Opthalmology Flashcards
(199 cards)
1
Q
What is the vitreous chamber of the eye? Describe the anatomy.
A
The largest chamber of the eye, located behind the lens and in front of the optic nerve. It is filled with vitreous humour.
2
Q
What is the anterior chamber of the eye? Describe the anatomy.
A
Located between the cornea and iris. It is filled with aqueous humour.
3
Q
What is the posterior chamber of the eye? Describe the anatomy.
A
Located between the lens and iris. It is filled with aqueous humour.
4
Q
Where is aqueous humour produced?
A
Ciliary body.
5
Q
Describe the flow of aqueous humour in the eye.
A
Flows from the ciliary body around the lens and under the iris, through the anterior chamber, through the trabecular meshwork and into the canal of Schlemm.
6
Q
What is normal intraocular pressure?
A
10-21 mmHg.
7
Q
Define glaucoma.
A
Optic nerve damage secondary to raised intraocular pressure.
8
Q
Describe the pathophysiology of open-angle glaucoma.
A
Gradual increase in resistance through the trabecular meshwork. It is more difficult for aqueous humour to exit the eye and pressure increases within the eye.
9
Q
Give examples of risk factors for the development of open-angle glaucoma.
A
Increasing age, family history, black ethnicity, near-sightedness.
10
Q
How does open-angle glaucoma present clinically?
A
Loss of peripheral vision that eventually develops into tunnel vision. Fluctuating pain, headaches, blurred vision and halos.
11
Q
Open-angle glaucoma: What are halos?
A
Bright circles of light that surround lights, particularly at night.
12
Q
How is open-angle glaucoma diagnosed?
A
Measure intraocular pressure by non-contact tonometry or contact tonometry.
13
Q
What investigations (other that tonometry) should be performed in suspected open-angle glaucoma?
A
Visual field assessment.
Fundoscopy.
14
Q
Open-angle glaucoma: What is the difference between non-contact tonometry and contact tonometry?
A
Non-contact tonometry uses air to estimate pressure whereas contact tonometry makes direct contact with the cornea.
15
Q
What might fundoscopy reveal in open-angle glaucoma?
A
Optic disc cupping.
16
Q
What is the first-line management of open-angle glaucoma?
A
Prostaglandin analogue drops such as latanoprost.
17
Q
Describe how latanoprost treats open-angle glaucoma.
A
Increases uveoscleral outflow.
18
Q
Open-angle glaucoma: What are two side effects of latanoprost use?
A
Eyelash growth.
Eye discolouration.
19
Q
What medications (other than latanoprost) can be used in the management of open-angle glaucoma?
A
Beta-blockers (timolol).
Carbonic anhydrase inhibitors (acetazolamide).
20
Q
Describe how timolol and acetazolamide treat open-angle glaucoma.
A
Reduces production of aqueous humour.
21
Q
What is acute angle-closure glaucoma?
A
Ophthalmology emergency. Optic nerve damage secondary to raised intraocular pressure.
22
Q
Describe the pathophysiology of acute angle-closure glaucoma?
A
The iris bulges forward and seals of the trabecular meshwork from the anterior chamber, preventing drainage of aqueous humour and resulting in a continual build-up of pressure in the eye.
23
Q
Give examples of risk factors for acute angle-closure glaucoma.
A
Increasing age, female sex, family history, East-Asian ethnicity.
24
Q
Give examples of medications which increase the risk of developing acute angle-closure glaucoma?
A
Adrenergic medications (noradrenaline). Anticholinergic medications (oxybutynin, solifenacin). Tricyclic antidepressants (amitriptyline).
25
How does acute angle-closure glaucoma present clinically?
Short history of severely painful red eye.
26
What does examination reveal in acute angle-closure glaucoma?
Hazy cornea, decreased visual acuity, fixed dilated pupil, firm eyeball.
27
How is acute angle-closure glaucoma managed?
```
Lay the patient flat.
Give pilocarpine eye drops.
Give acetazolamide.
Give timolol.
Definitive management - laser iridotomy.
```
28
Describe how pilocarpine, acetazolamide and timolol treat acute angle-closure glaucoma.
Pilocarpine causes pupil constriction.
| Acetazolamide and timolol both reduce production of aqueous humour.
29
Describe how laser iridotomy is used in the treatment of acute angle-closure glaucoma.
A hole is made in the iris to allow aqueous humour to flow from the posterior chamber into the anterior chamber.
30
What is the most common cause of blindness in the UK?
Age-related macular degeneration (AMD).
31
What is the pathophysiology of age-related macular degeneration?
Macular degeneration that causes progressive deterioration in vision.
32
Describe the structure of the macula (from bottom to top).
Choroid layer containing blood vessels.
Bruch's membrane.
Retinal pigment epithelium.
Photoreceptors.
33
Give examples of risk factors for the development of age-related macular degeneration.
Increasing age, smoking history, family history, cardiovascular disease.
34
What is the presentation of age-related macular degeneration?
Gradually worsening central vision loss, reduced visual acuity and crooked/wavy appearance of straight lines.
35
What are the two types of AMD?
Dry age-related macular degeneration (90% of cases).
| Wet age-related macular degeneration (more severe).
36
Describe the pathophysiology of dry AMD.
Characterised by the degeneration of retinal photoreceptors and the formation of drusen.
37
What are drusen and where in the macula do they form?
Yellow deposits of lipids and proteins. Deposition occurs between Bruch's membrane and the retinal pigment epithelium.
38
How is dry AMD managed?
Reduce progression. Encourage smoking cessation, control blood pressure and supplement vitamins.
39
Describe the pathophysiology of wet AMD?
Development of new vessels from the choroid layer into the retina. The vessels leak fluid or blood and cause oedema.
40
How does the presentation of wet AMD differ from dry AMD?
Patients complain of more rapid vision loss in wet AMD.
41
How is wet AMD managed?
Anti-vascular endothelial growth factor (anti-VEGF) injections such as ranibizumab... which block VEGF and and the development of new blood vessels.
42
What investigations are performed in AMD?
Snellen chart.
Automated visual field testing.
Amsler grid test.
Fundoscopy.
43
What does Snellen chart reveal in AMD?
Reduced visual acuity.
44
What does automated visual field testing reveal in AMD?
Scotoma (central patch of vision loss).
45
What does Amsler grid test reveal in AMD?
Distortion of straight lines.
46
What does fundoscopy reveal in AMD?
Presence of drusen.
47
What is diabetic retinopathy?
Complication of prolonged exposure to high blood glucose.
48
Describe the pathophysiology of diabetic retinopathy.
High blood sugar leads to damage of the retinal small vessels and endothelial cells... increased vascular permeability leads to leakage, blot haemorrhages and the formation of hard exudates (yellow/white deposits of lipids in the retina).
49
What investigation is performed in the assessment of diabetic retinopathy?
Fundoscopy.
50
What might fundoscopy show in diabetic retinopathy?
```
Blot haemorrhages.
Hard exudates.
Cotton wool spots.
Microaneurysms.
Intraretinal microvascular abnormalities.
Neovascularisation.
```
51
What do cotton wool spots represent in diabetic retinopathy?
Damage to nerve fibres.
52
How is diabetic retinopathy classified?
Non-proliferative diabetic retinopathy.
| Proliferative diabetic retinopathy.
53
What is the difference between proliferative and non-proliferative diabetic retinopathy?
Proliferative includes neovascularisation and vitreous haemorrhage (presents as sudden vision loss).
54
What is the management of diabetic retinopathy?
Laser photocoagulation.
Ranibizumab (anti-VEGF).
Vitreoretinal surgery.
55
Give examples of complications of diabetic retinopathy.
Retinal detachment.
Vitreous haemorrhage.
Optic neuropathy.
Cataracts.
56
What is hypertensive retinopathy?
Damage to the small blood vessels of the retina relating to systemic hypertension. Can develop due to years of chronic hypertension or quickly as a result of malignant hypertension.
57
What investigation is performed in the assessment of hypertensive retinopathy?
Fundoscopy.
58
What might fundoscopy reveal in hypertensive retinopathy?
```
Silver wiring.
Arteriovenous nipping.
Cotton wool spots.
Hard exudates.
Retinal haemorrhage.
Papilloedema.
```
59
Hypertensive retinopathy: What is silver wiring (on fundoscopy)?
Arteriole wall thickening, sclerosis... increased reflection of light.
60
Hypertensive retinopathy: What is arteriovenous nipping (on fundoscopy)?
Arteriole sclerosis leads to compression of adjacent veins.
61
Hypertensive retinopathy: What is retinal haemorrhage (on fundoscopy)?
Damaged vessels rupture and leak blood into the retina.
62
Hypertensive retinopathy: What is papilloedema (on fundoscopy)?
Optic nerve ischaemia leads to swelling and blurring of the optic disc margins.
63
How is hypertensive retinopathy managed?
Control blood pressure.
Control blood lipid levels.
Encourage smoking cessation.
64
Describe the pathophysiology of cataracts.
Condition of reduced visual acuity that occurs as the lens becomes cloudy and opaque (reducing the amount of light that can enter).
65
What is the normal function of the lens in the eye?
To focus light onto the retina. Held in place by suspensory ligaments attached to the ciliary body, which contract and relax to focus the lens.
66
What are risk factors for the development of cataracts?
Increasing age, smoking, alcohol consumption, diabetes, steroid use, hypocalcaemia.
67
How do cataracts present clinically?
Asymmetrical, slow reduction in vision with progressive blurring. Patients complain of change in colour vision (more brown/yellow) and starburst that appear around lights.
68
What does examination reveal in people with cataracts?
Loss of red reflex.
69
What is the definitive management of cataracts?
Surgery - removal of diseased lens and implantation of artificial lens into the eye.
70
What is a rare complication of cataract surgery?
Endophthalmitis (inflammation of the inner contents of the eye, typically due to infection).
71
What muscles control pupil constriction?
Circular muscles in the iris.
72
What neurotransmitter stimulates the circular muscles of the eyes as part of the parasympathetic nervous system?
Acetylcholine.
73
What muscles control pupil dilation?
Dilator muscles.
74
What neurotransmitter stimulates the dilator muscles of the eyes as part of the sympathetic nervous system?
Adrenaline.
75
Give examples of causes of mydriasis (dilated pupil).
```
Third nerve palsy
Holmes-Adie syndrome
Raised ICP
Trauma
Stimulants (cocaine)
Anticholinergics
```
76
Give examples of causes of miosis (constricted pupil).
```
Horners syndrome.
Cluster headaches
Neurosyphilis (Argyll-Robertson pupil)
Opiates
Nicotine
Pilocarpine
```
77
How does third nerve palsy present?
Ptosis.
Dilated non-reactive pupil
Divergent strabismus (down and out position).
78
Give two causes of third nerve palsy.
Cavernous sinus thrombosis
| Posterior communicating artery aneurysm
79
What is the triad of Horner syndrome?
Ptosis
Miosis
Anhidrosis
80
What causes Horner syndrome?
Damage to sympathetic nervous system supplying the face.
81
How are the causes of Horner syndrome grouped?
Central lesions
Pre-ganglionic lesions
Post-ganglionic lesions
82
How do central lesions of Horner syndrome present?
Anhidrosis of the arm, trunk and face
83
Give four causes of central lesion Horner syndrome.
```
Stroke
Multiple Sclerosis
Swelling (tumours)
Syringomyelia
Remember: Four Ss
```
84
Give four causes of pre-ganglionic Horner syndrome
```
Tumour
Trauma
Thyroidectomy
Top rib
Remember: Four Ts
```
85
Give four causes of post-ganglionic Horner syndrome.
```
Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache
Remember: Four Cs
```
86
How do pre-ganglionic lesions of Horner syndrome present?
Anhidrosis of the face
87
How do post-ganglionic lesions of Horner syndrome present?
Do not cause anhidrosis.
88
What is blepharitis?
Inflammation of the eyelid margins.
89
How does blepharitis present clinically?
Gritty, itchy, dry sensation in the eyes.
90
Blepharitis may be associated with dysfunction of what?
Meibomian glands.
91
What are Meibomian glands?
Glands responsible for secreting oil onto the surface of the eye.
92
Blepharitis may lead to the development of what conditions?
Styes.
| Chalazions.
93
How is blepharitis managed?
Hot compresses and gentle cleaning of the eyelid margins to remove debris using cotton wool dipped in sterilised water and baby shampoo. Can also use lubricating eye drops (hypromellose) to relieve symptoms.
94
What are the two types of stye?
```
Hordeolum externum (an infection of the glands of Zeis or glands of Moll).
Hordeolum internum (an infection of the Meibomian glands).
```
95
What are the glands of Zeis?
Sebaceous glands at the base of the eyelashes, secrete oily/waxy matter.
96
What are the glands of Moll?
Sweat glands at the base of the eyelashes.
97
How do styes present?
Tender, red lump along the eyelid (may contain pus).
98
How are styes managed?
Hot compresses and analgesia. Consider topical antibiotics (chloramphenicol) if associated with conjunctivitis or persistent.
99
What is a chalazion?
Meibomian cyst that occurs when a Meibomian gland becomes blocked and swells up.
100
How does chalazion present clinically?
Non-tender swelling in the eyelid.
101
How are chalazion managed?
Hot compresses and analgesia. Consider topical antibiotics (chloramphenicol) if acutely inflamed.
102
What is entropion?
Condition characterised by eyelid turned inwards with the lashes against eyeball.
103
How does entropion present clinically?
Pain.
104
What are complications of entropion?
Corneal damage.
| Ulceration.
105
How is entropion managed?
Initially taping the eyelid down to prevent it turning inwards. Apply regular lubricating eye drops while taped down. Definitive management is surgical intervention.
106
What is ectropion?
Condition characterised by eyelid turning outwards with the inner aspect of the eyelid exposed (usually the bottom eyelid).
107
What is a complication of ectropion?
Exposure keratopathy (eyelid exposed and not adequately lubricated and protected).
108
What is the management of ectropion?
Regular lubricating eye drops. Significant cases may require surgical intervention.
109
What is trichiasis?
Inward growth of eyelashes.
110
How does trichiasis present clinically?
Pain.
111
What are complications of trichiasis?
Corneal damage.
| Ulceration.
112
What is the management of trichiasis?
Epilation (removal of eyelashes).
| Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent the lash regrowing.
113
What is periorbital cellulitis?
An eyelid and skin infection in front of the orbital septum.
114
How does periorbital cellulitis present clinically?
Swelling.
Redness/erythema
Hot skin around the eyelids and eye.
115
How is periorbital cellulitis differentiated from orbital cellulitis?
CT scan.
116
What is the treatment of periorbital cellulitis?
Systemic antibiotics.
117
What is orbital cellulitis?
An infection around the eyeball that involves tissues behind the orbital septum (the membrane that acts as the anterior boundary to the orbit).
118
How does orbital cellulitis present clinically?
```
Pain on eye movement.
Reduced eye movement.
Change in vision.
Abnormal pupil reaction.
Proptosis.
```
119
What is the treatment of orbital cellulitis?
Intravenous antibiotics.
| Surgical drainage if an abscess forms.
120
What is conjunctivitis?
Inflammation of the conjunctiva.
121
What is the conjunctiva?
Thin layer of tissue that covers the inside of the eyelid and the sclera of the eye.
122
How does conjunctivitis present clinically?
Unilateral/bilateral red eyes, bloodshot, itchy/gritty sensation with discharge from the eye.
123
What are the three main types of conjunctivitis?
Bacterial conjuncitivitis.
Viral conjuncitivitis.
Allergic conjunctivitis.
124
How does bacterial conjunctivitis present?
Purulent discharge along with general symptoms of conjunctivitis (red eyes, bloodshot, itchy/gritty).
Worse in the morning when eyes may be stuck together.
125
What is the management of bacterial conjunctivitis?
Highly contagious - advise good hygiene. Most cases improve spontaneously but some may require chloramphenicol eye drops.
126
How does viral conjunctivitis present?
Clear discharge along with general symptoms of conjunctivitis (red eyes, bloodshot, itchy/gritty).
May be associated with symptoms of viral infection (dry cough, sore throat, blocked nose).
127
What is allergic conjunctivitis?
Due to contact with allergens... swelling of the conjunctival sac and eye lid with significant watery discharge and itch.
128
What is the management of allergic conjunctivitis?
Oral or topical antihistamines.
129
What is anterior uveitis?
Inflammation of the anterior part of the uvea.
130
What makes up the uvea?
Iris, ciliary body and choroid.
131
Acute anterior uveitis is associated with what conditions?
HLA B27 related:
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
132
Chronic anterior uveitis (> 3 months) is associated with what conditions?
```
Sarcoidosis.
Syphilis.
Lyme disease.
Tuberculosis.
Herpes virus.
```
133
What is the presentation of anterior uveitis?
Unilateral, without history of trauma or precipitating events. Dull, aching, painful red eye with reduced visual acuity, visual floaters and photophobia.
134
What is found on examination of a patient with anterior uveitis?
Ciliary flush (ring of red spreading from cornea outwards).
Miosis.
Abnormally shaped pupil.
Hypopyon.
135
What is hypopyon?
Collection of white blood cells in the anterior chamber, seen as yellowish collection.
136
How is anterior uveitis investigated?
Slit lamp.
137
What does slit lamp reveal in anterior uveitis?
Conjunctival injection.
Keratic precipitates
Anterior chamber cells
Posterior synechiae
138
What is the management of anterior uveitis?
Steroids
| Cycloplegic/mydriatic eye drops
139
What is episcleritis?
Benign inflammation of the episclera.
140
What is the episclera?
Outermost layer of the sclera, beneath the conjunctiva.
141
Episcleritis is associated with what conditions?
Rheumatoid arthritis.
| Inflammatory bowel disease.
142
What is the presentation of episcleritis?
Unilateral painless superficial red eye. Patients may describe foreign body discomfort.
143
Describe how redness in episcleritis presents?
Segmental rather than diffuse, usually a patch in the lateral sclera.
144
How can episcleritis be differentiated from scleritis?
Phenylephrine drops - application improves eye redness in episcleritis but not scleritis.
145
Explain how phenylephrine drops differentiate between episcleritis and scleritis.
Phenylephrine drops blanch the conjunctival and episcleral vessels but not the scleral vessels.
146
What is the management of episcleritis?
Mostly self-limiting, conservative management. Consider lubricating eye drops to improve symptoms.
147
What is scleritis?
Inflammation of the full thickness of the sclera.
148
Scleritis is more common in which groups of people?
People with autoimmune conditions:
Rheumatoid arthritis
SLE
Inflammatory bowel disease
149
What is the presentation of scleritis?
Severe eye pain (worse on movement), photophobia, reduced visual acuity, deep diffuse redness.
150
What is the management of scleritis.
Same day ophthalmology assessment. Consider oral/topical NSAIDs or oral/topical steroids.
151
What are corneal abrasions?
Scratches or damages to the cornea.
152
Give examples of causes of corneal abrasions.
```
Contact lenses
Foreign bodies
Fingernails
Eyelashes
Entropion
```
153
What are clinical features of corneal abrasions?
History of contact lens use or foreign body exposure.
| Painful red eye, foreign body sensation, watering eye, blurring vision and photophobia.
154
How are corneal abrasions investigated?
Fluorescein staining.
155
What does fluorescein staining show in corneal abrasions?
The stain collects in the abrasions or ulcers and highlights them as a yellow-orange colour.
156
What is the management of corneal abrasions?
Removal of foreign body.
Simple analgesia.
Lubricating eye drops.
Antibiotic eye drops.
157
What is the management of chemical corneal abrasions?
irrigation for 20-30 minutes and urgent referral to ophthalmology.
158
What is keratitis?
Inflammation of the cornea.
159
Give five causes of keratitis.
Viral infection with herpes simplex.
Bacterial infection with pseudomonas or staphylococcus.
Fungal infection with candida or aspergillus.
Contact lens acute red eye (CLARE).
Exposure keratitis.
160
What is the most common cause of keratitis?
Herpes simplex - herpes simplex keratitis.
161
How does herpes simplex keratitis present?
Painful red eye, photophobia, vesicles around the eye, watering, foreign body sensation, reduced acuity.
162
How can herpes simplex keratitis be investigated?
Fluorescein stain.
Slit lamp.
Corneal swabs/scrapings.
163
What does fluorescein stain reveal in herpes simplex keratitis?
Dendritic corneal ulcer (appearances of branching and spreading of the ulcer).
164
What is the management of herpes simplex keratitis?
Topical/oral acyclovir.
165
Bacterial keratitis most commonly occurs in which groups of people?
Contact lens wearer.
Smoker.
Poor hygiene.
Immunocompromised.
166
How does bacterial keratitis present?
Unilateral, moderate-to-severe eye pain, red eye, photophobia, eye discharge.
167
What does examination reveal in patients with bacterial keratitis?
Epiphora, lid oedema, hypopyon.
168
What is the management of bacterial keratitis?
Antibiotics.
169
What is subconjunctival haemorrhage?
Relatively common condition where one of the small blood vessels within the conjunctiva ruptures and releases blood into the space between the sclera and conjunctiva.
170
Give examples of triggers of subconjunctival haemorrhage?
Heavy coughing.
Weightlifting.
Straining when constipated.
Trauma.
171
How does subconjunctival haemorrhage present?
Patch of bright red blood underneath the conjunctiva covering the white of the eye. It is painless and does not affect vision.
172
How is subconjunctival haemorrhage managed?
Spontaneous resolution within two weeks. Investigate for predisposing factors such as hypertension and bleeding disorders.
173
What is posterior vitreous detachment?
Condition where the vitreous body comes away from the retina.
174
What is the function of the vitreous body?
Responsible for maintaining the structure of the eyeball and keeping the retina pressed on the choroid.
175
What is the presentation of posterior vitreous detachment?
Painless spots of vision loss, floaters and flashing lights in vision.
176
What is the management of posterior vitreous detachment?
No treatment is necessary.
177
Posterior vitreous detachment can predispose to what conditions?
Retinal tears.
| Retinal detachment.
178
What is retinal detachment?
Separation of retina from the choroid underneath. The outer retina relies on the blood vessels of the choroid body... detachment is a sight-threatening emergency.
179
What predisposes to retinal detachment?
Retinal tears.
180
Describe how retinal tears can predispose to retinal detachment.
Retinal tear allows vitreous fluid to get under the retina and fill the space between the retina and choroid.
181
What is the presentation of retinal detachment?
Painless, peripheral vision loss described as a sudden shadow coming across the visual field. There is also blurred or distorted vision as well as flashes and floaters,
182
How are retinal tears managed?
Laser therapy or cryotherapy are used to create adhesions between the retina and choroid to prevent detachment.
183
How is retinal detachment managed?
Vitrectomy.
Scleral bulking.
Pneumatic retinoplexy.
184
Describe the pathophysiology of retinal vein occlusion.
Blood clot forms in the retinal veins and blocks the drainage of blood from the retina... causing pooling of blood which results in leakage of fluid and blood causing macular oedema and retinal haemorrhages.
185
Give examples of risk factors for retinal vein occlusion.
```
Hypertension.
Hypercholesterolaemia.
Diabetes.
Smoking.
Glaucoma.
```
186
What is the presentation of retinal vein occlusion?
Sudden painless loss of vision (extent of which determined by which vein is blocked).
187
What does fundoscopy reveal in retinal vein occlusion?
Flame + blot haemorrhages, optic disc oedema and macular oedema.
188
What is the management of retinal vein occlusion?
Laser photocoagulation.
Intravitreal steroids.
Ranibizumab (anti-VEGF)
189
What is centra retinal artery occlusion?
Occurs when flow of blood through central retinal artery (responsible for supplying blood to retina) is obstructed.
190
The central retinal artery is formed from which arteries?
Ophthalmic artery which is a branch of the internal carotid.
191
What causes central retinal artery occlusion?
Atherosclerosis.
| Giant cell arteritis.
192
What is the presentation of central retinal artery occlusion ?
Sudden painless loss of vision. Relative afferent pupillary defect.
193
Central retinal artery occlusion: Describe retinal afferent pupillary defect.
Affected eye constricts more when light is shone in the other eye (due to input not being sensed by the ischaemic retina).
194
What investigation is performed in central retinal artery occlusion?
Fundoscopy.
195
What does fundoscopy reveal in central retinal artery occlusion?
Pale retina (due to lack of perfusion) with cherry-red spot (macula with thinner surface shows red-coloured choroid below).
196
What is the management of central retinal artery occlusion?
Ocular massage
Removing fluid form the anterior chamber
Inhaling carbogen (high oxygen conc. gas)
Sublingual isosorbide dinitrate
197
What is retinitis pigmentosa?
Congenital inherited condition where there is degeneration of the rods and cones in the retina
198
What is the first symptom of retinitis pigmentosa?
Night blindness
199
What are the clinical features of retinitis pigmentosa?
Night blindness, peripheral vision loss followed by central vision loss.
