillage: can block causing a Meibomian cyst - not infected - glands becomeblocked and there is some inflammation.swelling is a little bit deeper inside the eyelid. Not particularly painful
Eyelash follicles can also block (infection-staph) causing styes - painful, white head visible in the area of swelling, on the tip of the eyelid

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10
Q

What is the orbital septum

A

Thin sheet of fibrous tissue originating from orbital rim periosteum blends with tarsal plates
• Orbital septum & tarsal plates separate subcutaneous tissue
of eyelid and orbicularis oculi muscle from intra-orbital
contents
• Acts as a barrier against superficial infection spreading from
the pre-septal to post-septal space (orbital cavity proper)
Blends with tarsal plates and tendon of lps

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11
Q

What is periorbital (pre-septal) cellulitis

A

Difficultto tell the difference between peri orbital or orbital - need to refer to specialist - peri - oral antibiotics, orbital need surgical drainage and antibiotics?
• Secondary to superficial infections e.g. from bites, wounds,
– May be secondary to bacterial sinusitis (fronto-ethmoidal sinuses) in children
• Confined to tissues superficial to orbital septum (and tarsal plates)
• Ocular function (eye movements/vision) remains unaffected
• Can be difficult to differentiate between peri-orbital and the more severe orbital cellulitis
• If any doubt, urgently refer (high dose IV antibiotics + surgical drainage)
Infection in front of septum - subcutaneous tissues of eyelid - t is very red or swollen - may be sendary to bite or break in thhe skin. Confined in front of septum and plates. Does not affect structures to do with ocular function. Eye movements and vision is normal.

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12
Q

What is orbital cellulitis

A

Infection WITHIN the orbit* posterior or deep to the orbital septum
*involving orbital tissue/fat and extraocular muscles not the globe of the eye itself
Orbital veins drain to cav sinus -> pterygoid v plexus -> facicalveins - potental route for infection to spread - > cav sinus thrombosis, meningitis, SSSSS

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13
Q

What are the contents of the orbital xvaoty

A

• Eyeball • Fat • Associated extra-ocular muscles • Nerves and blood vessels • Lacrimal apparatus

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14
Q

What is the lacrimal apparatus

A

Structures involved in tear film production and drainage
• Lacrimal gland (tear production), lacrimal sac and ducts (tear drainage)
– Ducts = canaliculi and nasolacrimal duct
• Blinking (orbicularis oculi-palpebral part) washes tear film across front of eye, rinsing and lubricating conjunctivae and cornea
• Tears are ultimately drained into nasal cavity
• Obstruction to the drainage system leads to epiphora (overflow of tears over lower eyelid)
Spr

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15
Q

Describe teh anatomy of the eyeball

A

• Eyeball has three layers
• Outer: sclera (white of eye) continuous
anteriorly as transparent cornea- Choroid, becomes ciliary body, becomes iris - all the choroid layer
• Middle: choroid, ciliary body and iris (vascular) - Choroid, becomes ciliary body, becomes iris - all the choroid layer
• Inner: retina (inner photosensitive layer lying on an outer pigmented layer)
• Eyeball is maintained in position by
• Suspensory ligament (sits underneath like a sling)
• Extra-ocular muscles
• Orbital fat ++ Lots of fat to hold eye off the floor of the orbit

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16
Q

What is teh conjunctiva

A

• Conjunctiva is a transparent mucous membrane
– Produces mucous and tears
• Covers white of eye (sclera) and lines inside of eyelids (forming a conjunctival sac); does not cover over cornea
– Limbus (junction of conjunctivae with cornea)
• Highly vascular with small blood vessels within the membrane A
• Inflammed and injected in infections e.g. conjunctivitis - Conjunctivitis - infection - itchy, engorgement of blood vessels
• Haemorrhage from blood vessels readily visible as a subconjunctival haemorrhage - not to worry

17
Q

Descrbe how light is focused

A

• Need transparent structures and medium

• Need to refract light* (bending of light) to
bring to a focal point - macula

  • Several structures refract light (all transparent)
  • Cornea and its associated tear film - very important
  • Lens
  • Aqueous humour and vitreous humour
  • Shape of your eyeball also effects ability to focus light appropriately onto retina
  • Myopia (short-sighted) - eyeball too long
  • Hypermetropia (long-sighted)
18
Q

What are rods and cones

A

• Rods (active at low light levels, do not
mediate colour vision)
• Abundant in peripheral parts of retina • Cones (high definition, colour vision- active
at high light levels) • Concentrated within the macula of the retina • Fovea = only cones

19
Q

How are apps interpreted

A

Photoreceptors - photosensitive part of the yes - rods and cones
• Action potentials generated in response to
light pass via retinal ganglion cells (RGC)

• RGC axons collect in area of optic disc forming the optic nerve
– Optic disc = blind spot as no
photoreceptors present here

• Action potentials propagated along visual pathway to occipital lobe for interpretation

20
Q

What is the accommodation reflex

A

Focusing Near Objects Requires Greater Refraction of Light
F• Light rays from near-objects are more divergent
• Greater refraction, beyond capabilities of cornea (which is fixed in shape) to bring into focus on retina
• Eye accommodates
– Pupil constricts (limits amount of light coming through)
– Eyes converge (to ensure image remains focused on same point of retina in both eyes)
– Lens becomes more biconvex (fatter) by contraction of ciliary muscle
• Note, as we age the lens becomes stiffer and less able to change shape
– Presbyopia (age-related inability to focus near-object)

21
Q

What can cause blurring of vision

A

Pathology affecting
• transparency of structures anterior to retina
- e.g. opacity in lens such as cataract,
• ability of structures to refract light
- e.g. irregularity of corneal surface
(astigmatism), ability of lens to change shape (presbyopia), or shape of eyeball
• and the retina (including macula) or optic nerve
• E.g. retinal detachment, age-related macular
degeneration, optic neuritis
• will cause blurring of vision/ decreased acuity

22
Q

What are the fluids which help maintain the shape o the eyball

A

Aqueous humour filling anterior and posterior chambers

Vitrous humour within vitreous chamber

23
Q

Scribe the production and drainage of aqueous humorist

A

• Aqueous humour secreted by ciliary
processes within ciliary body
• Flows from posterior chamber, through pupil into anterior chamber
• Nourishes lens and cornea
• Drains through iridocorneal angle (between iris and cornea)
• Via trabecular meshwork into canal of
Schlemm (circumferential venous channeldraining into venous circulation)

24
Q

What si glaucoma

A

Optic nerve Damage Secondary to Raised Intraocular Pressure
• Drainage of aqueous humour from anterior chamber blocked causing rise in intra-ocular pressure
– Can develop chronically or acutely
• Chronic=open-angle glaucoma [most common]
– Trabecular meshwork deteriorates as we age
– Many asymptomatic [picked up on routine eye tests]
– Increased IOP -> ↑ optic disc cupping
– Gradual loss of peripheral vision
• Acute-=closed-angle glaucoma [less common]
– Narrowing of iridocorneal angle
– Ophthalmological emergency
• Sight-threatening - Something has caused the pressure to increase. This needs attention much sooner. Iris plushies forward and narrows he angle. Obstructing the outflow so pressure rises very quickly - immediate detrimental effect - damagopting nerve - sight loss

25
Q

Describe the presentation fo acute angle closure glaucoma

A
  • Older patient 55 years + (most common 70s-80s)
  • Acutely painful red eye ++
  • Irregular oval-shaped pupil (fixed)
  • Blurring of vision
  • Halo’s around lights (due to corneal oedema)
  • Nausea and vomiting
  • Medical (drugs to reduce IOP) then surgical treatment
26
Q

Which are the muscles that move the eyeball

A

• Six muscles move the eyeball and have attachment to the sclera
– Superior, inferior, medial and lateral rectus
– Superior and inferior oblique
• Four muscles (the recti) arise from a common tendinous ring at the apex of the orbit
• Nerve innervation can be remembered by LR6 SO4

27
Q

What happens at resting gaze

A

Primary Resting Gaze (position of rest) Equal and opposite pull of all extra ocular muscles
• Constancy of activity in all extra ocular muscles on the eyeball,
even at rest
• Each muscle has antagonist of its movement but during resting gaze their actions are balanced allowing for forward gaze

28
Q

What happens when oen extra oxxular muscles contract

A

• Moving eye position involves exerting greater pull through action of certain extraocular muscles, while its antagonist relaxes
• Muscles moving both eyes must be highly co-ordinated and move simultaneously - Communication at level of brain stem that les other eye know hitch way moving
– Malalignment causes diplopia

29
Q

What are the actions of SR

A
Superior rectus (SR) will
IR
– Elevate
– Slightly intorts (internally rotates)
– Slight adducts (pull eye medially)
30
Q

What are the cations of inferior rectus

A
  • depress
  • slightly extort
  • slightly adduct
31
Q

What are teh actions of superior and inferior obliges

A

• Superior* and inferior oblique (IO) approach eyeball from anteromedial corner of orbit IO
– *consider the functional pull of SO being from
the area of its trochlea
• Superior oblique will
– Intort (internally rotate)
– Depress
– Slightly abducts(pull eye laterally) SO

• Inferior oblique will
– Extort (externally rotate) 
– Elevate
IO
– Slightly abduct (pulls eye laterally)
32
Q

What happens if one muscle is weaknened

A
  • If a muscle is weakened, its ‘influence’/pull on the eyeball is lost- other muscle actions no longer antagonised (“balanced”)
  • Resting position of eyeball changes = strabismus (squint)
  • Can be congenital or acquired e.g. cranial nerve lesions
33
Q

Describe he clinical examination of eye movement

A

Need to Isolate Each Muscle to Test Them .. Clinical Examination of Eye Movements
• Lateral and medial rectus
– Straight forward as each only performs one action on the eye
– Abduction and adduction of the eye
Why the ‘H’?
• elevation and depression (in midline) involves two muscles each

• Move starting position of eye
– Medially (adducting) first or laterally (abducting) first
– before elevating and depressing
• Changing starting position (abducted vs adducted) changes line of pull for
superior/inferior recti and oblique muscles
– Dominant actions on eyeball therefore change
• Move the direction of gaze in line with pull of the muscle then elevate and
depress

34
Q

What are the stations poistion to test each muscle

A

Lateral placed elevation - sup and inf rectus

Medial placed elevation - obliques

35
Q

What can affect the cranial nerves that innervate the axtraccular muscles

A

• Abnormalities of eye movements and diplopia (double vision due to
malalignment of the eyes)
– May be obvious from initial inspection of the eye
– And/or become more apparent on testing eye movements
• Cranial nerves III, IV, VI innervate muscles that move the eyeball
• The cranial nerves can be affected by raised intracranial pressure (e.g.
intracranial haemorrhage or tumour)
– CN VI most commonly affected of the three in this context
• But all can also be affected by vascular disease (microvascular complications) from diabetes and hypertension

36
Q

Describe cn iii palsies

A

• Most extra-ocular eye muscles innervated by CN III (except LR and SO) Dow and out bc lr and so onopposed
• Innervates majority of muscle of eyelid (LPS)
• Carries parasympathetic function to the sphincter pupillae muscle causing constriction
– Run on outside of nerve
• Compressive lesions (raised ICP tumour, aneurysm
– Pupil involved
• Vasculopathic (microvascular) lesions (e.g. diabetes/hypertension)
– Pupil spared
Bc tends to involved blood vessels supplying deeper parts of the nerve. Parasympathetics aren’t involved as early.

37
Q

Describe cn ivpalsies

A

• Innervates superior oblique muscle only
• Superior oblique muscle acts to INTORT, and depress and abduct eye
• Lose these actions so eyeball is held EXTORTED, slightly elevated and adducted
• Compensate for the slight extortion of eyeball by tilting the head
slightly (not seen in image)
• Abnormality in gaze can be very subtle and often missed
• Worsening diplopia (on downward vertical gaze) especially looking
down and medially e.g. walking down stairs, reading
– Remember SO is main depressor of the eyeball when in adduction

38
Q

Descrbe cn vi palsies

A
• Innervates lateral rectus • Unopposed pull of medial rectus muscle 
• Unable to abduct the eye on affected
side 
• Report diplopia, made worse on
horizontal gaze
39
Q

What s the mostly likely cause for cn iii iv vi lesions

A

• Most likely cause for CN III, IV and VI lesions is vasculopathic
– Patients will be otherwise asymptomatic (apart from signs/symptoms directly relating to CN
lesion)
– Lesions usually self-resolve within few months)
• History will help give a clearer indication for more concerning underlying cause
– Headache (+/-) vomiting could suggest raised ICP (secondary to tumour or haemorrhage)
– Recent head injury
– Presence of pupil involvement in CN III lesions is of immediate concern