Ophthalmology Flashcards

Conditions and presentations

1
Q

What is glaucoma

A

Glaucoma is a group of disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP).

Not all patients with raised I have glaucoma and vice versa

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2
Q

Factors which predispose to AACG (Acutely angle-closure glaucoma)

A

hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

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3
Q

Features of AACG

A
  • severe pain: may be ocular or headache
  • decreased visual acuity
  • symptoms worse with mydriasis (e.g. watching TV in a dark room)
  • hard, red-eye
  • haloes around lights
  • semi-dilated non-reacting pupil
  • corneal oedema results in dull or hazy cornea
  • systemic upset may be seen, such as nausea and vomiting and even abdominal pain
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4
Q

Investigations of AACG

A

tonometry to assess for elevated IOP
gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle

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5
Q

Management of AACG

A
  • typically an emergency and should prompt urgent referral to ophthalmology

Emergency medical treatment is required to lower the IOP with more definitive surgical treatment given once the acute attack has settled.

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6
Q

Example regime of managing AACG

A

combination of eye drops, for example:
a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
a beta-blocker (e.g. timolol, decreases aqueous humour production)
an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
intravenous acetazolamide
reduces aqueous secretions
some guidelines also recommend the use of topical steroids to reduce inflammation

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7
Q

Definitive management of AACG

A

laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

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8
Q

Age-related macular degeneration

A

most common cause of blindness in the UK

Degeneration of the central retina (macula) is the key feature with changes usually bilateral.

ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography

It is more common with advancing age and is more common in females.

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9
Q

Risk factors of ARMD

A
  • advancing age (greatest risk)
  • smoking
  • current smokers are twice as likely as non-smokers
  • family history
  • ischaemic cardiovascular disease
  • hypertension
  • dyslipidaemia
  • diabetes mellitus.
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10
Q

Investigation of ARMD

A
  • slit-lamp microscopy (any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD)
    This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
    fluorescein angiography is utilised if neovascular 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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11
Q

Signs of ARMD during investigation

A

distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

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12
Q

Clinic features of ARMD

A

Patients typically present with a subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
gradual in dry ARMD
subacute in wet ARMD
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
visual hallucinations may also occur resulting in Charles-Bonnet syndrome

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13
Q

Treatment of ARMD

A

combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.

vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.

laser photocoagulation does slow progression of ARMD

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14
Q

Risk of laser photocoagulation

A

risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

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15
Q

Allergic conjunctivitis features

A

Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis)
Itch is prominent
the eyelids may also be swollen
May be a history of atopy
May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens)

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16
Q

Management of allergic conjunctivitis

A

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

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17
Q

Anterior uveitis

A

important differentials of a red eye

also referred to as iritis.

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

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18
Q

What genes is associated with anterior uveitis

A

HLA-B27

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19
Q

Features of anterior uveitis

A

acute onset
ocular discomfort & pain (may increase with use)
pupil may be small +/- irregular due to sphincter muscle contraction
photophobia (often intense)
blurred vision
red eye
lacrimation
ciliary flush: a ring of red spreading outwards
hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level
visual acuity initially normal → impaired

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20
Q

Associated conditions with anterior uveitis

A

ankylosing spondylitis
reactive arthritis
ulcerative colitis, Crohn’s disease
Behcet’s disease
sarcoidosis: bilateral disease may be seen

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21
Q

Management of anterior uveitis

A

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

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22
Q

Argyll-Robertson pupil

A

Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis.

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23
Q

What conditions are associated with HLA-B27

A
  • Ankylosing spondylitis
  • Reactive arthritis (Reiter’s syndrome)
    -psoriatic arthritis
    -enteropathic arthritis (associated with IBD)
    Juvenile idiopathic arthritis
    Acute anterior uveitis
    Axial spondyloarthritis
    Behçet’s disease (in some populations)
    Reactive arthritis following certain infections, such as Chlamydia trachomatis or Salmonella spp.
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24
Q

Argyll-Robertson pupil ARP—>PRA

A

Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

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25
Q

Features of Argyll-Robertson pupil

A

small, irregular pupils
no response to light but there is a response to accommodate

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26
Q

Causes of Argyll-Robertson pupil

A

diabetes mellitus
syphilis

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27
Q

Blepharitis

A

Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).

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28
Q

What condition is most associated with blepharitis

A

Rosacea

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29
Q

Function of the meibomian gland

A

The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film.

Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation

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30
Q

Features of blepharitis

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

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31
Q

Management of blepharitis

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
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

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32
Q

Blurred vision

A

Loss of clarity or sharpness of vision
Patients who have it will have long-term refractive errors
Make sure to assess for other symptoms such as visual loss, double vision and floaters

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33
Q

Causes of blurred vision (7)

A

refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax

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34
Q

Assessment of blurred vision

A

visual acuity with a Snellen chart
pinhole occluders are a useful way to check for whether the blurred vision is due to a refractive error or not
if the blurring improves with a pinhole occluder then likely cause is a refractive error
visual fields
fundoscopy

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35
Q

Management of blurred vision

A

depends on the suspected underlying cause
if gradual onset, corrected by pinhole occluder and no other associated symptoms then an optician review would be the next step
other patients should be seen by ophthalmology. If there are associated symptoms such as visual loss or pain this should be urgent

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36
Q

Thyroid eye disease

A

Grave’s disease

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37
Q

Pathophysiology of grave’s disease

A

it is thought to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
the inflammation results in glycosaminoglycan and collagen deposition in the muscles

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38
Q

Prevention of grave’s eye disease

A
  • smoking
  • radioiodine treatment
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39
Q

Features of grave’s eye disease

A
  • eu/ hypo/ hyperthyroid at time of presentation
  • exophthalmos
    conjunctival oedema
    optic disc swelling
    ophthalmoplegia
    inability to close the eyelids
    Dry eye
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40
Q

Managment of grave’s eye disease

A

smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure
steroids
radiotherapy
surgery

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41
Q

Complications of grave’s eye disease

A
  • exposure kerathopathy
  • optic neuropathy
    -strabismus and dipolopia
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42
Q

Exposure kerathopathy

A
  • eye lid retraction and proptosis causes cornea to become excessively exposed

Causes dryness and imitation and corneal ulceration

Pt may report a foreign body experience

Photophobia

Can cause scarring and vision impairment as well

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43
Q

Optic neuropathy

A

enlarged extraocular muscles compress the optic nerve at the apex of the orbit → a reduction in visual acuity, colour vision deficits, and visual field defect
it requires urgent medical intervention to prevent permanent vision loss.

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44
Q

Strabismus and diplopia

A

fibrosis and enlargement of the extraocular muscles can result in restrictive strabismus → misalignment of the eyes → double vision (diplopia)
this not only affects visual function but can also significantly impair the quality of life.

45
Q

When to urgently review someone with grave’s disease?

A

unexplained deterioration in vision
awareness of change in intensity or quality of colour vision in one or both eyes
history of eye suddenly ‘popping out’ (globe subluxation)
obvious corneal opacity
cornea still visible when the eyelids are closed
disc swelling
(EUGOGO guidelines)

46
Q

Optic neuritis

A

Inflammation of the optic nerve

47
Q

Causes of optic neuritis

A
  • MS
  • diabetes
    -syphilis
48
Q

Features of ON

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

49
Q

Investigation of ON

A

MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

50
Q

Managment of ON

A
  • high dose steroid (usually takes 4-6 weeks to recover )
51
Q

Prognosis of ON

A

MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

52
Q

Scleritis

A

Full thickness inflammation of the sclera
Non- infective cause and associated with red painful eye

53
Q

Risk factors for scleritis

A

rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis

54
Q

Features of scleritis

A

red eye
classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present
watering and photophobia are common
gradual decrease in vision

55
Q

Managment of scleritis

A
  • same day assessment by ophalmologist

oral NSAIDs are typically used first-line
oral glucocorticoids may be used for more severe presentations
immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)

56
Q

Corneal abrasion

A

Defect of the corneal epithelium and usually has occurred due to recent local trauma

57
Q

Feaures of corneal abrasion

A

eye pain
lacrimation
photophobia
foreign body sensation and conjunctival injection
decreased visual acuity in the affected eye

58
Q

Investigation for corneal abrasion

A
  • fluorescein staining
  • visualisation can be enhanced using cobalt blue filter or a wood’s lamp
59
Q

Managment of corneal abrasion

A

a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.

60
Q

Hyphema definition

A

Blood in the anterior chamber of the eye

61
Q

Managment of hyphema

A
  • required urgent referral to opthlamic specialist for review and managment
62
Q

Why do hyphema risk sight?

A
    • raised IOP
  • can cause blockage of the trabecular mesh work with erythrocytes
63
Q

Managment of hyphema

A
  • strict bed rest and reduce excessive movements
  • high risk classes often require admission
  • assessment should also be made for orbital compartmental syndrome (e.g retrobulbar haemorrhage)
64
Q

Features of orbital compartmental syndrome

A

eye pain/swelling
proptosis
‘rock hard’ eyelids
relevant afferent pupillary defect

65
Q

Managment of orbital compartmental syndrome

A

urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit

66
Q

Subconjunctival haemorrhage

A

result from the bleeding of blood vessels into the subconjunctival space.

Vessels which usually bleed are responsible for supplying conjunctiva or episclera

Cases are typically traumatic or idiopathic (e.g valsalva manoeuvres and several systemic diseases)

Look sinister but rarely are

67
Q

Epidemiology of subconjuctival haemorrhage

A
  • more common in women than men when no he of trauma
  • newborns and elderly at high risk.
68
Q

Risk factors for subconjunctival haemorrhage

A
  • trauma
  • control lens
  • idiopathic
  • valsalva manoeuvre
  • hypertension
  • bleeding disorders
  • drugs (aspirin, NSAID, anticoag)
  • diabetes
  • Arterial disease and hyperlipidaemia
69
Q

Symptoms of subconjunctival haemorrhage

A

Red-eye, usually unilateral
Subconjunctival haemorrhages are mostly asymptomatic,
mild irritation may be present

70
Q

Signs of subconjunctival haemorrhage

A
  • flat, red patch on conjunctiva
  • well defined edges with normal conjunctiva round it

Traumatic haemorrhages are most common in the temporal region

inferior conjunctiva as the next most commonly affected area

Normal vision and eye movement, normal fundus

71
Q

Investigations of subconjunctival haemorrhage

A
  • clinical diagnosis
  • check no obvious trauma cause
  • check pt blood pressure
  • if pt takes warfarin, check INR and make appropriate adjustments
  • may need to refer to CT to rule out brain bleed
  • if recurrent, spontaneous or bilateral suboconjunctival haemorrhage, check for bleeding disorder of other pathology
72
Q

Managment of subconjuctival haemorrhage

A
  • reassure pt it will resolve in 2-3 weeks
  • patch will change colour like a bruise
  • if cause is traumatic consider a referral to the ophthalmologist to ensure no other damage has been caused to the eye
  • advise pt to contact GP if happens again
  • use artificial tears if any mild irritation
73
Q

Posterior vitreous detachment

A
  • separation of the membrane from the retina.

-This occurs due to natural changes to the vitreous fluid of the eye with ageing

No pain or vision loss but can cause tears to the retina

74
Q

Epidemiology of PVD

A

Occur in over 75% of people over the age of 65
More common in females

75
Q

Risk factors for PVD

A
  • ageing
  • highly myopic patients
76
Q

Symptoms of PVD

A
  • Floaters (ring of floaters temporal to central vision)
  • flashes of light in vision
  • blurred vision
  • cobweb across vision
  • dark curtain descending (can also indicate retinal detachment)
77
Q

Signs of PVD

A
  • Weiss ring on ophalamscope
78
Q

Investigation of PVD

A
  • Examined by ophthalmologist within 24hrs
79
Q

Managment of PVD

A

-no tx needed as usually improves in around 6 months
- may need surgery if retinal detachment

80
Q

Retinal detachment

A

neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.

  • it is reversible cause of vision loss
81
Q

Risk factors for RD

A
  • diabetes mellitus
  • myopia
  • age
  • prev surgery for cataracts
  • eye trauma
82
Q

Signs and symptoms of RD

A
  • new flashers and floaters
  • painless and progressive visual field loss
    if the macula is involved, central visual acuity and visual outcomes become much worse
    peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached
    the swinging light test may highlight a relative afferent pupillary defect if the optic nerve is involved
    fundoscopy
    the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
    if the break is small, however, it may appear normal.
83
Q

Managment of RD

A
  • referr urgently under 24hr to ophthalmologist for assessment
  • slit lamp and indirect ophthalmoscope for pigment cell and haemorrhage
84
Q

Vitreous haemorrhage

A
  • bleeding into the vitreous humour
  • sudden painless vision loss
  • can range from floaters to complete loss
  • when bleeding stops it starts to clear
85
Q

Epidemiology of vitreous haemorrhage

A

Spontaneous vitreous haemorrhage has an incidence of around 7 cases per 100000 patient-years1
Incidence by age and sex varies according to the incidence of the underlying causes

86
Q

Common cause of vitreous haemorrhage

A

proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults

87
Q

Patient acute presentation of vitreous haemorrhage

A

painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision

88
Q

Signs of vitreous haemorrhage

A

decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage

89
Q

Investigation of vitreous haemorrhage

A

dilated fundoscopy: may show haemorrhage in the vitreous cavity
slit-lamp examination: red blood cells in the anterior vitreous
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury

90
Q

Corneal foreign body features

A

eye pain
foreign body sensation
photophobia
watering eye
red eye

91
Q

When to refer to ophthalmology for corneal foreign body

A

Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)
Significant orbital or peri-ocular trauma has occurred.
A chemical injury has occurred (irrigate for 20-30 mins before referring)
Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications
Foreign bodies in or near the centre of the cornea
Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.

92
Q

Keratitis

A

Inflammation of the cornea
Potentially fight threatening and should therefore be urgently evaluated and treated

93
Q

Causes of keratitis

A

bacterial
typically Staphylococcus aureus
Pseudomonas aeruginosa is seen in contact lens wearers
fungal
amoebic
acanthamoebic keratitis
accounts for around 5% of cases
increased incidence if eye exposure to soil or contaminated water
pain is classically out of proportion to the findings
parasitic: onchocercal keratitis (‘river blindness’)

Viral: herpes simplex keratitis

Environmental
- photokeratitis e.g. welder’s arc eye
exposure keratitis
contact lens acute red eye (CLARE)

94
Q

Features of keratitis

A

red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen

95
Q

When to refer cases of keratitis

A

contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis

96
Q

Managment of keratitis

A

stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate

97
Q

Complications of keratitis

A

corneal scarring
perforation
endophthalmitis
visual loss

98
Q

Cataracts

A

common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy.

This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision.

Cataracts are the leading cause of curable blindness worldwide.

99
Q

Epidemiology of cataracts

A

Cataracts are more common in women than in men
The incidence of cataracts increases with age. One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes

100
Q

Causes of cataracts

A
  • normal ageing process
    -smoking
    -increased alcohol consumption
  • trauma
  • DM
  • Long-term corticosteroids
    -Radiation exposure
    -Myotonic dystrophy
    -Metabolic disorders: hypocalcaemia
101
Q

Patients with cataracts gradual onset of…

A

Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights

102
Q

Signs of cataracts

A
  • reduced red reflex
103
Q

Investigations for cataracts

A

Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract

104
Q

Classification of cataracts

A

Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy

105
Q

Managment of cataracts

A
  • provide pt with stronger glasses and encourage brighter light use
  • surgical tx

the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice.

106
Q

Complications following cataract surgery

A

Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour

107
Q

Optic atrophy

A

Pale, well demarcated disc on fundoscopy
- causes gradual loss of vision
- can be congenital or acquired

108
Q

Acquired causes of optic atrophy

A

multiple sclerosis
papilloedema (longstanding)
raised intraocular pressure (e.g. glaucoma, tumour)
retinal damage (e.g. choroiditis, retinitis pigmentosa)
ischaemia
toxins: tobacco amblyopia, quinine, methanol, arsenic, lead
nutritional: vitamin B1, B2, B6 and B12 deficiency

109
Q

Congenital causes of optic atrophy

A

Friedreich’s ataxia
mitochondrial disorders e.g. Leber’s optic atrophy
DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)