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Y4 Neuro and Special Senses > Opthalmology 1 > Flashcards

Opthalmology 1 Flashcards

1
Q

What is glaucoma?

A

optic nerve damage caused by a rise in intraocular pressure (IOP) due to a blockage in aqueous humour trying to escape the eye.

There are two types of glaucoma:
Open-angle glaucoma
Acute angle-closure glaucoma

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2
Q

What is normal intraocular pressure?

A

10-21 mmHg

It is created by the resistance to flow of aqueous humour through the trabecular meshwork

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3
Q

What is the difference between the pathophysiology of open angle glaucoma and acute closed angle glaucoma?

A

With open-angle glaucoma, there is a gradual increase in resistance to flow through the trabecular meshwork. The pressure slowly builds within the eye.

With acute angle-closure glaucoma, the iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining. This causes an acute build up of pressure.

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4
Q

Raised intraocular pressure causes cupping of the optic disc.

What is this?

A

In the centre of the optic disc is an indent called the optic cup, which is usually less than 50% of the size of the optic disc.

Raised intraocular pressure causes this indent to become wider and deeper, described as “cupping”. A cup-disk ratio greater than 0.5 is abnormal.

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5
Q

Risk factors for open-angle glaucoma include:

A

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Hypertension
Diabetes mellitus
Corticosteroids

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6
Q

In open-angle glaucoma, the rise in IOP may be asymptomatic for a long time and diagnosed by routine eye testing.

How may it present if symptomatic?

A

Peripheral visual field loss
Decreased visual acuity (blurred vision)
Fluctuating pain
Headaches
Halos around lights, particularly at night

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7
Q

What are the methods for measuring intraocular pressure?

A

Non-contact tonometry:
shooting a “puff of air” at the cornea and measuring the corneal response
less accurate but good for general screening purposes

Goldmann applanation tonometry:
gold-standard
device mounted on a slip lamp that makes contact with the cornea and applies various pressures

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8
Q

How can open-angle glaucoma be investigated?

A

Visual field assessment for peripheral vision loss
Goldmann applanation tonometry for the intraocular pressure
Slit lamp assessment for the cup-disk ratio and optic nerve health
Gonioscopy to assess the angle between the iris and cornea
Central corneal thickness assessment

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9
Q

How does open-angle glaucoma present on fundoscopy?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7, loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
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10
Q

When is treatment initiated for open-angle glaucoma?

A

at an intraocular pressure of 24 mmHg or above

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11
Q

How can open-angle glaucoma be managed?

A

Prostaglandin analogue eye drops (e.g., latanoprost) are the first-line medical treatment - increase uveoscleral outflow

360° selective laser trabeculoplasty - laser is directed at the trabecular meshwork, improving drainage

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12
Q

What are the potential side effects of prostaglandin analogue eye drops e.g. lantanoprost?

A

eyelash growth, eyelid pigmentation and iris pigmentation (browning)

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13
Q

Other than prostaglandin analogues, what eye drops may be used in the mx of open angle glaucoma?

A

Beta-blockers (e.g., timolol) reduce the production of aqueous humour

Carbonic anhydrase inhibitors (e.g., dorzolamide) reduce the production of aqueous humour

Sympathomimetics (e.g., brimonidine) reduce the production of aqueous fluid and increase the uveoscleral outflow

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14
Q

Risk factors for acute angle-closure glaucoma include:

A

Increasing age
Family history
Female (four times more likely than males)
Chinese and East Asian ethnic origin
Shallow anterior chamber

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15
Q

What medications can precipitate acute angle-closure glaucoma?

A

Adrenergic medications (e.g., noradrenaline)

Anticholinergic medications (e.g., oxybutynin and solifenacin)

Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects

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16
Q

How do patients with acute angle-closure glaucoma present?

A

Severely painful red eye
Decreased visual acuity (blurred vision)
Halos around lights
Associated headache, nausea and vomiting
Symptoms worse with mydriasis (e.g. watching TV in a dark room)

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17
Q

What may be seen on examination of patients with acute angle-closure glaucoma?

A

Red eye
Hazy cornea
Semi-dilated non-reactive pupil
Hard eyeball on gentle palpation
Decreased visual acuity

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18
Q

How can acute angle closure glaucoma be investigated?

A

tonometry to assess for elevated IOP

gonioscopy (looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle

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19
Q

How can acute angle closure glaucoma be managed in the community?

A

Acute angle-closure glaucoma requires immediate admission!

Measures while waiting for an ambulance are:

Lying the patient on their back without a pillow
Pilocarpine eye drops (2% for blue and 4% for brown eyes)
Acetazolamide 500 mg orally
Analgesia and an antiemetic, if required

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20
Q

How does pilocarpine work?

A

acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent)

also causes ciliary muscle contraction

opens up the pathway for the flow of aqueous humour

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21
Q

How does Acetazolamide work?

A

a carbonic anhydrase inhibitor that reduces the production of aqueous humour

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22
Q

How can acute angle closure glaucoma be managed in secondary care?

A

Pilocarpine eye drops

IV Acetazolamide

Hyperosmotic agents (e.g. IV mannitol)

Timolol, Dorzolamide - both reduce the production of aqueous humour via different mechanisms

Brimonidine - reduces aqueous humour production and increases uveoscleral outflow

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23
Q

What is usually required as definitive mx for acute angle closure glaucoma once the initial attack has settled ?

A

Laser iridotomy - involves making a hold in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber

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24
Q

What is the most common cause of blindness in the UK?

A

Age-related macular degeneration (AMD)

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25
Q

Age-related macular degeneration (AMD) is a progressive condition affecting the macula. What are the two types?

A

Wet (also called neovascular), accounting for 10% of cases - characterised by choroidal neovascularisation

Dry (also called non-neovascular), accounting for 90% of cases - characterised by drusen

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26
Q

The macula is found in the centre of the retina. It generates high-definition colour vision in the central visual field.

What are its 4 layers?

A

Choroid layer (at the base), which contains the blood vessels that supply the macula

Bruch’s membrane

Retinal pigment epithelium

Photoreceptors (towards the surface)

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27
Q

What are Drusen?

A

yellowish deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane

A few small drusen can be normal in older patients

Frequent and larger drusen can be an early sign of macular degeneration

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28
Q

What features are common to wet and dry AMD?

A

Atrophy of the retinal pigmented epithelium
Degeneration of the photoreceptors

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29
Q

What is the pathophysiology of wet AMD?

A

new vessels develop from the choroid layer and grow into the retina (neovascularisation)

these vessels can leak fluid or blood, causing oedema and faster vision loss

vascular endothelial growth factor (VEGF) is the target of medications for AMD

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30
Q

Give some risk factors for AMD?

A

Older age
Family history
Smoking (x2 risk)
Cardiovascular disease (e.g., hypertension)
Obesity
Poor diet (low in vitamins and high in fat)

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31
Q

How does AMD typically present?

A

Visual changes associated with AMD tend to be unilateral, with:

Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphopsia)
Worsening night vision

Patients often present with a gradually worsening ability to read small text.

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32
Q

How does wet AMD present differently to dry AMD?

A

Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years.

It often progresses to bilateral disease.

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33
Q

What are the key points used to differentiate between glaucoma and AMD?

A

Glaucoma is associated with peripheral vision loss and halos around lights

AMD is associated with central vision loss and a wavy appearance to straight lines

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34
Q

What are the key examination findings for AMD?

A

Reduced visual acuity using a Snellen chart

Scotoma (an enlarged central area of vision loss)

Amsler grid test can be used to assess for the distortion of straight lines seen in AMD

Drusen may be seen during fundoscopy

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35
Q

What is the name for the visual hallucination syndrome associated with AMD?

A

Charles-Bonnet syndrome

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36
Q

What investigations can be done for AMD?

A

slit-lamp microscopy is the initial investigation of choice

fluorescein angiography if wet ARMD is suspected

optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone

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37
Q

How can dry AMD be managed?

A

Management involves monitoring and reducing the risk of progression by:

Avoiding smoking
Controlling blood pressure
Vitamin supplementation has some evidence in slowing progression

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38
Q

How can wet AMD be managed?

A

Anti-VEGF medications (e.g., ranibizumab, aflibercept and bevacizumab) - injected directly into the vitreous chamber of the eye, usually about once a month.

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39
Q

What is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia (high blood sugar) damages the retinal small vessels and endothelial cells.

Damage to the blood vessel walls leads to microaneurysms and venous beading

Increased vascular permeability leads to leaking blood vessels, blot haemorrhages and hard exudates

Damage to nerve fibres in the retina causes fluffy white patches called cotton wool spots to form on the retina

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40
Q

Diabetic retinopathy is classified based on the findings on fundus examination.

What are the different types?

A

non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy

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41
Q

What are the key features of non proliferative diabetic retinopathy?

A

due to direct damage to vessels:
microaneurysms
venous beading
intraretinal microvascular abnormalities (IRMA)

due to increased vascular permeability:
blot haemorrhages
hard exudates

due to damage to nerves:
cotton wool spots

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42
Q

What do cotton wool spots represent?

A

they are soft exudates
they represent infarction in the nerve fibre layer

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43
Q

What are the key features of proliferative diabetic retinopathy?

A

retinal neovascularisation - may lead to vitreous haemorrhage
fibrous tissue forming anterior to retinal disc

more common in Type I DM, 50% blind in 5 years

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44
Q

What does diabetic maculopathy involve?

A

Exudates within the macula
Macular oedema

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45
Q

What are the potential complications of diabetic retinopathy?

A

Vision loss
Retinal detachment
Vitreous haemorrhage (bleeding into the vitreous humour)
Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
Optic neuropathy
Cataracts

46
Q

Non-proliferative diabetic retinopathy requires close monitoring and careful diabetic control.

What are the treatment options for proliferative diabetic retinopathy?

A

Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels

Anti-VEGF medications by intravitreal injection

Surgery (e.g., vitrectomy) may be required in severe disease

47
Q

What are the potential complications of Pan-retinal photocoagulation?

A

50% of patients develop reduction in their visual fields due to the scarring of peripheral retinal tissue

decrease in night vision (majority of rod cells - which are responsible for night vision - are located in the peripheral retina which is targeted by PRP)

48
Q

What can be used to treat macular oedema?

A

An intravitreal implant containing dexamethasone

49
Q

Outline the Keith Wagner Classification of hypertensive retinopathy

A

Stage 1: Mild narrowing of the arterioles
Stage 2: Focal constriction of blood vessels and AV nicking
Stage 3: Cotton-wool patches, exudates and haemorrhages
Stage 4: Papilloedema

50
Q

What are the different types of retinal haemorrhage?

A

Dot and blot haemorrhages: occur deeper, in the inner nuclear layer or outer plexiform layer

Flame haemorrhages: occur in the nerve fiber layer

51
Q

What are cataracts?

A

a progressively opaque eye lens, which reduces the light entering the eye and visual acuity

most develop in older age, apart from congenital cataracts, which can be identified by testing the red reflex in the neonatal exam

52
Q

Give some risk factors for developing cataracts

A

Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia

53
Q

How do cataracts present?

A

Symptoms are usually asymmetrical, as both eyes are affected separately.

It presents with:
Slow reduction in visual acuity
Progressive blurring of the vision
Colours becoming more faded, brown or yellow
Starbursts can appear around lights, particularly at night

54
Q

Key examination findings for cataracts?

A

Loss of the red reflex

55
Q

How can cataracts be managed?

A

Cataract surgery : drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens

Can be performed as a day case under local anaesthetic

56
Q

Give a complication of cataract surgery

A

Endophthalmitis : inflammation of the inner contents of the eye, usually caused by infections

Can lead to vision loss

Treated with intravitreal antibiotics injected directly into the eye

57
Q

What controls pupillary constriction?

A

The circular muscles in the iris are responsible for pupil constriction

They are stimulated by the parasympathetic nervous system (via the oculomotor nerve - CN III) using acetylcholine as a neurotransmitter

picture a PARrot sitting on the arch of the circular muscles -PARasympathetic

58
Q

What controls pupillary dilation?

A

dilator muscles in the iris

stimulated by the sympathetic nervous system, using adrenalin as a neurotransmitter

59
Q

Give 6 causes of an abnormal pupil shape

A

Acute angle-closure glaucoma

Rubeosis iridis (neovascularisation in the iris)

Coloboma

Tadpole pupil

Trauma to the sphincter muscles in the iris (e.g., during cataract surgery)

Anterior uveitis can cause adhesions (scar tissue) in the iris

60
Q

How does acute angle closure glaucoma cause an abnormal pupil shape?

A

Acute angle-closure glaucoma can cause ischaemic damage to the muscles of the iris

This can cause an abnormal pupil shape, usually a vertical oval.

61
Q

What is Rubeosis iridis?

A

Rubeosis iridis (neovascularisation in the iris) can distort the shape of the iris and pupil. This is usually associated with poorly controlled diabetes and diabetic retinopathy.

62
Q

What is Coloboma?

A

a congenital malformation that can cause a hole in the iris and an irregular pupil shape.

63
Q

What is tadpole pupil?

A

muscle spasm in part of the dilator muscle of the iris, causing a misshapen pupil

It is a temporary condition and may be associated with migraines and Horner syndrome.

64
Q

Give some causes of Mydriasis (Dilated Pupil)

A

Trauma
Third nerve palsy
Raised ICP
Acute angle-closure glaucoma
Stimulants (e.g., cocaine)
Anticholinergics (e.g., oxybutynin)
Holmes-Adie syndrome

65
Q

Give some causes of Miosis (Constricted Pupil)

A

Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine

66
Q

A palsy in the third cranial nerve (the oculomotor nerve) causes:

A

Ptosis (drooping upper eyelid)

Dilated non-reactive pupil

Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye

67
Q

A third nerve palsy that does not affect the pupil (sparing of the pupil) suggests what cause?

A

a microvascular cause, as the outer parasympathetic fibres that supply the pupil are spared

when the central fibres are compromised but the peripheral fibres are not, this suggests that the problem is with the blood supply as opposed to extrinsic compression

This may be due to:
Diabetes
Hypertension
Ischaemia

68
Q

What can cause a full third nerve palsy? (involves the pupil)

A

caused by compression of the nerve, including compression of the parasympathetic fibres.

This may be due to:
Tumour
Trauma
Cavernous sinus thrombosis
Posterior communicating artery aneurysm
Raised intracranial pressure

69
Q

What is Horner syndrome?

A

Triad of:
Ptosis
Miosis
Anhidrosis (loss of sweating)

may also have enophthalmos (sunken eye)

caused by damage to the sympathetic nervous system supplying the face

70
Q

How can you determine the location of the lesion in Horner syndrome?

A

can be determined by the anhidrosis (loss of sweating)

Central lesions (occurring before the nerves exit the spinal cord) cause anhidrosis of the arm, trunk and face

Pre-ganglionic lesions cause anhidrosis of the face

Post-ganglionic lesions do not cause anhidrosis.

71
Q

How can you remember the causes of Horner syndrome?

A

S for Sentral, T for Torso (pre-ganglionic) and C for Cervical (post-ganglionic)

72
Q

What are the central causes of Horner syndrome?

A

S – Stroke
S – Multiple Sclerosis
S – Swelling (tumours)
S – Syringomyelia (cyst in the spinal cord)

73
Q

What are the pre-ganglionic causes of Horner syndrome?

A

T – Tumour (Pancoast tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib and clavicle)

74
Q

What are the post-ganglionic causes of Horner syndrome?

A

C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache

75
Q

How can you test for Horner syndrome?

A

Cocaine eye drops:
acts on the eye to stop noradrenalin re-uptake at the NMJ which causes a normal eye to dilate

In Horner syndrome, the nerves are not releasing noradrenalin, so blocking re-uptake makes no difference, and there is no pupil reaction.

Alternatively, low-dose adrenalin eye drops (0.1%) will dilate the pupil in Horner syndrome but not a normal pupil.

76
Q

What is seen in congenital Horner syndrome?

A

heterochromia (difference in iris colour)

77
Q

What is a Holmes Adie pupil?

A

aDI- DIlated pupil

benign condition that is more common in women , caused by damage to the post-ganglionic parasympathetic fibres

Presentation:
unilateral dilated pupil
Sluggish to react to light
Responsive to accommodation (the pupils constrict well when focusing on a near object)
Slow to dilate following constriction (“tonic” pupil)

78
Q

What is Holmes-Adie syndrome ?

A

a Holmes-Adie pupil with absent ankle and knee reflexes

79
Q

What is Argyll-Robertson pupil?

A

finding in neurosyphilis

a constricted pupil that accommodates when focusing on a near object but does not react to light

often irregularly shaped

commonly called a “prostitute’s pupil” due to its relation to neurosyphilis and because “it accommodates but does not react”.

80
Q

What are the 2 causes of Argyll Robertson pupil?

A

diabetes mellitus
syphilis

81
Q

What is blepharitis?

A

inflammation of the eyelid margins leading to a red eye

due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)

82
Q

Which patient group is at greater risk of blepharitis?

A

patients with rosacea

83
Q

How does blepharitis present?

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
swollen eyelids may be seen in staphylococcal blepharitis

84
Q

Complications of blepharitis?

A

can lead to styes and chalazions
can get secondary conjunctivitis

85
Q

How can blepharitis be managed?

A

softening of the lid margin using hot compresses twice a day

‘lid hygiene’ - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used

artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

86
Q

What is a stye?

A

infection of a gland on the eyelid

external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum) or glands of Moll (sweat)

internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)

internal are deeper, tend to be more painful and may point inwards towards the eyeball

87
Q

How can styes be managed?

A

hot compresses and analgesia

CKS only recommend topical antibiotics if there is an associated conjunctivitis

88
Q

What is a Chalazion?

A

also called a Meibomian cyst
retention cyst of the Meibomian gland

presents as a firm painless lump in the eyelid

majority of cases resolve spontaneously but some require surgical drainage

89
Q

What are entropions and ectropions?

A

entropion: in-turning of the eyelids
ectropion: out-turning of the eyelids

90
Q

What is Trichiasis?

A

inward growth of the eyelashes
results in pain and can cause corneal damage and ulceration

Mx = removing the affected eyelashes
Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent them from regrowing

91
Q

What is conjunctivitis?

A

inflammation of the conjunctiva
may be bacterial, viral or allergic

Presentation:
Red, bloodshot eye
Itchy or gritty sensation
Discharge

92
Q

How do bacterial and viral conjunctivitis present differently?

A

Bacterial conjunctivitis
Purulent discharge
Eyes may be ‘stuck together’ in the morning

Viral conjunctivitis
Serous discharge
Recent URTI
Preauricular lymph nodes

93
Q

How can infective conjunctivitis be managed?

A

normally a self-limiting condition that settles within 1-2 weeks

topical antibiotic therapy is commonly offered e.g. Chloramphenicol
topical fusidic acid is an alternative for pregnant women

advice should be given not to share towels

school exclusion is not necessary

94
Q

Advice for contact lens users during an epsiode of infective conjunctivits?

A

topical fluoresceins should be used to identify any corneal staining

contact lens should not be worn

95
Q

How does allergic conjunctivitis present?

A

Bilateral symptoms
Conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy

96
Q

How can allergic conjunctivitis be managed?

A

first-line: topical or systemic antihistamines

second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil

97
Q

Causes of an acute painful red eye include:

A

Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Keratitis
Corneal abrasions or ulceration
Foreign body
Traumatic or chemical injury

98
Q

Causes of an acute painless red eye include:

A

Conjunctivitis
Episcleritis
Subconjunctival haemorrhage

99
Q

What is anterior uveitis?

A

important ddx for a red eye

inflammation of the anterior portion of the uvea - iris and ciliary body

associated with HLA-B27

autoimmune process usually causes it, but it can be due to infection, trauma, ischaemia or malignancy

100
Q

How does anterior uveitis typically present?

A

acutely painful red eye
excessive lacrimation
photophobia (due to ciliary muscle spasm)
reduced visual acuity
small pupil

101
Q

What may you find on examination of anterior uveitis?

A

Ciliary flush (a ring of red spreading from the cornea outwards)

Miosis (a constricted pupil due to sphincter muscle contraction)

Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes

Hypopyon (inflammatory cells collected as a white fluid in the anterior chamber)

102
Q

What conditions are associated with anterior uveitis?

A

HLA-B27 linked conditions:
ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

103
Q

How may anterior uveitis be managed?

A

urgent review by ophthalmology
cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate
steroid eye drops

104
Q

What is episcleritis?

A

acute onset of inflammation in the episclera of one or both eyes

The majority of cases are idiopathic, associated conditions include:
inflammatory bowel disease
rheumatoid arthritis

105
Q

How does episcleritis typically present?

A

red eye

classically not painful (in comparison to scleritis), but mild pain/irritation is common

watering and mild photophobia may be present

Dilated episcleral vessels

106
Q

How can you differentiate between episcleritis and scleritis?

A

in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera
in scleritis, vessels are deeper, hence do not move

phenylephrine drops may also be used to differentiate:

phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels

if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made

107
Q

How can episcleritis be managed?

A

analgesia (e.g., ibuprofen) and lubricating eye drops

More severe cases may be treated with steroid eye drops.

108
Q

What is scleritis?

A

inflammation of the sclera

most severe type of scleritis is called necrotising scleritis, which can lead to perforation of the sclera

109
Q

What can cause scleritis?

A

Most cases are idiopathic

Can be associated with an underlying systemic inflammatory condition:
RA (most common)
SLE
sarcoidosis
vasculitis, particularly granulomatosis with polyangiitis

Less commonly, it can be due to infection (e.g., Pseudomonas or Staphylococcus aureus)

110
Q

How does scleritis present?

A

Red, inflamed sclera with congested vessels
Severe pain (typically a boring pain)
Pain with eye movement
Photophobia
Reduced visual acuity
Epiphora (excessive tear production)
Tenderness to palpation of the eye

111
Q

How may scleritis be managed?

A

same-day assessment by an ophthalmologist

oral NSAIDs are typically used first-line

oral glucocorticoids may be used for more severe presentations

immunosuppressive drugs for resistant cases

Y4 Neuro and Special Senses (21 decks)

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