Ophthalmology Flashcards
(198 cards)
1
Q
What is glaucoma?
A
- Optic nerve damage caused by a rise in intraocular pressure
2
Q
What causes intraocular pressure to rise?
A
- A blockage in aqueous humour trying to escape the eye
3
Q
What are the 2 types of glaucoma?
A
- Open angle glaucoma
- Acute angle closure glaucoma
4
Q
Which part of the eye is filled with vitreous humour?
A
- Vitreous chamber
5
Q
Which parts of the eye are filled with aqueous humour?
A
- Anterior chamber (between the cornea and iris)
- Posterior chamber (between the lens and iris)
6
Q
What is the function of the aqueous humour and where is it produced?
A
- Supplies nutrients to the cornea
- Produced by the ciliary body
7
Q
Outline the flow of aqueous humour from the ciliary body to the general circulation:
A
- Produced by the ciliary body
- Flows through the posterior chamber and around the iris to the anterior chamber
- Drains through the trabecular meshwork to the canal of Schlemm at the angle between the cornea and the iris and enters the general circulation
8
Q
What is the normal range for intraocular pressure?
A
- 10 to 21 mmHg, created by the resistance to flow through the trabecular meshwork
9
Q
Outline the pathophysiology of open angle glaucoma:
A
- There is a gradual increase in resistance to flow through the trabecular meshwork
- The pressure slowly builds within the eye
10
Q
Outline the pathophysiology of acute angle closure glaucoma:
A
- The iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining
- There is a continual build up of pressure and an acute onset of symptoms
11
Q
Which type of glaucoma is an ophthalmological emergency?
A
- Acute angle closure glaucoma
12
Q
What change is seen in the optic disc in eyes with high intraocular pressure?
A
- Cupping of the optic disc (cup disc ratio above 0.5)
13
Q
State 3 risk factors for open angle glaucoma:
A
- Increasing age
- Black ethnic origin
- Myopia
14
Q
What is the difference in the onset of symptoms of open angle glaucoma and acute angle closure glaucoma?
A
- Open angle glaucoma: gradual onset
- Acute angle closure: sudden onset
15
Q
What is the most common 1st symptom of open angle glaucoma?
A
- Gradual onset of peripheral vision loss (tunnel vision)
16
Q
Other than tunnel vision, state 3 symptoms of open angle glaucoma:
A
- Headaches
- Blurred vision
- Halos around lights, particularly at night
17
Q
State 2 methods for measuring intraocular pressure:
A
- Non contact tonometry (less accurate)
- Goldmann applanation tonometry (gold standard)
18
Q
Other than goldmann applanation tonometry, state and explain 4 investigations for diagnosing glaucoma:
A
- Slit lamp assessment (for the cup-disk ratio and optic nerve health)
- Visual field assessment (for peripheral vision loss)
- Gonioscopy (to assess the angle between the iris and cornea)
- Central corneal thickness assessment
19
Q
Glaucoma treatment is typically started at an intraocular pressure of 24 mmHg or above. State and explain 2 surgical treatments for open angle glaucoma:
A
- 360° selective laser trabeculoplasty: a laser is directed at the trabecular meshwork, improving drainage
- Trabeculectomy: creating a new channel from the anterior chamber through the sclera to a location under the conjunctiva, causing a bleb on the conjunctiva (from here, it is reabsorbed into the general circulation)
20
Q
What is the 1st line medical treatment for open angle glaucoma and how does it work?
A
- Prostaglandin analogue eye drops (e.g. latanoprost)
- Increase uveoscleral outflow
21
Q
State 3 potential side effects of prostaglandin analogue eye drops (e.g. latanoprost):
A
- Eyelash growth
- Eyelid pigmentation
- Iris pigmentation (browning)
22
Q
Other than latanoprost eye drops, state and explain 3 other medical treatments for 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
23
Q
State 3 risk factors for acute angle closure glaucoma:
A
- Increasing age
- Female
- East Asian ethnicity
24
Q
State 3 types of medications that 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
25
State 4 symptoms and 2 signs of acute angle closure glaucoma:
- Painful red eye, blurred vision, headache nausea/vomiting
- Fixed dilated pupil, hazy cornea
26
State 5 treatments for acute angle closure glaucoma:
- Pilocarpine (cholinergic agonist)
- Acetazolamide (carbonic anhydrase inhibitor)
- IV mannitol
- Timolol (beta blocker)
- Laser iridotomy (definitive)
27
What is the most common cause of blindness in the UK?
- Age related macular degeneration (AMD)
28
What is age related macular degeneration (AMD)?
- A progressive medical condition which may result in blurred or no vision in the centre of the visual field
29
State the 2 types of AMD:
- Wet (neovascular): 10% of cases
- Dry (non neovascular): 90% of cases
30
Where in the eye is the macula located?
- In the centre of the retina
31
What is the function of the macula?
- Generates high definition colour vision in the central visual field
32
What are the 4 layers of the macula?
- Choroid layer (base): contains blood vessels that supply the macula
- Bruch’s membrane
- Retinal pigment epithelium
- Photoreceptors (surface)
33
Drusen are an important finding with AMD. What are Drusen?
- Yellowish deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane (a few small Drusen can be normal in elderly patients)
34
Other than the presence of Drusen, state 2 findings common to both types of AMD:
- Atrophy of the retinal pigment epithelium
- Degeneration of the photoreceptors
35
Outline the pathophysiology of wet (neovascular) AMD:
- 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
36
Outline the pathophysiology of dry (non neovascular) AMD:
- Slow, progressive degeneration of the retinal pigment epithelium (RPE), photoreceptors, and Bruch’s membrane in the macula, which leads to central vision loss over time
37
State 1 chemical that stimulates the development of new vessels in wet (neovascular) AMD:
- Vascular endothelial growth factor (VEGF)
38
State 4 risk factors for AMD:
- Older age
- Smoking
- Cardiovascular disease
- Obesity
39
Visual changes associated with AMD tend to be unilateral. State 3 visual changes associated with AMD and state how these visual changes commonly present:
- Gradual loss of central vision
- Reduced visual acuity
- Metamorphopsia
- Gradually worsening ability to read small text
40
Which type of AMD presents more acutely?
- Wet AMD presents more acutely than dry AMD
- Vision loss can develop within days and progress to complete vision loss within 2-3 years (often progresses to bilateral disease)
41
In terms of visual changes, outline the differences between AMD and glaucoma:
- Glaucoma: peripheral vision loss and halos around lights
- AMD: central vision loss and wavy appearance to straight lines
42
State 4 key findings of AMD on examination:
- 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
43
State and explain 1 investigation for diagnosing and monitoring AMD:
- Optical coherence tomography: gives a cross sectional view of the layers of the retina
44
There is no specific treatment for dry AMD. State 3 management options for dry AMD:
- Smoking cessation
- Controlling blood pressure
- Vitamin supplementation
45
State 1 class of medication that can be used to treat wet AMD and give 1 example of a medication in this medication class:
- VEGF inhibitors
- Ranibizumab
46
How are VEGF inhibitors (e.g. ranibizumab) administered for wet AMD?
- Intravitreal injection
- Usually about once a month
47
What is diabetic retinopathy?
- Damage to the retinal blood vessels (endothelial cells) due to prolonged high blood sugar levels
48
State and explain 5 potential findings of a fundoscopy of a patient with diabetic retinopathy:
- Microaneurysms: increased vascular permeability
- Blot haemorrhages: increased vascular permeability
- Hard exudates (of lipid and protein): increased vascular permeability
- Cotton wool spots: damage to retinal nerve fibres
- Neovascularisation: due to release of growth factors in the retina
49
State the 3 grades of diabetic retinopathy:
- Background
- Pre-proliferative
- Proliferative
50
What is the main distinction between non proliferative (background and pre proliferative) and proliferative diabetic retinopathy?
- The key feature of proliferative diabetic retinopathy is the development of new blood vessels (neovascularisation)
51
State 2 findings of diabetic maculopathy:
- Exudates within the macula
- Macular oedema
52
State 4 potential complications of diabetic retinopathy:
- Retinal detachment
- Vitreous haemorrhage
- Rubeosis iridis
- Cataracts
53
Non proliferative diabetic retinopathy requires close monitoring and careful diabetic control. State 3 treatments for proliferative diabetic retinopathy:
- Pan retinal photocoagulation (PRP)
- Anti VEGF medications
- Vitrectomy
54
State 1 treatment for macular oedema:
- Intravitreal implant containing dexamethasone
55
What is the function of the sclera?
- Provides attachment to the extraocular muscles
56
What is the function of the cornea?
- Refracts incoming light so it can be focused on the retina
57
In the context of the cornea, what is refraction?
- The bending of light as it passes from air (less dense medium) into the cornea (denser, transparent tissue at the front of the eye)
58
What is the function of the choroid?
- Provides nourishment to the outer layers of the retina
59
What is the function of the ciliary body?
- Controls the shape of the lens, and contributes to the formation of aqueous humour
60
What is the function of the iris?
- Controls the diameter of the pupil
61
What is the function of the retina?
- Converts light into electrical signals that the brain can interpret
62
Explain the difference between the retina, macula and fovea:
- Retina: entire light sensitive layer at the back of the eye
- Macula: central area of the retina, responsible for central vision
- Fovea: tiny pit in the centre of the macula, responsible for high acuity colour vision
63
What is the difference between the function of rod and cone cells?
- Rod cells: night vision
- Cone cells: colour vision
64
Describe the relative distributions of rod and cone cells in the retina:
- Peripheral retina: mostly rods
- Macula: mostly cones
- Fovea: all cones
65
What is the function of the conjunctiva?
- Provides protection and lubrication of the eye by the production of mucus and tears
66
What is hypertensive retinopathy?
- Damage to the small blood vessels in the retina caused by hypertension
67
State and explain 5 potential findings of a fundoscopy of a patient with diabetic retinopathy:
- Silver wiring or copper wiring: arteriole walls become thickened and sclerosed and reflect more light on examination
- Arteriovenous nipping (AV nipping): is where the arterioles cause compression of the veins where they cross due to sclerosis and hardening of the arterioles
- Hard exudates (of lipid and protein): increased vascular permeability
- Cotton wool spots: damage to retinal nerve fibres
Retinal haemorrhages: caused by damaged vessels rupturing
- Papilloedema: caused by ischaemia to the optic nerve, resulting in optic nerve swelling (oedema)
68
What is the classification system for hypertensive retinopathy called?
- The Keith Wagener classification
69
State and explain the 4 stages of the Keith Wagener classification:
- 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
70
What are cataracts?
- A progressively opaque eye lens, which reduces the light entering the eye and visual acuity
71
What is visual acuity?
- The ability to distinguish details or shapes at a specific distance
72
What is the function of the lens?
- To focus light on the retina
73
What is the lens held in place by and how is it nourished?
- Held in place by suspensory ligaments attached to the ciliary body
- Nourished by the aqueous humour
74
What reflex is tested for during the neonatal examination to screen for congenital cataracts?
- The red reflex
75
State 4 risk factors for developing cataracts:
- Increasing age
- Diabetes
- Steroids
- Hypocalcaemia
76
Symptoms of cataracts are usually asymmetrical. State 4 symptoms of cataracts:
- 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
77
State 1 key examination finding in patients with cataracts:
- Loss of the red reflex
78
Why is the red reflex "red" in a healthy eye and "grey" in an unhealthy eye?
- Healthy eye: clear lens, light reaches the retina (which is rich in blood vessels)
- Unhealthy eye: cloudy lens, light blocked or scattered
79
What does cataract surgery involve?
- Drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens
80
Why might a patient with cataracts still have reduced visual acuity after the cataract is treated?
- Cataracts can prevent the detection of other pathology, such as macular degeneration or diabetic retinopathy, which can become apparent after surgery
81
How can cataracts mask macular degeneration and diabetic retinopathy?
- Cataracts cloud the lens, making it hard to see clearly into the back of the eye during fundoscopy
82
State and explain 1 potential complication of cataract surgery:
- Endophthalmitis: inflammation of the inner contents (humours) of the eye, usually caused by infections, and is a rare but serious complication of cataract surgery that can lead to vision loss
83
State 1 treatment for endophthalmitis:
- Intravitreal antibiotics
84
The pupil is a small hole in the centre of the iris. Which muscles of the iris constrict and dilate the pupil?
- Pupil constriction: circular muscles of the iris
- Pupil dilation: dilator muscles of the iris
85
Describe the innervation of the circular and dilator muscles of the iris:
- Circular: parasympathetic fibres of CN3
- Dilator: sympathetic nervous system
86
Trauma to the sphincter muscles in the iris can cause an irregular pupil shape. State 5 examples of pathologies that can cause an irregular pupil shape:
- Anterior uveitis: scar tissue in the iris
- Acute angle-closure glaucoma: vertical oval pupil
- Rubeosis iridis: neovascularisation in iris
- Coloboma (congenital): hole in the iris
- Tadpole pupil: muscle spasm in part of the dilator muscle of the iris (temporary condition associated with migraines)
87
State 4 potential causes of mydriasis:
- Anticholinergics (e.g. oxybutynin)
- Third nerve palsy
- Raised ICP
- Acute angle closure glaucoma
88
State 4 potential causes of miosis:
- Horner syndrome
- Cluster headache
- Opiates
- Pilocarpine
89
State 3 manifestations of a full CN3 palsy:
- Ptosis
- Dilated non reactive pupil (concerning)
- Divergent strabismus (squint, down and out eye)
90
Why does a CN3 palsy cause ptosis?
- Because the oculomotor nerve supplies the levator palpebrae superioris, which is responsible for lifting the upper eyelid
91
Why does a CN3 palsy cause a dilated non reactive pupil (concerning)?
- Because the oculomotor nerve carries parasympathetic fibres that innervate the circular muscles of the iris
92
Why does a CN3 palsy cause divergent strabismus?
- Because the oculomotor nerve supplies all the extraocular muscles except the lateral rectus and superior oblique
93
Explain why a full CN3 palsy is much more concerning than a CN3 palsy where the pupil is sparred:
- CN3 parasympathetic fibres (for pupil): located on the outer part of the nerve
- CN3 motor fibres (for eye muscles): located on the inner part of the nerve
- Pupil sparring CN3 palsy: caused by ischaemia to the core of the nerve (microvascular causes, outer parasympathetic fibres are sparred)
- Full CN3 palsy: caused by compression of the entire nerve (compression causes, outer parasympathetic fibres affected)
94
State 3 potential causes of a pupil sparring CN3 palsy:
- (Microvascular:)
- Diabetes
- Hypertension
- Ischaemia
95
State 4 potential causes of a full CN3 palsy:
- (Compression:)
- Posterior communicating artery aneurysm
- Tumour
- Raised ICP
- Cavernous sinus thrombosis
96
Why can cavernous sinus thrombosis or posterior communicating artery aneurysm cause nerve compression?
- Because the oculomotor nerve travels directly from the brainstem to the eye in a straight line, through the cavernous sinus and close to the posterior communicating artery
97
What is the triad of symptoms in Horner's syndrome?
- Ptosis
- Miosis
- Anhidrosis
98
What causes Horner's syndrome?
- A disruption of the 3 neuron sympathetic nerve pathway to the face
99
Outline the 3 neuron sympathetic nerve pathway to the face:
- Sympathetic nerves arise from the spinal cord in the chest (pre ganglionic nerves)
- They enter the sympathetic ganglion at the base of the neck and exit as post ganglionic nerves
- The post ganglionic nerves travel to the head alongside the internal carotid artery
100
What might anhidrosis tell you about the type of lesion responsible for a patient's Horner syndrome?
- 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
101
The causes of Horner syndrome can be remembered as the 4 Ss, 4 Ts and 4 Cs mnemonic. S for sentral, T for torso (pre ganglionic) and C for cervical (post ganglionic). What are they?
- Sentral lesions: stroke, multiple sclerosis, swelling (tumours), syringomyelia (cyst in the spinal cord)
- Torso (pre ganglionic) lesions: tumour (Pancoast tumour), trauma, thyroidectomy, top rib (a cervical rib growing above the first rib and clavicle)
- Cervical (post ganglionic) lesions: carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache
102
What phenotypical abnormality is associated with congenital Horner syndrome?
- Heterochromia (a difference in iris colour on the affected side)
103
State and explain 2 eye drops that can be used to test for Horner syndrome:
- Cocaine eye drops (normal pupil dilates, Horner eye does not dilate)
- Adrenalin eye drops (normal pupil does not dilate, Horner pupil does)
104
A Holmes Adie pupil is caused by damage to the post ganglionic parasympathetic fibres. State 6 features of a Holmes Adie Pupil:
- 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)
- Absent knee reflex
- Absent ankle reflex
105
What is Argyll Robertson Pupil?
- A specific finding in neurosyphilis, a constricted pupil that accommodates when focusing on a near object but does not react to light
106
What is blepharitis?
- Inflammation of the eyelid margins
107
Blepharitis is often associated with the dysfunction of which glands?
- Meibomian glands, which are responsible for secreting meibum (oil) onto the surface of the eye
108
State 2 complications of blepharitis:
- Styes (hordeolum externum)
- Chalazions
109
Describe the management of blepharitis:
- Warm compresses and gentle cleaning of the eyelid margins to remove debris
110
What is stye (hordeolum externum)?
- An infection of the glands of Zeis or glands of Moll
111
What are the glands of Zeis and the glands of Moll?
- Glands of Moll: sweat glands at the base of the eyelashes
- Glands of Zeis: sebaceous glands at the base of the eyelashes
112
What is the difference between stye (Hordeolum externum) and Hordeolum internum?
- Hordeolum internum is an infection of the Meibomian glands
- They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid
113
Describe the symptoms associated with blepharitis:
- Gritty, itchy, dry sensation in the eyes
114
State 1 symptom of stye (Hordeolum externum):
- Tender red lump along the eyelid that may contain pus
115
State 3 treatments for stye:
- Hot compresses
- Analgesia
- Topical antibiotics (e.g. chloramphenicol)
116
What is a Chalazion?
- A chalazion occurs when a Meibomian gland becomes blocked and swells (often called a Meibomian cyst)
117
State 3 treatments for Chalazion:
- Warm compresses
- Gentle massage towards the eyelashes (to encourage drainage)
- Surgical drainage may be required
118
What is entropion?
- When the eyelid turns inwards with the lashes pressed against the eye, which can cause corneal ulceration
119
What is the initial management for entropion?
- Taping the eyelid down to prevent it from turning inwards (when the eyelid is taped down, it is essential to prevent the eye from drying out by using regular lubricating eye drops)
120
What is ectropion?
- When the eyelid turns outwards, exposing the inner aspect
121
State 1 potential complication of ectropion:
- It usually affects the bottom lid
- This can result in exposure keratopathy, as the eyeball is exposed and not adequately lubricated and protected
122
What is trichiasis?
- Inward growth of the eyelashes
- It results in pain and can cause corneal damage and ulceration
123
State 3 treatments for trichiasis:
- Electrolysis
- Cryotherapy
- Laser treatment
124
What is periorbital cellulitis?
- An eyelid and skin infection in front of the orbital septum (in front of the eye)
125
How does periorbital cellulitis present?
- Swollen, red, hot skin around the eyelid and eye
126
What life threatening emergency must periorbital cellulitis be differentiated from?
- Orbital cellulitis
127
What is orbital cellulitis?
- An infection around the eyeball involving the tissues behind the orbital septum
128
What investigation can help to distinguish between periorbital and orbital cellulitis?
- CT scan
129
State 5 symptoms of orbital cellulitis:
- Pain with eye movement
- Reduced eye movements
- Vision changes
- Abnormal pupil reactions
- Proptosis
130
State 2 treatments for orbital cellulitis:
- IVN antibiotics
- Surgical drainage
131
State 3 symptoms of conjunctivitis:
- Red, bloodshot eye
- Itchy or gritty sensation
- Discharge
132
State 3 symptoms which are not associated with conjunctivitis:
- Pain
- Photophobia
- Reduced visual acuity
133
State 1 difference between viral and bacterial conjunctivitis:
- Viral: clear discharge
- Bacterial: purulent discharge
134
State 3 causes of painful red eye and 3 causes of non painful red eye:
- Painful red eye: acute angle closure glaucoma, scleritis, foreign body
- Non painful red eye: conjunctivitis, episcleritis, subconjunctival haemorrhage
135
Conjunctivitis usually resolves in 1-2 weeks without needing treatment. State 2 treatments for persistent bacterial conjunctivitis:
- Chloramphenicol eye drops
- Fusidic acid eye drops
136
Why do neonates under 1 month with conjunctivitis need an urgent ophthalmology assessment?
- Neonatal conjunctivitis may be caused by gonococcal infection, which can cause serious complications (e.g. permanent vision loss)
137
Allergic conjunctivitis is caused by contact with allergens, causing itching and watery discharge. State 2 treatments for allergic conjunctivitis:
- Antihistamines
- Mast cell stabilisers
138
What does the uvea consist of?
- The uvea consists of the iris, ciliary body and choroid
139
What is anterior uveitis?
- Inflammation in the anterior chamber of the eye
140
What is hypopyon?
- A fluid collection containing inflammatory cells seen at the bottom of the anterior chamber on inspection
141
142
State 4 symptoms of anterior uveitis:
- Painful red eye (typically a dull, aching pain)
- Reduced visual acuity
- Photophobia (due to ciliary muscle spasm)
- Excessive lacrimation (tear production)
143
State 4 examination findings of anterior uveitis:
- 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)
144
State 2 treatments for anterior uveitis:
- Steroids (eye drops, oral or intravenous)
- Cycloplegics (e.g. cyclopentolate or atropine eye drops)
145
What are cycloplegics?
- Medications that paralyse the ciliary muscles
- Cycloplegics dilate the pupil and reduce pain associated with ciliary spasm
146
Episcleritis is associated with inflammatory disorders (e.g. IBD). What is episcleritis?
- Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera, just below the conjunctiva
147
State 2 features of episcleritis:
- Localised or diffuse redness (often a patch of redness in the lateral sclera)
- Dilated episcleral vessels
148
Explain how phenylephrine eye drops helps differentiate between episcleritis and scleritis:
- They will cause blanching of episcleral vessels causing the redness to disappear
- It will not affect scleral vessels and will not impact the redness in scleritis
149
State 3 symptoms that can be used to differentiate between episcleritis and scleritis:
- Scleritis: photophobia, discharge, reduced visual acuity (none of these in episcleritis)
150
Episcleritis is usually self-limiting and will resolve in 1-2 weeks. State 3 treatments for episcleritis:
- Analgesia
- Lubricating eye drops
- Steroid eye drops
151
What is the most severe form of scleritis and what can it lead to?
- Necrotising scleritis
- Can lead to perforation of the sclera
152
There is an associated systemic condition in around 50% of patients presenting with scleritis. State 2 examples of these conditions:
- Rheumatoid arthritis
- Vasculitis, particularly granulomatosis with polyangiitis)
153
State 6 symptoms of scleritis:
- Red, inflamed sclera (localised or diffuse)
- Severe pain (typically a boring pain)
- Pain with eye movement
- Photophobia
- Epiphora (excessive tear production)
- Reduced visual acuity
154
State 3 treatments for scleritis:
- NSAIDs (oral)
- Steroids (topical or systemic)
- Immunosuppression appropriate to the underlying systemic condition (e.g. methotrexate in rheumatoid arthritis)
155
State 3 potential causes of corneal abrasions:
- Damaged contact lenses
- Fingernails
- Entropion
156
Corneal abrasions caused by contact lenses are associated with what type of infection?
- Pseudomonas infection
157
State 5 symptoms of corneal abrasions:
- Painful red eye
- Photophobia
- Foreign body sensation
- Epiphora (excessive tear production)
- Blurred vision
158
Explain how staining can help to diagnose corneal abrasions:
- A fluorescein stain can be applied to the eye to help diagnose a corneal abrasion
- This is a yellow orange colour and collects in abrasions or ulcers, highlighting them, particularly when viewed under cobalt blue light
159
State 3 treatments for corneal abrasions:
- Simple analgesia (e.g. paracetamol)
- Lubricating eye drops
- Antibiotic eye drops (e.g. chloramphenicol)
160
Lubricating eye drops vary in their viscosity. State and describe 3 examples of lubricating eye drops:
- Hypromellose drops are the least viscous (the effects last around 10 minutes)
- Polyvinyl alcohol drops are the middle viscous choice
- Carbomer drops are the most viscous (the effects last about 30 to 60 minutes)
161
What is keratitis?
- Inflammation of the cornea
162
State 5 types of causes of keratitis:
- Viral infection (e.g. herpes simplex)
- 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)
163
What is the single most common cause of keratitis?
- Herpes simplex virus (HSV) infection
164
Herpes simplex keratitis can be primary or recurrent. What causes recurrent herpes keratitis?
- Recurrence is caused by the virus travelling to the trigeminal ganglion, where it becomes latent (dormant) and can reactivate later
165
What layer of the cornea does herpes keratitis typically affect?
- Epithelial layer of the cornea
166
What is stromal keratitis?
- Inflammation of the stroma (the layer between the epithelium and endothelium)
167
State 2 complications associated with stromal keratitis:
- Stromal necrosis
- Corneal blindness
168
Primary herpes keratitis often involves mild symptoms of blepharoconjunctivitis. State 6 symptoms of recurrent herpes keratitis:
- Painful red eye
- Photophobia
- Vesicles (fluid filled blisters)
- Foreign body sensation
- Watery discharge
- Reduced visual acuity
169
Explain how herpes keratitis is diagnosed:
- Slit lamp examination: fluorescein staining shows a dendritic (branching) corneal ulcer
- (Corneal scrapings can be used for viral testing)
170
State 2 treatments for herpes keratitis:
- Topical or oral antivirals (e.g. aciclovir or ganciclovir)
- Corneal transplant is an option to treat permanent scarring and vision loss after keratitis
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What is a subconjunctival haemorrhage?
- When a small blood vessel within the conjunctiva ruptures, releasing blood into the space between the sclera and the conjunctiva
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State 4 causes of subconjunctival haemorrhage:
- Straining (constipated)
- Hypertension
- Medications (e.g. DOCS)
- Trauma
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Subconjunctival haemorrhages does not affect vision and is painless. State 1 symptom of subconjunctival haemorrhage:
- Bright red blood under the conjunctiva
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Subconjunctival haemorrhages are harmless and will resolve spontaneously without treatment. State 2 investigations to determine the cause of a subconjunctival haemorrhage:
- Checking the blood pressure
- Checking the INR in patients taking warfarin
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What is posterior vitreous detachment?
- When the vitreous body comes away from the retina
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Why is posterior vitreous detachment common in older age?
- The vitreous humour is the gel inside the vitreous chamber of the eye
- It maintains the structure of the eyeball and keeps the retina pressed on the choroid
- With age, it becomes less firm and able to maintain its shape
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Posterior vitreous detachment is often asymptomatic. State 3 symptoms of posterior vitreous detachment:
- Floaters
- Flashing lights
- Blurred vision
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No treatment is necessary for posterior vitreous detachment. State 2 complications of posterior vitreous detachment:
- Retinal tears
- Retinal detachment
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What is retinal detachment?
- When the neurosensory layer of the retina (containing photoreceptors and nerves) separates from the retinal pigment epithelium (the base layer attached to the choroid)
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What is the most common cause of retinal detachment?
- Retinal tears
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What is a retinal tear?
- A tear in the retina, allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
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Why is retinal detachment sight threatening?
- The neurosensory retina relies on the blood vessels of the choroid for its blood supply so retinal detachment can disrupt the blood supply and cause permanent damage to the photoreceptors
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State 5 risk factors for retinal detachment:
- Lattice degeneration (thinning of the retina)
- Posterior vitreous detachment
- Diabetic retinopathy
- Retinal malignancy
- Family history
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Retinal detachment is painless. State 3 symptoms of retinal detachment:
- Peripheral vision loss (often sudden and described as a shadow coming across the vision)
- Blurred or distorted vision
- Flashes and floaters
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Management of retinal tears aims to create adhesions between the retina and the choroid. State 2 treatments for retinal tears:
- Laser therapy
- Cryotherapy
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Management of retinal detachment aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. State 3 treatments for retinal detachment:
- Vitrectomy
- Scleral buckle
- Pneumatic retinopexy
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Explain how vitrectomy treats retinal detachment:
- Vitrectomy involves keyhole surgery on the eye, removing the vitreous fluid, fixing the tear, and then inserting gas or oil into the eye to hold the retina in place
188
Explain how scleral buckling treats retinal detachment:
- Scleral buckling involves using a silicone “buckle” to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina
- It acts like a corset, squeezing the eye contents together
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Explain how pneumatic retinopexy treats retinal detachment:
- Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place
190
What is a retinal vein occlusion?
- When a blood clot 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
191
Outline the venous drainage of the retina:
- The branch retinal veins drain into the central retinal vein, which runs through the optic nerve to drain into either the superior ophthalmic vein or cavernous sinus
- Blockage of one of the branch veins affects the area drained by that branch
- Blockage in the central vein causes problems with the whole retina
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Which areas are more prone to retinal vein occlusion?
- Sites where the retinal arteries cross over the top of the veins because this can cause narrowing of the vein
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Explain how retinal vein occlusion can cause macular oedema and retinal haemorrhages:
- 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
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Retinal vein occlusion can be categorised as ischaemic or non ischaemic. Explain the difference between them:
- Retinal ischaemia leads to the release of vascular endothelial growth factor (VEGF), resulting in new blood vessel development (neovascularisation in ischaemic)
195
In retinal vein occlusion, which branch is affected in patients presenting with central vision loss?
- The branch draining the macula
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State 5 features of retinal vein occlusion on fundoscopy:
- Dilated tortuous retinal veins
- Flame and blot haemorrhages
- Retinal oedema
- Cotton wool spots
- Hard exudates
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State 3 treatments for retinal vein occlusion:
- Anti-VEGF therapies (e.g. ranibizumab and aflibercept)
- Dexamethasone intravitreal implant (to treat macular oedema)
- Laser photocoagulation (to treat new vessels)
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