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Y4 Neuro and Special Senses > Opthalmology 1 > Flashcards

Opthalmology 1 Flashcards

1
Q

What is glaucoma?

A

optic nerve damage caused by a rise in intraocular pressure (IOP) due to a blockage in aqueous humour trying to escape the eye.

There are two types of glaucoma:
Open-angle glaucoma
Acute angle-closure glaucoma

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2
Q

What is normal intraocular pressure?

A

10-21 mmHg

It is created by the resistance to flow of aqueous humour through the trabecular meshwork

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3
Q

What is the difference between the pathophysiology of open angle glaucoma and acute closed angle glaucoma?

A

With open-angle glaucoma, there is a gradual increase in resistance to flow through the trabecular meshwork. The pressure slowly builds within the eye.

With acute angle-closure glaucoma, the iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining. This causes an acute build up of pressure.

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4
Q

Raised intraocular pressure causes cupping of the optic disc.

What is this?

A

In the centre of the optic disc is an indent called the optic cup, which is usually less than 50% of the size of the optic disc.

Raised intraocular pressure causes this indent to become wider and deeper, described as “cupping”. A cup-disk ratio greater than 0.5 is abnormal.

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5
Q

Risk factors for open-angle glaucoma include:

A

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Hypertension
Diabetes mellitus
Corticosteroids

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6
Q

In open-angle glaucoma, the rise in IOP may be asymptomatic for a long time and diagnosed by routine eye testing.

How may it present if symptomatic?

A

Peripheral visual field loss
Decreased visual acuity (blurred vision)
Fluctuating pain
Headaches
Halos around lights, particularly at night

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7
Q

What are the methods for measuring intraocular pressure?

A

Non-contact tonometry:
shooting a “puff of air” at the cornea and measuring the corneal response
less accurate but good for general screening purposes

Goldmann applanation tonometry:
gold-standard
device mounted on a slip lamp that makes contact with the cornea and applies various pressures

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8
Q

How can open-angle glaucoma be investigated?

A

Visual field assessment for peripheral vision loss
Goldmann applanation tonometry for the intraocular pressure
Slit lamp assessment for the cup-disk ratio and optic nerve health
Gonioscopy to assess the angle between the iris and cornea
Central corneal thickness assessment

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9
Q

How does open-angle glaucoma present on fundoscopy?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7, loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
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10
Q

When is treatment initiated for open-angle glaucoma?

A

at an intraocular pressure of 24 mmHg or above

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11
Q

How can open-angle glaucoma be managed?

A

Prostaglandin analogue eye drops (e.g., latanoprost) are the first-line medical treatment - increase uveoscleral outflow

360° selective laser trabeculoplasty - laser is directed at the trabecular meshwork, improving drainage

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12
Q

What are the potential side effects of prostaglandin analogue eye drops e.g. lantanoprost?

A

eyelash growth, eyelid pigmentation and iris pigmentation (browning)

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13
Q

Other than prostaglandin analogues, what eye drops may be used in the mx of 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

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14
Q

Risk factors for acute angle-closure glaucoma include:

A

Increasing age
Family history
Female (four times more likely than males)
Chinese and East Asian ethnic origin
Shallow anterior chamber

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15
Q

What medications 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

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16
Q

How do patients with acute angle-closure glaucoma present?

A

Severely painful red eye
Decreased visual acuity (blurred vision)
Halos around lights
Associated headache, nausea and vomiting
Symptoms worse with mydriasis (e.g. watching TV in a dark room)

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17
Q

What may be seen on examination of patients with acute angle-closure glaucoma?

A

Red eye
Hazy cornea
Semi-dilated non-reactive pupil
Hard eyeball on gentle palpation
Decreased visual acuity

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18
Q

How can acute angle closure glaucoma be investigated?

A

tonometry to assess for elevated IOP

gonioscopy (looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle

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19
Q

How can acute angle closure glaucoma be managed in the community?

A

Acute angle-closure glaucoma requires immediate admission!

Measures while waiting for an ambulance are:

Lying the patient on their back without a pillow
Pilocarpine eye drops (2% for blue and 4% for brown eyes)
Acetazolamide 500 mg orally
Analgesia and an antiemetic, if required

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20
Q

How does pilocarpine work?

A

acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent)

also causes ciliary muscle contraction

opens up the pathway for the flow of aqueous humour

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21
Q

How does Acetazolamide work?

A

a carbonic anhydrase inhibitor that reduces the production of aqueous humour

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22
Q

How can acute angle closure glaucoma be managed in secondary care?

A

Pilocarpine eye drops

IV Acetazolamide

Hyperosmotic agents (e.g. IV mannitol)

Timolol, Dorzolamide - both reduce the production of aqueous humour via different mechanisms

Brimonidine - reduces aqueous humour production and increases uveoscleral outflow

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23
Q

What is usually required as definitive mx for acute angle closure glaucoma once the initial attack has settled ?

A

Laser iridotomy - involves making a hold in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber

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24
Q

What is the most common cause of blindness in the UK?

A

Age-related macular degeneration (AMD)

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25
Age-related macular degeneration (AMD) is a progressive condition affecting the macula. What are the two types?
Wet (also called neovascular), accounting for 10% of cases - characterised by choroidal neovascularisation Dry (also called non-neovascular), accounting for 90% of cases - characterised by drusen
26
The macula is found in the centre of the retina. It generates high-definition colour vision in the central visual field. What are its 4 layers?
Choroid layer (at the base), which contains the blood vessels that supply the macula Bruch’s membrane Retinal pigment epithelium Photoreceptors (towards the surface)
27
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 older patients Frequent and larger drusen can be an early sign of macular degeneration
28
What features are common to wet and dry AMD?
Atrophy of the retinal pigmented epithelium Degeneration of the photoreceptors
29
What is the pathophysiology of wet 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 vascular endothelial growth factor (VEGF) is the target of medications for AMD
30
Give some risk factors for AMD?
Older age Family history Smoking (x2 risk) Cardiovascular disease (e.g., hypertension) Obesity Poor diet (low in vitamins and high in fat)
31
How does AMD typically present?
Visual changes associated with AMD tend to be unilateral, with: Gradual loss of central vision Reduced visual acuity Crooked or wavy appearance to straight lines (metamorphopsia) Worsening night vision Patients often present with a gradually worsening ability to read small text.
32
How does wet AMD present differently to dry AMD?
Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years. It often progresses to bilateral disease.
33
What are the key points used to differentiate between glaucoma and AMD?
**Glaucoma** is associated with **peripheral vision loss** and halos around lights **AMD** is associated with **central vision loss** and a wavy appearance to straight lines
34
What are the key examination findings for AMD?
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
35
What is the name for the visual hallucination syndrome associated with AMD?
Charles-Bonnet syndrome
36
What investigations can be done for AMD?
**slit-lamp microscopy** is the initial investigation of choice fluorescein angiography if wet ARMD is suspected optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren't visible using microscopy alone
37
How can dry AMD be managed?
Management involves monitoring and reducing the risk of progression by: Avoiding smoking Controlling blood pressure Vitamin supplementation has some evidence in slowing progression
38
How can wet AMD be managed?
**Anti-VEGF medications** (e.g., ranibizumab, aflibercept and bevacizumab) - injected directly into the vitreous chamber of the eye, usually about once a month.
39
What is the pathophysiology of diabetic retinopathy?
Hyperglycaemia (high blood sugar) damages the retinal small vessels and endothelial cells. Damage to the blood vessel walls leads to **microaneurysms** and **venous beading** **Increased vascular permeability** leads to leaking blood vessels, **blot haemorrhages** and **hard exudates** Damage to nerve fibres in the retina causes fluffy white patches called **cotton wool spots** to form on the retina
40
Diabetic retinopathy is classified based on the findings on fundus examination. What are the different types?
non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy
41
What are the key features of non proliferative diabetic retinopathy?
due to direct damage to vessels: microaneurysms venous beading intraretinal microvascular abnormalities (IRMA) due to increased vascular permeability: blot haemorrhages hard exudates due to damage to nerves: cotton wool spots
42
What do cotton wool spots represent?
they are soft exudates they represent infarction in the nerve fibre layer
43
What are the key features of proliferative diabetic retinopathy?
retinal neovascularisation - may lead to vitreous haemorrhage fibrous tissue forming anterior to retinal disc more common in Type I DM, 50% blind in 5 years
44
What does diabetic maculopathy involve?
Exudates within the macula Macular oedema
45
What are the potential complications of diabetic retinopathy?
Vision loss Retinal detachment Vitreous haemorrhage (bleeding into the vitreous humour) Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma Optic neuropathy Cataracts
46
Non-proliferative diabetic retinopathy requires close monitoring and careful diabetic control. What are the treatment options for proliferative diabetic retinopathy?
Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels Anti-VEGF medications by intravitreal injection Surgery (e.g., vitrectomy) may be required in severe disease
47
What are the potential complications of Pan-retinal photocoagulation?
50% of patients develop reduction in their visual fields due to the scarring of peripheral retinal tissue decrease in night vision (majority of rod cells - which are responsible for night vision - are located in the peripheral retina which is targeted by PRP)
48
What can be used to treat macular oedema?
An intravitreal implant containing dexamethasone
49
Outline the Keith Wagner Classification of hypertensive retinopathy
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
50
What are the different types of retinal haemorrhage?
Dot and blot haemorrhages: occur deeper, in the inner nuclear layer or outer plexiform layer Flame haemorrhages: occur in the nerve fiber layer
51
What are cataracts?
a progressively opaque eye lens, which reduces the light entering the eye and visual acuity most develop in older age, apart from congenital cataracts, which can be identified by testing the red reflex in the neonatal exam
52
Give some risk factors for developing cataracts
Increasing age Smoking Alcohol Diabetes Steroids Hypocalcaemia
53
How do cataracts present?
Symptoms are usually asymmetrical, as both eyes are affected separately. It presents with: 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
54
Key examination findings for cataracts?
Loss of the red reflex
55
How can cataracts be managed?
Cataract surgery : drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens Can be performed as a day case under local anaesthetic
56
Give a complication of cataract surgery
Endophthalmitis : inflammation of the inner contents of the eye, usually caused by infections Can lead to vision loss Treated with intravitreal antibiotics injected directly into the eye
57
What controls pupillary constriction?
The circular muscles in the iris are responsible for pupil constriction They are stimulated by the parasympathetic nervous system (via the oculomotor nerve - CN III) using acetylcholine as a neurotransmitter picture a PARrot sitting on the arch of the circular muscles -PARasympathetic
58
What controls pupillary dilation?
dilator muscles in the iris stimulated by the sympathetic nervous system, using adrenalin as a neurotransmitter
59
Give 6 causes of an abnormal pupil shape
Acute angle-closure glaucoma Rubeosis iridis (neovascularisation in the iris) Coloboma Tadpole pupil Trauma to the sphincter muscles in the iris (e.g., during cataract surgery) Anterior uveitis can cause adhesions (scar tissue) in the iris
60
How does acute angle closure glaucoma cause an abnormal pupil shape?
Acute angle-closure glaucoma can cause ischaemic damage to the muscles of the iris This can cause an abnormal pupil shape, usually a vertical oval.
61
What is Rubeosis iridis?
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.
62
What is Coloboma?
a congenital malformation that can cause a hole in the iris and an irregular pupil shape.
63
What is tadpole pupil?
muscle spasm in part of the dilator muscle of the iris, causing a misshapen pupil It is a temporary condition and may be associated with migraines and Horner syndrome.
64
Give some causes of Mydriasis (Dilated Pupil)
Trauma Third nerve palsy Raised ICP Acute angle-closure glaucoma Stimulants (e.g., cocaine) Anticholinergics (e.g., oxybutynin) Holmes-Adie syndrome
65
Give some causes of Miosis (Constricted Pupil)
Horner syndrome Cluster headaches Argyll-Robertson pupil (neurosyphilis) Opiates Nicotine Pilocarpine
66
A palsy in the third cranial nerve (the oculomotor nerve) causes:
Ptosis (drooping upper eyelid) Dilated non-reactive pupil Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye
67
A third nerve palsy that does not affect the pupil (sparing of the pupil) suggests what cause?
a microvascular cause, as the outer parasympathetic fibres that supply the pupil are spared when the central fibres are compromised but the peripheral fibres are not, this suggests that the problem is with the blood supply as opposed to extrinsic compression This may be due to: Diabetes Hypertension Ischaemia
68
What can cause a full third nerve palsy? (involves the pupil)
caused by compression of the nerve, including compression of the parasympathetic fibres. This may be due to: Tumour Trauma Cavernous sinus thrombosis Posterior communicating artery aneurysm Raised intracranial pressure
69
What is Horner syndrome?
Triad of: Ptosis Miosis Anhidrosis (loss of sweating) may also have enophthalmos (sunken eye) caused by damage to the sympathetic nervous system supplying the face
70
How can you determine the location of the lesion in Horner syndrome?
can be determined by the anhidrosis (loss of sweating) 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.
71
How can you remember the causes of Horner syndrome?
S for Sentral, T for Torso (pre-ganglionic) and C for Cervical (post-ganglionic)
72
What are the central causes of Horner syndrome?
S – Stroke S – Multiple Sclerosis S – Swelling (tumours) S – Syringomyelia (cyst in the spinal cord)
73
What are the pre-ganglionic causes of Horner syndrome?
T – Tumour (Pancoast tumour) T – Trauma T – Thyroidectomy T – Top rib (a cervical rib growing above the first rib and clavicle)
74
What are the post-ganglionic causes of Horner syndrome?
C – Carotid aneurysm C – Carotid artery dissection C – Cavernous sinus thrombosis C – Cluster headache
75
How can you test for Horner syndrome?
Cocaine eye drops: acts on the eye to stop noradrenalin re-uptake at the NMJ which causes a normal eye to dilate In Horner syndrome, the nerves are not releasing noradrenalin, so blocking re-uptake makes no difference, and there is no pupil reaction. Alternatively, low-dose adrenalin eye drops (0.1%) will dilate the pupil in Horner syndrome but not a normal pupil.
76
What is seen in congenital Horner syndrome?
heterochromia (difference in iris colour)
77
What is a Holmes Adie pupil?
aDI- DIlated pupil benign condition that is more common in women , caused by damage to the post-ganglionic parasympathetic fibres Presentation: unilateral 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)
78
What is Holmes-Adie syndrome ?
a Holmes-Adie pupil with absent ankle and knee reflexes
79
What is Argyll-Robertson pupil?
finding in neurosyphilis a constricted pupil that accommodates when focusing on a near object but does not react to light often irregularly shaped commonly called a “prostitute’s pupil” due to its relation to neurosyphilis and because “it accommodates but does not react”.
80
What are the 2 causes of Argyll Robertson pupil?
diabetes mellitus syphilis
81
What is blepharitis?
inflammation of the eyelid margins leading to a red eye due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)
82
Which patient group is at greater risk of blepharitis?
patients with rosacea
83
How does blepharitis present?
symptoms are usually bilateral grittiness and discomfort, particularly around the eyelid margins eyes may be sticky in the morning swollen eyelids may be seen in staphylococcal blepharitis
84
Complications of blepharitis?
can lead to styes and chalazions can get secondary conjunctivitis
85
How can blepharitis be managed?
softening of the lid margin using hot compresses twice a day 'lid hygiene' - mechanical removal of the debris from lid margins cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
86
What is a stye?
infection of a gland on the eyelid external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum) or glands of Moll (sweat) internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst) internal are deeper, tend to be more painful and may point inwards towards the eyeball
87
How can styes be managed?
hot compresses and analgesia CKS only recommend topical antibiotics if there is an associated conjunctivitis
88
What is a Chalazion?
also called a Meibomian cyst retention cyst of the Meibomian gland presents as a firm painless lump in the eyelid majority of cases resolve spontaneously but some require surgical drainage
89
What are entropions and ectropions?
entropion: in-turning of the eyelids ectropion: out-turning of the eyelids
90
What is Trichiasis?
inward growth of the eyelashes results in pain and can cause corneal damage and ulceration Mx = removing the affected eyelashes Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent them from regrowing
91
What is conjunctivitis?
inflammation of the conjunctiva may be bacterial, viral or allergic Presentation: Red, bloodshot eye Itchy or gritty sensation Discharge
92
How do bacterial and viral conjunctivitis present differently?
Bacterial conjunctivitis Purulent discharge Eyes may be 'stuck together' in the morning Viral conjunctivitis Serous discharge Recent URTI Preauricular lymph nodes
93
How can infective conjunctivitis be managed?
normally a self-limiting condition that settles within 1-2 weeks topical antibiotic therapy is commonly offered e.g. Chloramphenicol topical fusidic acid is an alternative for pregnant women advice should be given not to share towels school exclusion is not necessary
94
Advice for contact lens users during an epsiode of infective conjunctivits?
topical fluoresceins should be used to identify any corneal staining contact lens should not be worn
95
How does allergic conjunctivitis present?
Bilateral symptoms Conjunctival erythema, conjunctival swelling (chemosis) Itch is prominent the eyelids may also be swollen May be a history of atopy
96
How can allergic conjunctivitis be managed?
first-line: topical or systemic antihistamines second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil
97
Causes of an acute painful red eye include:
Acute angle-closure glaucoma Anterior uveitis Scleritis Keratitis Corneal abrasions or ulceration Foreign body Traumatic or chemical injury
98
Causes of an acute painless red eye include:
Conjunctivitis Episcleritis Subconjunctival haemorrhage
99
What is anterior uveitis?
important ddx for a red eye inflammation of the anterior portion of the uvea - iris and ciliary body associated with HLA-B27 autoimmune process usually causes it, but it can be due to infection, trauma, ischaemia or malignancy
100
How does anterior uveitis typically present?
acutely painful red eye excessive lacrimation photophobia (due to ciliary muscle spasm) reduced visual acuity small pupil
101
What may you find on examination 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)
102
What conditions are associated with anterior uveitis?
HLA-B27 linked conditions: ankylosing spondylitis reactive arthritis ulcerative colitis, Crohn's disease Behcet's disease sarcoidosis: bilateral disease may be seen
103
How may anterior uveitis be managed?
urgent review by ophthalmology cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate steroid eye drops
104
What is episcleritis?
acute onset of inflammation in the episclera of one or both eyes The majority of cases are idiopathic, associated conditions include: inflammatory bowel disease rheumatoid arthritis
105
How does episcleritis typically present?
red eye classically not painful (in comparison to scleritis), but mild pain/irritation is common watering and mild photophobia may be present Dilated episcleral vessels
106
How can you differentiate between episcleritis and scleritis?
in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera in scleritis, vessels are deeper, hence do not move phenylephrine drops may also be used to differentiate: phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made
107
How can episcleritis be managed?
analgesia (e.g., ibuprofen) and lubricating eye drops More severe cases may be treated with steroid eye drops.
108
What is scleritis?
inflammation of the sclera most severe type of scleritis is called necrotising scleritis, which can lead to perforation of the sclera
109
What can cause scleritis?
Most cases are idiopathic Can be associated with an underlying systemic inflammatory condition: RA (most common) SLE sarcoidosis vasculitis, particularly granulomatosis with polyangiitis Less commonly, it can be due to infection (e.g., Pseudomonas or Staphylococcus aureus)
110
How does scleritis present?
Red, inflamed sclera with congested vessels Severe pain (typically a boring pain) Pain with eye movement Photophobia Reduced visual acuity Epiphora (excessive tear production) Tenderness to palpation of the eye
111
How may scleritis be managed?
same-day assessment by an ophthalmologist oral NSAIDs are typically used first-line oral glucocorticoids may be used for more severe presentations immunosuppressive drugs for resistant cases

Y4 Neuro and Special Senses (21 decks)

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