OPHTHALM Flashcards

1
Q

What structures are contained in the bony orbits?

A
  1. The eyeballs
  2. Extra-ocular muscles
  3. Nerves
    => Optic, oculomotor, trochlear, trigeminal and abducens
  4. Blood vessels
  5. (Most of) the Lacrimal apparatus.
  6. Orbital fat
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2
Q

What is the purpose of orbital fat?

A

Fills any space that is not occupied by other structures

Cushions the eye and stabilises the extraocular muscles.

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3
Q

What are the three main pathways by which structures can enter and leave the orbit?

A
  1. Optic canal
  2. Superior orbital fissure
  3. Inferior orbital fissure

(There are other minor openings into the orbital cavity.)

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4
Q

What goes through the optic canal?

A

transmits the optic nerve and ophthalmic artery.

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5
Q

What goes through the superior orbital fissure?

A

transmits the lacrimal, frontal, trochlear (CN IV), oculomotor (CN III), nasociliary and abducens (CN VI) nerves.

It also carries the superior ophthalmic vein.

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6
Q

What goes through the inferior orbital fissure?

A

transmits the:

Zygomatic branch of the maxillary nerve,
Inferior ophthalmic vein,
Sympathetic nerves.

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7
Q

How can the layers of the eyeball be divided?

A

Fibrous
Vascular
Inner

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8
Q

What makes up the Fibrous layer of the eyeball?

What is the main function?

A

The outermost layer.
Consists of the sclera and cornea

Their main functions are to provide shape to the eye and support the deeper structures

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9
Q

What is the main function of the sclera?

A

The sclera provides attachment to the extraocular muscles; it is visible as the white part of the eye.

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10
Q

What is the main function of the cornea?

A

The cornea is transparent and positioned centrally at the front of the eye; it refracts the light entering the eye

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11
Q

What does the vascular layer of the eyeball consist of?

A

the choroid, ciliary body and iris

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12
Q

What is the Choroid ?

A

= layer of connective tissue and blood vessels.

provides nourishment to the outer layers of the retina.

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13
Q

What is the ciliary body?

A

= comprised of two parts – the ciliary muscle and ciliary processes.

=> The ciliary muscle = a collection of smooth muscles fibres.

=> These are attached to the lens of the eye by the ciliary processes.

The ciliary body controls the shape of the lens, and contributes to the formation of aqueous humour.

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14
Q

What is the iris?

A

= circular structure, with an aperture in the centre (the pupil).

The diameter of the pupil is altered by smooth muscle fibres within the iris, which are innervated by the autonomic nervous system.

It is situated between the lens and the cornea.

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15
Q

What is the inner layer of the eyeball?

A

= the retina

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16
Q

What are the 2 layers of the retina?

A
  1. Pigmented (outer) layer

2. Neural (inner) layer

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17
Q

Neural/inner layer of retina

A

Consists of photoreceptors, the light detecting cells of the retina.

It is located posteriorly and laterally in the eye.

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18
Q

Pigmented/outer layer of retina

A

Formed by a single layer of cells.

Attached to the choroid and supports the choroid in absorbing light (preventing scattering of light within the eyeball).

It continues around the whole inner surface of the eye.

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19
Q

Where is the non-visual retina?

A

Anterior of the retina

the pigmented layer continues but the neural layer does not

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20
Q

Where is the optic part of the retina?

A

Posteriorly and laterally

Both layers of the retina are present.

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21
Q

What is the macula?

A

The centre of the retina is marked by an area known as the macula.

It is yellowish in colour, and highly pigmented.

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22
Q

What is the fovea?

A

The macula contains the fovea, which has a high concentration of light detecting cells.

It is the area responsible for high acuity vision.

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23
Q

What is the optic disc?

A

= the area where the optic nerve enters the retina

it contains no light detecting cells.

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24
Q

What is the vitreous humour?

A

= a transparent gel which fills the posterior segment of the eyeball.

has three main functions:
• Contributes to the magnifying power of the eye
• Supports the lens
• Holds the layers of the retina in place

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25
Q

What is the hyaloid canal ?

A

a narrow canal on the vitreous humour, which runs from the optic disc to the lens

this is a foetal remnant which was involved in oxygenation of the lens

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26
Q

Lens of the eye

A

The lens of the eye is located anteriorly, between the vitreous humour and the pupil.

The shape of the lens is altered by the ciliary body, altering its refractive power.

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27
Q

What fills the anterior and posterior chambers of the eye?

What does this do?

A

Aqueous humour

=> Nourishes and protects the eye.

It is produced constantly, and drains via the trabecular meshwork, an area of tissue at the base of the cornea, near the anterior chamber.

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28
Q

Where is the anterior chamber of the eye?

A

The anterior chamber is located between the cornea and the iris

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29
Q

Where is the posterior chamber of the eye?

A

The posterior chamber between the iris and ciliary processes

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30
Q

Arterial supply of the eyeball

A

receives arterial blood primarily via the ophthalmic artery (branch of internal carotid a.)

The ophthalmic artery gives rise to many branches

The central artery of the retina is the most important branch - supplying the internal surface of the retina

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31
Q

What is the venous drainage of the eyeball?

A

the superior and inferior ophthalmic veins.

These drain into the cavernous sinus.

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32
Q

What are the 7 extra-ocular muscles?

What are their general functions?

A
  1. Levator palpebrae superioris
  2. Superior rectus,
  3. Inferior rectus,
  4. Medial rectus,
  5. Lateral rectus,
  6. Inferior oblique
  7. Superior oblique.

LPS = superior eyelid movement
All others = eye movement

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33
Q

Levator Palpebrae Superioris - attachments

A

Originates from the lesser wing of the sphenoid bone, immediately above the optic foramen.

It attaches to the superior tarsal plate of the upper eyelid

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34
Q

Levator Palpebrae Superioris - innervation

A

oculomotor nerve (CN III)

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35
Q

What is the superior tarsal muscle ?

A

= a small portion of the LPS muscle, which contains a collection of smooth muscle fibres

HAS SYMPATHETIC INNERVATION

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36
Q

Superior Rectus - attachments

A

Originates from the superior part of the common tendinous ring.

Attaches to the superior and anterior aspect of the sclera.

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37
Q

Superior Rectus - innervation

A

Oculomotor nerve (CN III)

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38
Q

Superior Rectus - actions

A

Mainly elevation of eye.

Also contributes to adduction and medial rotation.

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39
Q

Inferior rectus - attachments

A

Originates from the inferior part of the common tendinous ring

Attaches to the inferior and anterior aspect of the sclera.

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40
Q

Inferior rectus - innervation

A

Oculomotor nerve (CN III)

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41
Q

Inferior rectus - actions

A

Mainly depression of the eye

Also contributes to adduction and lateral rotation.

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42
Q

Medial Rectus - attachments

A

Originates from the medial part of the common tendinous ring

Attaches to the anteromedial aspect of the sclera.

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43
Q

Medial Rectus - innervation

A

Oculomotor nerve (CN III)

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44
Q

Medial Rectus - actions

A

Adduction

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45
Q

Lateral rectus - attachments

A

Originates from the lateral part of the common tendinous ring

Attaches to the anterolateral aspect of the sclera.

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46
Q

Lateral rectus - innervation

A

Abducens nerve (CN VI).

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47
Q

Lateral rectus - actions

A

Abduction

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48
Q

Superior Oblique - attachments

A

Originates from the body of the sphenoid bone.

Its tendon passes through a trochlea and then attaches to the sclera of the eye, posterior to the superior rectus.

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49
Q

Superior Oblique - innervation

A

Trochlear nerve (CN IV).

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50
Q

Superior Oblique - actions

A

Depresses, abducts and medially rotates the eyeball.

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51
Q

Inferior Oblique - attachments

A

Originates from the anterior aspect of the orbital floor.

Attaches to the sclera of the eye, posterior to the lateral rectus

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52
Q

Inferior Oblique - actions

A

Elevates, abducts and laterally rotates the eyeball.

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53
Q

Inferior Oblique - innervation

A

Oculomotor nerve (CN III)

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54
Q

Monocular Causes of Acute Painless Vision Loss

A
Acute corneal disease
Acute cataract
Optic neuritis
Vitreous haemorrhage
Ischaemic optic neuropathy
Retinal vein/artery occlusion
Retinal detachment
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55
Q

Binocular Causes of Acute Painless Vision Loss

A
Pituitary tumour
Optic neuritis
Severe papilloedema
CVA
Migraine
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56
Q

What is retinal detachment?

A

= the retina at peels away from its underlying layer of support tissue.

Initial detachment may be localised, but without rapid treatment the entire retina may detach, leading to vision loss and blindness.

It is a surgical emergency.

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57
Q

Causes of retinal detachment

A
  • Age
  • Post-op/trauma
  • Diabetic retinopathy
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58
Q

Symptoms of retinal detachment

A
  • Floaters
  • Flashes
  • Field Loss
  • Fall in acuity

+ absent red reflex

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59
Q

Treatment of retinal detachment

A

Refer for urgent surgery (vitrectomy and reattachment)

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60
Q

What is vitreous haemorrhage?

A

= the extravasation of blood into the areas in and around the vitreous humour of the eye

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61
Q

Causes of vitreous haemorrhage

A
  • Proliferative diabetic retinopathy
  • Retinal tear
  • Retinal detachment
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62
Q

Symptoms of vitreous haemorrhage

A
  • Floaters = small black dots in vision

- Absent red reflex (if large bleed)

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63
Q

Treatment of vitreous haemorrhage

A

Vitrectomy and reattachment if necessary

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64
Q

What is a vitrectomy?

A

= removal of the vitreous and replacement it with saline

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65
Q

Central Retinal Artery Occlusion - symptoms

A

Sudden, profound, entire vision loss

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66
Q

Central Retinal Artery Occlusion - signs

A

Relative Afferent Pupillary Defect (RAPD)
Retinal Oedema
Pale retina (ischaemic)
Cherry red spots

+/- carotid bruits

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67
Q

Central/Branch Retinal Artery Occlusion - Investigations

A

To r/o causes of: HTN, DM, Heart problems, GCA

  • BP
  • FBC, ESR, glucose
  • Carotid USS
  • Cardiac Echo
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68
Q

Central Retinal Artery Occlusion - management

A

REFER to eye casualty (&TIA clinic)

Rebreathe into paper bag (CO2 dilates vessels)

Ocular massage
Acetazolamide (to decrease IOP)
Paracentesis (to decrease IOP)

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69
Q

in which class of drugs is Acetazolamide?

A

carbonic anhydrase inhibitors

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70
Q

Branch Retinal Artery Occlusion - symptoms

A

Sudden central or sectoral vision loss

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71
Q

Branch Retinal Artery Occlusion - signs

A

RAPD
Field Defect
Signs of hypertensive retinopathy

+/- carotid bruits

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72
Q

Branch Retinal Artery Occlusion - management

A

Refer to eye casualty & TIA clinic

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73
Q

Central Retinal Venous Occlusion - symptoms

A

Blurred, widespread vision loss

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74
Q

Central Retinal Venous Occlusion - signs

A

Widespread retinal haemorrhages
Oedema
Disc swelling
Tortuous veins

+/- cotton wool spots

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75
Q

Central/Branch Retinal Venous Occlusion - investigations

A

To r/o causes of: HTN, DM, Glaucoma, Blood problems

  • BP
  • FBC, ESR, glucose
  • Intraocular Pressure
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76
Q

Central/Branch Retinal Venous Occlusion - management

A

Refer to eye casualty

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77
Q

Branch Retinal Venous Occlusion - symptoms

A

Blurred, central vision loss

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78
Q

Branch Retinal Venous Occlusion - signs

A

Focal retinal haemorrhages

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79
Q

Branch Retinal Venous Occlusion - management

A

Refer to eye casualty

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80
Q

What are Mydriatic eye drops?

A

Dilate the pupil

Short-acting, relatively weak mydriatics, such as TROPICAMIDE (action lasts for up to 6 hours), facilitate the examination of the fundus of the eye.

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81
Q

What causes the fundal/red reflex?

A

caused by light reflecting back from the vascularised retina

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82
Q

When might the fundal/red reflex be absent?

A

ADULTS - cataracts, vitreous haemorrhage, retinal detachment.

CHILDREN - congenital cataracts, retinal detachment, vitreous haemorrhage, retinoblastoma.

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83
Q

Haemorrhages causing red eye

A
  1. Sub-conjunctival = blood pools behind the conjunctiva

2. Retrobulbar = blood pools behind the eyeball

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84
Q

Risk factors for sub-conjunctival haemorrhage

A

post-surgery,
anticoagulants,
trauma,
URTI

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85
Q

Risk factors for retrobulbar haemorrhage

A

anaesthetic injection,

trauma/perforation => ask if have been using hammer/chisel

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86
Q

sub-conjunctival haemorrhage - symptoms

A

= asymptomatic and harmless

POSTERIOR BORDER VISIBLE

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87
Q

sub-conjunctival haemorrhage - management

A

reassure, resolution in 2 weeks

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88
Q

retrobulbar haemorrhage - symptoms

A

proptosis, decreased eye movement, increased IOP

POSTERIOR BORDER NOT VISIBLE

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89
Q

retrobulbar haemorrhage - management

A

= CT scan needed

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90
Q

What are the causes of red eye?

A

Haemorrhages - subconjunctival/retrobulbar

Vascular congestion - localised/generalised

Acute glaucoma

Trauma

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91
Q

Conjunctivitis

A

= inflamed conjunctiva with bacterial/viral/allergic cause

  • Redness in conjunctival fornixes
  • Discharge
  • Photophobia
  • Blanches

• Normal vision, normal pupil, no pain

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92
Q

Keratitis

A

= inflammation of the cornea

  • Ciliary redness
  • Does not blanche
  • Vision blurry/impaired
  • Constricted pupil
  • Discharge
  • Moderate/severe pain
  • Photophobia
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93
Q

Keratitis - Management

A
  • Steroids (PO/topical) +/- ABX
  • Analgesia

UNLESS HSV KERATITIS - DO NOT GIVE STEROIDS (topical acyclovir)

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94
Q

Uveitis

A

= inflamed iris, ciliary body, choroid

  • Ciliary redness
  • Does not blanche
  • Vision blurry/impaired
  • Constricted pupil
  • No discharge
  • Moderate/achy pain
  • Photophobia
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95
Q

Uveitis - Management

A
  • Steroids (PO/topical) +/- ABX

- Analgesia

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96
Q

Viral causes of conjunctivitis

A

= Adenovirus, HSV, molluscum

“Gritty” sensation
Watery discharge
Lymphadenopathy

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97
Q

How is viral/bacterial conjunctivitis managed?

A

Chloramphenicol/fusidic acid drops and eye hygiene

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98
Q

Bacterial causes of conjunctivitis?

A

= S. aureus, S. pneumoniae

“Gritty” sensation
Purulent discharge
Lymphadenopathy

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99
Q

Allergic conjunctivitis

A

= hay fever, pollen, dust

Itchy/stingy eyes

Tx = antihistamines

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100
Q

When would you consider chlamydial conjunctivitis?

A

consider if prolonged in young adults

=> STI history

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101
Q

Neonatal conjunctivitis

A

gonococcal/chlamydial infection

can cause permanent scarring and vision loss

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102
Q

What can cause keratitis?

A

Infection – pseudomonas, HSV*

Trauma – foreign body, post-op, perforation

Inflammation – RA/SLE/Wegner’s

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103
Q

Risk factors for developing keratitis

A

contact lenses, dry eyes

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104
Q

How is HSV keratitis different from other keratitis?

A

Causes Dendritic ulcers

DO NOT GIVE STEROIDS (Tx = acyclovir)

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105
Q

Complications of keratitis

A

= corneal ulcer

Can perforate, so needs URGENT REFERRAL and STEROIDS

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106
Q

Assessment of Ocular Trauma

A
  1. Thorough Hx – hammer and chisel?
  2. Visual Acuity
  3. Ophthalmoscopy
  4. Slit lamp – check for abrasions
  5. Systemic examination (esp. CNS)
  6. CT
    => AVOID MRI if possibility of forgein body
107
Q

What is episcleritis?

What is it sometimes associated with?

A

= Superficial inflammation of episclera

Associated with autoimmune disease (e.g. SLE)

108
Q

Symptoms of episcleritis

A

Red Eye
Usually no pain (or if pain, only mild/achy)

Vision not affected
Blanches with phenylephrine

109
Q

Management of episcleritis

A

Steroid drops/NSAIDs

=> self-limiting

110
Q

What is scleritis?

A

Deeper inflammation of sclera + episclera

Associated with Infection and connective tissue diseases

111
Q

Symptoms of scleritis

A

Red eye
Moderate/severe pain
Blurring of vision and photophobia

No blanching with phenylephrine

112
Q

Management of scleritis

A

Oral steroids

=> needs referral

113
Q

Uveitis

A

= inflamed iris, ciliary body, choroid

  • Ciliary redness (does not blanche)
  • Vision blurry/impaired
  • Constricted pupil
  • No discharge
  • Moderate/achy pain
  • Photophobia
114
Q

Uveitis - Management

A
  • Steroids (PO/topical) +/- ABX

- Analgesia

115
Q

How is viral/bacterial conjunctivitis managed?

A

Chloramphenicol/fusidic acid drops and eye hygiene

116
Q

Foreign body in eye - symptoms and management

A

Sx = Sudden onset irritation + photophobia

Mx:
=> Eye Casualty
=> FB removal, analgesia, prophylactic ABX

117
Q

Chemical Eye Burn - Signs and Sx

A
  • Pain, redness, irritation, tears
  • Inability to keep the eye open
  • Sensation of something in the eye
  • Swelling of the eyelids

• Blurred vision
=> Complete loss of vision indicates a severe burn

118
Q

Immediate management of chemical burn to the eye

A
  1. Immediate irrigation with water
  2. Determine if acid/alkali:
    => Alkali is worse (penetrates the eye more readily to damage external and internal structures)
  3. Careful eye inspection
  4. Ophthalmology referral – topical ABX and steroids, topical dilators, analgesia, artificial tears.
119
Q

Common causes of blunt trauma to the eye?

A

= sports injury, automobile accident, fight, job-related injury.

120
Q

Presentations of blunt trauma to the eye?

A
Can present in many ways:
•	Hyphaema (can cause acute glaucoma if blocks drainage)
•	Periorbital haematoma
•	Retinal tear/haemorrhage/detachment
•	Traumatic cataract
•	BLOWOUT FRACTURE
121
Q

What is hyphaema?

A

blood in anterior chamber of the eye

122
Q

Blowout fracture

A

Increased pressure in orbital cavity causes floor fracture into maxillary sinus => eye muscles can get trapped

Sx = restricted eye movement, periorbital swelling

Ix = X-ray, CT

Mx = Conservative (unless muscle trapped)

123
Q

Thyroid eye disease

A

Periorbital oedema,
Eyelid retraction,
Exophthalmos,
Diplopia

124
Q

Orbital cellulitis - symptoms and complications

A
  • Eyelid oedema + erythema
  • Painful eye movements/ visual disturbance/ proptosis.
  • Systemically unwell

Complications:
• Optic neuropathy
• Orbital abscess,
• Brain abscess/meningitis

125
Q

Orbital cellulitis - management

A
  • Admit to hospital for systemic ABX

* Monitor optic nerve function

126
Q

Endophthalmitis

A

= inflammation of the internal eye

Causes:
- Post-op/trauma

RFs

  • Immunocompromised
  • Blepharitis (=inflammation along the edges of the eyelids)
127
Q

What is blepharitis?

A

=inflammation along the edges of the eyelids

128
Q

Management of Endophthalmitis?

A

Intravitreal ABX

129
Q

Idiopathic orbital inflammatory disease

A

= non-infectious/neoplastic inflammation
(therefore a diagnosis of exclusion)

Symptoms:

  • Rapid onset, painful, periorbital oedema
  • Eye muscle paralysis

Management:
- Steroids

130
Q

Features of a swollen optic disc on fundoscopy

A
  • Blurred disc margin
  • Haemorrhages around disc
  • Smaller cup:disc ratio
131
Q

Causes of swollen optic disc

A
  • Optic neuritis
  • Papilloedema
  • Malignant HTN
  • GCA / Arteritic anterior Ischemic Optic Neuropathy
  • Non-arteritic AION
132
Q

What is optic neuritis?

What can cause it?

A

Inflammation of the optic nerve,

caused by:

  • Idiopathic
  • Infection – syphilis, HSV, mumps
  • Demyelination – MS
  • SLE/sarcoid, DM
  • Ischaemia (GCA)
133
Q

Optic neuritis - symptoms

A

UNTILATERAL:

  • Blurred vision and decreased acuity
  • Central scotoma
  • Red desaturation
  • RAPD
  • Pain on eye movement+/- neuro Sx like numbness
134
Q

Optic neuritis - management

A

= steroids

135
Q

What is papilloedema?

A

Swollen optic disc due to raised ICP.

Causes:

  • Brain tumour/abscess
  • Head injury/brain bleed
  • Meningitis/encephalitis
  • Idiopathic
136
Q

Papilloedema - symptoms

A

BILATERAL:

  • Transient blurred vision
  • Gradual, progressive field loss
  • Enlarged blind spot
  • Headache/vomiting
137
Q

Papilloedema - management

A

= investigate and treat underlying cause

138
Q

Swollen optic disc due to Malignant HTN

A

= swollen disc due to rapid increase in BP to >180/120, and fundoscopy features of hypertensive retinopathy

139
Q

What are fundoscopy features of hypertensive retinopathy?

A

Grade I – subtle arterial narrowing

Grade 2 – AV nipping

Grade 3 – cotton wool spots, haemorrhages, exudates

Grade 4 (malignant) – above features and also swollen optic disc.

140
Q

Malignant HTN - Sx

A

BILATERAL:

  • Decreased acuity
  • Headache
  • Eye pain
  • +/- focal neuro signs
141
Q

Malignant HTN - Mx

A

= hospital admission and antihypertensives.

142
Q

GCA / Arteritic AION

A

= Inflammation and occlusion of vessels supplying the optic nerve, causing infarction.

UNILATERAL (may become bilateral):

  • Headache
  • Jaw/temportal pain
  • SUDDEN VISION LOSS
143
Q

GCA / Arteritic AION - Diagnosis and Mx

A

Investigations:

  • Raised ESR/CRP
  • Also check cholesterol/TGs, glucose, BP

Mx = EMERGENCY, high-dose steroids

144
Q

Non-arteritic AOIN

A

= occluded posterior cerebral artery causing optic nerve infarction

Caused by atherosclerosis (DM, HTN, increased lipids).

Symptoms – UNILATERAL SUDDEN VISION LOSS

145
Q

Non-arteritic AOIN - diagnosis and Mx

A

Investigations:

  • ESR (norma)
  • Cholesterol/TGs, glucose, BP

Management = Treat cause, aspirin

146
Q

Optic nerve atrophy

A

= death of optic nerve fibres

Cause = Compression or decreased blood supply

  • Optic neuritis, ischaemia, glaucoma
  • Chronic papilloedema

Ix = MRI/CT

147
Q

What is the most common cause of vision loss in the younger population?

A

Diabetic retinopathy

148
Q

Diabetic retinopathy - pathophysiology

A
  1. Hypoperfusion of retinal vessels
    => ischaemia
  2. Pericyte death in vessels
    => Causes weakened walls, causing microaneurysms and oedema
  3. Macrophage accumulation to clear debris
    => Causes exudates.
  4. A-V shunts open to overcome hypoxia
    => Causes intra-retinal microvascular abnormalities
  5. Neovascularisation:
    => Release of VEGF due to hypoxia causes growth of abnormal, weak vessels
    => Leads to haemorrhages
149
Q

Diabetic retinopathy - Risk factors

A
  • Duration and poor control of DM
  • HTN / renal disease
  • Pregnancy
  • Age
  • Lifestyle – smoking/alcohol/diet
150
Q

What are the forms of diabetic retinopathy?

A
  1. Non-proliferative (NPDR)
  2. Pre-proliferative
  3. Proliferative (PDR)
  4. Diabetic Maculopathy
151
Q

Non-proliferative DR - Features

A

Asymptomatic

Features:

  • microaneurysms,
  • exudates,
  • haemorrhages (dot, blot, flame),
  • cotton wool spots (infarcted axons)

If severe or pre-proliferative – intraretinal microvascular abnormalities (IRMAs)

152
Q

Non-proliferative DR - Management

A
  • Diabetes control = most important!

- Careful monitoring

153
Q

Proliferative DR - Features

A

Asymptomatic until haemorrhage occurs.

Features:

  • Irregular new vessels (over disc or elsewhere)
  • Haemorrhage (vitreous or pre-retinal)
  • Neovascularised iris
154
Q

Proliferative DR - Management

A
  • Diabetes control = most important!

- Pan-retinal laser photocoagulation (PRP)

155
Q

Pan-retinal laser photocoagulation (PRP)

A

= use of a laser to burn away peripheral photoreceptors, to decrease O2 demand and decrease VEGF release and creation of new vessels.

Start far out, review in 4-6 weeks and then burn further if needed.

156
Q

Diabetic Maculopathy

A

When retinopathy affects the macula.

Features:

  • Focal or widespread retinal oedema.
  • Affects vision
157
Q

What eye diseases other than retinopathy does DM pre-dispose people to?

A
  • Increased risk of eyelid infections
  • Increased risk of cataracts
  • Delayed healing of abrasions/ulcers/wounds
158
Q

What is the most common cause of vision loss in the UK?

What kind of vision loss does this condition cause?

A

Age-related Macular Degeneration

Causes progressive, irreversible, CENTRAL vision loss.

159
Q

Investigations in ?AMD

A
  1. Eye examination – fundoscopy, acuity, central visual field test (Amsler grid).
  2. Fundus Photos
160
Q

Dry AMD

A

~90% of AMD

Gradual vision loss (years)

Pathophysiology:
=> Lipid debris thickens Bruch’s membrane = DRUSEN
=> Retinal Pigment Epithelium atrophy = pale areas on retina

161
Q

Dry AMD - Management

A

Ophthalmology referral

Counsel patient:
• Cannot predict how bad it will get
• Tx does not reverse damage, just stops progression
• Impact – struggle to recognise faces, difficulty reading & driving, increased falls risk
• Smoking cessation

Low-level visual aids

Consider antioxidant supplements

162
Q

Wet AMD

A

~10% of AMD

Sudden, severe vision loss (months), starting with distorted images.

Pathophysiology:

  • New, abnormal vessels pierce Bruch’s membrane
  • Leak fluid and blood = oedema, haemorrhage & RPE detachment
  • Fibrotic tissue
163
Q

Wet AMD - Management

A

Anti-VEGF

Focal laser photocoagulation – destroy areas of neovascularisation

164
Q

Cataracts

A

= clouded opacity on/within the lens due to liquefaction of lens content.

165
Q

Causes of cataracts

A

Age = leading cause

Trauma
Metabolic – DM, Wilson’s disease
Toxins
Systemic disease 
Maternal infection
Hereditary
166
Q

General symptoms of cataracts

A
  • Decreased acuity and blurring
  • Increased myopia
  • Faded colours
  • Trouble with bright lights and night vision
167
Q

Cataracts - diagnosis

A

Hx

Slit lamp examination

168
Q

Cataracts - management

A

depends on the impact on the patient’s life (occupation/driving/ADLs)

  1. Patient Assessment
    => Assess refractive power of current lens
    => Eye health (?any concurrent glaucoma/AMD)
  2. Phacoemulsification:
    => US waves emulsify cataract, which is then removed via incision
    => Corrective intraocular lens inserted
169
Q

Possible complications of cataracts op

A
Possible complications:
•	Post-capsule opacification
•	Retinal detachment
•	Vitreous loss
•	Endophthalmitis
170
Q

Glaucoma

A

= diseases causing characteristic damage to the optic disc, usually use to increased IOP (>21mmHg).

171
Q

Normal-tension glaucoma

A

there is normal IOP but the disc is damaged

172
Q

Normal cycle of aqueous fluid

A
  1. Ciliary bodies secrete aqueous into the posterior chamber.
  2. Passes through the iris into the anterior chamber
  3. Drained via the trabecular meshwork in the anterior angle
173
Q

Where is the anterior angle?

A

= the angle between the iris and the cornea.

174
Q

Open Angle Glaucoma

A

Wide anterior angle allows increased aqueous entry but there is decreased drainage (aging may cause sclerosis of meshwork).

=> Increased IOP damages optic nerve fibres.

175
Q

Open Angle Glaucoma - symptoms

A

Asymptomatic until almost blind => need screening

Visual field loss
=> Superior arcuate scotoma
=> Progress to tunnel vision => blindness.

176
Q

Open Angle Glaucoma - investigations

A

Visual fields – progressive decrease

Fundoscopy – optic disc changes

IOP (tonometer) – >21 mmHg

177
Q

Optic Disc Changes in Glaucoma

A

• Increased cup:disc ratio (>0.3/0.4)

• Oval cup
=> Normally the neuro-retinal rim is thickest Inferiorly and thinnest Temporally (I > S > N > T)
=> If the optic disc doesn’t follow the ISNT rule, then there may be glaucomatous damage.

• Disc atrophy

178
Q

Open Angle Glaucoma - management

A

aim is to prevent further loss, not reverse!

  1. Medical Eye Drops (in order of use)
    • PG analogues (e.g. iatanoprost) = increase drainage
    • Beta-blockers (Timolol) = decreased production
    • Carbonic anhydrase inhibitors (Acetozolamide) = decreased production
    • Alpha agonist = increase drainage and decreased production
  2. Laser Trabeculoplasty
  3. Surgical Trabeculectomy
179
Q

What is a surgical trabeculectomy?

A

involves making a hole in the sclera so the aqueous can drain into reservoir/bleb under the surface.

180
Q

What is a laser trabeculoplasty?

A

use a laser to unblock the trabecular meshwork

181
Q

Angle Closure Glaucoma

A

Narrow anterior angle becomes suddenly blocked, preventing drainage.

= EMERGENCY

Trigger is usually entering darkness and pupil dilating.

182
Q

Angle Closure Glaucoma - presentation

A

Sudden onset:

  • Acute pain + red eye
  • Blurred and decreased vision
  • Headache, nausea, vomiting
  • +/- prodromal “halos” around bright lights

Signs:

  • Sudden increase in IOP (to 70/80 mmHg)
  • Red eye
  • Clouded lens
  • Fixed, mid-dilated pupil
183
Q

Risk factors for angle closure glaucoma

“CLOSE”

A
Children (FHx)
Long-sighted
Old age
Shallow anterior chamber
Ethnicity (Asian)
184
Q

Angle Closure Glaucoma - Management

A
  1. URGENT HOSPITAL ADMISSION
  2. Medical:
    => Acetazolamide +/- timolol (decrease aqueous production)
    => Pilocarpine (pupil constriction opens drainage angle)

!!! also give prophylactically to other eye !!!

  1. Surgical:
    => Peripheral laser iridotomy
    => Trabectulectomy.
185
Q

Peripheral laser iridotomy

A

involves burning a hole in iris to allow drainage and the angle to reopen in angle closure glaucoma

also done prophylactically in other eye

186
Q

What is orthoptics?

A

= diagnosis and management of binocular vision and eye motility disorders.

187
Q

Manifest Squint

A

Heterotropia

= the visible deviation of one eye when eyes are open

=> ALWAYS PATHOLOGICAL

188
Q

Manifest Squint - Sx

A

diplopia in adults,

suppression in children.

189
Q

Manifest Squint - Dx

A

= cover test (bad eye fixes centrally when good eye is covered)

190
Q

Concomitant squint

A

Squint is the same irrespective of the gaze direction.

Causes = retinoblastoma, congenital cataract, Down’s

Childhood onset and lifelong

191
Q

Incomitant squint

A

degree of squint varies with gaze direction (increases when looking in the direction of affected muscles).

Causes = nerve palsies (CN 3, 4, 6) causing EOM paralysis
=> Sudden diplopia +/- neuro signs.

192
Q

Exotropia

A

Eye points temporally/outwards at rest

Moves nasally/inwards when opposite eye is occluded

193
Q

Esotropia

A

Eye points nasally/inwards at rest

Moves temporally/outwards when opposite eye is occluded

194
Q

Hypertropia

A

Eye points superiorly at rest

Moves inferiorly when opposite eye is occluded

195
Q

Hypotropia

A

Eye points inferiorly at rest

Moves superiorly when opposite eye is occluded

196
Q

CN III Palsy - signs

A

Ptosis – levator palpebrae

Down & out – SR, IR, MR, IO affected

There can be an efferent pupil defect (DILATED) or can be PUPIL-SPARING

197
Q

CN III Palsy - causes

A
Tumour
CVA
Orbital trauma
Demyelination
Posterior Cerebral Artery aneurysm
198
Q

CN IV Palsy - signs

A

Up & in – SO muscle affected

Compensatory head tilt

199
Q

CN IV Palsy - causes

A

Trauma = most common

Also:
Tumour
CVA
Demyelination
PCA aneurysm
200
Q

CN VI Palsy - signs

A

Eye Adducted – LR muscle affected

201
Q

CN VI Palsy - causes

A
Tumour
CVA
Orbital trauma
Demyelination
PCA aneurysm
202
Q

Latent Squint

A

Heterophoria

= tendency for eye deviation, BUT normally compensated

This is present in most people

203
Q

Latent Squint - Sx

A

If decompensated, can get:

  • headache,
  • eye strain,
  • diplopia
204
Q

Latent Squint - Dx

A

cover-uncover test

bad eye deviates to “rest” when covered, returns to central when uncovered

205
Q

Latent Squint - Mx

A

If symptomatic - orthoptic exercises and prism

206
Q

Management of squints

A
  1. Correct refractive error
    => CONVEX lenses for CONVERGENT squints
    => CONCAVE lenses for DIVERGENT squints
  2. Surgery to realign EOM
    => If no refractive error/lenses don’t help
207
Q

What is amblyopia?

A

“Lazy Eye”

= reduced vision in one eye.

208
Q

Causes of amblyopia

A

= lack of stimulation during critical period of visual development

  • Strabismic – brain ignored image from squinting eye (suppression)
  • Stimulus deprivation – something blocks image reaching retina (e.g. ptosis, cataract)
  • Anisometropic – difference in refractive errors of >1 dioptre (worse eye becomes “lazy”)
209
Q

When is the critical period of visual development?

A

birth – 7/8 years

210
Q

Amblyopia - Management

A

If treated in critical period, can reverse amblyopia.

=> Occlusion of good eye with eye patch

211
Q

What causes pupil dilation/mydriasis?

A

Dilator Pupillae muscle - Sympathetic innervation

212
Q

What causes pupil constriction/miosis?

A

Sphincter Pupillae - parasympathetic innervation

213
Q

Afferent and Efferent pathway of pupillary light reflex

A

Afferent = optic nerve (CN II)

Efferent = fibres running ALONG the oculomotor nerve (CN III)

214
Q

Consensual Pupil reflex

A

= light in one eye stimulates the efferent pathways to both.

2nd order neurons connect pretectal nucleus to BOTH Erdinger-Westphal Nuclei, stimulating efferent pathways

215
Q

Efferent pupillary defect

A

the affected pupil will never constrict

216
Q

Afferent pupillary defect

A

= both pupils will constrict a bit, but the “bad” eye less.

217
Q

Accommodation Reflex

A

Initiated by blurred vision +/- close object

  • Ciliary muscles contract
  • Zonula fibres relax
  • Lens becomes more globular
    => Leads to increased refractive power.
218
Q

What does maximum accommodation depend on?

A

depends on lens flexibility (this decreases with age).

219
Q

Components of accommodation reflex

A

Components:

  1. Accommodation – constrict ciliary muscle (= CN 3)
  2. Constriction – sphincter pupillae (= CN 3)
  3. Convergence – medial and lateral rectus (= CN 3 and 6)
220
Q

Horner’s Syndrome - Sx

A
Miosis (constriction)
Partial Ptosis (tarsal muscle affected, but not LPS)
Anhidrosis
221
Q

Horner’s Syndrome - causes

A

LESION OF SYMPATHETIC CHAIN:

Pancoast tumour
Cervical rib
Carotid aneurysm
Neck trauma
CNS disease
222
Q

Adie Pupil - Sx

A

Mydriasis
Light-near dissociation

+/- decreased tendon reflexes

223
Q

Adie Pupil - causes

A

Post-ganglionic parasympathetic lesion

=> Mostly post-viral/bacterial Infection

224
Q

Argyll-Robertson Pupil - Sx

A

Small, irregular pupils

Light-near dissociation

225
Q

Argyll-Robertson Pupil - Causes

A

Neurosyphilis

226
Q

What is Marcus-Gunn Pupil

A

= Relative Afferent Pupillary Defect

pupils respond differently to light stimuli shone in one eye at a time in a swinging flashlight test

227
Q

Marcus-Gunn Pupil / RAPD - Causes

A

Optic neuritis
MS (demyelination)
Ischaemia to optic nerve (e.g. GCA)

Trauma
Tumour
CVA

228
Q

What is light-near dissociation?

A

Pupillary light reaction is impaired while the near reaction (accommodative response) remains intact

229
Q

What is visual acuity?

What is normal distance VA?

A

= the ability of the eye to distinguish shapes and the details of objects at a given distance.

6/6 Snellen = average vision

230
Q

What is the range of visual acuity?

A

6/4 => 6/60 => 3/60 => 1/60

=> Count Fingers => Hand movements

=> Perception of light (PL) => No Perception of Light

231
Q

Conditions for Emmetropia

A

= perfect focussing onto retina

  • 60D = 40D (Cornea) + 20D (Lens)
  • Axial length: 22.22mm
232
Q

Ametropia

A

= some form of refractive error

Hypermetropia/ Myopia

233
Q

Myopia

A

Short-sighted – light focusses in front of the retina.

=> Refractive – eye refraction too strong (>60D)
=> Axial – eyeball too long (>22.22mm)

234
Q

Myopia - risk factors

A

Chinese ethnicity

Lots of close work/time indoors?

235
Q

Myopia - complications

A

increased risk of retinal detachment

236
Q

Myopia - correction

A

DIVERGENT/CONCAVE (negative) lens

237
Q

Hypermetropia

A

Long-sighted – light focuses behind the retina.

=> Refractive – eye refraction too weak (<60D)
=> Axial – eyeball too short (<22.22mm)

238
Q

Hypermetropia - risk factors

A

infants (but corrects as eyeball grows)

239
Q

Hypermetropia - complications

A

acute angle closure glaucoma

240
Q

Hypermetropia - correction

A

CONVERGENT/CONVEX (positive) lens

241
Q

Astigmatism

A

= unevenly shaped eyeball

=> asymmetry causes different degrees of refraction and 2 focus points

242
Q

Astigmatism - correction

A

Cylindrical lens

  • Has refractive power in only 1 meridian
  • Can be used in conjunction with a spherical (convex/concave) lens

=> Combination of spherical and cylindrical lens = toric lens

243
Q

Presbyopia

A

= loss of accommodation due to thickening and sclerosis of lens with age (>40 years).
=> At ~55 years accommodation is essentially zero.

Correction = “add on” positive lens for reading
=> combined with distance prescription = bi/varifocals

244
Q

Vision rules for driving

A

Minimum 6/12 vision with glasses and both eyes open

Read number plate from 20m

Sufficient visual fields

CANNOT DRIVE WITH DOUBLE VISION

245
Q

Stereopsis

A

= the overlap between the eyes, allowing depth perception

246
Q

Blind spot

A

= where the optic nerve leaves the retina

Not normally noticed due to overlap in visual fields

247
Q

What is the Visual Pathway?

A
  • Axons of retina converge to become optic nerve
  • Behind the retina, it becomes myelinated.
  • Passes through the optic chiasm and becomes optic tract
  • Fibres reach Lateral geniculate nucleus in thalamus
  • Rotation of fibres 90o inwards
    => Superior retinal fibres => medial
    => Inferior retinal fibres => lateral
  • Fibres rejoin to form optic radiation and rotate back to original position.
248
Q

Blood supply to visual cortex

A

= posterior cerebral artery

The medial part is also supplied by occipital branch of middle cerebral artery (protects fibres from macula in the event of a PCA occlusion).

249
Q

general rules of visual field loss

A

Any lesion in optic chiasm = BILATERAL LOSS

Any ONE-SIDED LOSS (homonymous) = retro-chiasmal and will be contralateral to the lesion

QUADRANTANOPIAS = temporal or parietal lobe lesions

250
Q

Where is the location of the lesion causing bitemporal hemianopia?

A

= optic chiasm lesion

  • Pituitary tumour,
  • Rathke’s pouch meningioma
  • Craniopharyngioma
251
Q

Where is the location of the lesion causing homonymous hemianopia?

A

= optic tract lesion

Defect will be on opposite side to lesion

252
Q

Where is the location of the lesion causing Superior Quadrantanopia ?

A

= temporal lobe lesion (inferior fibres capture superior visual field)

Defect will be on opposite side to lesion

253
Q

Where is the location of the lesion causing Inferior Quadrantanopia ?

A

= parietal lobe lesion (superior fibres capture inferior visual field)

Defect will be on opposite side to lesion

254
Q

Where is the location of the lesion causing visual field defect with macular sparing ?

A

Lesion of PCA but spared MCA

255
Q

Red Flag Eye Symptoms

A
  • Eye pain (moderate-severe)
  • Photophobia
  • Sudden and persistent (>60 minutes) visual loss
  • Red eye (especially if associated with pain and/or loss of vision)
  • Trauma to the eye
256
Q

Questions to ask about visual disturbance

A
  • One or both eyes affected?
  • Onset – sudden or gradual?
  • Constant or does it come and go?
  • How severe is the disturbance?
  • Does anything make it worse / better?
  • Does the visual disturbance affect distance or near vision, or both?
  • Is a specific area of vision affected? (e.g. peripheral, central)
  • Any double vision?
    => Images side by side / on top of each other / oblique angle?
  • Any positive visual symptoms?
  • Any visual distortions?
257
Q

What are “positive” visual symptoms?

A
  • Flashing lights or floaters
  • Presence of a “black curtain” across field of vision
  • Glare from low sun/car headlights
  • Halos around lights
258
Q

What are some visual distortions?

A

Straight lines appearing wavy

Sparkling lights moving across the visual field

Objects appearing larger or smaller than they really are

259
Q

Questions to ask about Eye Pain

A
  • Site (one/both, where?)
  • Onset (how, when, sudden/gradual)
  • Character (dull/achey/throbbing/sharp/worse on movement?)
  • Radiation
  • Associated Sx (N&V, headache, eye Sx)
  • Time course (change? getting worse?)
  • Exacerbating/relieving Factors:
  • Severity of pain
260
Q

Questions to ask about Eye Trauma

A

Determine mechanism of injury
=> Blunt, chemical, sharp

Document use of power tools/hammer and chisel/absence of safety goggles

Determine the size, speed and nature of the flying object

261
Q

Past Ocular Hx

A

Ask about previous episodes similar to their current presenting complaint.

Other eye problems/diagnoses.

Ask if the patient uses prescription glasses and if these are used for distance or near vision.

Ask if the patient uses contact lenses

262
Q

What does red desaturation indicate?

A

Optic neuritis

loss of colour vision (especially red) in the affected eye

263
Q

Periorbital vs. Orbital cellulitis

A

Have overlapping symptoms (e.g. swelling, erythema) but orbital cellulitis will present with more eye symptoms

=> pain on eye movement / visual disturbance / proptosis.

264
Q

Management of blepharitis

A

Hot compresses to eyelid margin and removal of debris with cotton buds dipped in cooled boiled water

+ Artificial tears if patients report dry eyes.