OPHTHALMOLOGY Flashcards
(231 cards)
1
Q
GLAUCOMA
what are the two types of glaucoma?
A
open angle glaucoma
acute angle closure glaucoma
2
Q
GLAUCOMA
what is it?
A
optic nerve damage caused by a rise in intraocular pressure
increased pressure is caused by a blockage in aqueous humour
3
Q
GLAUCOMA
what is the role of aqueous humour in the eye?
A
supplies nutrients to the cornea
4
Q
GLAUCOMA
what produces aqueous humour?
A
ciliary body
5
Q
GLAUCOMA
what is the normal flow of aqueous humour in the eye?
A
- produced by ciliary body
- flows through posterior chamber and around iris to the anterior chamber
- drains through the trabecular meshwork to the canal of Schlemm where it enters general circulation
6
Q
GLAUCOMA
what is normal eye pressure?
A
10-21mmHg
7
Q
OPEN-ANGLE GLAUCOMA
what is the pathophysiology?
A
gradual increased resistance to flow through the trabecular meshwork
pressure slowly builds in the eye
progressive loss of retinal nerve fibres and optic nerve atrophy
8
Q
OPEN-ANGLE GLAUCOMA
what are the risk factors?
A
increased age
family history
black
myopia (nearsighted)
hypertension + CVD
diabetes mellitus
corticosteroid use
9
Q
OPEN-ANGLE GLAUCOMA
what is the clinical presentation?
A
often presents insidiously + detected during routine eye exams
SYMPTOMS
- asymptomatic
- peripheral vision loss (progressive)
SIGNS
- raised intraocular pressure
- visual field defect (peripheral loss, leading to tunnel vision)
- decreased visual acuity
- open iridocorneal angle
- fundoscopic findings (optic disc cupping, bayonetting of vessels, cup notching, optic disc haemorrhages and disc haemorrhages)
10
Q
OPEN-ANGLE GLAUCOMA
what are the fundoscopic findings?
A
- optic disc cupping
- bayonetting of vessels
- cup notching
- optic disc pallor
- disc haemorrhages
11
Q
GLAUCOMA
what is the gold standard way to measure intraocular pressure?
A
Goldmann applanation tonometry
12
Q
OPEN-ANGLE GLAUCOMA
what are the investigations?
A
- standard automated perimetry (for visual field assessment)
- goldmann applanation tonometry (for intraocular pressure measurement)
- slit lamp (assess optic nerve health)
- gonioscopy (assess peripheral anterior chamber)
- central corneal thickness assessment
13
Q
OPEN-ANGLE GLAUCOMA
what is the management?
A
1st line
- topical prostaglandin analogue (LATANOPROST) or prostamide (BIMATOPROST)
- topical beta-blocker (TIMOLOL)
2nd line
- switch to drug in other 1st line drug class
- combine topical prostaglandin analogue/prostamide with topical beta-blocker
- switch to/add in one of following drugs:
= topical sympathomimetic (BRIMONIDINE TARTRATE)
= topical carbonic anhydrase inihibitor (BRINZOLAMIDE)
= topical miotic (PILOCARPINE HYDROCHLORIDE)
refractory cases
- laser (selective laser trabeculoplasty)
- surgery (trabeculectomy)
14
Q
GLAUCOMA MEDICATIONS
how does prostaglandin analogues (e.g. latanoprost) work?
A
increases the uveosceral outflow of aqueous humour
15
Q
GLAUCOMA MEDICATIONS
what are the side effects of prostaglandin analogue drops (e.g. latanoprost)?
A
- eyelash growth
- eyelid pigmentation
- iris pigmentation (browning)
16
Q
GLAUCOMA MEDICATIONS
how do prostamides (e.g. bimatoprost) work?
A
increases uveoscleral outflow of aqueous humour and acts via trabecular meshwork
17
Q
GLAUCOMA MEDICATIONS
how do beta-blockers (e.g. timolol) work?
A
decreases aqueous humour production
18
Q
GLAUCOMA MEDICATIONS
what are the side effects of beta-blockers (e.g. timolol)?
A
may cause corneal disorders
avoid in asthma + heart block
19
Q
GLAUCOMA MEDICATIONS
how do sympathomimetics (e.g. brimonidine) work?
A
decreases aqueous humour production
20
Q
GLAUCOMA MEDICATIONS
what are the side effects of sympathomimetics (e.g. brimonidine)?
A
- hyperaemia
- burning + stinging eyes
- dry mouth
avoid in CVD, raynauds + if taking MAOIs or TCAs
21
Q
ACUTE ANGLE CLOSURE GLAUCOMA
what is the pathophysiology?
A
the iris bulges forwards and seals off the trabecular meshwork, preventing aqueous humour from draining
pressure builds in the posterior chamber which pushes the iris forward further
22
Q
ACUTE ANGLE CLOSURE GLAUCOMA
what are the risk factors?
A
Increasing age
Family history
Female (four times more likely than males)
Chinese and East Asian ethnic origin
Shallow anterior chamber
Mydriatic drugs (anticholinergics, anti-histamines, TCAs)
23
Q
ACUTE ANGLE CLOSURE GLAUCOMA
which medications can precipitate it?
A
- Adrenergic medications (e.g., noradrenaline)
- Anticholinergic medications (e.g., oxybutynin and solifenacin)
- Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
24
Q
ACUTE ANGLE CLOSURE GLAUCOMA
what is the clinical presentation?
A
SYMPTOMS
- unilateral red, painful eye
- pain worse in the dark
- blurred vision
- haloes around lights
- headache (may be severe)
- nausea and vomiting
SIGNS
- hard, red eye
- fixed, dilated pupil
- corneal oedema (dull, hazy cornea)
- reduced visual acuity
25
ACUTE ANGLE CLOSURE GLAUCOMA
what are the investigations?
must be urgently referred to ophthalmologist
- slit lamp = shallow anterior chamber, optic disc cupping, optic disc pallor
- gonioscopy (GOLD STANDARD)
- tonometry
26
ACUTE ANGLE CLOSURE GLAUCOMA?
what is the initial management?
- lie patient flat
- analgesia + antiemetics
following may be given in combination:
- 1st line = carbonic anhydrase inhibitor (ACETAZOLAMIDE)
- topical beta-blocker (TIMOLOL)
- topical alpha-2-agonist (BRIMONIDINE)
- topical cholinergic (PILOCARPINE)
DEFINITIVE TREATMENT
- iridotomy
27
GLAUCOMA MEDICATIONS
how does miotics (e.g. pilocarpine) work?
- Pupil constriction
- pulls iris away from trabecular meshwork increasing drainage of aqueous humour
28
GLAUCOMA MEDICATIONS
what are the side effects of miotics (e.g. pilocarpine)?
- constricted pupil
- retinal detachment
- vitreous haemorrhage
- headache
29
GLAUCOMA MEDICATIONS
how does carbonic anhydrase inhibitors (e.g. acetazolamide) work?
decreases the production of aqueous humour.
30
GLAUCOMA MEDICATIONS
what are the side effects of carbonic anhydrase inhibitors (e.g. acetazolamide)?
- dry mouth
- change in taste
- tingling feeling in extremities
- stevens-johnson syndrome
not for long term use orally
do not use in hyperchloremic acidosis or sulphonamide sensitivity
31
ACUTE ANGLE CLOSURE GLAUCOMA
what is the definitive treatment?
Laser iridotomy
This involves making a hole in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber.
32
ACUTE ANGLE CLOSURE GLAUCOMA
what are the complications?
- irreversible visual loss
- contralateral eye affected (40-80% risk)
- central retinal vein occlusion
33
AGE RELATED MACULAR DEGENERATION
what is the most common cause of blindness in the UK?
age related macular degeneration
34
AGE RELATED MACULAR DEGENERATION
what is the main characteristic found on fundoscopy and retinal photography?
drusen formation - yellowish deposits of proteins and lipids
35
AGE RELATED MACULAR DEGENERATION
what are the risk factors?
- increasing age
- smoking (doubles risk of developing ARMD)
- family history
- cardiovascular disease
- obesity
- poor diet (low in vitamin and high in fat)
36
AGE RELATED MACULAR DEGENERATION
what are the two different types?
dry (90%) and wet (10%)
37
AGE RELATED MACULAR DEGENERATION
what is dry age related macular degeneration?
also known as atrophic
is 85-90% of cases
characterised by drusen
progresses slowly over decades
38
AGE RELATED MACULAR DEGENERATION
what is wet age related macular degeneration?
10-15% of cases
also known as exudative or neovascular
characterised by choroidal neovascularisation
leakage of serous fluid and blood result in rapid loss of vision
has worse prognosis
39
AGE RELATED MACULAR DEGENERATION
what is the clinical presentation?
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)
- poor vision at night
- photopsia (perceived flickering of lights)
- gradually worsening ability to read small text.
SIGNS
- visual distortion (particularly line perception- metamorphopsia)
- drusen (yellow spots) in dry ARMD
- subretinal/intraretinal haemorrhages in wet ARMD
40
how do you tell the difference between glaucoma and age related macular degeneration?
AMD = central vision loss and wavy appearance to straight lines
glaucoma = peripheral vision loss and halos around lights
41
AGE RELATED MACULAR DEGENERATION
what are the investigations?
- slit lamp = identification of exudative, pigmentary or haemorrhagic changes in retina
- colour fundus photography = monitor progression
- Fluorescein angiography = to identify neovascular ARMD + guide anti-VEGF therapy
- OCT scan = assess all layers of retina + identification of disease not visible by slit lamp
42
AGE RELATED MACULAR DEGENERATION
what is the management?
smoking cessation important
WET = anti-VEGF medications e.g. ranibizumab injected into vitrous chamber each month
DRY = no specific treatment, can reduce risk of progression by avoiding smoking, control BP and vitamin supplementation (zinc, vits A, C and E)
43
ANTERIOR UVEITIS
what is it?
describes inflammation of the anterior portion of the uvea - iris and ciliary body
44
ANTERIOR UVEITIS
what is the pathophysiology?
pain is due to irritation of ciliary nerves
photophobia is due to irritation of trigeminal nerve from ciliary spasm
45
ANTERIOR UVEITIS
what is it associated with?
HLA-B27
Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis)
Inflammatory bowel disease
Sarcoidosis
Behçet’s disease
46
ANTERIOR UVEITIS
what is the clinical presentation?
SYMPTOMS
- painful, red eye
- photophobia
- tear formation
- blurred vision, then a reduction in visual acuity
SIGNS
- red eye
- presence of hypopyon (pus cells in anterior chamber which can show fluid level)
- presence of keratic precipitates
- ciliary flush (dilated ciliary vessels spreading outwards from pupil)
- small or irregular pupil
47
ANTERIOR UVEITIS
what are the investigations?
- physical exam (visual fields, acuity, CN assessment)
- slit lamp
to consider
- infection/autoimmune screen
48
ANTERIOR UVEITIS
what is the management?
urgently refer to ophthalmologist for review within 24hrs
1st line
- corticosteroids (topical, orally, IV, or ocular injections)
- cycloplegic-mydriatic drug (CYCLOPENTOLATE 1% or ATROPINE 1%)
- antimicrobials
2nd line
- immunosuppressants (DMARDS)
- surgical intervention (laser phototherapy, cryotherapy, vitrectomy)
49
BLEPHARITIS
what is it?
inflammation of the eyelid margins
50
BLEPHARITIS
what are the causes?
meibomian gland dysfunction (common, posterior blepharitis)
seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).
51
BLEPHARITIS
what are the clinical features?
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
52
BLEPHARITIS
what is the management?
- 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
53
CATARACTS
what is it?
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
54
CATARACTS
what is the epidemiology?
Cataracts are more common in women than in men
The incidence of cataracts increases with age
55
CATARACTS
what are the risk factors?
Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia
56
CATARACTS
what is the clinical presentation?
usually asymmetrical, as both eyes are affected separately.
SYMPTOMS
It presents with:
- gradual painless loss of vision
- difficulty reading/watching TV
- Progressive blurring of the vision
- Colours becoming more faded, brown or yellow
- Starbursts (haloes around lights) can appear around lights, particularly at night
SIGNS
- loss of red reflex
- brown/white appearance of lens on slit-lamp
57
CATARACTS
what are the investigations and findings?
Loss of the red reflex is a key examination finding.
The lens can appear grey or white using an ophthalmoscope, even from a distance. This is also seen on photographs taken with a flash.
58
CATARACTS
what is the management?
Cataract surgery (pseudophakia) involves drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens
59
CATARACTS
what are the complications of cataract surgery?
endophthalmitis
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
60
CENTRAL RETINAL ARTERY OCCLUSION
what is it?
sudden obstruction to blood flow through the central retinal artery. The central retinal artery is a branch of the ophthalmic artery, which is a branch of the internal carotid artery.
61
CENTRAL RETINAL ARTERY OCCLUSION
what are the causes?
main cause is atherosclerosis (causes an embolism)
others = giant cell arteritis,
62
CENTRAL RETINAL ARTERY OCCLUSION
what are the risk factors?
- smoking
- HTN
- diabetes
- raised cholesterol
- white
- older age
- male
- polymyalgia rheumatica
63
CENTRAL RETINAL ARTERY OCCLUSION
what is the clinical presentation?
typically sudden, painless, monocular vision loss occurring over seconds
patients may report transient vision loss prior to event (amaurosis fugax)
SYMPTOMS
- sudden painless vision loss in one eye
SIGNS
- reduced visual acuity
- afferent pupillary defect
- pale retina and 'cherry red spot' on fundoscopy
64
CENTRAL RETINAL ARTERY OCCLUSION
what are the investigations?
- ESR/CRP (to investigate temporal arteritis)
to consider
- vasculitis screening
- coagulation screen
- HbA1c/lipid profile
65
CENTRAL RETINAL ARTERY OCCLUSION
what is the management?
1st line
- reperfusion therapy (PENTOXIFYLLINE or HYPERBARIC OXYGEN)
- reduction in intraocular pressure (ACETAZOLAMIDE)
- IV methylprednisolone
- thrombolytic therapy (tissue plasminogen activator)
2nd line
- surgical intervention
long term management
- reduction in CVD risk (weight loss, aspirin + statins)
- inform DVLA
66
CONJUNCTIVITIS
what is it?
inflammation of the conjunctiva
67
CONJUNCTIVITIS
what are the causes?
BACTERIA
- s.aureus
- h.influenzae
- s.pneumoniae
- chlamydia + n.gonorrhoeae
VIRUSES
- adenovirus
- coxsackie
- enterovirus
- herpes simplex (HSV)
NON-INFECTIVE
- allergic conjunctivitis
68
CONJUNCTIVITIS
what is the clinical presentation?
SYMPTOMS
- itchiness in one or both eyes
- conjunctival injection (redness)
- discharge (bacterial = purulent, viral = watery)
- difficulty opening eyes in morning (due to crusting)
SIGNS
- conjunctival follicles
- superficial punctate keratopathy
- periauricular lymph nodes
NO PAIN, PHOTOPHOBIA OR REDUCED VISUAL ACUITY
69
CONUNCTIVITIS
what is the difference in presentation of viral and bacterial conjunctivitis?
BACTERIAL
- purulent discharge
- eyes stuck together in the morning
VIRAL
- recent URTI
- watery discharge
- preauricular lymph nodes
70
what are the differentials for a painful red eye?
Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Corneal abrasions or ulceration
Keratitis
Foreign body
Traumatic or chemical injury
71
what are the differentials for painless red eye?
Conjunctivitis
Episcleritis
Subconjunctival haemorrhage
72
CONJUNCTIVITIS
what is the management?
1st line
- watch and wait (most resolve in 7 days)
- practice good hygiene
- no exclusion period required
- artificial tears
- mast cell stabilisers (in allergic conjunctivitis)
2nd line = topical antibiotics
- chloramphenicol 0.5% eye drops (2hrly for 2 days, then QDS for 5 days)
- chloramphenicol 1% ointment (QDS for 2 days, then BD for 5 days)
- fusidic acid 1% eye drops (2nd line, BD for 7 days)
73
CONJUNCTIVITIS
what is allergic conjunctivitis?
Allergic conjunctivitis is caused by contact with allergens. It causes swelling of the conjunctival sac and eyelid with itching and a watery discharge.
74
CONJUNCTIVITIS
what is the management of allergic conjunctivitis?
Antihistamines (oral or topical) can help symptoms.
Topical mast-cell stabilisers can be used in patients with chronic seasonal symptoms.
75
DIABETIC RETINOPATHY
what is the pathophysiology?
Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes
Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms.
Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
76
DIABETIC RETINOPATHY
what are the different types?
non-proliferative
proliferative
maculopathy
77
DIABETIC RETINOPATHY
what are the key features of non-proliferative diabetic retinopathy?
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots ('soft exudates' - represent areas of retinal infarction),
venous beading/looping
intraretinal microvascular abnormalities (IRMA)
78
DIABETIC RETINOPATHY
what are the key features of proliferative diabetic retinopathy?
retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM
79
DIABETIC RETINOPATHY
what are the key features of maculopathy diabetic retinopathy?
based on location rather than severity, anything is potentially serious
hard exudates and other 'background' changes on macula
check visual acuity
more common in Type II DM
80
DIABETIC RETINOPATHY
what are the complications?
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
81
DIABETIC RETINOPATHY
what is the management for all patients?
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
82
DIABETIC RETINOPATHY
what is the management for non-proliferative diabetic retinopathy?
regular observation
if severe/very severe consider panretinal laser photocoagulation
83
DIABETIC RETINOPATHY
what is the management for maculopathy diabetic retinopathy?
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
84
DIABETIC RETINOPATHY
what is the management for proliferative diabetic retinopathy?
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
85
KERATITIS
what are the causes?
Viral infection (e.g., herpes simplex = most common)
Bacterial infection (e.g.,
Pseudomonas or Staphylococcus)
Fungal infection (e.g., Candida or Aspergillus)
Contact lens-induced acute red eye (CLARE)
Exposure keratitis, caused by inadequate eyelid coverage (e.g., ectropion)
86
KERATITIS
what is it?
refers to inflammation of the cornea.
87
KERATITIS
what are the clinical features?
red eye: pain and erythema
photophobia
foreign body sensation , gritty sensation
hypopyon may be seen
88
KERATITIS
what are the investigations?
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
89
KERATITIS
what is the management?
stop using contact lens until the symptoms have fully resolved
topical antibiotics (quinolones = first-line)
cycloplegic for pain relief
e.g. cyclopentolate
90
KERATITIS
what are the complications?
corneal scarring
perforation
endophthalmitis
visual loss
91
HERPES KERATITIS
what is the pathophysiology?
Herpes simplex keratitis usually affects only the epithelial layer of the cornea
92
HERPES KERATITIS
what is the clinical presentation of primary and recurrent herpes keratosis?
Primary infection often involves mild symptoms of blepharoconjunctivitis (inflammation of the eyelid margins and conjunctiva).
Recurrent infection may present with:
Painful red eye
Photophobia
Vesicles (fluid-filled blisters)
Foreign body sensation
Watery discharge
Reduced visual acuity
93
HERPES KERATITIS
what are the investigations?
Slit lamp examination is required to diagnose keratitis.
Fluorescein staining shows a dendritic corneal ulcer. Dendritic describes the branching appearance of the ulcer.
Corneal scrapings can be used for viral testing.
94
HERPES KERATITIS
what is the management?
Patients should be referred for urgent assessment and management by an ophthalmologist.
Specialist management involves topical or oral antivirals (e.g., aciclovir or ganciclovir).
Corneal transplant is an option to treat permanent scarring and vision loss after keratitis.
95
OPTIC NEURITIS
what are the causes?
- multiple sclerosis: the commonest associated disease
- diabetes
- syphilis
96
OPTIC NEURITIS
what are the clinical features
- acute painful vision loss
- periocular pain, particularly on eye movement
- unilateral decrease in visual acuity over hours or days
- poor discrimination of colours, 'red desaturation' (dyschromatopsia)
- relative afferent pupillary defect
- central scotoma
97
OPTIC NEURITIS
what are the investigations?
- visual function tests = acuity, colour vision + visual fields
- MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases
- lumbar puncture = if MS is considered
98
OPTIC NEURITIS
what is the management?
high-dose steroids = IV methylprednisolone
recovery usually takes 4-6 weeks
99
OPTIC NEURITIS
what is the prognosis?
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%
100
RETINAL DETACHMENT
what is it?
involves the neurosensory layer of the retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (the base layer attached to the choroid).
This is usually due to a retinal tear, allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers.
101
RETINAL DETACHMENT
why is it sight-threatening?
The neurosensory retina relies on the blood vessels of the choroid for its blood supply. Therefore, retinal detachment can disrupt the blood supply and cause permanent damage to the photoreceptors
102
RETINAL DETACHMENT
what are the risk factors?
Lattice degeneration (thinning of the retina)
Posterior vitreous detachment
Trauma
Diabetic retinopathy
Retinal malignancy
Family history
103
RETINAL DETACHMENT
what is the clinical presentation?
SYMPTOMS
- floaters (dots, lines or haze)
- recurrent flashes
- painless
- progressive vision loss (starts at periphery + progresses towards centre)
- blurred vision
SIGNS
- decreased visual acuity
- peripheral visual field loss
- relative afferent pupillary defect
- fundoscopic findings (asymmetric red reflex, detached retinal folds appear pale, opaque + wrinkled)
104
RETINAL DETACHMENT
what are the investigations?
- slit lamp
- fundoscopy
to consider
- B-scan ultrasonography
- CT/MRI orbit
105
RETINAL DETACHMENT
what is the management?
immediate referral to ophthalmologist, should be seen within 24hrs
SURGERY
- vitrectomy
- scleral buckle
- pneumatic retinopexy
106
SCLERITIS
what is it?
involves inflammation of the sclera. The sclera is the outer layer of connective tissue surrounding most of the eye (excluding the cornea). It forms the visible white part of the eye.
107
SCLERITIS
what are the causes?
- idiopathic = most common
- systemic conditions - RA, vasculitis (granulomatosis with polyangiitis)
- infection - pseudomonas or s.aureus
- ocular trauma
- ocular surgery
- systemic infection
108
SCLERITIS
what is the clinical presentation?
SYMPTOMS
- severe eye pain (worse on eye movement, can awaken from sleep)
- red eye
- eye watering (but no other discharge)
- photophobia
- blurred vision
- may have history of recurrent episodes
SIGNS
- red eye (do not blanch with phenylephrine + not mobile)
- visual acuity normal or reduced (depends on severity)
109
SCLERITIS
what is the difference in clinical presentation of episcleritis vs scleritis?
EPISCLERITIS
- mild discomfort/grittiness
- superficial inflamed vessels
- vessels blanch with topical phenylephrine
- mobile vessels with cotton tip
SCLERITIS
- severe pain, worse on eye movement
- deep inflamed vessels
- vessels do not blanch
- vessels are immobile
110
SCLERITIS
what are the risk factors?
rheumatoid arthritis: the most commonly associated condition
systemic lupus erythematosus
sarcoidosis
granulomatosis with polyangiitis
111
SCLERITIS
what are the investigations?
- baseline bloods (FBC, U&Es, LFTs, bone profile)
- ESR + CRP
- autoimmune screen
- urine dipstick
- B scan ultrasonography
112
SCLERITIS
what is the management?
1st line
- NSAIDS (ibuprofen 400mg TDS)
- corticosteroids (topical, oral or IV)
REFRACTORY CASES
- DMARDs (methotrexate, ciclosporin)
- biological agents (infliximab)
- surgical intervention
113
THYROID EYE DISEASE
how many patients does it affect?
25-50% of patients with graves disease
114
THYROID EYE DISEASE
what is the pathophysiology?
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
115
THYROID EYE DISEASE
how can it be prevented?
smoking is the most important modifiable risk factor for the development of thyroid eye disease
radioiodine treatment may increase the inflammatory symptoms seen in thyroid eye disease. Prednisolone may help reduce the risk
116
THYROID EYE DISEASE
what is the clinical presentation?
the patient may be eu-, hypo- or hyperthyroid at the time of presentation
exophthalmos
conjunctival oedema
optic disc swelling
ophthalmoplegia
inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
117
THYROID EYE DISEASE
what is the management?
smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure
steroids
radiotherapy
surgery
118
THYROID EYE DISEASE
what are the complications?
exposure keratopathy
optic neuropathy
strabismus
diplopia
119
ORBITAL CELLULITIS
what is it?
Orbital cellulitis is an infection around the eyeball involving the tissues behind the orbital septum.
120
ORBITAL CELLULITIS
what is the most common cause?
It is usually caused by a spreading upper respiratory tract infection from the sinuses and carries a high mortality rate.
Most common bacterial causes - Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
121
ORBITAL CELLULITIS
what are the risk factors?
Childhood - Mean age of hospitalisation 7-12 years
Previous sinus infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection
122
ORBITAL CELLULITIS
what is the clinical presentation?
SYMPTOMS
- swelling and redness of eyelids
- pain on ocular movement
- diplopia
- fever
- malaise
SIGNS
- restricted ocular motility (ophthalmoplegia)
- RAPD
- chemosis
- proptosis
- reduced visual acuity
- impaired colour vision
- ptosis
123
ORBITAL CELLULITIS
what are the investigations?
- FBC = leukocytosis
- CRP = elevated
- blood cultures
- VBG = acidosis + raised lactate
- CT orbit + sinuses with contrast
to consider
- swab
- MRI
124
ORBITAL CELLULITIS
what is the management?
MEDICAL MANAGEMENT
- hospital admission
- elevation of head of the bed
- regular neurological + eye observations
- analgesia
- IV antibiotics (IV CO-AMOXICLAV or CEFTRIAXONE (clindamycin + metronidazole if penicillin allergic))
- topical decongestants
- daily ophthalmology + ENT reviews
SURGICAL MANAGEMENT
- surgical drainage +/- sinus washout
- lateral canthotomy
125
ORBITAL CELLULITIS
what are the complications?
- central retinal artery or vein occlusion
- optic neuropathy
- endophthalmitis
- subperiosteal abscess
- meningitis
- cavernous sinus thrombosis
- cerebral abscess
126
PERIORBITAL CELLULITIS
what is it also known as?
preseptal cellulitis
127
PREORBITAL CELLULITIS
what is it?
is an eyelid and skin infection in front of the orbital septum (in front of the eye). This includes the eyelids, skin and subcutaneous tissue of the face, but not the contents of the orbit.
128
PREORBITAL CELLULITIS
what are the most common causes?
most commonly from breaks in the skin or local infections such as sinusitis or other respiratory tract infections.
The most frequently causative organisms are Staph. aureus, Staph. epidermidis, streptococci and anaerobic bacteria
129
PREORBITAL CELLULITIS
what is the epidemiology?
occurs most commonly in children - 80% of patients are under 10 and the median age of presentation is 21 months
It is more common in the winter due to the increased prevalence of respiratory tract infections.
130
PREORBITAL CELLULITIS
what are the symptoms?
The patient presents with a red, swollen, painful eye of acute onset. They are likely to have symptoms associated with fever.
131
PREORBITAL CELLULITIS
what are the clinical signs?
Erythema and oedema of the eyelids, which can spread onto the surrounding skin
Partial or complete ptosis of the eye due to swelling
132
PREORBITAL CELLULITIS
what are the investigations?
Bloods - raised inflammatory markers
Swab of any discharge present
Contrast CT of the orbit may help to differentiate between preseptal and orbital cellulitis. It should be performed in all patients suspected to have orbital cellulitis
133
PREORBITAL CELLULITIS
what is the management?
All cases should be referred to secondary care for assessment
Oral antibiotics are frequently sufficient - usually co-amoxiclav
Children may require admission for observation
134
PREORBITAL CELLULITIS
what are the complications?
Bacterial infection may spread into the orbit and evolve into orbital cellulitis
135
STYE
what is it?
Hordeolum externum is an infection of the glands of Zeis or glands of Moll.
The glands of Moll are sweat glands at the base of the eyelashes.
The glands of Zeis are sebaceous glands at the base of the eyelashes.
A stye causes a tender red lump along the eyelid that may contain pus
136
STYE
what are the clinical features?
painful red hot lump on eyelid that points outwards
causes localised inflammation
137
STYE
how is it managed?
treated with hot compresses and analgesia.
Topical antibiotics (e.g., chloramphenicol) may be considered if it is associated with conjunctivitis or if symptoms are persistent.
138
CHALAZION
what is it?
A chalazion occurs when a Meibomian gland becomes blocked and swells. It is often called a Meibomian cyst.
139
CHALAZION
how does it present?
a swelling in the eyelid that is typically not tender (however, it can be tender and red).
points inwards
140
CHALAZION
what is the management?
warm compresses and gentle massage towards the eyelashes (to encourage drainage). Rarely, surgical drainage may be required.
141
ENTROPION
what is it?
Entropion refers to when the eyelid turns inwards with the lashes pressed against the eye.
This causes pain and can result in corneal damage and ulceration.
142
ENTROPION
what are the clinical features?
- inverted eyelid
- eye irritation
- excessive tearing
143
ENTROPION
what is the management?
INITIAL MANAGEMENT
- taping (must use lubricating eye drops)
DEFINITIVE MANAGEMENT
- surgical repair
144
ECTROPION
what is it?
Ectropion refers to when the eyelid turns outwards, exposing the inner aspect.
This can result in exposure keratopathy, as the eyeball is exposed and not adequately lubricated and protected.
145
ECTROPION
what are the clinical features?
- everted eyelid
- exposure of palpebral conjunctiva
- excessive tearing
- conjunctival hyperaemia
146
ECTROPION
what is the management?
Mild cases may not require treatment.
Regular lubricating eye drops are used to protect the surface of the eye.
More significant cases may require surgery to correct the defect.
A same-day referral to ophthalmology is required if there is a risk to sight
147
TRICHIASIS
what is it?
Trichiasis refers to inward growth of the eyelashes. It results in pain and can cause corneal damage and ulceration.
148
TRICHIASIS
what is the management?
removing the affected eyelashes.
Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent them from regrowing. A same-day referral to ophthalmology is required if there is a risk to sight.
149
CORNEAL ABRASIONS
what are the common causes?
Damaged contact lenses
Fingernails
Foreign bodies (e.g., metal fragments)
Tree branches
Makeup brushes
Entropion (inward turning eyelid)
chemical abrasions
contract lenses (associated with pseudomonas infection)
150
CORNEAL ABRASIONS
what is the clinical presentation?
Painful red eye
Photophobia
Foreign body sensation
Epiphora (excessive tear production)/lacrimation
Blurred vision
151
CORNEAL ABRASIONS
what are the investigations?
fluorescein staining
- examination typically reveals a yellow-stained abrasion (representative of the de-epithelialized surface) which is usually visible to the naked eye
- visualisation is enhanced by the use of a cobalt blue filter (available on an ophthalmoscope) or a Wood's lamp
152
CORNEAL ABRASIONS
what is the management?
a topical antibiotic is recommended for these patients in order to prevent secondary bacterial infection.
153
OCULAR TRAUMA
what is hyphema?
blood in the anterior chamber of the eye
154
OCULAR TRAUMA
what is the risk of hyphema?
raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes.
155
OCULAR TRAUMA
what is the management of hyphema?
Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted.
Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient.
156
OCULAR TRAUMA
what are the clinical features of orbital compartment syndrome?
eye pain/swelling
proptosis
'rock hard' eyelids
relevant afferent pupillary defect
157
OCULAR TRAUMA
what is the management of orbital compartment syndrome?
urgent lateral canthotomy (before diagnostic imaging) to decompress the orbit
158
SUBCONJUNCTIVAL HAEMORRHAGE
what is it?
Subconjunctival haemorrhages result from the bleeding of blood vessels into the subconjunctival space. The vessels that bleed are usually the ones responsible for supplying the conjunctiva or episclera.
159
SUBCONJUNCTIVAL HAEMORRHAGE
what are the causes?
cause is most commonly traumatic followed by spontaneous idiopathic cases, Valsalva manoeuvres and several systemic diseases.
160
SUBCONJUNCTIVAL HAEMORRHAGE
what is the epidemiology?
more common in women than in men when there has been no history of trauma
risk increases with age as the risk factors are more common in elderly patients. Newborns are also more susceptible
161
SUBCONJUNCTIVAL HAEMORRHAGE
what are the risk factors?
Trauma and contact lens usage (68%): these are the most common causes generally, as well as being often the sole risk factor in younger patients
Idiopathic
Valsalva manoeuvre e.g. coughing, straining
Hypertension
Bleeding disorders
Drugs such as aspirin, NSAIDs and anticoagulants
Diabetes
Arterial disease and hyperlipidaemia
162
SUBCONJUNCTIVAL HAEMORRHAGE
what are the symptoms?
Red-eye, usually unilateral
Subconjunctival haemorrhages are mostly asymptomatic, however mild irritation may be present
163
SUBCONJUNCTIVAL HAEMORRHAGE
what are the signs?
Flat, red patch on the conjunctiva. It will have well-defined edges and normal conjunctiva surrounding it. Patches can vary in size depending on the size of the bleed, and can involve the whole conjunctiva
Traumatic haemorrhages are most common in the temporal region (40.5%), with the inferior conjunctiva as the next most commonly affected area
Vision should be normal, including acuity, visual fields and range of eye movements
On examination, the fundus should be normal
164
SUBCONJUNCTIVAL HAEMORRHAGE
what are the investigations?
clinical diagnosis
165
SUBCONJUNCTIVAL HAEMORRHAGE
what is the management?
should resolve on its own within 2-3 weeks
166
POSTERIOR VITREOUS DETACHMENT
what is it?
Posterior vitreous detachment is the separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing
167
POSTERIOR VITREOUS DETACHMENT
what is the epidemiology?
Occur in over 75% of people over the age of 65
More common in females
168
POSTERIOR VITREOUS DETACHMENT
what are the risk factors?
- increasing age
- highly myopic
169
POSTERIOR VITREOUS DETACHMENT
what are the symptoms?
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
170
POSTERIOR VITREOUS DETACHMENT
what are the signs?
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
171
POSTERIOR VITREOUS DETACHMENT
what are the investigations?
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
172
POSTERIOR VITREOUS DETACHMENT
what is the management?
Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
173
VITREOUS HAEMORRHAGE
what is it?
Vitreous haemorrhage is bleeding into the vitreous humour. It is one of the most common causes of sudden painless loss of vision.
It causes disruption to vision to a variable degree, ranging from floaters to complete visual loss.
The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas.
Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day.
174
VITREOUS HAEMORRHAGE
what are the common causes?
proliferative diabetic retinopathy (over 50%)
posterior vitreous detachment
ocular trauma: the most common cause in children and young adults
175
VITREOUS HAEMORRHAGE
what are the symptoms?
painless visual loss or haze (commonest)
red hue in the vision
floaters or shadows/dark spots in the vision
176
VITREOUS HAEMORRHAGE
what are the clinical signs?
decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
visual field defect if severe haemorrhage
177
VITREOUS HAEMORRHAGE
what are the investigations?
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
178
CORNEAL FOREIGN BODY
what are the clinical features?
eye pain
foreign body sensation
photophobia
watering eye
red eye
179
CORNEAL FOREIGN BODY
what are the indications for referral to ophthalmology?
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.
180
BLURRED VISION
what are the causes?
refractive error: most common
cataracts
retinal detachment
age-related macular degeneration
acute angle closure glaucoma
optic neuritis
amaurosis fugax
181
BLURRED VISION
how is it assessed?
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
182
OPTIC ATROPHY
what is it?
Optic atrophy is seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision*. Causes may be acquired or congenital
183
OPTIC ATROPHY
what are the acquired causes?
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
184
OPTIC ATROPHY
what are the congenital causes?
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)
185
STRABISMUS
what is it?
Squint (strabismus) is characterised by misalignment of the visual axes.
186
STRABISMUS
what are the different types?
concomitant
paralytic
187
STRABISMUS
what is concomitant strabismus?
Due to imbalance in extraocular muscles
Convergent is more common than divergent
188
STRABISMUS
what is paralytic strabismus?
Due to paralysis of extraocular muscles
189
STRABISMUS
what are the investigations?
cover test
ask the child to focus on an object
cover one eye
observe movement of uncovered eye
cover other eye and repeat test
190
STRABISMUS
what is the management?
referral to secondary care
eye patches may help prevent amblyopia
191
SUDDEN LOSS OF VISION
what are the causes?
- ischaemic (amaurosis fugax)
- central retinal vein occlusion
- central retinal artery occlusion
- vitreous haemorrhage
- retinal detachment
192
RETINAL VEIN OCCLUSION
what is it?
Retinal vein occlusion occurs when a blood clot (thrombus) forms in the retinal veins, blocking the drainage of blood from the retina. The thrombus may form in the central retinal vein or branch retinal veins.
193
RETINAL VEIN OCCLUSION
what are the risk factors?
Hypertension
High cholesterol
Diabetes
Smoking
High plasma viscosity (e.g., myeloma)
Myeloproliferative disorders
Inflammatory conditions (e.g., SLE)
194
RETINAL VEIN OCCLUSION
what is the clinical presentation?
SYMPTOMS
- blurred vision
- painless
- unilateral and sudden
- metamorphopsia (image distortion)
SIGNS
- stormy sunset appearance on fundoscopy (vascular dilatation + tortuosity, dot + flame haemorrhages, cotton wool spots, macular oedema)
- relative afferent pupillary defect
195
RETINAL VEIN OCCLUSION
what is the pathophysiology?
Blockage of a retinal vein causes venous congestion in the retina. Increased pressure in the retinal veins results in fluid and blood leaking into the retina, causing macular oedema and retinal haemorrhages. This results in retinal damage and vision loss.
196
RETINAL VEIN OCCLUSION
what are the fundoscopic findings?
Dilated tortuous retinal veins
Flame and blot haemorrhages
Retinal oedema
Cotton wool spots
Hard exudates
197
RETINAL VEIN OCCLUSION
what are the investigations?
- slit lamp
- fluorescein angiogram
to consider
- OCT scan
- screen for risk factors
198
RETINAL VEIN OCCLUSION
what is the management?
UNCOMPLICATED CRVO
- observe + manage risk factors
EVIDENCE OF MACULAR OEDEMA
- intravitreal VEGF inhibitor
- intravitreal corticosteroid injections
EVIDENCE OF NEOVASCULARISATION
- panretinal photocoagulation
199
VISUAL FIELD DEFECTS
what is the effect of lesions to the optic nerve?
unilateral vision loss
200
VISUAL FIELD DEFECTS
what is the effect of lesions to optic chiasm?
bitemporal hemianopia
201
VISUAL FIELD DEFECTS
where is the location if there is bitemporal hemianopia where upper quadrant defect > lower quadrant defect?
inferior chiasm - pituitary tumour
202
VISUAL FIELD DEFECTS
where is the location if there is bitemporal hemianopia where lower quadrant defect > upper quadrant defect?
superior chiasm - craniopharyngioma
203
VISUAL FIELD DEFECTS
what is the effect of a lesion to the optic tract?
contralateral homonymous hemianopia to side of lesion
204
VISUAL FIELD DEFECTS
what is the effect of a lesion in optic radiations
contralateral homonymous quadrantanopia
205
VISUAL FIELD DEFECTS
where is the lesion located in a inferior homonymous quadrantanopia?
Baum's loop in parietal lobe
206
VISUAL FIELD DEFECTS
where is the lesion located in a superior homonymous quadrantanopia?
Meyers loop in the temporal lobe
207
VISUAL FIELD DEFECTS
where is the lesion in left homonymous hemianopia with macular sparing?
calcarine sulcus
208
VISUAL FIELD DEFECTS
what pathway is affected in monocular vision loss?
optic nerve
209
VISUAL FIELD DEFECTS
what are the causes of monocular vision loss?
- retinal disorders
- optic nerve disorders
- corneal disorders
210
VISUAL FIELD DEFECTS
what part of the vision pathway is affected in a bitemporal hemianopia?
optic chiasm
211
VISUAL FIELD DEFECTS
what are the causes of bitemporal hemianopias?
pituitary tumours
212
VISUAL FIELD DEFECTS
what part of the vision pathway is affected in contralateral homonymous hemianopias?
optic tracts
213
VISUAL FIELD DEFECTS
what part of the vision pathway is affected in quadrantanopias?
optic radiations
214
UVEITIS
what are the different types of uveitis?
- anterior uveitis (iritis) = iris + ciliary body
- intermediate uveitis = posterior ciliary body + pars plana
- posterior uveitis = posterior vitreous, retina, choroid + optic nerve
- panuveitis = anterior, intermediate + posterior segments
215
UVEITIS
what are the clinical features of intermediate uveitis?
SYMTPOMS
- worsening floaters
- decreased vision
SIGNS
- vitreous haze
- snowballs
- macular oedema
216
UVEITIS
what are the clinical features of posterior uveitis?
SYMPTOMS
- decreased vision
- visual field changes
SIGNS
- chorioretinal lesions
- retinal whitening
217
UVEITIS
what are the clinical features of panuveitis?
have all features of anterior, intermediate and posterior uveitis
- decreased vision
- floaters
- red, painful eye
218
UVEITIS
what are the investigations?
PHYSICAL EXAMINATION
- visual fields
- visual acuity
- cranial nerve assessment
- reflexes
SLIT LAMP
- snowballs = intermediate
- retinal whitening = posterior
to consider
- infection/autoimmune screen
219
UVEITIS
what is the management?
- assessment with ophthalmologist within 24hrs
1st line
- corticosteroids (topical, oral, IV or ocular injections)
- antimicrobials (if fungal/bacterial/viral source suspected)
2nd line
- immunosuppressant +/- DMARDs
- surgical intervention (laser phototherapy, cryotherapy or vitrectomy)
220
UVEITIS
what are the complications?
- visual loss or impairment
- secondary cataracts or glaucoma
- retinal detachment
- vitreous haemorrhage
221
FUNDOSCOPY
what does this show?
pre-proliferative diabetic retinopathy
222
FUNDOSCOPY
what does this show?
age related macular degeneration
223
FUNDOSCOPY
what does this show?
branch retinal vein occlusion
224
FUNDOSCOPY
what does this show?
central retinal artery occlusion
225
FUNDOSCOPY
what does this show?
central retinal artery occlusion
226
FUNDOSCOPY
what does this show?
central retinal vein occlusion
227
FUNDOSCOPY
what does this show?
retinal branch vein occlusion
228
FUNDOSCOPY
what does this show?
proliferative diabetic retinopathy
229
FUNDOSCOPY
what does this show?
pre-proliferative diabetic retinopathy
230
FUNDOSCOPY
what does this show?
panretinal photocoagulation
231
FUNDOSCOPY
what does this show?
papilloedema
