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Module 3C - Neuro / Ophthal > OPHTHAL - clinical > Flashcards

OPHTHAL - clinical Flashcards

1
Q

What is glaucoma?

A

Optic nerve damage caused by raised intraocular pressure due to blocked aqueous humour drainage
.
There are two types:
- Open-angle glaucoma
- Acute angle-closure glaucoma

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2
Q

What fills the vitreous chamber of the eye + what is the function of this?

A

Vitreous humour - provides nutrients to your eye and helps your eye keep its shape, it sticks to your retina at the back of your eye and lets light in

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3
Q

Vitreous humour VS Aqueous humour

A
  • Vitreous humour (lies behind lens) - maintains shape of eye, not continuously replaced
  • Aqueous humour (lies in front of lens) - provides nutrients to cornea and lens, continuously produced by ciliary body and drains via trabecular meshwork
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4
Q

Where is aqueous humour located?

A

In the anterior chamber (between the cornea and iris) and posterior chamber (between the lens and iris).

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5
Q

What is the function of aqueous humour?

A

Supplies nutrients to the cornea.

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6
Q

Where is aqueous humour produced and how does it drain?

A

Produced by the ciliary body –> flows from posterior to anterior chamber (around iris) –> drains via trabecular meshwork into the canal of Schlemm (at angle between cornea and iris) –> enters circulation

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7
Q

What is the normal intraocular pressure (IOP)?

A

10-21 mmHg

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8
Q

What causes open-angle glaucoma?

A

A gradual increase in resistance to aqueous humour outflow through the trabecular meshwork, leading to a slow rise in IO

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9
Q

What is the difference between open-angle and acute angle-closure glaucoma?

A
  • Open-angle –> gradual increase in IOP
  • Acute angle-closure –> sudden blockage of the trabecular meshwork (iris bulges forward), leading to rapid IOP rise
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10
Q

What is optic disc cupping?

A

Increased intraocular pressure causes widening and deepening of the optic cup (indent in centre of optic disc) –> leading to a cup-to-disc ratio > 0.5

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11
Q

What are key risk factors for open-angle glaucoma?

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Myopia (nearsightedness) - myopic eyes are larger than normal, which can make the optic nerve more vulnerable
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12
Q

Why is open-angle glaucoma often diagnosed late?

A

The rise in IOP may be asymptomatic for a long time and is often diagnosed on routine eye testing

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13
Q

What is the main visual symptom of open-angle glaucoma + what are some other possible symptoms?

A

Peripheral vision loss (tunnel vision)
.
Other symptoms:
- Fluctuating pain
- Headaches
- Blurred vision
- Halos around lights (particularly at night)

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14
Q

What is non-contact tonometry?

A

A screening test that estimates IOP by shooting a puff of air at the cornea and measures corneal response

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15
Q

What is the gold-standard test for IOP measurement?

A

Goldmann applanation tonometry

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16
Q

What investigations confirm open-angle glaucoma?

A
  • Goldmann applanation tonometry - IOP measurement
  • Slit lamp examination - cup-to-disc ratio + optic nerve health
  • Visual field assessment - peripheral vision loss
  • Gonioscopy - assess the angle between the iris and cornea (drainage angle)
  • Central corneal thickness assessment - can affect IOP readings (thicker –> falsely high IOP) + thinner cornea is risk factor for glaucoma
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17
Q

At what IOP level is treatment typically started?

A

24 mmHg or higher

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18
Q

What is the first-line treatment for open-angle glaucoma?

A

360° selective laser trabeculoplasty (SLT) - a laser procedure that improves drainage

(basically works by acting on trabecular meshwork to improve drainage of aqueous humour)

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19
Q

What is the first-line medical treatment for open-angle glaucoma?

A

Prostaglandin analogue eye drops (e.g., latanoprost) - increase uveoscleral outflow

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20
Q

What are side effects of prostaglandin analogues (eg. latanoprost)?

A
  • Eyelash growth
  • Eyelid pigmentation
  • Iris pigmentation (browning)
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21
Q

Other than prostaglandin analogues (eg. latanoprost), what are other eye drop options for open-angle glaucoma?

A
  • Beta-blockers (e.g., timolol) - reduce aqueous humour production
  • Carbonic anhydrase inhibitors (e.g., dorzolamide) - reduce aqueous humour production
  • Sympathomimetics (e.g., brimonidine) - reduce aqueous humour production and increase uveoscleral outflow
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22
Q

What surgical option is available if medications and laser therapy fail in the treatment of open-angle glaucoma?

A

Trabeculectomy - creates a new drainage channel from anterior chamber, through sclera, under conjunctiva, here it drains into general circulation

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23
Q

Why is it important to check if glaucoma patients have asthma?

A

One of the IOP lowering medications used in the management of glaucoma is timolol (topical beta-blocker) –> can cause bronchoconstriction or reduce effectiveness of salbutamol

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24
Q

What is the pathophysiology of acute angle-closure glaucoma?

A
  • The iris bulges forward, sealing off the trabecular meshwork from the anterior chamber, preventing aqueous humour drainage –> this causes intraocular pressure to rise
  • the pressure builds in the posterior chamber, pushing the iris forward and exacerbating the angle closure
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25
Q

Why is acute angle-closure glaucoma an ophthalmological emergency?

A

It requires rapid treatment to prevent permanent vision loss due to sustained high intraocular pressure damaging the optic nerve

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26
Q

What are the risk factors for acute angle-closure glaucoma?

A
  • Increasing age
  • Family history
  • Female sex (4× more likely than males)
  • Chinese & East Asian ethnic origin
  • Shallow anterior chamber
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27
Q

How do the risk factors for open-angle and angle-closure glaucoma differ in relation to ethnic origin?

A
  • Open-angle glaucoma is more common in Black individuals, whereas angle-closure glaucoma is rare in this group and more common in Chinese and East Asian populations

(Ethnic origin is an important risk factor to consider in exam questions)

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28
Q

Which medications can precipitate acute angle-closure glaucoma?

A
  • Adrenergic medications (e.g., noradrenaline) - causes mydriasis (blocks outflow of aqueous humour), ciliary muscle relaxation (can cause anterior displacement of lens-iris diaphragm), and increased aqueous humour production (but it cannot drain properly)
  • Anticholinergic medications (e.g., oxybutynin and solifenacin) - causes mydriasis (pupil dilation), which can lead to pupillary block, and closure of the iridocorneal angle
  • Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects - causes mydriasis (pupil dilation), which can lead to pupillary block, and closure of the iridocorneal angle
    .
    (particularly an issue in people with anatomically narrow iridocorneal angles as they are more vulnerable)
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29
Q

What are the typical symptoms of acute angle-closure glaucoma + what are the key examination findings?

A

Typical symptoms:
- Severely painful red eye
- Blurred vision
- Halos around lights
- Associated headache, nausea and vomiting
.
Signs O/E:
- Red eye
- Hazy cornea
- Decreased visual acuity
- Fixed, dilated pupil
- Hard eyeball on gentle palpation

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30
Q

What are the immediate management steps for acute angle-closure glaucoma?

A
  • Lay patient on their back without a pillow
  • Pilocarpine eye drops (2% for blue eyes, 4% for brown eyes)
  • Acetazolamide 500 mg orally
  • Analgesia and antiemetics as needed
  • Urgent ophthalmology admission
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31
Q

What is the mechanism of action of pilocarpine in acute angle-closure glaucoma?

A
  • It is a miotic agent (constricts the pupil) –> acts on muscarinic receptors in the sphincter muscles in the iris
  • it also causes ciliary muscle contraction
    .
    These two effects open up the drainage pathway for aqueous humour
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32
Q

What is the mechanism of action of acetazolamide in acute angle-closure glaucoma?

A

It is a carbonic anhydrase inhibitor –> reduces aqueous humour production

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33
Q

What are the key secondary care treatments for acute angle-closure glaucoma?

A
  • Pilocarpine eye drops
  • Acetazolamide (oral/IV)
  • Hyperosmotic agents (e.g. IV mannitol) - increase osmotic gradient between blood and eye
  • Timolol (beta-blocker) - reduces aqueous humour production
  • Dorzolamide (carbonic anhydrase inhibitor) - reduces aqueous humour production
  • Brimonidine (sympathomimetic) - reduces aqueous humour production and increases uveoscleral outflow
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34
Q

What is the definitive treatment for acute angle-closure glaucoma?

A

Laser iridotomy - laser creates hole in iris, allowing aqueous humour to flow directly from posterior chamber to anterior chamber, this relieves the pressure pushing iris forward against the cornea and opens up the pathway for the aqueous humour to drain

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35
Q

Why is glaucoma symptoms worse in low night (evening/night)?

A

Due to dilation of the pupils, which further reduces the iridocorneal angle –> worsening symptoms

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36
Q

What is age-related macular degeneration (AMD)?

A

A progressive condition affecting the macula –> it is the most common cause of blindness in the UK

  • Often unilateral, but can be bilateral
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37
Q

What are the two types of AMD, and how common are they?

A
  • Dry (non-neovascular) AMD - 90% of cases
  • Wet (neovascular) AMD - 10% of cases
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38
Q

What is the function of the macula, and what are its four layers?

A

The macula is responsible for high-definition colour vision in the central visual field.
.
Its four layers are:
- Choroid layer (at the base) - contains the blood vessels that supply the macula
- Bruch’s membrane
- Retinal pigment epithelium
- Photoreceptors

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39
Q

What are drusen, and how are they related to AMD + what are two other features that are common to both wet and dry AMD?

A

Drusen are yellowish deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane

  • a few small Drusen is normal in older patients, but frequent and larger drusen can be an early sign of macular degeneration
    .
    Other features:
  • Atrophy of retinal pigment epithelium
  • Degeneration of the photoreceptors
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40
Q

What is the key pathological difference between wet and dry AMD?

A

Wet AMD is characterised by neovascularisation from the choroid layer (blood vessels grow into retina)

  • these vessels can leak fluid or blood, causing oedema and faster vision loss
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41
Q

What stimulates neovascularisation in wet AMD, and what is its treatment target?

A

Vascular endothelial growth factor (VEGF) stimulates neovascularisation in wet AMD

  • Anti-VEGF medications target this factor to slow disease progression
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42
Q

What are the risk factors for AMD?

A
  • Older age
  • Smoking
  • Family history
  • Cardiovascular disease (e.g., hypertension)
  • Obesity
  • Poor diet (low in vitamins and high in fat)
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43
Q

How does AMD typically present?

A
  • Gradual loss of central vision
  • Reduced visual acuity
  • Metamorphopsia (wavy or crooked appearance of straight lines)
  • Difficulty reading small text
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44
Q

How does wet AMD differ in its presentation/progression compared to dry AMD?

A

Wet AMD presents more acutely than dry AMD, with vision loss developing over days and potentially leading to complete blindness within 2-3 years

  • often progresses to bilateral disease
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45
Q

How can you differentiate glaucoma from AMD based on vision changes in an exam question?

A
  • Glaucoma –> Peripheral vision loss + Halos around lights
  • AMD –> Central vision loss + Wavy appearance of straight lines (metamorphopsia)
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46
Q

What examination findings are seen in AMD?

A
  • Reduced visual acuity - using a Snellen chart
  • Scotoma (an enlarged central area of vision loss)
  • Amsler grid test - shows distortion of straight lines (metamorphosis)
  • Drusen - on fundoscopy
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47
Q

What investigations are used to diagnose AMD?

A
  • Slit lamp examination - gives detailed view of retina and macula
  • Optical coherence tomography (OCT) - gives cross-sectional view of layers of retina, can be used to diagnose AND monitor AMD
  • Fluorescein angiography (fluorescein contrast given and retina is photographed to assess blood supply) - identifies oedema and neovascularization in wet AMD
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48
Q

What is the management of dry AMD?

A
  • No specific treatment available
  • Lifestyle modifications - avoid smoking, control BP, consider vitamin supplementation to slow progression
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49
Q

What is the management of wet AMD?

A

Anti-VEGF injections (e.g., ranibizumab, aflibercept, bevacizumab) –> block VEGF and slow development of new vessels
.
(they are injected directly into the vitreous chamber (intravitreal), usually once a month)

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50
Q

What is diabetic retinopathy?

A

damage to the retinal blood vessels due to prolonged high blood sugar levels

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51
Q

What are the key pathological changes in diabetic retinopathy?

A
  • Hyperglycaemia –> damages retinal blood vessels + endothelial cells
  • Increased vascular permeability (leaking blood vessels) –> blot hemorrhages + hard exudates
  • Blood vessel wall damage –> microaneurysms + venous beading
  • Damage to nerve fibres in retina –> cotton wool spots (fluffy, white patches on retina)
  • Intraretinal microvascular abnormalities (IRMA) –> dilated and torturous capillaries in the retina
  • Neovascularisation –> growth of new blood vessels, due to release of growth factors in the retina
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52
Q

What is the key distinction between non-proliferative (background and pre-proliferative) and proliferative diabetic retinopathy?

A

Neovascularisation (new blood vessel formation) is the key feature of proliferative diabetic retinopathy

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53
Q

How is diabetic retinopathy graded?

A
  • Background - microaneurysms, retinal haemorrhages, hard exudates , and cotton wool spots
  • Pre-proliferative - venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA)
  • Proliferative - neovascularisation, vitreous haemorrhage
    .
    Diabetic maculopathy exists separately and involves:
  • exudates within the macula
  • macular oedema
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54
Q

What are the differences between drusen and hard exudates?

A
  • Drusen –> yellow deposits of proteins and lipids, located between retinal pigment epithelium and Bruch’s membrane (seen in AMD)
    .
  • Hard exudates –> yellow-white deposits of lipids and proteins, located in the retinal layers due to leaky blood vessels (seen in diabetic retinopathy
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55
Q

What are the complications of diabetic retinopathy?

A
  • Vision loss
  • Retinal detachment
  • Vitreous haemorrhage (bleeding into the vitreous humour)
  • Rubeosis iridis (new blood vessel formation in the iris) –> can lead to neovascular glaucoma
  • Optic neuropathy
  • Cataracts
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56
Q

How is diabetic retinopathy managed?

A

Non-proliferative –> close monitoring and strict diabetic control
.
Proliferative:
- Pan-retinal photocoagulation (PRP) –> laser treatment across the retina to suppress new vessels

  • Intravitreal anti-VEGF injections
  • Surgery (e.g. vitrectomy) - for severe cases
    .
    Macular oedema –> intravitreal dexamethasone implant
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57
Q

What is one of the main reasons to perform cataract surgery in diabetic patients?

A

To be able to see the retina on fundoscopy more clearly and therefore monitor diabetic retinopathy changes (cataracts obscure fundoscopy view)

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58
Q

What is hypertensive retinopathy?

A

Damage to the retinal blood vessels due to hypertension, which can develop slowly with chronic hypertension or rapidly in malignant hypertension

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59
Q

What are the key features of hypertensive retinopathy?

A
  • Silver wiring/copper wiring - walls of arterioles become thickened and sclerosed reflecting more light O/E
  • Arteriovenous (AV) nipping - arterioles compress veins at crossings (due to sclerosis and hardening of arterioles)
  • Cotton wool spots - caused by ischaemia and infarction of retina, causing damage to nerve fibres
  • Hard exudates - caused by damaged vessels leaking lipids onto retina
  • Retinal haemorrhages - caused by damaged vessels rupturing and releasing blood in the retina (dot/blot occur deeper, flame haemorrhages occur in nerve fibre layer)
  • Papilloedema - caused by ischaemia of optic nerve, resulting in optic nerve swelling (oedema)
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60
Q

What are the stages of the Keith-Wagener classification for hypertensive retinopathy?

A
  • Stage 1: Mild narrowing of arterioles
  • Stage 2: Focal constriction of blood vessels and AV nipping
  • Stage 3: Cotton-wool spots, haemorrhages, and exudates
  • Stage 4: Papilloedema (malignant hypertension)
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61
Q

What is the mainstay of management for hypertensive retinopathy?

A

BP control and management of CVD risk factors (eg. smoking cessation and lipid control)

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62
Q

What are cataracts?

A

A progressively opaque lens that reduces the light entering the eye and visual acuity

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63
Q

What is the role of the lens in the eye?

A

To focus light on the retina - it is held in place by the suspensory ligaments attached to the ciliary body, which changes its shape to adjust focus
.
(note: the lens has no blood supply and is nourished by the aqueous humour)

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64
Q

How does the ciliary body affect the lens?

A
  • Contracts –> suspensory ligaments loosen –> lens thickens (near vision).
  • Relaxes –> suspensory ligaments tighten –> lens narrows (distance vision)
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65
Q

What is tested during the neonatal examination to screen for congenital cataracts?

A

The red reflex

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66
Q

What are the risk factors for cataracts?

A
  • Increasing age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypocalcaemia
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67
Q

What are the key symptoms of cataracts?

A

Symptoms are usually asymmetrical:
- 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)

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68
Q

What is a key examination finding in cataracts?

A

Loss of the red reflex, with the lens also appearing grey/white on ophthalmoscopy

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69
Q

How are cataracts managed?

A
  • No intervention if symptoms are manageable
    .
    Cataract surgery (day case with good results):
  • Breaking up and removing the lens
  • Implanting an artificial lens
    .
    (note: cataracts can prevent the detection of other pathology (eg. AMD or diabetic retinopathy), which can become apparent after surgery if the patient still has visual symptoms)
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70
Q

What is a rare but serious complication of cataract surgery?

A

Endophthalmitis - inflammation of inner eye, usually caused by infections, can lead to vision loss

  • Treated with intravitreal antibiotics injected directly into the eye
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71
Q

What are the 3 types of cataracts?

A
  • Nuclear - affects central nucleus of lens
  • Posterior subcapsular - affects back surface of lens
  • Cortical - affects outer edge (cortex) of lens
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72
Q

Why should all children with cataracts be urgently referred?

A

To rule out a tumour - commonly associated with retinoblastoma

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73
Q

Name of this sign and what is the most serious cause?

A

Leukocoria (aka. white pupillary reflex) - retinoblastoma (malignant tumour of retina)
.
(congenital cataract is also a cause)

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74
Q

Which muscles are responsible for pupil constriction, and what is their innervation?

A

Circular muscles in the iris (sphincter pupillae), innervated by the parasympathetic nervous system, using acetylcholine as a neurotransmitter

  • parasympathetic fibres travel along the oculomotor nerve (CN III)
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75
Q

What are five causes of an irregular pupil shape?

A
  • Trauma to the sphincter muscles in the iris –> e.g. during cataract surgery
  • Anterior uveitis –> can cause adhesions (scar tissue) in the iris
  • Acute angle-closure glaucoma –> can cause ischaemic damage to muscles of iris (usually a vertical oval)
  • Rubeosis iridis –> neovascularisation in the iris (usually due to poorly controlled diabetes and diabetic retinopathy)
  • Coloboma –> congenital hole in the iris + irregular pupil shape
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76
Q

Which muscles are responsible for pupil dilation, and what is their innervation?

A

Dilator muscles in the iris (dilator pupillae), innervated by the sympathetic nervous system, using adrenalin as a neurotransmitter

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77
Q

What is tadpole pupil, and what conditions is it associated with?

A

Temporary, misshapen pupil due to muscle spasm in part of the dilator muscle

  • may be associated with migraines and Horner syndrome
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78
Q

List causes of mydriasis (dilated pupil)

A
  • Congenital
  • Stimulants (e.g. cocaine)
  • Anticholinergics (e.g. oxybutynin)
  • Trauma
  • Third nerve palsy
  • Holmes-Adie syndrome
  • Raised intracranial pressure
  • Acute angle-closure glaucoma
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79
Q

What are the key features of a third nerve (oculomotor) palsy?

A
  • Ptosis (drooping upper eyelid) - due to paralysis of the levator palpebrae superioris

-Dilated non-reactive pupil - due to paralysis of sphincter pupillae

  • Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye - due to unopposed lateral rectus and superior oblique
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80
Q

List causes of miosis (constricted pupil)

A
  • Horner syndrome
  • Cluster headaches
  • Argyll-Robertson pupil (neurosyphilis)
  • Opiates
  • Nicotine
  • Pilocarpine
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81
Q

What is the difference between pupil-sparing and pupil-involving third nerve palsy?

A

Pupil-sparing –> suggests a microvascular cause:
- diabetes
- hypertension
- ischaemia
.
Pupil-involving –> suggests nerve compression:
- tumour
- trauma
- cavernous sinus thrombosis
- posterior communicating artery aneurysm
- raised ICP
.
(pupillary fibres are located at the periphery of the nerve, microvascular causes lead to infarct of central nerve fibres first)

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82
Q

How does the course of the oculomotor nerve (CN III) make it vulnerable to compression, particularly in relation to the posterior communicating artery (PCOM)?

A
  • The oculomotor nerve (CN III) travels directly from the brainstem to the eye in a straight line
  • it passes through the cavernous sinus and runs close to the posterior communicating artery (PCOM) –> making it susceptible to compression from cavernous sinus thrombosis or a PCOM aneurysm
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83
Q

What is the classic triad of Horner syndrome + what additional sign may be present?

A
  • Ptosis (drooping eyelid)
  • Miosis (constricted pupil)
  • Anhidrosis (loss of sweating)
    .
    (enopthalmos (sunken eye) may be present, light/accommodation reflexes are not affected)
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84
Q

What causes Horner syndrome?

A

Damage to the sympathetic nervous system supplying the face

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85
Q

Describe the sympathetic nerve pathway involved in Horner syndrome

A

First order neurons (central neurons):
- originate in hypothalamus
- descend through brainstem to spinal cord (C8-T2)
.
Second-order neurons (pre-ganglionic neurons):
- exit spinal cord and travel to superior cervical ganglion
- pass through apex of lung

(note: sympathetic chain runs along each side of the spinal cord)
.
Third-order neurons (post-ganglionic neurons):
- travel from superior cervical ganglion along internal carotid artery to the eye

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86
Q

How does the location of a lesion in Horner syndrome affect anhidrosis (loss of sweating)?

A
  • Central (first-order) lesions –> anhidrosis of the arm, trunk, and face
  • Pre-ganglionic (second-order) lesions –> anhidrosis of the face
  • Post-ganglionic (third-order) lesions –> no anhidrosis (due to the sweat gland fibres have already branched off with the external carotid artery before the lesion occur)
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87
Q

The causes of Horner syndrome can be split into central, pre-ganglionic, and post-ganglionic, name some causes for each.

A

Central lesions (4Ss):
- S - Stroke
- S - Multiple Sclerosis
- S - Swelling (tumours)
- S - Synringomyelia (cyst in spinal cord)
.
Pre-ganglionic (4Ts):
- T - Tumour (Pancoast tumour)
- T - Trauma
- T - Thyroidectomy
- T - Top rib (a cervical rib growing above first rib and clavicle)
.
Post-ganglionic (4Cs):
- C - Carotid aneurysm
- C - Carotid artery dissection
- C - Cavernous sinus thrombosis
- C - Cluster headache

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88
Q

What is congenital Horner syndrome associated with?

A

Heterochromia (difference in iris colour on the affected side)

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89
Q

How can Horner syndrome be tested pharmacologically?

A
  • Cocaine eye drops –> normal pupil dilates, Horner pupil does not

. In Horner syndrome, the nerves are not releasing noradrenaline, so blocking re-uptake makes no difference, and there is no pupil change)
.
- Low-dose adrenaline (0.1%) –> dilates Horner pupil, but not normal pupil

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90
Q

What is the mechanism of the cocaine eye drop test in Horner’s syndrome?

A
  • Cocaine blocks the reuptake of noradrenaline (or norepinephrine) at the NMJ, which leads to increased noradrenaline in the synaptic cleft, and consequently pupil dilation (noradrenaline stimulates dilator muscles of the iris)
    .
  • Normal pupil –> pupil dilates
  • Horner pupil –> pupil does not dilate effectively (sympathetic pathway is impaired, preventing normal adrenergic response)
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91
Q

What is the mechanism of the low-dose adrenaline (0.1%) eye drop test in Horner’s syndrome?

(note: apraclonidine can be used as an alternative to adrenaline)

A
  • Adrenaline (epinephrine) is a sympathomimetic drug that normally causes pupil dilation (mydriasis) by stimulating alpha-1 adrenergic receptors on the iris dilator muscle
  • In Horner syndrome, due to disruption of the sympathetic pathway, the affected pupil becomes hypersensitive to adrenergic stimuli, this occurs because of upregulatoin of alpha-1 receptors (denervation hypersensitivity) on the dilator muscle
  • When a low dose (0.1%) of adrenaline is applied to the eye, the pupil in someone with Horner syndrome will show a dilation response due to this hypersensitivity (however, a normal pupil with normal sensitivity will not dilate with such a low dose)
    .
    (note: post-ganglionic lesions will show the most prominent response)
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92
Q

What is the characteristic feature of a Holmes-Adie pupil?

A
  • Dilated pupil
  • Sluggish light response
  • Normal accommodation response
  • Slow redilation after constriction (“tonic” pupil)
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93
Q

What syndrome is associated with a Holmes-Adie pupil?

A

Holmes-Adie syndrome, which also features absent ankle and knee reflexes.

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94
Q

What condition is associated with an Argyll-Robertson pupil?

A

Neurosyphilis - commonly called a “prostitute’s pupil” due to its relation to neurosyphilis and because “it accommodates but does not react”

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95
Q

How does an Argyll-Robertson pupil behave?

A
  • Constricted pupil
  • Accommodates on near object, but does not react to light (“prostitute’s pupil”)
  • Irregularly shaped
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96
Q

What is blepharitis, and what are its symptoms?

A

Blepharitis is inflammation of the eyelid margins, causing a gritty, itchy, dry sensation in the eyes

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97
Q

What gland dysfunction is associated with blepharitis?

A

Dysfunction of the Meibomian glands (which secrete meibum (oil) onto the surface of the eye)

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98
Q

What complications can arise from blepharitis?

A

Styes and chalazions

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99
Q

How is blepharitis managed?

A

Warm compresses and gentle cleaning of the eyelid margins to remove debris - e.g. with a cotton bud and baby shampoo

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100
Q

What is a hordeolum internum?

A

A stye that results from infection of the Meibomian glands, which are deeper and often more painful

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101
Q

What is a stye (hordeolum externum)?

A

An infection of the glands of Zeis (sebaceous glands) or glands of Moll (sweat glands) at the base of the eyelashes, presenting as a tender, red lump

102
Q

What is a chalazion?

A

A blocked and swollen Meibomian gland, also called a Meibomian cyst

103
Q

How are styes treated?

A
  1. Warm compresses and analgesia
  2. Topical antibiotics (e.g., chloramphenicol) may be considered if conjunctivitis is present or symptoms persist
104
Q

How is a chalazion treated?

A

Warm compresses and gentle massage towards the eyelashes to encourage drainage

(rarely, surgical drainage may be required)

105
Q

How does a chalazion present?

A

A swelling in the eyelid that is usually not tender, but can occasionally be red and painful

106
Q

What is entropion?

A

Inward turning of the eyelid, causing the lashes to press against the eye

107
Q

What complications can arise from entropion?

A

Corneal damage and ulceration

108
Q

How is entropion managed?

A
  1. Initial management involves taping the eyelid down (to prevent it from turning inwards)
  2. Definitive treatment is surgical –> same-day referral to ophthalmology is required if there is a risk to sight
109
Q

What must be used when taping the eyelid in entropion?

A

Lubricating eye drops to prevent the eye from drying out

110
Q

What is ectropion?

A

Outward turning of the eyelid, exposing the inner surface

111
Q

What complications can arise from ectropion?

A

Exposure keratopathy - as the eyeball is inadequately lubricated and protected

112
Q

How is ectropion managed?

A
  • Mild cases –> regular lubricating eye drops
  • Severe cases –> surgical correction

(note: same-day ophthalmology referral if there is a risk to sight)

113
Q

What is trichiasis?

A

Inward growth of the eyelashes

114
Q

What are the risks of trichiasis?

A

Pain, corneal damage, and ulceration

115
Q

How is trichiasis managed?

A
  • Removal of affected eyelashes
  • Recurrent cases may need electrolysis, cryotherapy, or laser treatment (to prevent eyelashes from regrowing)

(same-day ophthalmology referral if there is a risk to sight)

116
Q

What is periorbital cellulitis (preseptal cellulitis)?

A

An infection of the eyelid and skin in front of the orbital septum (anterior to orbital septum)

117
Q

How does periorbital cellulitis present?

A

Swollen, red, hot skin around the eyelid and eye

(no visual changes/eye pain)

118
Q

Why is it important to differentiate periorbital from orbital cellulitis?

A

Orbital cellulitis is a sight- and life-threatening emergency

(CT scan can help distinguish them)

119
Q

How is periorbital cellulitis managed?

A
  • Urgent ophthalmology referral
  • Systemic antibiotics (oral or IV)
  • Severe cases or vulnerable patients (e.g., children) may require admission - due to risk of developing into orbital cellulitis
120
Q

What is orbital cellulitis?

A

An infection behind the orbital septum (posterior to orbital septum) affecting the tissues around the eye

121
Q

How does orbital cellulitis present?

A

Similar appearance to periorbital cellulitis, but with additional symptoms:
- Pain with eye movement
- Reduced eye movements
- Vision changes
- Abnormal pupil reactions
- Proptosis (bulging eye)

122
Q

How is orbital cellulitis treated?

A
  • Emergency admission under ophthalmology
  • IV antibiotics
  • Surgical drainage if an abscess forms
123
Q

What is conjunctivitis (“pink eye”)?

A

Inflammation of the conjunctiva, the thin tissue covering the inside of the eyelids and the sclera

  • can be bacterial, viral, or allergic
  • can be unilateral or bilateral
    .
    (conjunctiva protects and lubricates the eye)
124
Q

What are the main symptoms of conjunctivitis + negative symptoms

A
  • Red, bloodshot eye
  • Itchy or gritty sensation
  • Discharge
    .
    There is NO pain, photophobia, or reduced visual acuity
    .
    (discharge covering the eye may cause blurry vision, but this should return to normal when the discharge is cleared)
125
Q

How does bacterial conjunctivitis present?

A
  • Purulent discharge
  • Worse in the morning (eyes stuck together)
  • Typically starts in one eye and spreads to the other (highly contagious)
126
Q

How does viral conjunctivitis present?

A
  • Clear discharge
  • Associated with viral symptoms (dry cough, sore throat, blocked nose)
  • Tender pre-auricular lymph nodes
    .
    (viral conjunctivitis is also contagious)
127
Q

What are causes of an acute painful red eye?

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
    -Keratitis
  • Foreign body
  • Traumatic or chemical injury
128
Q

What are causes of an acute painless red eye?

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
129
Q

What red eye conditions require same-day emergency referral to ophthalmology?

(ie. not specific conditions, but symptoms)

A

Conditions that cause pain or reduced visual acuity

130
Q

Does conjunctivitis usually require treatment?

A

No, it usually resolves in 1–2 weeks without treatment (even bacterial cases)

131
Q

What hygiene measures help prevent the spread of conjunctivitis?

A
  • Avoid sharing towels
  • Avoid close contact
  • Regular hand washing
  • Clean the eyes with cooled boiled water and cotton wool (can help clear the discharge)
132
Q

What treatment options exist for bacterial conjunctivitis if necessary?

A

Chloramphenicol or fusidic acid eye drops

133
Q

Why do neonates with conjunctivitis need urgent ophthalmology assessment?

A

It could be gonococcal conjunctivitis, which can cause permanent vision loss

134
Q

Allergic conjunctivitis is caused by contact with allergens, how does alergic conjunctivitis present?

A
  • Swelling of the conjunctival sac and eyelid
  • Itching
  • Watery discharge
135
Q

What treatments are used for allergic conjunctivitis?

A
  1. Antihistamines (oral or topical)
  2. Topical mast-cell stabilisers (for chronic seasonal symptoms) - work by preventing mast cells from releasing histamine
136
Q

What is anterior uveitis?

A

Inflammation of the anterior uvea - which includes the iris, ciliary body, and choroid

137
Q

What part of the eye is affected in anterior uveitis?

A

The anterior chamber - where inflammatory cells (neutrophils, lymphocytes, macrophages) accumulate

138
Q

What is hypopyon?

A

A fluid collection of inflammatory cells seen at the bottom of the anterior chamber

139
Q

What is the most common cause of anterior uveitis + name some other factors that can cause anterior uveitis

A

Autoimmune disease
.
Other factors - infection, trauma, ischaemia, or malignancy

140
Q

What autoimmune conditions are associated with anterior uveitis?

A
  • Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis) - HLA-B27 associated
  • Inflammatory bowel disease
  • Sarcoidosis
  • Behçet’s disease
141
Q

What clinical signs may be seen in anterior uveitis?

A
  • Ciliary flush - ring of red spreading from the cornea outwards
  • Miosis - 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
142
Q

What are the symptoms of anterior uveitis?

A
  • Painful red eye (dull, aching pain)
  • Reduced visual acuity
  • Photophobia (due to ciliary muscle spasm)
  • Excessive lacrimation (tear production)
143
Q

What is the initial management + first-line treatments for anterior uveitis?

A
  • Urgent referral to ophthalmology
    .
    1. Steroids (eye drops, oral, or IV)
  1. Cycloplegics (e.g., cyclopentolate, atropine) - dilate pupil and reduce pain by paralysing the ciliary muscles (reducing ciliary spasm)
144
Q

What do cycloplegics (eg. cyclopentolate or atropine eye drops) do in the management of anterior uveitis?

A

They dilate the pupil and reduce pain by paralysing the ciliary muscles (reducing ciliary spasm)

  • cyclopentolate and atropine are antimuscarinic drugs that reduce the action of the iris sphincter muscles and ciliary muscles
145
Q

What treatments may be needed for recurrent anterior uveitis?

A

DMARDs or anti-TNF medications

146
Q

What is episcleritis?

A

Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera beneath the conjunctiva

147
Q

What is episcleritis often associated with?

A

Inflammatory disorders –> RA, inflammatory bowel disease

(it is not usually caused by an infection)

148
Q

What symptoms are not present in episcleritis that help distinguish it from scleritis?

A
  • No photophobia
  • No discharge
  • Normal visual acuity
149
Q

What are the typical features of episcleritis?

A

Acute-onset unilateral features:

  • Localised or diffuse redness (often in the lateral sclera)
  • No pain (or mild pain)
  • Dilated episcleral vessels
150
Q

What test helps differentiate episcleritis from scleritis?

A

Phenylephrine eye drop test –> causes blanching of episcleral vessels (redness disappears in episcleritis but remains in scleritis)

151
Q

What is the typical management of episcleritis?

A
  • Self-limiting –> usually resolves in 1-2 weeks
  • Mild cases –> no treatment needed
  • Symptom relief –> analgesia (e.g. ibuprofen) and lubricating eye drops
  • Severe cases –> may require steroid eye drops
152
Q

What is scleritis?

A

Inflammation of the sclera, the outer connective tissue layer surrounding most of the eye (excluding the cornea)

  • it forms the visible white part of the eye
153
Q

What is the most severe type of scleritis?

A

Necrotising scleritis –> can lead to perforation of the sclera

(perforation of sclera can lead to infection, vision loss (due to damage to cornea or retina), and sometimes loss of the eye)

154
Q

What are the most common causes of scleritis + are men or women more affected?

A
  1. Idiopathic (no clear cause)
  2. Underlying systemic inflammatory conditions
  3. Less commonly, infection (e.g., Pseudomonas or Staphylococcus aureus)
    .
    - more common in women
155
Q

There is an associated systemic condition in around 50% of patients with scleritis, what systemic conditions are associated with scleritis?

A
  • Rheumatoid arthritis
  • Vasculitis (particularly granulomatosis with polyangiitis)
156
Q

Why is scleritis associated with rheumatoid arthritis?

A

The connective tissue of the sclera is similar to joint connective tissue, so it may be affected by rheumatoid arthritis

157
Q

How do the conditions associated with scleritis differ from those associated with anterior uveitis?

A
  • Scleritis –> associated with rheumatoid arthritis & vasculitis
  • Anterior uveitis –> associated with seronegative spondyloarthropathies (e.g. ankylosing spondylitis)
158
Q

What are the key features of scleritis?

A
  • Red, inflamed sclera (localised or diffuse)
  • Congested vessels
  • Severe “boring” pain
  • Pain with eye movement
  • Photophobia
  • Epiphora (excessive tear production)
  • Reduced visual acuity
  • Tenderness to palpation of the eye
159
Q

What are the management steps for scleritis?

A
  • Urgent referral to ophthalmology
  • Screening for an underlying systemic condition (eg. RA or vasculitis)
    .
    Treatments:
  • NSAIDs (oral)
  • Steroids (topical or systemic)
  • Immunosuppression (appropriate to underlying systemic condition) –> eg. methotrexate for RA
160
Q

How is infectious scleritis managed?

A

Antimicrobial treatment appropriate to the infecting organism

161
Q

What is a corneal abrasion?

A

A scratch or damage to the cornea –> causes a red, painful eye and photophobia

162
Q

What are common causes of corneal abrasions?

A
  • Damaged contact lenses
  • Fingernails
  • Foreign bodies (e.g., metal fragments)
  • Tree branches
  • Makeup brushes
  • Entropion (inward-turning eyelid)
163
Q

What is an important differential diagnosis for corneal abrasions?

A

Herpes keratitis, which requires antiviral treatment

164
Q

Why are corneal abrasions associated with contact lenses concerning?

A

They may be associated with Pseudomonas infection, which can cause serious corneal damage

165
Q

What is the immediate management of chemical corneal abrasions (e.g., from acid exposure)?

A
  • Immediate, extensive irrigation
  • Urgent ophthalmology referral - can cause severe damage and vision loss
166
Q

What is the typical history in a patient with a corneal abrasion?

A

A history of trauma followed by:

  • Painful red eye
  • Photophobia
  • Foreign body sensation
  • Epiphora (excessive tear production)
  • Blurred vision
167
Q

ow can corneal abrasions be diagnosed?

A
  • Fluorescein staining - yellow-orange dye collects in abrasions or ulcers, highlighting them
  • Cobalt blue light - used to enhance the fluorescein stain
168
Q

How are uncomplicated corneal abrasions managed?

A

Usually heal over 2-3 days.

  • Foreign body removal (if present)
  • Simple analgesia (eg. paracetamol)
  • Lubricating eye drops
  • Antibiotic eye drops (e.g., chloramphenicol)
  • Close follow-up
169
Q

When should a patient with a corneal abrasion be referred to ophthalmology?

A

If the abrasion is:
- complicated
- not healing
- associated with contact lens use, chemical injury, or infection

170
Q

What are the three types of lubricating eye drops used in corneal abrasions?

  • least viscous
  • medium viscosity
  • most viscous
A
  • Hypromellose drops - least viscous (lasts ~10 min)
  • Polyvinyl alcohol drops - medium viscosity
  • Carbomer drops - most viscous (lasts 30-60 min)
171
Q

How is a corneal foreign body managed?

A
  1. Anaesthesia
  2. Foreign body removal - (irrigation OR needle technique OR Jeweller’s forceps OR Alger brush (if residual rust rings or iron deposits)*
  3. Post-removal care - antibx prophylaxis +/- cycloplegics +/- analgesia +/- tetanus prophylaxis
  4. Pain relief - lubricant drops +/- oral analgesia
  5. Follow-up -24-48hrs post-procedure
172
Q

What is keratitis?

A

Inflammation of the cornea (also referred to as a corneal ulcer)

173
Q

What are the main causes of keratitis?

A
  • 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)
174
Q

What is the main risk factor for bacterial keratitis + which causative organism?

A

Contact lens wearer - due to natural barrier of eye being disrupted (especially if lens hygiene is poor/wear lenses overnight)

  • Pseduomonas aeruginosa
175
Q

What is the most common cause of keratitis?

A

Herpes simplex virus (HSV) infection, also called herpes simplex keratitis

  • most commonly affects epithelial layer of cornea
176
Q

What are the two types of herpes simplex keratitis?

A
  • Primary infection - often mild, may present as blepharoconjunctivitis
  • Recurrent infection - due to reactivation of latent virus in the trigeminal ganglion
177
Q

Where does HSV become latent after primary infection?

A

Trigeminal ganglion

178
Q

What is stromal keratitis and its associated complications?

A

Inflammation of the stromal layer of the cornea (between epithelium and endothelium), leading to:

  • Stromal necrosis
  • Vascularisation
  • Scarring
  • Risk of corneal blindness (due to above)
179
Q

What are the symptoms of primary herpes simplex keratitis?

A

Mild symptoms of blepharoconjunctivitis (inflammation of eyelid margins and conjunctiva)

180
Q

What are the symptoms of recurrent herpes simplex keratitis?

A
  • Painful red eye
  • Photophobia
  • Vesicles (fluid-filled blisters)
  • Foreign body sensation
  • Watery discharge
  • Reduced visual acuity
181
Q

What is the key diagnostic finding of herpes keratitis on fluorescein staining?

A

Dendritic corneal ulcer (branching appearance)

182
Q

What is the initial management step for suspected herpes keratitis + what is the main treatment for herpes keratitis?

A
  • Initial management step –> Urgent opthalmology referral
  • Main treatment –> Topical/oral antivirals (eg. aciclovir or ganciclovir)
183
Q

What topical medication (which is used in the management of some eye conditions) should be avoided in herpes simplex keratitis?

A

Topical steroids –> increases herpes load and worsens condition

(eg. risk of corneal perforation)

184
Q

What test can confirm viral keratitis?

A

Corneal scrapings for viral testing

185
Q

What is the treatment for permanent scarring and vision loss after herpes keratitis?

A

Corneal transplant

186
Q

Most cases of subcnjunctival haemorrhage are idiopathic in otherwise healthy patients, however, several factors may predispose to the condition.
What are some predisposing factors for subconjunctival haemorrhage?

A
  • Hypertension
  • Bleeding disorders (e.g., thrombocytopenia)
  • Whooping cough
  • Medications (e.g., antiplatelets, DOACs or warfarin)
  • Non-accidental injury (NAI)
187
Q

What causes a subconjunctival haemorrhage + name some common triggers for a subconjunctival haemorrhage

A

A small blood vessel within the conjunctiva ruptures, releasing blood into the space between the sclera and conjunctiva
.
Common triggers:
- Strenuous activity (e.g. heavy coughing, weightlifting, straining from constipation)
- Trauma to the eye

188
Q

What does a subconjunctival haemorrhage look like?

A

A bright red patch underneath the conjunctiva, covering the white of the eye

189
Q

What symptoms are associated with a subconjunctival haemorrhage?

A
  • Painless
  • No impact on vision
  • Possible history of precipitating event (e.g., coughing, heavy lifting)
190
Q

How is a subconjunctival haemorrhage diagnosed + what investigations might be necessary for underlying causes?

A

Clinical diagnosis based on history and examination
.
- Check BP - for hypertension
- Check INR - in patients taking Warfarin

191
Q

What is the treatment for subconjunctival haemorrhage?

A

No treatment required –> it resolves spontaneously in ~2 weeks

  • Lubricating eye drops can be used for mild irritation
192
Q

What is posterior vitreous detachment (PVD)?

A

when the vitreous body comes away from the retina

193
Q

Why does posterior vitreous detachment occur with age?

A

The vitreous humour becomes less firm, making it unable to maintain its shape and adhesion to the retina
.
(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)

194
Q

What are the key symptoms of posterior vitreous detachment (PVD)?

A

PVD is painless and may be asymptomatic, but can present with key symptoms such as:
- Floaters
- Flashing lights
- Blurred vision

195
Q

What is the treatment for posterior vitreous detachment?

A

No treatment is needed - symptoms improve as the brain adjusts

196
Q

Why is it important to assess for retinal tears or detachment in patients with posterior vitreous detachment?

A

PVD can predispose patients to these conditions, which can present with flashes, floaters, and vision loss

(a thorough assessment of the retina should be done in these cases)

197
Q

What is retinal detachment?

A

Separation of the neurosensory retina (photoreceptors and nerves) from the retinal pigment epithelium (base layer attached to the choroid)

198
Q

How does a retinal tear lead to retinal detachment?

A

A tear allows vitreous fluid to enter between the neurosensory retina and the retinal pigment epithelium, separating them

199
Q

Why is retinal detachment sight-threatening?

A
  • The neurosensory retina relies on the choroid for its blood supply
  • Detachment can disrupt blood flow, leading to permanent photoreceptor damage
200
Q

What are risk factors for retinal detachment?

A
  • Lattice degeneration (thinning of the retina)
  • Posterior vitreous detachment
  • Trauma
  • Diabetic retinopathy
  • Retinal malignancy
  • Family history
201
Q

What are the key symptoms of retinal detachment?

A

Painless condition, but key symptoms are:
- Peripheral vision loss (described as a shadow coming across the vision)
- Blurred or distorted vision
- Flashes and floaters

202
Q

What should be done if a patient presents with painless flashes and floaters?

A

A detailed retinal assessment to check for retinal tears or detachment –> any suspicion of retinal detachment requires immediate ophthalmology referral

203
Q

What are the treatments for retinal tears?

A

Aims to create adhesions between the retina and the choroid:
- Laser therapy
- Cryotherapy

204
Q

What are the options for reattaching the retina in retinal detachment?

A

(aim is to reattach retina and reduce any traction/pressure that may cause it to detach again)

  1. Vitrectomy - removes vitreous fluid, fixes the tear, and inserts gas or oil to hold the retina in place
  2. Scleral buckle - a silicone band is placed around the eye to push the sclera inward, reconnecting the retina (acts like a corset, squeezing the eye contents together)
  3. Pneumatic retinopexy - a gas bubble is injected into the vitreous body to press the retina back into place (head must be positioned in a specific way for an amount of time to ensure the bubble is pressing the separated layer back into place)
205
Q

What causes retinal vein occlusion?

A
  • Blood clot (thrombus) forms in a retinal vein - blocking venous drainage from the retina
  • Hardened arteries (atherosclerosis) can press on nearby veins, particularly where they cross - leading to vein narrowing and potential blockage
206
Q

What are the main types of retinal vein occlusion?

A
  1. Central retinal vein occlusion (CRVO) - affects the whole retina
  2. Branch retinal vein occlusion (BRVO) - affects the area drained by the blocked branch vein
    .
    These can further be classified as being either ischaemic or non-ischaemic:
    - Retinal ischaemia –> leads to release of VEGF, resulting in new vessel development (neovascularisation)
207
Q

Describe the venous drainage of the retina?

A

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

208
Q

Why are sites where retinal arteries cross veins at higher risk of occlusion?

A

The arteries can compress the veins, leading to narrowing and increased risk of clot formation

(atherosclerosis is the main cause of this)

209
Q

What happens when a retinal vein is blocked?

A
  1. Venous congestion in the retina
  2. Increased pressure in retinal veins
  3. Fluid and blood leak into retina –> causing macular oedema and retinal haemorrhages
  4. This results in retinal damage and vision loss
210
Q

What is the role of vascular endothelial growth factor (VEGF) in retinal vein occlusion?

A

Retinal ischaemia triggers VEGF release, leading to neovascularisation (new blood vessel growth)

211
Q

What are key risk factors for retinal vein occlusion?

A
  • Hypertension
  • High cholesterol
  • Diabetes
  • Smoking
  • High plasma viscosity (e.g., myeloma)
  • Myeloproliferative disorders
  • Inflammatory conditions (e.g., SLE)
212
Q

What is the main symptom of retinal vein occlusion?

A

Painless blurred vision or vision loss

213
Q

How does vision loss differ in BRVO vs. CRVO?

A
  • BRVO –> vision loss corresponds to the affected branch vein area
  • CRVO –> widespread vision loss
  • Macular involvement (ie. branch draining macula) –> loss of central vision
214
Q

What are the key fundoscopy features of retinal vein occlusion?

A

“Stormy sunset”:
- Dilated tortuous retinal veins
- Flame and blot haemorrhages
- Retinal oedema
- -Cotton wool spots
Hard exudates

215
Q

What should be done if retinal vein occlusion is suspected + what are the key treatment options?

A
  • Immediate referral to an ophthalmologist
    .
    Management in secondary care aims to treat macular oedema and prevent neovascularisation:
  1. Anti-VEGF therapies (e.g., ranibizumab, aflibercept) –> to reduce macular oedema
  2. Dexamethasone intravitreal implant –> to treat macular oedema
  3. Laser photocoagulation –> to treat neovascularisation
216
Q

What happens in central retinal artery occlusion (CRAO)?

A

There is an obstruction to blood flow through the central retinal artery –> leading to ischaemia of the retina

217
Q

What is the central retinal artery a branch of?

A

The ophthalmic artery, which is a branch of the internal carotid artery

218
Q

What are the main causes of CRAO?

A
  • Atherosclerosis (most common)
  • Giant cell arteritis (GCA) - vasculitis affecting the ophthalmic or central retinal artery reduces blood flow
219
Q

What are the main risk factors for CRAO?

A
  • Cardiovascular disease risk factors (smoking, hypertension, diabetes and raised cholesterol) –> increases risk of atherosclerosis
  • GCA risk factors - white ethnicity, older age, female and polymyalgia rheumatica
220
Q

What is the classic symptom of CRAO?

A

Sudden painless loss of vision, often described as a “curtain coming down” over vision

221
Q

What is a key pupil examination finding in CRAO?

A

Relative afferent pupillary defect (RAPD) - the affected pupil constricts less when light is shone directly in it compared to when light is shone in the unaffected eye

222
Q

What are the key fundoscopy findings in CRAO?

A
  • Pale retina - due to ischaemia and lack of perfusion
  • Cherry red spot - at the fovea, where the thinner surface allows the red choroid to be seen
223
Q

What is amaurosis fugax?

A

Temporary loss of vision due temporary interuption to the blood supply - usually caused by an embolus or due to carotid artery disease)

224
Q

What are the main differentials for sudden painless vision loss?

A
  • Retinal detachment
  • Central retinal artery occlusion
  • Central retinal vein occlusion
  • Vitreous haemorrhage (e.g., due to diabetic retinopathy)
225
Q

What are the management steps for a patient with CRAO suspected to be caused by GCA?

A

GCA is a potentially reversible cause:
- Investigations - ESR blood test (inflammation) and temporal artery biopsy
.
- Treatment - high-dose systemic steroids (eg. prednisolone), to prevent further vision loss

226
Q

How should CRAO be managed initially?

A

Immediate referral to ophthalmology, as it is a vision-threatening emergency

227
Q

Immediate management options for a centrla retinal artery occlusion (CRAO) involves attempting to dislodge/resolve the blockage, name some ways we can do this (not strong evidence/guidleines backing these).

A
  • Ocular massage - to move the embolus
  • Anterior chamber paracentesis - removing fluid from the anterior chamber to reduce the IOP
  • Inhaled carbogen (5% CO₂, 95% O₂) - to dilate the artery
  • Sublingual isosorbide dinitrate - to dilate the artery
  • Oral pentoxifylline - to dilate the artery
  • IV acetazolamide - to reduce IOP
  • IV mannitol - to reduce IOP
  • Topical timolol - to reduce IOP
228
Q

What is the long-term management of CRAO?

A
  • Identify and treat reversible risk factors
  • Secondary prevention of cardiovascular disease –> e.g. managing BP, lipids, and diabetes
229
Q

What is retinitis pigmentosa?

A

A genetic condition causing progressive degeneration of the photoreceptors in the retina - rods are affected more than cones

230
Q

What is the primary function of rods, and how does their degeneration affect vision?

A
  • Rods are responsible for night vision and peripheral vision –> degeneration leads to night blindness and peripheral vision loss
231
Q

How does retinitis pigmentosa vary between individuals?

A
  • It can occur in isolation or as part of systemic diseases
  • Different genetic mutations affect the age of onset and disease progression
232
Q

What are the two main symptoms of retinitis pigmentosa?

A
  • Night blindness (often the first symptom)
  • Peripheral vision loss (before central vision is affected) –> progressing to tunnel vision and potentially total blindness
233
Q

What are the key general management strategies for retinitis pigmentosa?

A

Currently there are no treatment options to slow the disease process.
.
- Ophthalmology referral for assessment and follow-up

  • Genetic counselling
  • Vision aids
  • Sunglasses to reduce retinal damage
  • Driving limitations - patients should inform the DVLA
234
Q

What are the characteristic fundoscopy findings in retinitis pigmentosa?

A
  • Bone-spicule pigmentation (sharp, pointed pigment resembling bone matrix)
  • Mid-peripheral pigment deposits
  • Narrowing of arterioles
  • Waxy or pale optic disc
235
Q

What are three systemic diseases associated with retinitis pigmentosa?

A
  • Usher syndrome - associated with hearing loss
  • Bassen-Kornzweig syndrome - associated with progressive neurological impairments
  • Refsum disease - associated with peripheral neuropathy, hearing loss, and ichthyosis (scaly skin)
236
Q

What symptom will a person with misaligned eyes experience?

A

Double vision - the images on the retina do not match

237
Q

How does the brain compensate for strabismus (squint) in childhood?

A
  • The brain suppresses signals from the less dominant eye –> leading to a “lazy eye” (ie. person has one dominant eye they use to see, and one eye they ignore)
  • If untreated, the “lazy eye” becomes progressively more disconnected from the brain and over time the problem becomes worse –> this is called amblyopia
238
Q

What is the difference between concomitant and paralytic squints?

A
  • Concomitant squint - due to differences in the control of the extra-ocular muscles (severity of squint can vary)
  • Paralytic squint (rare) - due to paralysis in one or more of the extra ocular muscles
239
Q

What is strabismus?

A

Misalignment of the eyes

240
Q

What is amblyopia (“lazy eye”)?

A

the affected eye becomes passive and has reduced function compared to the other dominant eye

241
Q

Define the different types of squint:

  • Esotropia
  • Exotropia
  • Hypertropia
  • Hypotropia
A
  • Esotropia - eye deviates inward (towards the nose)
  • Exotropia - eye deviates outward (towards the ear)
  • Hypertropia - eye deviates upward
  • Hypotropia - eye deviates downward
242
Q

What are causes of squint (strabismus)?

A
  • Idiopathic (most common in healthy children)
  • Neurological conditions (e.g., hydrocephalus, cerebral palsy)
  • Space-occupying lesions (e.g., retinoblastoma)
  • Trauma
243
Q

How is Hirschberg’s test performed (corneal light reflex)?

A
  • Shine a pen-torch at the patient from 1 metre away
  • Observe the corneal light reflex
    .
  • Central and symmetrical reflection = normal
  • Deviation from centre = indicates a squint
244
Q

How is the cover test performed?

A
  1. Cover one eye while the patient fixates on an object in front of them
  2. Move the cover to the opposite eye and observe the previously covered eye:
    - Moves inward –> had drifted outward when covered (exotropia)
    - Moves outward –> had drifted inward when covered (esotropia)
245
Q

Why must treatment of amblyopia start before 8 years old?

A

The visual fields are still developing –> early intervention prevents permanent squint

246
Q

What is the first-line treatment for amblyopia + what is an alternative treatment?

A
  1. 1st-line –> Occlusive patch over the good eye to force weaker eye to develop
  2. Atropine eye drops in good/dominant eye –> causes blurred vision (dilates eye), again forcing the weaker eye to develop
    .
    other things to consider:
    - treat underlying pathology (eg. cataracts)
    - corrective lenses for refractive errors
247
Q

Manifest squint VS Latent squint

A
  • Manifest squint (heterotropia) - where the eyes are visibly misaligned when the eyes are open and being used
  • Latent squint (heterophoria) - eyes are misaligned when eyes are closed or covered, but appear normal when open
248
Q

What is hyperopia (farsightedness) + main cause

A
  • distant objects seen more clearly than near ones - because light focuses behind the retina rather than directly on it
  • the eye is too short, or the cornea/lens is too flat, leading to insufficient focusing power
249
Q

What is myopia (nearsightedness) + main cause

A
  • near objects are seen more clearly than distant ones - because light focuses in front of the retina
  • eye is too long, or the cornea/lens is too steep, leading to excessive focusing power
250
Q

Treatment of hypermetropia (farsightedness) and myopia (nearsightedness)

A

Glasses OR Contact lenses:

  • Hyperopia - Convex (plus) lenses are used to help focus light onto the retina
  • Myopia - Concave (minus) lenses are used to diverge light, allowing it to focus on the retina
    .
    (Surgery: LASIK reshapes cornea to increase (hyperopia) or decrease (myopia) curvature
251
Q

Why does hypermetropia increase the risk of acute angle-closure glaucoma (AACG)?

A

Hypermetropic eyes often have a shallow anterior chamber and narrow drainage angles, increasing the likelihood of angle closure.

252
Q

Pseudosquint

A
  • A pseudosquint (also known as pseudostrabismus) refers to the appearance of a squint (strabismus) when the eyes are actually properly aligned
  • This condition is typically caused by facial or structural features around the eyes rather than an actual misalignment
  • It is common in children and does not require treatment.
    .
  • causes: wide nasal bridge

(this is why corneal light reflex is an important test for strabismus (squint)

Module 3C - Neuro / Ophthal (14 decks)

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