opthalmology Flashcards
1
Q
what sort of conditions lead to sudden loss of vision?
A
vascular occlusions:
- branch and central retinal artery occlusions
- branch and central retinal vein occlusions
- anterior ischaemic optic neuropathy
inflammatory disorders
- optic neuritis (MS or secondary)
retinal detachment
2
Q
what will patients who have retinal artery occlusion have?
A
patients will present with sudden, loss of vision (central retinal artery occlusion) or altitudinal loss (branch retinal artery occlusion)
they have a relative afferent pupillary defect
usually it is caused by atherosclerosis or emboli from the carotid or the heart
less frequently it can be caused by giant cell arteritis
vision can not be improved
management is directed to secondary prevention of myocardial or cerebrovascular events e.g.prescribe Aspirin
3
Q
what is transient monocular visual loss?
A
often referred to amaurosis fugax or TIA
patient describes curtain coming over vision
lasts around 30 minutes
resolves completely
investigate for TIA
manage with aspirin, clopidogrel etc
4
Q
what is conjunctivitis?
A
inflammation of the conjunctiva - this is a thin membrane that covers the front surface of the eye and the inner surface of the eye lids.
5
Q
what are the different types of conjunctivitis?
A
bacterial
viral
allergic
6
Q
how does conjunctivitis present?
A
can be unilateral or bilateral red eyes blood shot itchy or gritty sensation discharge from the eye
7
Q
how would bacterial and viral conjunctivitis present?
A
bacterial conjunctivitis presents with a purulent discharge and an inflamed conjunctiva. It is typically worse in the morning when the eyes may be stuck together, it usually starts in one eye and then can spread to the other because it is highly contagious.
viral conjunctivitis is common and usually presents with a clear discharge. It is often associated with other symptoms of a viral infection such a dry cough, sore throat and blocked nose. There may be tender preauricular lymph nodes (in front of the ears)
8
Q
what are the differential diagnosis for acute painless red eye?
A
conjunctivitis
episcleritis
subconjunctival haemorrhage
9
Q
what are the differential diagnosis for a painful acute red eye?
A
Glaucoma Anterior uveitis Scleritis Corneal abrasions or ulceration Keratitis Foreign body Traumatic or chemical injury
10
Q
how do you manage conjunctivitis?
A
often resolves without treatment after 1-2 weeks
advise on good hygiene to avoid spreading (avoid sharing towels or rubbing eyes and regularly wash hands) and avoid use of contact lenses. Cleaning the eyes with cooled boiled water and cotton wool can help clear the dischargee
Bacteriral: antibiotic eye drops can be considered - Chloramphenicol and fuscidic acid eye drops are both options
if under one month of age they need an urgent ophthalmology review
11
Q
what is allergic conjunctivitis?
what can be used to treat it?
A
it is caused by contact with allergens - it causes swelling of the conjunctival sec and eye lid with a significant watery discharge and itch
antihistamines - oral or topical can be used to reduce symptoms
2nd line - topical mast-cell stabilisers e.g. sodium cromoglicate and nedocromil
12
Q
what are glaucomas?
A
there is optic nerve damage that is caused by a significant rise intraocular pressure. The raised intraocular pressure is caused by a blockage aqueous humour trying to escape the eye.
There are two types of glaucoma - open angle and closed angle
13
Q
what happens in open angle glaucoma?
A
In open angle glaucoma, there is a gradual increase in resistance through the trabecular meshwork. This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.
there is a large angle between iris and cornea
14
Q
what happens in acute closure glaucoma?
A
In acute angle closure glaucoma the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away. This leads to a continual build up of pressure. This is an ophthalmology emergency
15
Q
what are the risk factors for open angle glaucoma?
A
increasing age family history black ethnic origin Nearsightedness (myopia) DM corticosteroids
16
Q
how does open angle glaucoma present?
A
Often the rise in intraocular pressure is asymptomatic for a long period of time. It is diagnosed by routine screening when attending optometry for an eye check.
the glaucoma will affect the peripheral vision first. Gradually the peripheral vision closes in until the experience tunnel vision
they will get optic disc cupping
17
Q
what signs would you see on fundoscopy in open angle glaucoma?
A
- Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
- Optic disc pallor - indicating optic atrophy
- Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
- Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
18
Q
what investigations would you perform for open angle glaucoma?
A
tonometry (will show elevated intra-ocular pressure)
ophthalmoscopy/fundoscopy to check the optic disc for cupping and optic nerve health
visual field testing
slit lamp biomicroscopy
19
Q
how do you manage open angle glaucoma
A
first line
- topical ophthalmic prostaglandin analogues (latanoprost) - increases outflow
second line
- topical ophthalmic beta blockers (timolol) - decreases production
- topical ophthalmic carbonic anhydrase inhibitors
- topical ophthalmic alpha-2 adrenergic agonists - brimonidone
eye drop failure :
laser trabeculoplasty
surgical interventoin
20
Q
what can be used to measure intraocular pressure?
A
Non-contact tonometry is the commonly used machine for estimating intraocular pressure by opticians. It involves shooting a “puff of air” at the cornea and measuring the corneal response to that air. It is less accurate but gives a helpful estimate for general screening purposes.
Goldmann applanation tonometry is the gold standard way to measure intraocular pressure. This involves a special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the front of the cornea to get an accurate measurement of what the intraocular pressure is.
21
Q
what are the risk factors for acute closed angle glaucoma?
A
increasing age female are affected around 4 time more often than males family history Chinese and east asian ethnic origin. shallow anterior chamber
22
Q
what medications may precipitate acute angle closure glaucoma?
A
Adrenergic medications such as noradrenalin
Anticholinergic medications such as oxybutynin and solifenacin
Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
23
Q
how will acute angle closure glaucoma present?
A
the patient will generally appear unwell in themselves
they have short history of
- severely painful eye
- blurred vision
- halos around lights
- associated headache, nausea and vomiting
24
Q
what would you see when examining a patient with acute angle closure glaucoma ?
A
Red eye Teary Hazy cornea Decreased visual acuity Dilatation of the affected pupil Fixed pupil size Firm eyeball on palpation
25
what investigations are performed for angle-closure glaucoma?
gonioscopy - examination of the anterior chamber angle is the definitive test for diagnosing angle-closure glaucoma
slit lamp examination can also be performed
automatic static perimetry
26
how is acute closed angle glaucoma managed?
NICE CKS 2019 states that patients with potentially life threatening causes of red eye should be referred for same day assessment by an ophthalmologist.
lie patient on their back without a pillow
give pilocarpine eye drops (2% for blue, 4% for brown)
give acetazolamide 500mg orally
give analgesia and antiemetic if required
Laser iridotomy is usually required as a definitive treatment. This involve using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
27
why are pilocarpine and acetazolamde given in acute angle closure glaucoma?
Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil. Therefore it is a miotic agent. It also causes ciliary muscle contraction. These two effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up.
Acetazolamide is a carbonic anhydrase inhibitor. This reduces the production of aqueous humour.
28
what is anterior uveitis?
aka iritis
Anterior uveitis is inflammation in the anterior part of the uvea. The uvea involves the iris, ciliary body and choroid. The choroid is the layer between the retina and the sclera all the way around the eye. Sometimes anterior uveitis is referred to as iritis.
It involves inflammation and immune cells in the anterior chamber of the eye. The anterior chamber of the eye becomes infiltrated by neutrophils, lymphocytes and macrophages. This is usually caused by an autoimmune process but can be due to infection, trauma, ischaemia or malignancy. Inflammatory cells in the anterior chamber cause floaters in the patient’s vision.
Anterior uveitis can be acute or chronic. Chronic anterior uveitis is more granulomatous (has more macrophages) and has a less severe and longer duration of symptoms, lasting more than 3 months.
29
what is acute and chronic anterior uveitis associated with?
Acute anterior uveitis is associated with HLA B27 related conditions:
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis
```
Chronic anterior uveitis is associated with:
Sarcoidosis
Syphilis
Lyme disease
Tuberculosis
Herpes virus
```
30
what is the presentation of anterior uveitis?
it usually presents with unilateral symptoms that start spontaneously without a history of trauma or precipitating events. They may occur with a flare of an associated disease such as reactive arthritis.
Symptoms Include:
- dull aching painful red eye
- ciliary flush - a ring of red spreading from the cornea outwards
- reduced visual acuity
- floaters and flashes
- sphincter muscle contraction causing miosis (contracted pupil)
- photohobiadue to ciliary muscle spasm
- pain on movement
- abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes
31
how should anterior uveitis be managed?
urgent review by ophthalmology - same day assessment - they need fully slit lamp assessment of the different structures of the eye and intraocular pressure to establish the diagnosis
Slit lamp exam
hypopyon - inflammatory cells and pus collecting
kerartic precipitates
ciliary flush
treatment choices
- steroids
- cycloplegic-mydriatic medications such as atropine - Cycloplegic means paralysing the ciliary muscles. Mydriatic means dilating the pupils. Cyclopentolate and atropine are antimuscarinic medications that blocks to the action of the iris sphincter muscles and ciliary body. These dilate the pupil and reduce pain associated with ciliary spasm by stopping the action of the ciliary body.
- immunosupressants such as DMARD and TNF inhibitors
- laser therapy, cryotherapy or surgery may be needed in severe cases
32
what is blepharitis?
Blepharitis is inflammation of the eyelid margins.
common in patients with rosacea
33
what can cause blepharitis?
meibomian gland dysfunction (common, posterior blepharitis)
| seborrhoeic dermatitis/staph infection (anterior blepharitis)
34
how does blepharitis present?
```
burning sensation
itching sensation
grittiness and discomfort particularly around the eyelid margins
foreign body sensations
crusting of eyelids
dry eyes
```
35
how do you manage blepharitis?
soften the lid margin using hot compresses twice a day
lid hygiene
Lubricating eye drops can be used to relieve symptoms:
Hypromellose is the least viscous. The effect lasts around10 minutes.
Polyvinyl alcohol is the middle viscous choice. It is worth starting with these.
Carbomer is the most viscous and lasts 30 – 60 minutes.
36
what is a stye?
Stye, also known as hordeolum, is an acute infectious process involving abscess formation at the upper or lower eyelid. One of 3 glands is typically infected: the meibomian glands or the glands of Zeis and Moll (ciliary glands).
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.
Hordeolum internum is infection of the Meibomian glands. They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid.
37
what is chalazion?
acuteA chalazion occurs when a Meibomian gland becomes blocked and swells up. It is often called a Meibomian cyst. It presents with a swelling in the eyelid that is typically not tender. It can be tender and red.
38
how do you manage a stye?>
topical Abx - bacitracin ophthalmic or erythromycin ophthalmic
warm compresses plus massage
39
how is chalazion managed?
warm compress plus massage plus lid hygiene
40
what is entropion?
Entropion is where the eyelid turns inwards with the lashes against the eyeball. This results in pain and can result in corneal damage and ulceration.
Initial management is by taping the eyelid down to prevent it turning inwards. Definitive management is with surgical intervention. When the eyelid is taped down it is essential to prevent the eye drying out by using regular lubricating eye drops.
A same day referral to ophthalmology is required if there is a risk to sight.
41
what is ectropion ?
Ectropion is where the eyelid turns outwards with the inner aspect of the eyelid exposed. It usually affects the bottom lid. This can result in exposure keratopathy as the eyeball is exposed and not adequately lubricated and protected.
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.
42
what is trichiasis?
Trichiasis is inward growth of the eyelashes. This results in pain and can result in corneal damage and ulceration.
Management by a specialist is to remove the eyelash (epilation). Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent the lash regrowing.
A same day referral to ophthalmology is required if there is a risk to sight.
43
what is periorbital cellulitis?
Periorbital cellulitis (also known as preorbital cellulitis) is an eyelid and skin infection in front of the orbital septum (in front of the eye). It presents with swelling, redness and hot skin around the eyelids and eye.
It is essential to differentiate it from orbital cellulitis, which is a sight and life threatening emergency. CT scan can help distinguish between the two.
Treatment is with systemic antibiotics (oral or IV). Preorbital cellulitis can develop into orbital cellulitis so vulnerable patients (e.g. children) or severe cases may require admission for observation while they are treated.
44
what is orbital cellulitis ?
Orbital cellulitis is an infection around the eyeball that involves tissues behind the orbital septum.
Key features that differential this from periorbital celluitis is pain on eye movement, reduced eye movements, changes in vision, abnormal pupil reactions and forward movement of the eyeball (proptosis).
This is a medical emergency that requires admission and IV antibiotics. They may require surgical drainage if an abscess fo
45
what are cataracts?
Cataracts are where the lens in the eye gradually becomes cloudy and opaque. This reduces visual acuity by reducing the light that enters the eye.
46
what are the risk factors for cataracts ?
- age >65
- smoking
- long term UV exposure
- DM
- eye trauma
- long term corticosteroid use
- family history
- uveitis
- hypocalcaemia
47
how does a cataract present?
Patients typically present with a gradual onset of:
- Reduced vision
- Faded colour vision: making it more difficult to distinguish different colours
- Glare: lights appear brighter than usual
- Halos around lights
- defect in the red reflex
TOM TIP: It is useful in exams to distinguish the causes of visual problems based on the symptoms. Cataracts cause a generalised reduction in visual acuity with starbursts around lights. Glaucoma causes a peripheral loss of vision with halos around lights. Macular degeneration causes a central loss of vision with a crooked or wavy appearance to straight lines.
48
what are the investigations of cataracts ?
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
measurement of intra-ocular pressure - may be normal or elevated if there is associated glaucoma
49
what are the classifications of cataracts?
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
50
how are cataracts managed?
if symptoms are managemenable then no intervention may be necessary
Cataract surgery involves drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens into the eye. This is usually done as a day case under local anaesthetic. It usually gives good results.
51
what are the complications following cataract surgery
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
52
what is diabetic retinopathy?
Diabetic retinopathy is a condition where the blood vessels in the retina are damaged by prolonged exposure to high blood sugar levels (hyperglycaemia) causing a progressive deterioration in the health of the retina.
53
what is the pathophysiology of diabetic retinopathy?
Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells. Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and the formation of hard exudates. Hard exudates are yellow/white deposits of lipids in the retina.
Damage to the blood vessel walls leads to microaneurysms and venous beading. Microaneurysms are where weakness in the wall causes small bulges. Venous beading is where the walls of the veins are no longer straight and parallel and look more like a string of beads or sausages.
Damage to nerve fibres in the retina causes fluffy white patches to form on the retina called cotton wool spots.
Intraretinal microvascular abnormalities (IMRA) is where there are dilated and tortuous capillaries in the retina. These can act as a shunt between the arterial and venous vessels in the retina.
Neovascularisation is when growth factors are released in the retina causing the development of new blood vessels.
54
how is diabetic retinopathy classified?
Diabetic retinopathy can be split into two broad categories: non-proliferative and proliferative depending on whether new blood vessels have developed. Non-proliferative is often called background or pre-proliferative retinopathy as it can develop in to proliferative retinopathy. A condition called diabetic maculopathy also exists separate from non-proliferative and proliferative diabetic retinopathy.
55
what is the classification of non-proliferative diabetic retinopathy?
Mild: microaneurysms
Moderate: microaneurysms, blot haemorhages, hard exudates, cotton wool spots and venous beading
Severe: blot haemorrhages plus microaneurysms in 4 quadrants, venous beating in 2 quadrates, intraretinal microvascular abnormality (IMRA) in any quadrant
56
what are the 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, 50% blind in 5 years
57
what is diabetic maculopathy?
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
- macula oedema and ischaemic maculopathy
58
what are the complications of diabetic retinopathy?
Retinal detachment
Vitreous haemorrhage (bleeding in to the vitreous humour)
Rebeosis iridis (new blood vessel formation in the iris)
Optic neuropathy
Cataracts
59
what are the investigations for diabetic retinopathy?
photographs of the fundus
optical coherence tomography scanning
fluorescein angiography
B scan ultrasonography
60
how is diabetic retinopathy managed?
Laser photocoagulation
Anti-VEGF medications such as ranibizumab and bevacizumab
Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
61
what is optic neuritis?
inflammation of the optic nerve
is most commonly idiopathic
primarily a demyelinating disease occurring in isolation or as part of multiple sclerosis
62
what can cause optic neuritis?
idiopathic
MS
diabetes
syphilis
63
how does optic neuritis present?
unilateral decrease in visual acuity over hours or days
poor discrimination of colours - red desaturation
perti-orbital/retro-ocular pain worse on eye movement
relative afferent pupillary defect
central scotoma
64
what investigations would you perform for optic neuritis?
MRI of the optic nerves - swelling of the optic nerve, enhancement in optic nerve, white matter lesions in patients with MS
if the MRI shows >3 white matter lesions - 5 year risk of developing MS is 50%
65
how is optic neuritis managed?
high dose methylprednisolone orally or IV
66
what is age related macular degeneration?
Age related macular degeneration is a condition where there is degeneration in the macular that cause a progressive deterioration in vision. In the UK it is the most common cause of blindness
67
what are the types of macular degeneration?
dry (90% of cases, geographic atrophy) macular degeneration: characterised by drusen - yellow round spots in Bruch's membrane
wet (10% of cases, exudative, neovascular) macular degeneration: characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis
Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)
68
what are the risk factors for macular degeneration?
```
age
smoking
white or chinese ethnic origin
family history
CV disease
```
69
how does macular degeneration usually present?
gradual worsening of central visual field loss
reduced visual acuity
crooked or wavy appearance to straight lines
fluctuations in visual disturbance which may vary significantly from day to day
wet age related macular degeneration presents more acutely - it can present with a loss of vision of days and progress to full vision loss over 2-3 years - it often progresses to bilateral disease.
A sudden onset blurring or distortion of vision can indicate development of choroidal neovascularization with leakage of fluid in the macula
70
what investigations would you perform for age related macular degeneration?
Amsler grid testing - shows a focal area of distortion
optical coherence tomography - test for confirming the presence of subretinal and intraretinal fluid
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar
71
how is age related macular degeneration managed?
dry ARMD - lifestyle measure
antioxidant and zinc supplementation can reduce the disease progression
wet ARMD - anti-VEGF medications
vascular endothelial growth factor is involved in the development of new blood vessels in the retina. Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels. They are injected directly into the vitreous chamber of the eye once a month. They slow and even reverse the progression of the disease. They typically need to be started within 3 months to be beneficial
72
what is retinal detachment?
Retinal detachment (RD) is typically a progressive condition in which the neuroretina separates (detaches) from the retinal pigment epithelium. Sub-retinal fluid accumulates, and the retina temporarily loses its function
The outer retina relies on the blood vessels of the choroid (which is firmly attached to the retinal pigment epithelium) for its blood supply. This makes retinal detachment a sight threatening emergency unless quickly recognised and treated.
73
what causes retinal detachment?
several factors can lead to it
- increasing age
- myopia
- trauma
- cataract surgery
- ocular inflammation
- posterior vitreous detachment
74
how does retinal detachment present?
painless condition that presents with:
- loss or deterioration of central vision
- peripheral vision loss - this is often sudden and like a shadow coming across the vision
- blurred or distorted vision
- flashes and floaters
75
what investigations would you perform for retinal detachment?
- visual acuity testing
- slit-lamp examination - will show retinal detachment, retinal break, vitreoretinal pathology
- indirect ophthalmoscopy
76
how is retinal detachment managed?
if they have posterior vitreous detachment without a break or tear - giving proper prophylactic treatment such as laser cerclage dramatically reduces this risk of subsequent detachment
Management of retinal tears aims to create adhesions between the retina and the choroid to prevent detachment. This can be done using:
Laser therapy
Cryotherapy
Management of retinal detachment aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. This needs to be followed by treating retinal tears as above. Reattaching the retina can be done using one of three options:
Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas.
Scleral buckling involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina.
Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.
77
what is posterior vitreous detachment?
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. Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina.
is important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment, as they may result in permanent loss of vision.
Signs:Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
78
what is a squint?
Squint (strabismus) is characterised by misalignment of the visual axes.
79
what are the different types of squint?
Squints may be divided into concomitant (common) and paralytic (rare)
Concomitant - due to imbalance in the extraocular muscles
Paralytic - due to paralysis of extraocular muscles
80
how do squints present?
diplopia
eye misalignment
amblyopia
81
what test to you do for squints?
```
cover test
ask the child to focus on an object
cover one eye
observe movement of uncovered eye
cover other eye and repeat test
```
direction of a squint may be made by the corneal light reflection test - holding a light source 30 cm from the child's face to see of the light reflects symmetrically
82
how are quints managed?
referral to secondary care
| eye patches may help prevent amblyopia
83
How does the pupil constrict?
There are circular muscles in the iris that cause pupil constriction. They are stimulated by the parasympathetic nervous system using acetylcholine as a neurotransmitter. The fibres of the parasympathetic system innervating the eye travel along the oculomotor (third cranial) nerve.
84
How does the pupil dilate?
The dilator muscles of the pupil arranged like spokes on a bicycle wheel travelling straight from the inside to the outside of the iris. They are stimulated by the sympathetic nervous system using adrenalin as a neurotransmitter.
85
what can cause abnormal pupil
Trauma to the sphincter muscles in the iris can cause an irregular pupil. This could be caused by cataract surgery and other eye operations.
Anterior uveitis can cause adhesions (scar tissue) in the iris that make the pupils misshapen.
Acute angle closure glaucoma can cause ischaemic damage to the muscles of the iris causing an abnormal pupil shape, usually a vertical oval.
Rubeosis iridis (neovascularisation in the iris) can distort the shape of the iris and pupil. This is usually associated with poorly controlled diabetes and diabetic retinopathy.
Coloboma is a congenital malformation in the eye. This can cause a hole in the iris causing an irregular pupil shape.
Tadpole pupil is where there is spasm in a segment of the iris causing a misshapen pupil. This is usually temporary and associated with migraines.
86
what is mydriasis?
dilated pupil
87
what are some causes of mydriasis?
```
Third nerve palsy
Holmes-Adie syndrome
Raised intracranial pressure
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics
```
88
what is miosis?
constricted pupil
89
what are some causes of miosis?
```
Horners syndrome
Cluster headaches
Argyll-Robertson pupil (in neurosyphilis)
Opiates
Nicotine
Pilocarpine
```
90
what does a 3rd nerve palsy cause?
Ptosis - drooping of the eyelid
dilated non-reactove pupil
divergent strabismus in the effected eye - it will cause a down and out position of the eye
91
what is the function of the CN3?
The third cranial nerve is the oculomotor nerve. It supplies all of the extraocular muscles except the lateral rectus and superior oblique. Therefore when these muscles are no longer getting signals from the oculomotor nerve, the eyes moves outward and downward due to the effects of the lateral rectus and superior oblique still functioning without resistance.
It also supplies the levator palpebrae superioris, which is responsible for lifting the upper eyelid. Therefore third nerve palsy causes a ptosis.
The oculomotor nerve also contains parasympathetic fibres that innervate the sphincter muscle of the iris. Therefore third nerve palsy causes a dilated fixed pupil.
92
what can cause compression of CN3?
The oculomotor nerve travels directly from the brainstem to the eye in a straight line. It travels through the cavernous sinus and close to the posterior communicating artery. Therefore, cavernous sinus thrombosis and a posterior communicating artery aneurysm can cause compression of the nerve and a third nerve palsy.
93
what are some causes of third nerve palsy?
Third nerve palsy can be idiopathic, without a clear cause.
A third nerve palsy with sparing of the pupil suggests a microvascular cause as the parasympathetic fibres are spared. This may be due to:
Diabetes
Hypertension
Ischaemia
A full third nerve palsy is caused by compression of the nerve, including the parasympathetic fibres. This is called a “surgical third” due to the physical compression:
```
Idiopathic
Tumour
Trauma
Cavernous sinus thrombosis
Posterior communicating artery aneurysm
Raised intracranial pressure
```
94
what is Horner syndrome?
Horner syndrome is caused by damage to the sympathetic nervous system supplying the face.
Horner syndrome is a triad of:
Ptosis
Miosis
Anhidrosis (loss of sweating)
They may also have enopthalmos, which is a sunken eye. Light and accommodation reflexes are not affected.
95
why is the journey of the sympathetic nerves to the head relevant to the cause of Horner's syndrome?
The journey of the sympathetic nerves to the head is relevant for the causes of Horner syndrome. The sympathetic nerves arise from the spinal cord in the chest. These are pre-ganglionic nerves. They then enter into the sympathetic ganglion at the base of the neck and exit as post-ganglionic nerves. These post-ganglionic nerves then travel to the head, running alongside the internal carotid artery.
The location of the Horner syndrome can be determined by the anhidrosis. Central lesions cause anhidrosis of the arm and trunk as well as the face. Pre-ganglionic lesions cause anhidrosis of the face. Post-ganglionic lesions do not cause anhidrosis.
96
what are the causes of Horner's syndrome?
Central lesions (4 Ss)
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S – Stroke
S – Multiple Sclerosis
S – Swelling (tumours)
S – Syringomyelia (cyst in the spinal cord)
Pre-ganglionic lesions (4 Ts):
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T – Tumour (Pancoast’s tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib above the clavicle)
Post-ganglionic lesion (4 Cs)
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C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache
97
what is congenital horner syndrome?
Congenital Horner Syndrome is associated with heterochromia, which is a difference in the colour of the iris on the affected side.
98
what can be used to test for Horner's syndrome?
Cocaine eye drops can be used to test for Horner syndrome. Cocaine acts on the eye to stop noradrenalin re-uptake at the neuromuscular junction. This causes a normal eye to dilate because there is more noradrenalin stimulating the dilator muscles of the iris. In Horner syndrome, the nerves are not releasing noradrenalin to start with so blocking re-uptake does not make a difference and there is no reaction of the pupil.
Alternatively, a low concentration adrenalin eye drop (0.1%) won’t dilate a normal pupil but will dilate a Horner syndrome pupil.
99
what is Holmes Adie Pupil ?
A Holmes Adie pupil is a unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction. Over time the pupil will get smaller. This is caused by damage to the post-ganglionic parasympathetic fibres. The exact cause is unknown but may be viral.
Holmes Adie Syndrome is where there is a Holmes Adie pupil with absent ankle and knee reflexes.
100
what is Argyll robertson pupil?
An Argyll-Robertson pupil is a specific finding in neurosyphilis. It is a constricted pupil that accommodates when focusing on a near object but does not react to light. They are often irregularly shaped. It is commonly called “prostitutes pupil” due to the relation to neurosyphilis and because “it accommodates but does not react“.
101
what is marcus-gunn pupil?
aka relative afferent pupillary defect?
a relative afferent pupillary defect is found by the 'swinging light test'. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina
Finding
the affected and normal eye appears to dilate when light is shone on the affected
Causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Pathway of pupillary light reflex
afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
102
what is perimetry ?
automated visual field testing
103
investigations for open angle glaucoma?
corneal thickness
