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Special senses > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is a glaucoma? What are the two types?

A

Optic nerve damage caused by significant rise in intraocular pressure caused by blockage in aqueous humour trying to escape eye

Open-angle and closed-angle

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2
Q

Label the following:

A
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3
Q

Label:

A
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4
Q

What fills the vitreous chamber?

A

Vitreous humour

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5
Q

What fills the anterior chamber and posterior chamber?

A

Aqueous humour (supplies nutrients to the cornea)

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6
Q

What is the aqueous humour produced by? Where does it flow?

A

Ciliary body (flows from ciliary body, around lens, under iris through the anterior chamber through trabecular meshwork and into the canal of Schlemm - then into general circulation)

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7
Q

What is the normal intraocular pressure? How is this created?

A

10-21mmHg

Created by resistance to flow through the trabecular meshwork into the canal of Schlemm

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8
Q

What happens in open-angle glaucoma?

A

Gradual increase in resistance through the trabecular meshwork (slow and chronic onset)

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9
Q

What happens in acute angle-closure glaucoma?

A

Iris buldges forwards and seals off the trabecular meshwork from anterior chamber (emergency)

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10
Q

What happens to the optic disc when intraocular pressure is raised?

A

Cupping of the optic disc (greater than 0.5 is abnormal)

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11
Q

What are the risk factors for open angle glaucoma?

A

Increased age

FH

Black ethnic origin

Nearsightedness (myopia)

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12
Q

How does open-angle glaucoma present?

A

Asymptomatic (often diagnosed by routine screening)

Affects peripheral vision first creating tunnel vision, also:

  • Fluctuating pain
  • Headaches
  • Blurred vision
  • Halos appearing around lights
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13
Q

What are the two ways of measuring intraocular pressure?

A

Non-contact tonometry - shooting “puff of air” at cornea and measuring corneal response (less accurate, good for screening)

Goldmann applanation tonometry - device mounted on slip lamp which makes contact with cornea and applies different pressures to measure intraocular pressure (gold standard)

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14
Q

How is open angle glaucoma diagnosed?

A

Goldman applanation tonometry - check intraocular pressure

Fundoscopy - check optic disc cupping and optic nerve health

Visual field assessment - peripheral vision loss

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15
Q

At what intraocular pressure is treatment started?

A

24mmHg or above

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16
Q

What is the management of open angle glaucoma?

A

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

Other options:

  • Beta-blockers (timolol) reduces production of aqueous humour
  • Carbonic anhydrase inhibitors (e.g. dorzolamide) reduces the production of aqueous humour
  • Sympathomimetics (e.g. brimonidine) reduces production fo aqueous humour and increase uveoscleral outflow

Surgery

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17
Q

What are the side effects of prostaglandin analogue eye drops (e.g. latanoprost)?

A

Eyelash growth

Eyelid pigmentation

Iris pigmentation

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18
Q

What is the surgery for open angle glaucoma?

A

Trabeculectomy (if eyedrops ineffective)

Creat new channel from anterior chamber through sclera to a location under conjunctiva (creating “bleb”) where aqueous humour drains

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19
Q

Where is the pressure build up greatest in acute angle-closure glaucoma?

A

Posterior chamber causing pressure behind iris and worsening of closure of angle

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20
Q

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

A

Increasing age

Female (4:1)

FH

Chinese and east asian origin (unlike open-angle glaucome, rare in black ethnicity)

Hypermetropia (long sightedness)

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21
Q

Which medications can precipitate acute angle-closure glaucoma?

A

Adrenergic medications e.g. noradrenalin

Anticholinergic medications e.g. oxybutynin and solifenacin

TCA e.g. amitriptyline (have anti-cholinergic effects)

Mydriatic eye drops

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22
Q

How does acute angle-closure glaucoma present?

A

Severely painful red eye

Blurred vision

Halos around lights

Associated headache, nausea and vomiting

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23
Q

How does acute angle-closure glaucoma appear on examination?

A

Red-eye

Teary

Hazy cornea

Decreased visual acuity

Dilatation of affected pupul

Fixed pupil size

Film eyeball on palpation

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24
Q

What is the inital management of acute open-angle glaucoma?

A

Referred for same-day assessment by opthalmologist

  • Lie patient on back without pillow
  • Give pilocarpine eye drops (2% blue, 4% brown)
  • Acetazolamide 500mg orally
  • Analgesia and antiemetic if required
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25
Q

How does pilocarpine work?

A

On muscarinic receptors in sphincter muscles of iris causing constriction of pupil (miotic agent)

Causes ciliary muscle contraction

Opening up pathway from flow of aqueous humour from ciliary body around iris and into trabecular meshwork

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26
Q

How does acetazolamide work?

A

Carbonic anhydrase inhibitor (reducing production of aqueous humour)

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27
Q

What medical options are there in secondary care for acute angle-closure glaucoma?

A

Pilocarpine

Acetazolamide (oral / IV)

Hyperosmotic agents e.g. glycerol or mannitol increases osmotic gradient between blood and fluid in eye

Timolol = beta-blocker that reduces production of aqueous humour

Dorzolamide = carbonic anhydrase inhibitor reducing production of aqueous humour

Brimonidine = sympathomimetic reducing production of aqueous fluid and increasing uveoscleral outflow

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28
Q

What is the surgical management of acute angle-closure glaucoma?

A

Laser iridotomy (definitive treatment) - laser makes hole in iris to allow aqueous humour to flow from posterior chamber into anterior chamber relieving pressure

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29
Q

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

A

Age-related degeneration of the macular causing progressive deterioration in vision

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30
Q

What is a key fundoscopy finding in macular degeneration?

A

Drusen

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31
Q

What are the two types of age related macular degeneration?

A

Wet (worse prognosis)

Dry

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32
Q

What are the four layers of the macular?

A

Choroid layer (bottom = blood vessels to macula)

Bruch’s membrane

Retinal pigment epithelium

Photoreceptors

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33
Q

What are drusen?

A

Yellow deposits of protein and lipids that appear between retinal pigment epithelium and Bruch’s membrane

Some is normal (<63 micrometres) and hard

Larger and more = early sign of macular degeneration

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34
Q

What features are common to both wet and dry AMD?

A

Atrophy of the retinal pigment epithelium

Degeneration of the photoreceptors

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35
Q

What feature is unique to wet AMD?

A

Development of new vessels growing from choroid layer into retina - can leak fluid or blood and cause oedema and more rapid loss of vision

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36
Q

What is targeted in the treatment of wet AMD?

A

Vascular endothelial growth factor (VEGF)

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37
Q

What are the risk factors for AMD?

A

Age

Smoking

White / chinese ethnic origin

FH

CVD

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38
Q

How does AMD present?

A

Gradual worsening central visual field loss

Reduced visual acuity

Crooked or wavy appearance to straight lines

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39
Q

How does wet age-related macular degeneration present?

A

More acutely - loss of vision over days and progresses to full loss over 2-3 years (often progresses to bilateral)

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40
Q

What are the examination findings for AMD?

A

Reduced acuity using a Snellen chart

Scotoma (central patch of vision loss)

Amsler grid test - look for distortion of straight lines

Fundoscopy - drusen are key findings

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41
Q

What specialist investigations are there for AMD?

A

Slit-lamp biomicroscopic fundus examination by a specialist to diagnose AMD

Optical coherence tomography to gain cross-sectional view of layers of retina to diagnose wet AMD

Flurescein angiography - gives fluroscein contrast and photograph retina to look in detail at the blood supply to retina (useful to show up and oedema and neovascularisation) - used second line to diagnose wet AMD if optical coherence tomography doesn’t exclude wet AMD

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42
Q

What is the management of dry AMD?

A

No specific treatment for dry age-related macular degeneration, focus on slowing disease progression:

  • Avoid smoking
  • Control blood pressure
  • Vitamin supplementation (has evidence in slowing progression)
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43
Q

What is the treatment of wet AMD?

A

Anti-VEGF medicationse.g.ranibizumab,bevacizumabandpegaptanib

Injected directly into vitreous chamber of eye once a month (slow and reverse progression of disease)

Need to be started within 3 months to be beneficial

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44
Q

What is diabetic retinopathy?

A

Blood vessels in retina are damaged by prolonged exposure to high blood sugar levels

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45
Q

What happens in diabetic retinopathy?

A

Hyperglycaemia caused damage to retinal small vessels and endothelial cells = vascular permeability and blot haemorrhages and formation of hard exudates (yellow / white deposits of lipids in the retina)

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46
Q

What is the result of damage to blood vessels in diabetic retinopathy?

A

Microaneurysms and venous beading

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47
Q

What is the result of damage to nerve fibres in diabetic retinopathy?

A

Cotton wool spots = fluffy white patches on retina

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48
Q

What are the intraretinal microvascular abnormalities in diabetic retinopathy?

A

Dilated and tortous capillaries in retina, acting as shunt between arterial and venous vessels

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49
Q

What is neovascularisation?

A

Growth factors are released in the retina cauing development of new blood vessels

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50
Q

Label the following:

A
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51
Q

Label the following:

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52
Q

What are the two classificationsofdiabetic retinopathy?

A

Non-proliferative and proliferative (depending on if new blood vessels have developed)

Proliferative = background or pre-proliferative

Classified based on fundus examination

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53
Q

What are the categories of non-proliferative diabetic retinopathy?

A

Mild = microaneurysms

Moderate = microaneurysms, blot haemorrhages, hard exudates, cotton wool spots and venous bleeding

Severe = blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants, intraretinal microvascular abnormality (IMRA) in any quadrant

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54
Q

What categorises proliferative diabetic retinopathy?

A

Neovascularisation

Vitrous haemorrhage

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55
Q

What categorises diabetic maculopathy?

A

Macular oedema

Ischaemic maculopathy

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56
Q

What are some complications of diabetic retinopathy?

A

Retinal detachment

Vitreous haemorrhage (bleeding in to the vitreous humour)

Rebeosis iridis (new blood vessel formation in the iris)

Optic neuropathy

Cataracts

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57
Q

What is the management of diabetic retinopathy?

A

Laser photocoagulation

Anti-VEGF medications e.g. ranibizumab and bevacizumab

Vitreoretinal surgery (keyhole surgery on the eye) in severe disease

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58
Q

What is hypertensive retinopathy?

A

Damage to small blood vessels in retina related to systemic hypertension (result of chronic hypertension / quick in malignant hypertension)

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59
Q

What signs occur in the retina in response to hypertension?

A

Silver wiring / copper wiring = walls of arterioles become thickened and sclerosed causing increased reflection of light

Arteriovenous nipping = arterioles cause compression of veins where they cross (again due to sclerosing and hardening of arterioles)

Cotton wool spots = caused by ischaemia and infarction in retrina causing damage to nerve fibres

Hard exudates = caused by damaged vessels leaking lipids into the retina

Retinal haemorrhages = damaged vessels rupturing and releasing blood into retina

Papilloedema caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of margins

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60
Q

Label the following:

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61
Q

Label the following:

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62
Q

What are the stages to the Keith-Wagener Classification?

A

Stage 1: Mild narrowing of the arterioles

Stage 2: Focal constriction of blood vessels and AV nicking

Stage 3: Cotton-wool patches, exudates and haemorrhages

Stage 4: Papilloedema

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63
Q

What is the management of hypertensive retinopathy?

A

Controlling blood pressure and risk factors e.g. smoking, blood lipid levels

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64
Q

What is cataracts?

A

Lens in eye becomes cloudy and opaque reducing visual acuity and light that enters eye

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65
Q

What is the role of the lens?

A

Focus light coming into the eye onto the retina

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66
Q

What is the lens held in place by?

A

Suspensory ligaments attached to the ciliary body (this contracts and relaxes to focus the lens - contracts = releases tension and lens thickens)

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67
Q

What is the lens nourished by?

A

Surrounding fluid (no blood supply) - grows and develops through life

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68
Q

When does congenital cataracts form? How is it screened for?

A

Before birth - screened for using red reflex during neonatal examination

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69
Q

What are the risk factors for cataracts?

A

Increasing age

Smoking

Alcohol

Diabetes

Steroids

Hypocalcaemia

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70
Q

How does cataracts present?

A

Asymmetrical as both eyes are affected separately

  • Slow reduction in vision
  • Progressive blurring
  • Change in colour of vision = more brown / yellow
  • Starbursts can appear around lights (particularly at night)
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71
Q

What is a key sign of cataracts?

A

Loss of red reflex (might show up on photographs)

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72
Q

How to differentiate cataracts, glaucoma, macular degenration?

A

Cataracts = generalised reduction in visual acuity with starbursts around lights

Glaucoma = peripheral vision loss with halos around lights

Macular degeneration = central loss of vision with crooked or wavy appearance to straight lines

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73
Q

What is the management of cataracts?

At what level vision is this done?

A

If manageable then no intervention

Surgery = phaecoemulsification (dissolving lens with US) and implanting artifical lens into the eye (usually under local anaesthetic)

Vision = less than 6/12

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74
Q

Why may surgery not be successful for cataracts?

A

May prevent detection of other pathology e.g. macular degenration / diabetic retinopathy

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75
Q

What is endopthalmitis?

A

Rare but serious complication of cataracts surgery = inflammation of the inner contents of the eye usually caused by infection can be treated with intravitreal abx

Can cause loss of vision / eye itself

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76
Q

What stimulates the circular muscles in the iris?

A

Parasympathetic nervous system using acetylcholine as a neurotransmitter (nerve fibres travel along the oculomotor cranial nerve)

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77
Q

What stimulates the dilator muscles?

A

Parasympathetic nervous system using adrenaline as a neurotransmitter

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78
Q

What can cause an abnormal pupil shape?

A

Trauma to the sphincter muscles in the iris (cataracts surgery or other eye operations)

Anterior uveitis causing adhesions (scar tissue)

Acute angle closure glaucoma (ischaemic damage to the muscles = vertical oval pupil shape)

Rubeosis iridis (neovascularisation in the iris) distorts shape of iris and pupil - associated w diabetic retinopathy

Coloboma is a congenital malformation in eye - hole in iris

Tadpole pupil - spasm in a segment of iris causing misshapen pupil (temporary and associated with migraines)

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79
Q

What are some causes of mydriasis (dilated pupil) ?

A

Third nerve palsy

Holmes-Adie syndrome

Raised intracranial pressure

Congenital

Trauma

Stimulants, such as cocaine

Anticholinergics

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80
Q

What are some causes of miosis (constricted pupil)?

A

Horners syndrome

Cluster headaches

Argyll-Robertson pupil (in neurosyphilis)

Opiates

Nicotine

Pilocarpine

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81
Q

How does a third nerve palsy appear?

A

Ptosis (drooping upper eyelid)

Dilated non-reacrive pupil

Divergent strabismus (squint) in affected eye (down and out position)

82
Q

Why does the eye move outward and downwards in a 3rd nerve palsy?

A

Oculomotor nerve supplies all extraocular muscles except lateral rectus and superior oblique

83
Q

Why does third nerve palsy also cause ptosis?

(what supplies the obicularis oculi)?

A

It supplies levator palpebrae superioris responsible for lifting upper eyelid

Facial nerve = obuicularis oculi (unopposed so cant open eyelid)

84
Q

Why does a third nerve palsy also cause a dilated fixed pupil?

A

Supplies the parasympathetic fibres that innervates the sphincter muscle of the iris

85
Q

How does the oculomotor nerve travel from the brainstem?

What can cause compression of the nerve?

A

Straight line through cavernous sinus and close to posterior communicating artery

Cavernous sinus thromobis and posterior communicating artery aneurysm

86
Q

What can a third nerve palsy with sparing of the pupil suggest? What can cause it?

A

Suggests microvascular cause as parasympathetic fibres are spared:

  • Diabetes
  • Hypertension
  • Ischaemia
87
Q

What can cause a full third nerve palsy?

A

Idiopathic

Tumour

Trauma

Cavernous sinus thrombosis

Posterior communicating artery aneurysm

Raised intracranial pressure

(also called a surgical third)

88
Q

What is the triad in horner syndrome?

A

Ptosis

Miosis

Anhidrosis (loss of sweating)

(may also have enopthalmos)

89
Q

What causes horner’s syndrome? What journey do the fibres take?

A

Damage to the sympathetic nervous system

Arise from spinal cord (pre-ganglionic nerves) then enter into sympathetic ganglion at the base of the neck and exit as post-ganglionic nerves (travel to the head along internal carotid artery)

90
Q

How can the location of the Horner syndrome be determined?

A

By anhidrosis:

  • Central lesion = arm and trunk and face
  • Pre-ganglionic = face
  • Post-ganglionic = no anhidosis
91
Q

What are the causes of Horner syndrome?

A

4 S’s (sentral), 4 T’s (torso - pre-ganglionic) 4 C’s (cervical - post ganglionic)

  • Stroke
  • MS
  • Swelling (tumour)
  • Syringomyelia (cyst in the spinal cord)
  • Tumour (pancoast)
  • Trauma
  • Thyroidectomy
  • Top rib (cervical rib growing above the first rib above clavicle)
  • Carotid aneurysm
  • Carotid artery dissection
  • Cavernous sinus thrombosis
  • Cluster headache
92
Q

What is congenital Horner syndrome associated with?

A

Heterochromia (difference in colour of iris on affected side)

93
Q

What can be used to test for Horner syndrome?

A

Cocaine eye drops (stops noradrenaline re-uptake at neuromuscular junction)

Normal eye = dilation

Horner eye = nerves are not releaseing noradrenaline in the first place so no difference

ALTERNATIVELY low concentration adrenaline eye drop (0.1%) won’t dilate a normal pupil but will dilate a Horner syndrome pupil

94
Q

What is a Holmes Adie pupil?

A

Unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction (over time the pupil gets smaller)

Caused by damage to the post-ganglionic parasympathetic fibres (cause is unknown but may be viral)

95
Q

What is Holmes Adie syndrome?

A

Holmes Adie pupil with absent ankle and knee reflexes

96
Q

What is Argyll-Robertson Pupil?

A

Finding in neurosyphilis - constricted pupil that accommodates when focusing on near objects but no reaction to light

Prostitutes pupil = accommodates but does not react

97
Q

What is blepharitis?

A

Inflammation of the eyelid margins

98
Q

What are the features of blepharitis?

A

Gritty, itchy, dry sensation in the eyes - associated with dysfunction of Meibomian glands (these secrete oil onto surface of eye)

99
Q

What can blepharitis lead to?

A

Styes

Chalazions

100
Q

What is the management of blepharitis?

A

Hot compress and gentle cleaning of eyelid to remove debris using cotton wool dipped in sterilised water and baby shampoo

101
Q

What eyedrops can be used to relieve symptoms of blepharitis?

A

Hypromellose is least viscous (effect lasts around 10 mins)

Polyvinyl alcohol is middle viscous choice

Carbomer is most viscous (lasts 30-60 mins)

102
Q

What are the two types of styes (may contain pus)?

A

Hordeolum externum = infection of glands of Zeis (sebaceous glands at base of eyelashes) or glands of Moll (sweat glands at base of eyelids)

Hordeolum internum = infection of Meibomian glands (deeper and more painful, may be underneath eyelid)

103
Q

What are the treatment of styes?

A

Hot compresses and analgesia (consider topical antibiotics e.g. chloramphenicol) if its associated with conjunctivits or persistent

104
Q

What is a Chalazion?

A

Blocked Meibomian gland (often called Meibomian cyst) = swelling in eyelid that is non-tender

105
Q

What is the treatment of a chalazion?

A

Hot compress and analgesia (consider topical antibiotics e.g. chloramphemicol if acutely inflammed)

Sugical drainage may be required

106
Q

What is entropion?

A

Eyelid turns inwards with lashes against eyeball

107
Q

What can result from entropion?

A

Pain

Corneal damage

Ulceration

108
Q

What is the management of entropion?

A

Taping eyelid down to prevent turning inwards (use lubricating eye drops to prevent eye drying out)

Definitive = surgical intervention

109
Q

What is ectropion?

A

Eyelid turns outwards with inner aspect of eyelid exposed

110
Q

What can result from ectropion?

What is the treatment?

A

Exposure keratopathy (eyeball is exposed and not adequately lubricated)

Mild = no treatment (regular lubricating eyedrops)

Severe = surgery

111
Q

What is trichiasis?

A

Inward growth of the eyelashes (causes pain, corneal damage, ulceration)

112
Q

What is the management of trichiasis?

A

Removal of eyelash (epilation)

If recurrent = electrolysis, cryotherapy or laser treatment (prevents lash regrowing)

113
Q

What is periorbital cellulitis (aka preorbital cellulitis)?

A

Eyelid and skin infection in front of the orbital septum (in front of eye) presenting with swelling, redness and hot skin around eyelids and eye

114
Q

How to distinguish preorbital cellulitis from orbital cellulitis (sight and life threatening emergency)?

A

CT scan

115
Q

What is the treatment of preorbital cellulitis?

A

Systemic antibiotics (oral / IV)

Can develop into orbital cellulitis so vulnerable patients may require admission

116
Q

What is orbital cellulitis?

A

Infection around the eyeball involving tissue behind orbital septum

117
Q

What are the distinguishing features of orbital cellulitis?

A

Pain on eye movement

Reduced eye movements

Changes in vision

Abnormal pupil reactions

Forward movement of eye (proptosis)

118
Q

What is the management of orbital cellulitis?

A

Admission

IV abx

Surgical drainage if abscess forms

119
Q

What is conjunctivitis?

A

Inflammation of the conjunctiva (thin layer of tissue covering inside of eyelids and sclera of eye)

  • Bacterial
  • Viral
  • Allergic
120
Q

How does conjunctivitis present?

A

Unilateral or bilateral

Red eyes

Bloodshot

Itchy or gritty sensation

Discharge from the eye

121
Q

What eye symptoms does conjunctivitis not cause?

A

Pain, photophobia or reduced visual acuity (may be blurry when eye is covered with discharge, when this is cleared the acuity should be normal)

122
Q

How does bacterial conjunctivitis present?

A

Purulent discharge and inflammed conjunctiva (worse in morning, eyes stuck together)

Highly contagious

123
Q

How does viral conjunctivitis present?

A

Clear discharge

Dry cough sore throat, blocked nose

Tender preauricular lymph nodes (in front of ear)

Contagious

124
Q

What are the differential diagnoses of acute red eye?

A

Painless red eye

  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage

Painful red eye

  • Glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury
125
Q

What is the management of conjunctivitis?

A

Usually resolves without treatment after 1-2 weeks

Good hygiene (avoid sharing towels / rubbing eyes / contact lenses)

Clear eyes with cooled boiled water / cotton wool

Abx eye drops if bacterial cause (chloramphenicol and fuscidic acid eye drops are both options)

If under 1 month then urgent opthalmology review as neonatal conjunctivitis can be associated with gonococcal infection and can cause loss of sight and pneumonia

126
Q

What is allergic conjunctivitis cause by?

A

Contact with allergens causing swelling of the conjunctival sac and eye lid with significant watery discharge and itch

127
Q

What can be used to reduce symptoms of allergic conjunctivitis?

A

Antihistamines

Topical mast-cell stabilisers in patients with chronic seasonal symptoms (prevent mast cells releasing histamine - use for several weeks before benefit)

128
Q

What is anterior uveitis aka iritis?

A

Inflammation in anterior part of uvea (iris, ciliary body and choroid)

Choroid = layer between retina and sclera

129
Q

What cells infiltrate the anterior chamber of the eye?

What do they cause?

A

Neutrophils

Lymphocytes

Macrophages

Due to either autoimmune process, infection, trauma, ischaemia or malignancy

Causing floaters in patients vision

130
Q

How to differentiate chronic anterior uveitis from acute?

A

Chronic = granulomatous (more macrophages) and less severe and longer duration (lasts more than 3 months)

131
Q

What is acute anterior uveitis associated with?

A

HLA B27 conditions

  • Ankylosing spondylitis
  • IBD
  • Reactive arthritis
132
Q

What can chronic anterior uveitis associated with?

A
  • Sarcoidosis
  • Syphilis
  • Lyme disease
  • Tuberculosis
  • Herpes virus
133
Q

How does anterior uveitis present?

A

Unilateral symptoms starting spontaeously without history of trauma / precipitating event

With flare of associated disease e.g. reactive arthritis

134
Q

What are the symptoms of anterior uveitis?

A
  • Dull, aching, painful red eye
  • Ciliary flush (ring of red spreading from cornea outwards)
  • Reduced visual acuity
  • Floaters / flashes
  • Sphincter muscle contraction causing miosis (constricted pupil)
  • Photophobia due to ciliary muscle spasm
  • Pain on movement
  • Excessive tear formation (lacrimation)
  • Abnormally shaped pupil due to posterior synechiae(adhesions) pulling the iris into abnormal shapes
  • Hypopyon - collection of WBC in anterior chamber, seen as yellowish fluid collection settled in front of the lower iris with a fluid level
135
Q

Which investigations can help establish diagnosis of red eye?

A

Same day assessment by opthalmologist

  • Full slit lamp assessment of different structures
  • Intraocular pressures
136
Q

What are the treatment options for anterior uveitis?

A

Steroids (oral, topical or IV)

Cycloplegic (paralysing ciliary muscles)-mydriatic (dilating pupil) medications e.g. cyclopentolate or atropine eye drops (anti-muscarinic medications, blocking action of iris sphincter muscles and ciliary body) - dilate pupil and reduce pain associated with ciliary spasm

Immunosuppressants e.g. DMARDS and TNF inhibitors

Laser therapy, cryotherapy or surgery (vitrectomy)

137
Q

What is episcleritis?

A

Self-limiting inflammation of the episclera, outermost layer of the sclera (just underneath the conjunctiva)

Not usually caused by infection

138
Q

What is episcleritis associated with?

A

Inflammatory disorders e.g. RA and IBD

139
Q

How does episcleritis present?

A

Acute onset unilateral symptoms:

  • Typically not painful but there can be mild pain
  • Segmental redness (rather than diffuse). There is usually a patch of redness in the lateral sclera.
  • Foreign body sensation
  • Dilated episcleral vessels
  • Watering of eye
  • No discharge
140
Q

What is the management of episcleritis?

A

If in doubt, refer to ophthalmology

Usually self limiting and recovery in 1-4 weeks

Lubricating eye drops can help symptoms

Simple analgesia, cold compress and safetynet advice

Severe = systemic NSAIDs (e.g. naproxen) or topical steroid eye drops

141
Q

What is scleritis?

A

Inflammation of full thickness of sclera (more serious than episcleritis) usually not caused by infection

142
Q

What is the most severe type of scleritis?

A

Necrotising scleritis - normally have visual impairment but no pain (can lead to perforation of sclera)

143
Q

Which systemic conditions may be associated with scleritis?

A

Rheumatoid arthritis

SLE

IBD

Sarcoidosis

Granulomatosis with polyangiitis

144
Q

How does scleritis present?

A

Acute onset (50% = bilateral)

  • Severe pain
  • Pain with eye movement
  • Photophobia
  • Eye watering
  • Reduced visual acuity
  • Abnomal pupil reaction to light
  • Tenderness to palpation of eye
145
Q

What is the management of scleritis?

A

Potentially life threatening = referred for same day assessment by ophthalmologist

  • Consider underlying condition
  • NSAIDs (topical / systemic)
  • Steroids (topical / systemic)
  • Immunosuppression appropriate to underlying systemic condition (e.g. methotrexate in RA)
146
Q

What are corneal abrasions?

What supplies sensory supply to cornea?

A

Scratches or damage to the cornea (cause of red, painful eye)

Sensation = ophthalmic division of trigeminal nerve

147
Q

What are the causes of corneal abrasions?

A

Contact lenses

Foreign bodies

Finger nails

Eyelashes

Entropion (inward turning eyelid)

148
Q

What infection may be present in abrasion with contact lenses?

A

Pseudomonas

149
Q

What is an important differential to rule out in corneal abrasions?

A

Herpes keratitis

150
Q

How do corneal abrasions present?

A

History of contact lenses or foreign body

Painful red eye

Foreign body sensation

Watering eye

Blurring vision

Photophobia

151
Q

How are corneal abraisons diagnosed?

A

Fluorescein stain applied to eye - yellow - orange colour collects in abrasions or ulcers highlighting them

Slit lamp examination for more significant abrasions

152
Q

What is the managament of corneal abrasions in secondary care?

A

Simple analgesia (e.g. paracetamol)

Lubricating eye drops to improve symptoms

Antibiotic eye drops (i.e. chloramphenicol)

Bring patient back after 1 week to check healed

Cyclopentolate eye drops dilate the pupil and improve significant symptoms, particularly photophobia (usually not necessary)

Uncomplicated corneal abraisons = heal over 2-3 days

153
Q

What is keratitis? What are the causes?

A

Keratitis = inflammation of cornea

  • Viral infection with herpes simplex
  • Bacterial infection with pseudomonas or staphylococcus
  • Fungal infection with candida or aspergillus
  • Contact lens acute red eye (CLARE)
  • Exposure keratitis (caused by inadequate eyelid coverage e.g. eyelid ectropion)
154
Q

What is the most common cause of keratitis? What kind of inflammation can it cause?

A

Herpes simplex keratitis

Affects epithelial layer of cornea (can be primary or recurrent)

155
Q

What is inflammation in stroma called?

What can it lead to?

A

Stromal keratitis (stroma = layer between epithelium and endothelium)

Associated with stromal necrosis, vascularisation and scarring can lead to corneal blindness

156
Q

How does herpes keratitis present?

A

Painful red eye

Photophobia

Vesicles around the eye

Foreign body sensation

Watering eye

Reduced visual acuity (subtle to significant)

157
Q

What investigations are there for herpes keratitis?

A

Slit lamp examination to find and diagnose keratitis

Staining with fluorescein will show dendritic corneal ulcer (branching and spreading of ulcer)

Corneal swabs or scrapings can be used to isolate the virus using a viral culture or PCR

158
Q

What are the management options for Herpes Keratitis in secondary care?

A

Aciclovir (topical or oral)

Glanciclovir eye gel

Topical steroids (used alongside antivirals for stromal keratitis)

Corneal transplant (maybe after infection resolves to treat corneal scarring by stromal keratitis)

159
Q

What is a subconjunctival haemorrhage?

A

Small blood vessel in the conjunctiva ruptures between sclera and conjunctiva (often appearing after coughing, weight lifting, or straining when constipated)

160
Q

Which conditions may predisposed to subconjunctival haemorrhage?

A

HTN

Bleeding disorders e.g. thrombocytopaenia

Whooping cough

Medications (warfarin, NOAC, antiplatelet)

Non-accidental injury

161
Q

How does a subconjunctival haemorrhage present?

A

Bright red blood underneath conjunctiva

Painless

Doesn’t affect vision

162
Q

How is a subconjunctival haemorrhage diagnosed?

A

History and examination

163
Q

What is the managament of subconjunctival haemorrhage?

A

Resolves without treatment (2 weeks)

Investigate for possible causes?

Foreign body sensation = lubricating eye drops

164
Q

What is the vitreous humour?

A

Gel inside eye maintaining structure and keeping retina pressed on the choroid (made from collagen and water)

Aging = less firm and able to keep shape

165
Q

Who is posterior vitreous detachment most common in?

A

Older patients

166
Q

How may posterior vitreous detachment present?

A

Painless

Spots of vision loss

Floaters

Flashing lights

167
Q

What is the management of posterior vitreous detachement?

A

No treatment - brain adjusts over time

Can predispose to retinal tears or retinal detachment (assess retina to rule out)

168
Q

What is retinal detachment?

A

Retina separates from choroid underneath (due to retinal tear allowing vitreous fluid to get underneath retina)

169
Q

Why is retinal detachment a sight-threatening injury?

A

Outer retina relies on the blood vessels of the choroid for its blood supply

170
Q

What are the risk factors for retinal detachment?

A

Posterior vitreous detachment

Diabetic retinopathy

Trauma to the eye

Retinal malignancy

Older age

FH

171
Q

How does retinal detachment present?

A

Peripheral vision loss (sudden - like a curtain coming down vision)

Blurred and distored vision

Flashes and floaters

RAPD

172
Q

How should patients presenting with flashes / floaters be managed?

A

Assess retina for tears or detachment

173
Q

How are retinal tears managed?

A

Create adhesions between retina and choroid to prevent detachment:

  • Laser therapy
  • Cryotherapy
174
Q

How can retinal detachment be treated?

A

Vitrectomy - removing relevant parts of vitreous body and replace with oil / gas

Scleral buckling - using silicone“buckle” to put pressure on the outside of the eye (sclera) to outer eye indents to bring the choroid inwards and into contact with the detached retina

Pneumatic retinopexy - injecting gas bubble into vitreous body and positioning patient so bubble creates pressure that flattens retina against choroid

THEN TREAT RETINAL TEARS

175
Q

What is a central retinal vein occlusion?

A

Blood clot (thrombus) forms in the retinal veins and blocks drainage of blood from retina (central retinal vein runs through optic nerve)

176
Q

How many veins come together to form central retinal vein?

A

4

177
Q

What happens in blocking of retinal vein?

A

Pooling of blood

Leakage of fluid / blood = macular oedema and retinal haemorrhages

Release of VEGF causing neovascularisation

178
Q

How does retinal vein occulsion present?

A

Sudden painless loss of vision

179
Q

What are the risk factors for retinal vein occulsion?

A

Hypertension

High cholesterol

Diabetes

Smoking

Glaucoma

Systemic inflammatory conditions e.g. systemic lupus erythematosus

180
Q

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

A

Flame and blot haemorrhages (cheese and tomato pizza)

Optic disc oedema

Macula oedema

181
Q

Which associated conditions to test for in retinal vein occlusion?

A

Full medical history

FBC for leukaemia

ESR for inflammatory disorders

Blood pressure for hypertension

Serum glucose for diabetes

182
Q

What is the management of retinal vein occlusion?

A

Referred to ophthalmologist for assessment and management

To treat macular oedema and prevent complications e.g. neovascularisation of retina and iris and glaucoma:

  • Laser photocoagulation
  • Intravitreal steroids (e.g. dexamethasone intravitral implant)
  • Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)
183
Q

What is the central retinal artery a branch of?

A

Opthalmic artery (branch of internal carotid)

184
Q

What can cause occlusion of the retinal artery?

A

Atherosclerosis

Giant cell arthritis (vasculitis affecting the ophthalmic or central retinal artery)

185
Q

What are the risk factors for retinal artery occlusion by atherosclerosis?

A

Older age

FH

Smoking

Alcohol consumption

HTN

Diabetes

Poor diet

Inactivity

Obesity

186
Q

Who is at risk of retinal artery occlusion secondary to giant cell arteritis?

A

White patients

> 50

Female

Those affected by giant cell arteritis / polymyalgia rheumatica

187
Q

How does central retinal artery occlusion present?

A

Sudden painless loss of vision

Relative afferent pupillary defect (pupil in affected eye constricts more when light shone in other eye, input is not being sensed by the ischaemic retina when testing direct light reflex)

188
Q

What will fundoscopy show for central retina occlusion?

A

Pale retina with a cherry-red spot (macula = thinner surface showing red choroid and contrasting with pale retina)

189
Q

What is the management of suspected central retinal occlusion?

A

Referred immediately to ophthalmologist

Older patient = tested (ESR and temporal artery biopsy) and treated with high dose steroids (i.e. prednisolone 60mg)

190
Q

What is the immediate and long term management of central retinal artery occlusion?

A

Immediate (if presenting shortly after symptoms)

  • Ocular massage (to dislodge)
  • Remove fluid from anterior chamber to reduce intraocular pressure
  • Inhaling carbogen (mix 5% CO2 and 95% O2 to dilate artery)
  • Sublingual isosorbide dinitrate to dilate the artery

Long term

  • Treat reversible risk factors and secondary prevention
191
Q

What is retinitis pigmentosa?

A

Congenital inherited condition where there is degenration of the rods and cones in the retina (can occur with systemic disease or isolated)

Mostly rods degenerate more causing night blindness (decreased central and peripheral vision)

192
Q

How does retinitis pigmentosa present?

A

Night blindness (first symptom)

Peripheral vision is lost before central vision

FH is important

193
Q

What will fundoscopy show for retinitis pigmentosa?

A

Pigmentation - “bone-spicule” pigmentation (similar to bone matrix)

Concentrated around mid-peripheral area of the retina

Associated narrowing of the arterioles and waxy / pale appearance to optic disc

194
Q

Which conditions are associated with retinitis pigmentosa?

A

Usher’s Syndrome = hearing loss plus retinitis pigmentosa

Bassen-Kornzweig Syndrome = disorder of fat absorption and metabolism causing progressive neurological symptoms and retinitis pigmentosa

Refsum’s Disease = metabolic disorder of phytanic acid causing neurological, hearing and skin symptoms and retinitis pigmentosa

195
Q

What is the general management of retinitis pigmentosa?

A

Referral to ophthalmologist for assessment and diagnosis

Genetic counselling

Vision aids

Sunglasses to protect retina from accelerated damage

Driving limitations and informing DVLA

Regular follow up

196
Q

What options to slow disease progress in retinitis pigmentosa? (not lots of evidence)

A

Vitamin and antioxidant supplements

Oral acetazolamide

Topical dorzolamide

Steroid injections

Anti-VEGF injections

Gene therapy is a potential future treatment

197
Q

What are some causes of sudden painless loss of vision?

A

Retinal detachment

Temporal Arteritis

Vitreous haemorrhage

Retinal vein occlusion

Retinal artery occlusion

Wet age related macular degeneration

Anterior ischemic optic neuropathy

Optic neuritis

Posterior Vitreous Detachment

Cerebrovascular accident

Migraine

198
Q

What is a squint also known as?

A

Strabismus (misalignment of the visual axis)

199
Q

What are the two different types of squints?

A

Concomitant (imbalance in extraocular muscles - convergent more common than divergent)

Paralytic (paralysis of extraocular muscles)

200
Q

How is a squint detected?

A

Corneal light reflexion test (light source 30cm away to see if equal reflection)

Cover test elicits nature of squint: ask pt to focus on an object and cover one eye then look for movement of eye

201
Q

What is age related stiffening of the lens called?

A

Presbyopia

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