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Child Health > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Describe the 3 zones of the retina

A
  • Zone 1: includes the optic nerve and the macula.
  • Zone 2: from the edge of zone 1 to the ora serrata (the pigmented border between the retina and ciliary body).
  • Zone 3: outside the ora serrata.
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2
Q

Define glaucoma

A

Optic nerve damage due to raised intraocular pressure caused by a blockage of aqueous humour.

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3
Q

Anterior vs posterior chambers of the eye

A
  • Anterior chamber: between cornea and iris.
  • Posterior chamber: between lens and iris.
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4
Q

Describe the normal circulation of aqueous humour

A

The aqueous humour supplies nutrients to the cornea. It is produced by the ciliary body. It flows through the posterior chamber and around the iris to the anterior chamber. It drains through the trabecular meshwork to the canal of Schlemm at the angle between the cornea and the iris. From the canal of Schlemm, it eventually enters the general circulation.

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5
Q

What is the normal range of intraocular pressure?

A

10-21 mmHg

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6
Q

Describe the pathophysiology of open-angle glaucoma

A
  • Gradual increase in resistance to flow through the trabecular meshwork, causing pressure to slowly build up.
  • Raised intraocular pressure causes cupping of the optic disk —> cup-disk ratio >0.5.
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7
Q

Outline the risk factors for open-angle glaucoma

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Myopia (nearsightedness)
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8
Q

Describe the typical features of open-angle glaucoma

A
  • Gradual onset of peripheral vision loss (tunnel vision)
  • Fluctuating pain
  • Headaches
  • Blurred vision
  • Halos around lights, particularly at night
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9
Q

Name 2 investigations to measure intraocular pressure

A
  • Non-contact tonometry
  • Goldmann applanation tonometry (gold standard)
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10
Q

How would you go about diagnosing open-angle glaucoma?

A
  • Goldmann applanation tonometry for the intraocular pressure.
  • Slit lamp assessment for the cup-disk ratio and optic nerve health.
  • Visual field assessment for peripheral vision loss.
  • Gonioscopy to assess the angle between the iris and cornea.
  • Central corneal thickness assessment.
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11
Q

Describe the management of open-angle glaucoma

A
  • Treatment started at an intraocular pressure > 24 mmHg.
  • 360° selective laser trabeculoplasty (improves drainage of trabecular meshwork) - first line.
  • Prostaglandin analogue eye drops (e.g. latanoprost) are the first-line medical treatment after SLT. They increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).
  • Beta-blockers (e.g. timolol) eye drops, reduce the production of aqueous humour - second line medical.
  • Carbonic anhydrase inhibitors (e.g. dorzolamide) eye drops, reduce the production of aqueous humour - second line medical.
  • Sympathomimetics (e.g. brimonidine) eye drops reduce the production of aqueous fluid and increase the uveoscleral outflow - second line medical.
  • Trabeculectomy surgery may be required where other treatments are ineffective. Creates a new channel from the anterior chamber, through the sclera to under the conjunctiva (bleb).
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12
Q

Describe the pathophysiology of acute angle-closure glaucoma

A

Iris budges forwards and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining and leading to an increase in intraocular pressure. The pressure builds in the posterior chamber, pushing the iris forwards and exacerbating the angle closure. It is an ophthalmological emergency.

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13
Q

Outline the risk factors for acute angle-closure glaucoma

A
  • Increasing age.
  • Family history.
  • Female (four times more likely than males).
  • Chinese and East Asian ethnic origin (compared to black people in open-angle).
  • Shallow anterior chamber.
  • 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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14
Q

What are the symptoms and signs associated with acute angle-closure glaucoma?

A

Acute onset:

  • Severely painful red eye.
  • Blurred vision.
  • Halos around lights.
  • Associated headache, N+V.

Signs:

  • Red eye.
  • Hazy cornea.
  • Decreased visual acuity.
  • Fixed dilated pupil.
  • Hard eyeball on gentle palpation.
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15
Q

Outline the management of acute angle-closure glaucoma

A
  • Pilocarpine eye drops: muscarinic agonist causing pupil constriction (miotic agent) and ciliary muscle contraction, to open up pathway for the flow of aqueous humour.
  • Acetazolamide (oral or IV): carbonic anhydrase inhibitor that reduces the production of aqueous humour.
  • Hyperosmotic agents (e.g. IV mannitol): increase the osmotic gradient between the blood and the eye.
  • Timolol (beta blocker): reduces the production of aqueous humour.
  • Dorzolamide (carbonic anhydrase inhibitor).
  • Brimonidine (sympathomimetic): reduces aqueous humour production and increases uveoscleral outflow.
  • Laser iridotomy (definitive treatment): making a hole in the iris, allowing aqueous humour to flow from posterior chamber to anterior chamber, relieving the pressure.
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16
Q

Myopia vs. Hyperopia

A
  • Myopia: nearsightedness.
  • Hyperopia: farsightedness.
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17
Q

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

A

Age-related macular degeneration (AMD)

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18
Q

What is AMD?

A

Progressive unilateral (sometimes bilateral) condition affected the macula of the eye. It causes atrophy of the retinal pigment epithelium and degeneration of the photoreceptors.

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19
Q

What is the function of the macula?

A

Found in the centre of the retina and generates high-definition colour vision in the central visual field.

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20
Q

Describe the 2 types of AMD

A
  • Wet (neovascular), accounting for 10% of cases: new blood vessels develop from the choroid layer and grow into retina. These vessels leak fluid/blood causing oedema and faster vision loss. VEGF stimulates this neovascularisation.
  • Dry (non-neovascular), accounting for 90% of cases.
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21
Q

Outline the risk factors for AMD

A
  • Older age
  • Smoking
  • Family history
  • CVD (e.g. hypertension)
  • Obesity
  • Poor diet (low in vitamins and high in fat)
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22
Q

Describe the symptoms associated with AMD

A

Unilateral visual changes:

  • Gradual loss of central vision.
  • Reduced visual acuity.
  • Crooked or wavy appearance to straight lines (metamorphopsia).
  • Gradually worsening ability to read small text.
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23
Q

Glaucoma vs. AMD symptoms

A
  • Glaucoma: peripheral vision loss and halos around lights.
  • AMD: central vision loss and a wavy appearance to straight lines.
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24
Q

Describe the key examination findings associated with AMD

A
  • Reduced visual acuity (Snellen chart).
  • Scotoma (an enlarged central area of vision loss).
  • Amsler grid test: used to assess for the distortion of straight lines.
  • Drusen (yellowish deposits of proteins and lipids under the retina) may be seen during fundoscopy.
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25
Q

Name 3 tests used to help diagnose AMD

A
  • Slit lamp examination gives a detailed view of the retina and macula.
  • Optical coherence tomography gives a cross-sectional view of the layers of the retina and is used for diagnosing and monitoring AMD.
  • Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
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26
Q

Outline the management for AMD

A
  • No specific treatment for dry AMD. Management involves monitoring and reducing the risk of progression by: avoiding smoking, controlling BP and vitamin supplementation.
  • Wet AMD: anti-VEGF medications (e.g. ranibizumab, aflibercept and bevacizumab) block VEGF and slow the development of new vessels. They are injected directly into the vitreous chamber of the eye (intravitreal), usually about once a month.
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27
Q

Define diabetic retinopathy

A

Damage to retinal blood vessels due to prolonged hyperglycaemia.

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28
Q

Outline the changes seen on fundoscopy for diabetic retinopathy

A
  • Blot haemorrhages (due to increased vascular permeability).
  • Hard exudates (yellow-white deposits of lipid and proteins due to increased vascular permeability).
  • Microaneurysms and venous beading (due to vessel wall damage).
  • Cotton wool spots (due to damage to retinal nerve fibres).
  • Intraretinal microvascular abnormalities (IRMA): dilated and tortuous capillaries in the retina, acting as a shunt between the arterial and venous vessels.
  • Neovascularisation (only seen in proliferative diabetic retinopathy).
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29
Q

Name the complications associated with diabetic retinopathy

A
  • 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.
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30
Q

Describe the management of diabetic retinopathy

A

Non-proliferative diabetic retinopathy requires close monitoring and careful diabetic control.

Treatment options for proliferative diabetic retinopathy are:

  • 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.

An intravitreal implant containing dexamethasone is an option for macular oedema.

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31
Q

Describe the features associated with hypertensive retinopathy

A
  • Silver wiring or copper wiring: walls of the arterioles become thickened and sclerosed and reflect more light on examination.
  • AV nipping: arterioles cause compression of the veins where they cross due to sclerosis and hardening of the arterioles.
  • Cotton wool spots: damage to nerve fibres.
  • Hard exudates: damaged vessels leaking lipids onto the retina.
  • Retinal haemorrhages: damaged vessels rupturing and releasing blood in the retina. Dot and blot haemorrhages occur deeper, in the inner nuclear layer or outer plexiform layer. Flame haemorrhages occur in the nerve fiber layer.
  • Papilloedema: ischaemia to the optic nerve, resulting in optic nerve swelling.
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32
Q

What is the management for hypertensive retinopathy?

A
  • Control BP.
  • Managing risk factors e.g. smoking and lipids.
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33
Q

Describe the function of the eye lens

A

The role of the lens is to focus light on the retina. It is held in place by suspensory ligaments attached to the ciliary body. The ciliary body contracts and relaxes to change the shape of the lens. When the ciliary body contracts, it releases tension on the suspensory ligaments, and the lens thickens. When the ciliary body relaxes, the suspensory ligaments tension, and the lens narrows. The lens has no blood supply and is nourished by the aqueous humour.

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34
Q

What is cataracts?

A

Progressive opacification of the eye lens, which reduces the light entering the eye and visual acuity.

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35
Q

Outline the risk factors for cataracts

A
  • Increasing age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypocalcaemia
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36
Q

Describe the features of cataracts

A

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.
  • Loss of the red reflex on examination.
  • White/grey pupil.
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37
Q

How can cataracts be managed?

A
  • No intervention may be necessary if the symptoms are manageable.
  • Cataract surgery: involves drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens.
  • Cataracts can prevent the detection of other pathology, such as macular degeneration or diabetic retinopathy, which can become apparent after surgery. Therefore, they may still have reduced visual acuity after the cataract is treated.
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38
Q

Name one complication of cataracts surgery

A

Endophthalmitis - inflammation and infection of the inner contents of the eye (intra-ocular fluid, vitreous/aqueous). It can lead to vision loss. Treated with intravitreal antibiotics injected directly into the eye.

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39
Q

Describe how the lens plays a role in refraction and accommodation

A
  • Refraction: refers to the change in direction of light when it passes from one medium to another. Helps to converge light onto the retina.
  • Accommodation: refers to the ability to maintain focus on an image as distance varies. The lens achieves this by altering its shape through contraction or relaxation of the ciliary bodies.
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40
Q

What is the hallmark feature of cataracts?

A

Painless loss of vision.

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41
Q

Explain the physiology of pupil size

A
  • Pupil constriction stimulated by parasympathetic NS along the oculomotor nerve.
  • Pupil dilation stimulated by sympathetic NS.
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42
Q

Outline some causes of abnormal pupil shape

A
  • Trauma to sphincter muscles.
  • Anterior uveitis causing adhesions.
  • Acute angle-closure glaucoma - vertical oval.
  • Rubeosis iridis (neovascularisation in iris) in diabetic retinopathy.
  • Coloboma (congenital malformation).
  • Tadpole pupil - associated with migraines and Horner syndrome.
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43
Q

Causes of mydriasis (dilated pupil)

A
  • Congenital
  • Stimulants (e.g. cocaine)
  • Anticholinergics (e.g. oxybutynin)
  • Trauma
  • Third nerve palsy
  • Holmes-Adie syndrome (Holmes-Adie pupil with absent ankle and knee reflexes)
  • Raised intracranial pressure
  • Acute angle-closure glaucoma
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44
Q

Causes of mitosis (constricted pupil)

A
  • Horner syndrome
  • Cluster headaches
  • Argyll-Robertson pupil (neurosyphilis)
  • Opiates
  • Nicotine
  • Pilocarpine
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45
Q

Explain the 3 features of a third cranial nerve (oculomotor nerve) palsy

A
  • Ptosis - due to palsy of levator palpebrae superioris.
  • Dilated non-reactive pupil - due to palsy of parasympathetic fibres.
  • Divergent strabismus (squint) in the affected eye, with a ‘down and out’ position of the affected eye - due to palsy of extraocular muscles, but sparing of lateral rectus and superior oblique.
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46
Q

What is the cause of a third nerve palsy with pupil sparing?

A

Microvascular cause e.g. diabetes, hypertension, ischaemia.

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47
Q

What causes a full third nerve palsy?

A

Compression of nerve (including parasympathetic fibres) due to: tumour, trauma, cavernous sinus thrombosis, posterior communicating artery aneurysm, raised ICP.

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48
Q

Outline the triad of features in Horner Syndrome

A

MAP:

  • Miosis
  • Anhidrosis
  • Ptosis
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49
Q

Are light and accommodation reflexes affected in Horner Syndrome?

A

No - because these are controlled by parasympathetic NS.

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50
Q

What causes Horner Syndrome?

A

Damage to sympathetic NS supplying the face.

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51
Q

Describe the location of the sympathetic nerves supplying the head and neck

A
  • Pre-ganglionic nerves arise from the spinal cord in the chest and enter the sympathetic ganglion at the base of the neck.
  • Post-ganglionic nerves travel to the head alongside the internal carotid artery.
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52
Q

How can the location of the Horner Syndrome lesion be determined?

A
  • Central lesions (occurring before the nerves exit the spinal cord) cause anhidrosis of the arm, trunk and face e.g. stroke, syringomyelia, MS, tumour, encephalitis.
  • Pre-ganglionic lesions cause anhidrosis of the face e.g. pancoast tumour, cervical rib, thyroidectomy, trauma.
  • Post-ganglionic lesions don’t cause anhidrosis e.g. carotid artery, cluster headache.
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53
Q

List the causes of Horner Syndrome central lesions, pre-ganglionic lesions and post-ganglionic lesions

A

Central lesions (Sentral):

  • S – Stroke
  • S – Multiple Sclerosis
  • S – Swelling (tumours)
  • S – Syringomyelia (cyst in the spinal cord)

Pre-ganglionic lesions (Torso):

  • T – Tumour (Pancoast tumour)
  • T – Trauma
  • T – Thyroidectomy
  • T – Top rib (a cervical rib growing above the first rib and clavicle)

Post-ganglionic lesions (cervical):

  • C – Carotid aneurysm
  • C – Carotid artery dissection
  • C – Cavernous sinus thrombosis
  • C – Cluster headache
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54
Q

How can you test for Horner syndrome?

A
  • Cocaine eye drops acts on the eye to stop NA re-uptake at the NMJ. This causes a normal eye to dilate as NA stimulates the dilator muscles of the iris. In Horner syndrome, the nerves are not releasing NA, so blocking re-uptake makes no difference, and there is no pupil reaction.
  • Alternatively, low-dose adrenaline eye drops (0.1%) will dilate the pupil in Horner syndrome but not a normal pupil.
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55
Q

What causes a Holmes-Adie pupil?

A

Damage to the post-ganglionic parasympathetic fibres.

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56
Q

Describe the findings seen with an Argyll-Robertson pupil

A
  • A constricted pupil that accommodates when focusing on a near object but does not react to light.
  • ‘Prostitute’s pupil’ due to its relation to neurosyphilis and because ‘it accommodates but does not react’.
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57
Q

Define blepharitis and it’s cause

A

Inflammation of the eyelid margins associated with dysfunction of the Meibomian glands (responsible for secreting meibum/oil onto eye surface). It can lead to styles and chalazions.

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58
Q

What are the common presenting symptoms for blepharitis?

A

Gritty or burning sensation in both eyes, crusted eyelashes, red eyes, and swollen or greasy eyelids.

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59
Q

What is a common complication of blepharitis?

A

Dry eye disease

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60
Q

Management of blepharitis?

A

Warm compresses and gentle cleaning of the eyelid margins to remove debris (e.g., using a cotton bud and baby shampoo).

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61
Q

Types of stye

A
  • Hordeolum externum: infection of the glands of Zeis or glands of Moll. The glands of Moll are sweat glands at the base of the eyelashes. The glands of Zeis are sebaceous glands at the base of the eyelashes. A stye causes a tender red lump along the eyelid that may contain pus.
  • Hordeolum internum: infection of the Meibomian glands. They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid.
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62
Q

Treatment of styes

A
  • Hot compresses and analgesia.
  • Topical antibiotics (e.g. chloramphenicol) may be considered if it is associated with conjunctivitis or if symptoms are persistent.
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63
Q

Define a chalazion

A

When a Meibomian gland becomes blocked and swells (Meibomian cyst). It presents with a swelling in the eyelid that is typically not tender.

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64
Q

What’s the name for the condition where the eyelid turns inwards with the lashes pressed against the eye?

A

Entropion

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65
Q

Name two complications of entropion

A

Corneal damage and ulceration.

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66
Q

Management of entropion?

A
  • Taping down eyelid to prevent it turning inwards (with lubricating eye drops).
  • Surgery is definitive management.
  • Same day referral to ophthalmology if there’s a risk to sight.
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67
Q

What is eyelid ectropion?

A

When the eyelid turns outwards, exposing the inner aspect.

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68
Q

What are the complications of eyelid ectropion?

A

Exposure keratopathy (the eyeball is exposed and not adequately lubricated and protected).

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69
Q

When should a same day referral to ophthalmology be made?

A

When there is a risk to sight

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70
Q

What is the term for the inward growth of the eyelashes?

A

Trichiasis

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71
Q

Define periorbital cellulitis

A

An infection of the eyelid and skin in front of the orbital septum, causing swollen, red and hot skin around the eyelid and eye.

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72
Q

Investigations for periorbital cellulitis

A
  • Urgent referral to ophthalmology to rule out orbital cellulitis (sight and life-threatening).
  • CT scan.
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73
Q

Treatment of periorbital cellulitis?

A

Systemic antibiotics

74
Q

How does orbital cellulitis differ to periorbital cellulitis?

A

Orbital cellulitis is an infection around the eyeball involving the tissues behind the orbital septum.

75
Q

Describe the symptoms of orbital cellulitis

A
  • Pain with eye movement.
  • Reduced eye movements.
  • Vision changes.
  • Abnormal pupil reactions.
  • Proptosis (bulging forward of the eyeball).
76
Q

Treatment of orbital cellulitis?

A
  • Emergency hospital admission.
  • IV antibiotics.
  • Surgical drainage if abscess forms.
77
Q

Describe the presentation of conjunctivitis

A
  • Red, bloodshot eye.
  • Itchy or gritty sensation.
  • Discharge (bacterial - purulent, viral - clear).
78
Q

Which lymph nodes may be tender in viral conjunctivitis?

A

Pre-auricular

79
Q

List the 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
80
Q

Outline the causes of an acute painless red eye

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
81
Q

Describe the management of conjunctivitis

A
  • Usually resolves within 1-2 weeks without treatment.
  • Hygiene measures to reduce spread (as it’s contagious).
  • Cleaning eyes with cooled boiled water and cotton wool.
  • Chloramphenicol (first-line) or fusidic acid eye drops (for bacterial conjunctivitis if necessary).
82
Q

What can cause neonatal conjunctivitis?

A

Gonococcal infection. It can cause permanent vision loss so needs urgent ophthalmology assessment.

83
Q

How can allergic conjunctivitis be treated?

A
  • Antihistamines.
  • Topical mast-cell stabilisers.
84
Q

What is the main cause of viral conjunctivitis?

A

Adenovirus

85
Q

What are the red flags for an ophthalmology referral?

A
  • Reduced visual acuity.
  • Marked eye pain, headache or photophobia.
  • Red sticky eye in a neonate (within 30 days of birth).
  • History of trauma or possible foreign body.
  • Copious rapidly progressive discharge (indicative of gonococcal infection).
  • Infection with a herpes virus.
  • Soft contact lens use with corneal symptoms (such as photophobia and watering).
86
Q

Define anterior uveitis

A

Inflammation of anterior uvea (iris, ciliary body and choroid) - aka the middle layer of the eye.

87
Q

What are the causes of uveitis?

A
  • Autoimmune (most common) - HLA B27
  • Infection
  • Trauma
  • Ischaemia
  • Malignancy
88
Q

What is the hallmark feature of anterior uveitis?

A

Presence of leukocytes (neutrophils, lymphocytes and macrophages) in anterior chamber.

89
Q

Which autoimmune conditions are associated with anterior uveitis?

A
  • Seronegative spondyloarthropathies (e.g. ankylosing spondylitis, psoriatic arthritis and reactive arthritis)
  • IBD
  • Sarcoidosis
  • Behçet’s disease
90
Q

Describe the features of anterior uveitis

A
  • Painful red eye (typically a dull, aching pain).
  • Reduced visual acuity.
  • Photophobia (due to ciliary muscle spasm).
  • Excessive lacrimation (tear production).
  • 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).
91
Q

What is the usual first-line treatment for anterior uveitis?

A
  • Urgent review by ophthalmology!
  • Topical steroids.
  • Cycloplegics (e.g. cyclopentolate or atropine eye drops, antimuscarinics, which dilate the pupil by relaxing sphincter and ciliary muscles) - paralyse ciliary muscles.
92
Q

Define episcleritis

A

Inflammation of episclera, which is often associated with inflammatory conditions e.g. IBD and RA.

93
Q

Describe the presentation of episcleritis

A
  • Localised or diffuse redness (often in lateral sclera).
  • No pain.
  • Dilated episcleral vessels.
94
Q

How would you differentiate between episcleritis and scleritis?

A

Phenylephrine eye drops causes blanching of episcleral vessels, causing redness to disappear.

95
Q

Management of episcleritis?

A

Analgesia and lubricating eye drops.

96
Q

Define scleritis

A

Inflammation of sclera, most commonly idiopathic or associated with inflammatory conditions (RA, vasculitis). Less commonly due to infection.

97
Q

Describe the presentation of scleritis

A
  • Red, inflamed sclera (localised or diffuse)
  • Congested vessels
  • Severe pain (typically a boring pain)
  • Pain with eye movement
  • Photophobia
  • Epiphora (excessive tear production)
  • Reduced visual acuity
  • Tenderness to palpation of the eye
98
Q

Management of scleritis?

A
  • NSAIDs.
  • Steroids.
  • Immunosuppression appropriate to the underlying systemic condition.
99
Q

Outline the common causes of corneal abrasions

A
  • Damaged contact lenses (may be associated with pseudomonas infection)
  • Fingernails
  • Foreign bodies (e.g. metal fragments)
  • Tree branches
  • Makeup brushes
  • Entropion (inward turning eyelid)
100
Q

Describe the presentation of a corneal abrasion

A
  • Painful red eye
  • Photophobia
  • Foreign body sensation
  • Epiphora (excessive tear production)
  • Blurred vision
101
Q

What can be used to diagnose a corneal abrasion?

A

Fluorescein stain

102
Q

Outline the management for complicated corneal abrasions

A
  • Assessment and management by ophthalmology
  • Removing foreign bodies
  • Simple analgesia (e.g. paracetamol)
  • Lubricating eye drops (e.g. Hypromellose, Polyvinyl alcohol, Carbomer)
  • Antibiotic eye drops (e.g. chloramphenicol)
  • Close follow-up
103
Q

What is keratitis?

A

Inflammation of the cornea.

104
Q

What are the causes of keratitis?

A
  • Viral infection (e.g., herpes simplex - most common cause)
  • 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)
105
Q

Describe the features of herpes keratitis

A
  • Painful red eye
  • Photophobia
  • Vesicles (fluid-filled blisters)
  • Foreign body sensation
  • Watery discharge
  • Reduced visual acuity
106
Q

How would usually diagnose keratitis?

A

Slit lamp examination

107
Q

Fluorescein staining for herpes keratitis shows what?

A

Dendritic corneal ulcer

108
Q

What are the management options for herpes keratitis?

A
  • Same-day ophthalmic assessment.
  • Topical or oral antivirals (e.g. aciclovir or ganciclovir).
  • Corneal transplant is an option to treat permanent scarring and vision loss after keratitis.
109
Q

Peripheral curtain over vision + spider webs + flashing lights in vision

A

Retinal detachment

110
Q

Define Amaurosis fugax

A
  • Sudden loss of vision due to ischaemia, often due to thromboembolic disease.
  • Temporary loss of vision only, with episodes lasting less than 24 hours.
  • ‘Black curtain coming down vertically into the field of vision in one eye’.
  • Painless, transient monocular blindness together with the description of a ‘black curtain coming down’.
111
Q

Differentiate between posterior vitreous detachment, retinal detachment and vitreous haemorrhage

A

Posterior vitreous detachment:

  • Flashes of light (photopsia) - in the peripheral field of vision.
  • Floaters, often on the temporal side of the central vision.

Retinal detachment:

  • Dense shadow that starts peripherally progresses towards the central vision.
  • A veil or curtain over the field of vision.
  • Straight lines appear curved.
  • Central visual loss.

Vitreous haemorrhage:

  • Large bleeds cause sudden visual loss.
  • Moderate bleeds may be described as numerous dark spots.
  • Small bleeds may cause floaters.
112
Q

A relative afferent pupillary defect is associated with…

A

Optic neuritis

113
Q

Subacute unilateral visual loss and eye pain worse on movements?

A

Optic neuritis

114
Q

What is a subconjunctival haemorrhage?

A

When blood vessels within the conjunctiva rupture, releasing blood into space between sclera and conjunctiva. They’re often idiopathic in otherwise healthy patients and appear after trauma or strenuous activity e.g. coughing, weight lifting or straining when constipated.

115
Q

Which factors can predispose individuals to subconjunctival haemorrhages?

A
  • Hypertension
  • Bleeding disorders (e.g. thrombocytopenia)
  • Whooping cough
  • Medications (e.g. antiplatelets, DOACs or warfarin)
  • Non-accidental injury
116
Q

Describe the presentation of a subconjunctival haemorrhage

A
  • Painless patch of bright red blood underneath conjunctiva, covering the white of the eye.
  • Doesn’t affect vision.
117
Q

How long does it take for a subconjunctival haemorrhage to spontaneously resolve?

A

Around 2 weeks

118
Q

Define posterior vitreous detachment

A

When the vitreous body separates from the retina. It is common in old age.

119
Q

What are the key symptoms of posterior vitreous detachment?

A
  • Floaters
  • Flashing lights
  • Blurred vision
  • Painless
120
Q

Outline the management plan for posterior vitreous detachment

A
  • No treatment is necessary. Over time, the symptoms will improve as the brain adjusts.
  • However, it can predispose patients to develop retinal tears and retinal detachment. It is essential to exclude a retinal tear or retinal detachment with a thorough assessment of the retina, usually by an optometrist or ophthalmologist.
121
Q

Describe the pathophysiology of retinal detachment

A
  • Neurosensory layer of the retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (base layer attached to choroid).
  • Usually due to a retinal tear, allowing vitreous fluid to get under the neurosensory retina.
  • Disrupts the blood supply to the photoreceptors.
122
Q

What are the risk factors for retinal detachment?

A
  • Lattice degeneration (thinning of the retina)
  • Posterior vitreous detachment
  • Trauma
  • Diabetic retinopathy
  • Retinal malignancy
  • Family history
  • Myopia
  • Age
  • Previous surgery for cataracts
123
Q

Describe the presentation of retinal detachment

A
  • Painless peripheral vision loss (sudden onset shadow coming across the vision).
  • Blurred or distorted vision.
  • Flashes and floaters.
124
Q

Outline the management of retinal detachment

A

Retinal tears:

  • Laser therapy.
  • Cryotherapy.

Retinal detachment:

  • Aims to reattach the retina.
  • Vitrectomy : keyhole surgery on the eye, removing the vitreous fluid, fixing the tear, and then inserting gas or oil into the eye to hold the retina in place.
  • Scleral buckling: a silicone ‘buckle’ to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina. It acts like a corset, squeezing the eye contents together.
  • Pneumatic retinopexy: injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place.
125
Q

Describe the pathophysiology of retinal vein occlusion

A
  • Thrombus forms in retinal veins, blocking the drainage of blood from the retina, leading to venous congestion, increasing the pressure in the retinal veins, causing macular oedema and retinal haemorrhages.
  • Thrombus may form in central retinal vein or branch retinal veins.
126
Q

How can retinal vein occlusion be categorised?

A
  • Ischaemic: leads to VEGF release causing neovascularisation.
  • Non-ischaemic.
127
Q

List the 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)
128
Q

Describe the presentation of retinal vein occlusion

A
  • Painless blurred vision or vision loss.
  • Branch retinal vein occlusion involving branch draining macula —> central vision loss.
129
Q

What are the characteristic findings on fundoscopy for retinal vein occlusion?

A
  • Dilated tortuous retinal veins
  • Flame and blot haemorrhages
  • Retinal oedema
  • Cotton wool spots
  • Hard exudates
  • ‘Blood and thunder’ appearance.
130
Q

Management of retinal vein occlusion?

A

Management aims to treat macular oedema and prevent neovascularisation:

  • Anti-VEGF therapies (e.g. ranibizumab and aflibercept).
  • Dexamethasone intravitreal implant (to treat macular oedema).
  • Laser photocoagulation (to treat new vessels).
131
Q

The ‘pizza pie’ appearance on fundoscopy is characteristic of what?

A

CMV retinitis

132
Q

Define central retinal artery occlusion (CRAO)

A

Obstruction to blood flow through the central retinal artery, causing ischaemia of the retina and sudden monocular visual loss.

133
Q

Central retinal artery is a branch of?

A

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

134
Q

Describe the causes for CRAO

A
  • Atherosclerosis (most common): RF include smoking, hypertension, diabetes and raised cholesterol.
  • Giant cell arteritis (vasculitis): RF include white ethnicity, older age, female and polymyalgia rheumatica.
135
Q

Describe the presentation of CRAO

A

Sudden painless loss of vision - ‘curtain coming down’ over the vision.

136
Q

What are the signs associated with CRAO?

A
  • Relative afferent pupillary defect.
  • Pale retina with a cherry red spot on fundoscopy.
137
Q

How would you test for a relative afferent pupillary defect (RAPD)?

A

Swinging light test

138
Q

Differentials for sudden painless vision loss

A
  • Retinal detachment
  • Central retinal artery occlusion
  • Central retinal vein occlusion
  • Vitreous haemorrhage (due to diabetic retinopathy).
139
Q

What does RAPD indicate?

A

Unilateral or asymmetrical disease of the retina or optic nerve (but only optic nerve disease that occurs in front of the optic chiasm) e.g. glaucoma, retinal disease, or multiple sclerosis.

140
Q

Outline the management for CRAO

A

Identification of giant cell arteritis (ESR blood test and temporal artery biopsy) - treated urgently with high-dose steroids.

Immediate management options attempt to dislodge/resolve the blockage:

  • Intra-arterial thrombolysis (catheter-directed delivery of recombinant tissue plasminogen activator (tPA) via the ophthalmic artery).
  • Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure).
  • Ocular massage (massaging the eye).
  • Inhaled carbogen (5% carbon dioxide and 95% oxygen) (to dilate the artery).
  • Sublingual isosorbide dinitrate (to dilate the artery).
  • Oral pentoxifylline (to dilate the artery).
  • IV acetazolamide (to reduce the intraocular pressure).
  • IV mannitol (to reduce the intraocular pressure).
  • Topical timolol (to reduce the intraocular pressure).

Long-term management involves managing reversible risk factors and secondary prevention for CVD.

141
Q

Which genetic condition is characterised by degeneration of the photoreceptors in the retina, particularly the rods?

A

Retinitis pigmentosa

142
Q

Describe the typical presentation of retinitis pigmentosa

A
  • Symptoms start in childhood.
  • Night blindness (often the first symptom).
  • Peripheral vision loss (before the central vision is affected).
143
Q

What are the signs on fundoscopy for retinitis pigmentosa?

A

‘Bone-spicule’ pigmentation. The pigmentation is most concentrated around the mid-peripheral area of the retina.

144
Q

Which genetic, systemic diseases are associated with retinitis pigmentosa?

A
  • Usher syndrome also causes hearing loss.
  • Bassen-Kornzweig syndrome also causes progressive neurological impairments.
  • Refsum disease also causes peripheral neuropathy, hearing and ichthyosis (scaly skin).
145
Q

What is the general management for retinitis pigmentosa?

A
  • Referral to an ophthalmologist for assessment, diagnosis and follow-up.
  • Genetic counselling.
  • Vision aids.
  • Sunglasses to protect the retina from accelerated damage.
  • Driving limitations and informing the DVLA.
146
Q

Scleritis vs. Episcleritis

A

Scleritis is painful, episcleritis is not painful.

147
Q

What can be given to slow vision loss in dry AMD?

A

High dose of beta-carotene, vitamins C and E, and zinc.

148
Q

Define Herpes zoster ophthalmicus

A

Reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve.

149
Q

What complications are associated with Herpes zoster ophthalmicus?

A
  • Ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
  • Ptosis
  • Post-herpetic neuralgia
150
Q

Define optic neuritis

A

Inflammation of the optic nerve secondary to demyelination that leads to acute visual loss.

151
Q

Pathophysiology of optic neuritis

A

Immune-mediated demyelination of the optic nerve.

152
Q

Which condition is optic neuritis linked with?

A

MS

153
Q

Outline the symptoms and signs of optic neuritis

A

Symptoms:

  • Visual loss: the loss of vision is typically acute, central, and unilateral occurring over hours to days.
  • Eye pain: worse on visual movement.
  • Reduced colour vision (particularly reds).
  • Photopsia: this refers to flickering or flashes of light.

Signs:

  • Relative afferent pupillary defect (RAPD): refers to asymmetrical pupillary reaction to light due to optic nerve disease. Tested using the ‘swinging light test’.
  • Visual field defects: commonly a central scotoma (i.e. a partial loss of vision in an otherwise normal visual field), but many different visual field defects can be present.
  • Papillitis: seen in anterior optic neuritis. There is evidence of a swollen optic disc on fundoscopy that is similar to papilloedema but the key is that visual loss is markedly reduced in papillitis. In posterior optic neuritis the disc appears normal.
  • Optic atrophy: this is a chronic sign of optic neuritis that can be seen following an acute episode. The optic disc appears shrunken and pale on fundoscopy. The degree of atrophy depends on the number of attacks and severity.
154
Q

Describe the swinging light test

A

The swinging light test is completed to assess for a RAPD. The examiner shines a light into one of the pupils. Light shone into the unaffected eye leads to bilateral pupillary constriction as the afferent pathway is unaffected. When the light source is swung across into the affected eye there is mild pupillary constriction as some light is still sensed (depending on severity), but the contralateral unaffected pupil dilates due to an abnormal afferent pathway. In other words, the consensual light reflux is reduced due to abnormal function of the optic nerve.

155
Q

What imaging can be used to diagnose optic neuritis?

A

MRI

156
Q

LP findings for optic neuritis?

A
  • Elevated protein
  • Elevated lymphocytes
  • Oligoclonal bands (OCB)
157
Q

What is the treatment for optic neuritis?

A

High-dose IV steroids

158
Q

What is the prognosis for optic neuritis?

A

Visual recovery is common

159
Q

Differential for sudden vision loss in diabetics?

A

Vitreous haemorrhage

160
Q

Flashers and floaters are most commonly caused by what?

A

Posterior vitreous detachment

161
Q

List 2 risk factors for posterior vitreous detachment

A
  • Advancing age (>65).
  • Near-sighted (myopic).
162
Q

Why should IV antibiotics be given to a patient with orbital cellulitis?

A

Due to the risk of cavernous sinus thrombosis and intracranial spread.

163
Q

What is the pathophysiology behind cotton wool spots?

A

Retinal infarction

164
Q

Outline the causes of papilloedema

A
  • Space-occupying lesion: neoplastic, vascular
  • Malignant hypertension
  • Idiopathic intracranial hypertension
  • Hydrocephalus
  • Hypercapnia
165
Q

What is the medical term for unequal pupil size?

A

Anisocoria

166
Q

What is the medical term for blood in the anterior chamber of the eye?

A

Hyphema

167
Q

What is the emergency treatment for orbital compartment syndrome?

A

Lateral canthotomy

168
Q

What investigation should be used when suspecting any corneal damage to see the extent of damage and penetrating injury?

A

Fluorescein staining

169
Q

Papilloedema indicates which grade of hypertensive retinopathy?

A

Grade IV

170
Q

Cotton wool spots, blot and flame haemorrhages indicate which grade of hypertensive retinopathy?

A

Grade III

171
Q

Most likely cause of contact lens associated keratitis?

A

Pseudomonas aeruginosa

172
Q

What are the causes of pre-chiasmal field defects?

A

They’re due to abnormalities with the retina or optic nerve.

173
Q

Define scotoma

A

An area of reduced (or absent) vision in an otherwise normal visual field (i.e. a blind spot).

A central scotoma involves the macula leading to a defect in central vision.

174
Q

Define anopia

A

Absence of sight.

175
Q

Causes of a unilateral anopia?

A

Pre-chiasmal field defects e.g. monocular visual loss

176
Q

Describe the optic chiasm visual field defect

A

Bitemporal hemianopia

177
Q

Describe the post-chiasmal field defects

A
  • Homonymous hemianopia
  • Superior homonymous quadrantanopia
  • Inferior homonymous quadrantanopia
  • Macular sparing
178
Q

Causes of a superior homonymous quadrantanopia?

A

Lesion involving the temporal lobe optic radiations.

179
Q

Causes of an inferior homonymous quadrantanopia?

A

Lesion involving the parietal lobe optic radiations.

180
Q

What does Hutchinson’s sign indicate?

A

Vesicles extending to the tip of the nose. This is strongly associated with ocular involvement in shingles.

Child Health (9 decks)

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