Ophthalmology

Question 1

Acute angle-closure glaucoma

Pathophysiology of acute angle-closure glaucoma

Answer 1

• Posterior chamber of the eye produces aqueous humour > anterior chamber > drains via trabecular meshwork
• AACG = iris bulges forward > seals trabecular meshwork, aqueous humour unable to drain from anterior chamber > ↑intraocular pressure + optic nerve damage
• Ophthalmological emergency to prevent permenant vision loss
• RIsk factors: ↑age, FHx, female, Chinese and East Asian, Shallow anterior chamber

Basic eye anatomy

Question 2

Presentation of acute angle-closure glaucoma

Answer 2

• Generally unwell
• Severely painful red eye
• Blurred vision
• Halos around lights
• Headache, nausea + vomitimg (↑intraocular pressure)

On examination

• Red eye
• Hazy cornea
• Decreased visual acuity
• Mid-dilated pupil
• Fixed-size pupil
• Hard eyeball on gentle palpation

Question 3

Management of acute angle-closure glaucoma

Answer 3

Waiting for ambulance:

• Lie patient on back without pillow
• Pilocarpine eye drops (2% for blue, 4% brown) - miotic > pupil constriction and ciliary muscle contraction = open pathway for aqueous humour
• Acetazolamide 500mg PO ↓ aqueous humour production
• Admission

Once admitted

• Pilocarpine eye drops
• PO or IV acetazolamide
• Hyperosmotic agents (e.g. IV mannitol)
• Timolol (BB ↓aqueous humour)
• Dorzolamide (↓aqueous humour)
• Brimonidine (↓aqueous humour)
• Laser iridotomy - definitive, hole in iris to allow aqueous humour to drain

Question 4

Open-Angle Glaucoma (raised intraocular pressure causing optic nerve damage)

Answer 4

• Normal intraocular pressure = 10 - 21mmHg due to resistance to flow through trabecular meshwork
• OAG = gradual increase in resistance of this flow, pressure slow build within eye
• Raised IOP = cupping of optic disc (optic cup in centre normally < 50% size of optic disc), cup-disk ratio > 0.5 =abnormal

Question 5

Risk factors and presentation of open angle glaucoma

Answer 5

• RFs: ↑age, black, FHx, myopia (near-sighted)
  Features:
• Asymptomatic for long period and incidental finding on routine eye testing
• Peripheral vision affected first > tunnel vision
• Fluctuating pain
• Headaches
• Blurred vision
• Halos around lights

Cup: disc rato > 0.5 indicates open-angle glaucoma

Question 6

Diagnosis of open-angle glaucoma

Answer 6

• **Goldmann applanation tonometry: measures 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

Goldmann applanation tonometry is gold standard for measuring IOP

Question 7

Management of open angle glaucoma

Answer 7

• Tx begins IOP > 24mmHg
• NICE recommends all patients: 360 degrees selective laser trabeculoplasty, laser to improves drainage from trabecular meshwork

Medical

• 1st line: latanoprost (prostaglandin anglogue) increase uveoscleral outflow

Question 8

Cataracts

Answer 8

• Progressively opaque lens - reduces light entering the eye and visual acuity
• Lens focuses light onto retina
• Risk factors: ↑age, smoking, alcohol, diabetes, steroids, hypocalacaemia

Presentation

• Asymmetrical
• Slow reduction in visual acuity
• Progressive vision blurring
• Colours become faded, brown or yellow
• Starbursts around light
• Loss of red reflex on exam

Management

• Conservative if manageable
• Cataract surgery: break lens, remove and implant artifical lens
• Macular degen or diabetic retinopathy more obvious after cataracts fixed

Complication
Endophthalmitis - inflammation of inner eye content, due to infection post-op. Intravitreal abx injected into eye

Question 9

Central retinal artery occlusion

Answer 9

• Obstruction of blood flow through CRA (branch of ophthalmic artery, which is branch of internal carotid)
• Atherosclerosis or GCA
• Sudden, unilateral painless vision loss
• Relative afferent pupillary defect (affected eye pupil dilates when light shone into it)
• “Cherry red” spot on pale retina

Management

• Difficult, poor prognosis
• Tx underlying cause (e.g. IV steroids for temporal arteritis)
• No guidelines or consenus of tx, so unlikely to be on exam

Fundoscopic image of a typical cherry red spot in a patient with central retinal artery occlusion

Question 10

Diabetic retinopathy

Answer 10

• Damage to retinal blood vessels due to prolonged hyperglycaemia in retinal small vessels and endothelial cells
• Leaky vessels = blot haemorrhages, hard exudates
• Damage to vessel walls = microaneurysms (mini bulges), venous beading
• Damage to nerve nerves = fluffy white cotton wool spots
• Neovascularisation = growth factors in retina = new vascularisation

Findings in diabetic retinopathy

Question 11

Grading of diabetic retinopathy

Answer 11

• Based on fundus examination findings:
• Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots
• Pre-proliferative – venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA)
• Proliferative – neovascularisation (key feature) and vitreous haemorrhage

Diabetic maculopathy = seperate

• Macular exudates
• Macular oedema

Question 12

Management and complications of diabetic retinopathy

Answer 12

Non-proliferative: close monitoring and careful diabetic control

Proliferative:

• Pan-retinal photocoagulation (PRP): laser tx to suppress new vessels. Lots of yellow dots after tx :(
• Anti-VEGF injections

Complications: vision loss, retinal dettachment, vitreous haemorrhage

Anti-VEGF = anti-vascular endothelial growth factor

Question 13

Infective keratitis

Answer 13

• Inflammation of cornea, sight-threatening so urgent treatment

Causes:

• Viral: herpes simplex keratitis (most common)
• Bacterial: S.aueus, Pseudomonas aeruginosa in contact-lens wear (1st line: topoical quinolones - e.g. ciprofloxacin)
• Fungal: candida or aspergillus
• Contact lens-induced acute red eye (CLARE)
• Exposure keratitis: if eyelid does not close properly

Question 14

Herpes simplex keratitis

Answer 14

• Most commonly affect epithelial layer of cornea
• Primary or recurrent (dormant in trigeminal ganglion)
• Primary: mild symptoms of blepharoconjunctivitis (inflammation of the eyelid margins and conjunctiva)
• Recurrent: painful red eye, photophobia, vesicles, foreign body feeling, watery dischage, ↓visual acuity

Diagnosis: slit lamp exam, fluorescein stain = dendritic (branching) corneal ulcer, corneal scrapings for viral testing

Management

• Urgent assessment and mx by opthalmologist
• Topical/oral aciclovir or ganciclovir
• Corneal transplant if permanent scarring and vision loss

Question 15

Anterior uveitis (what comes up when I search iritis)

Answer 15

• Inflammation of anterior uvea and anterior chamber
• Uvea = layer between outer sclera and retina. Consists of iris, ciliary body, choroid (blood supply)
• Autoimmune, but can be triggered by infection, trauma, ischaemia or malignancy
• Associated with seronegative spondyloarthropathies, IBD

Question 16

Presentation of anterior uevitis

Answer 16

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

On examination:

• Ciliary flush (red ring spreading from cornea outwards)
• Miosis (constricted pupil)
• Abnormally shaped pupil (posterior synechiae (adhesions) pulling)
• Hypopyon (inflammatory cells collection as white fluid in anterior chamber)

Question 17

Management of anterior uveitis

Answer 17

• Referral for urgent assessment and management by ophthalmologist

1st line:

• Steroids (topical, oral or IV)
• Cycloplegics (cyclopentolate or atropine eye drops) for pain relief

Question 18

Age-related macular degeneration (AMD)

Answer 18

• Most common cause of blindness in the UK
• Often unilateral, sometimes bilateral

Two types:

• Wet (neovascular) 10%
• Dry (non-neovascular) 90%

Macula at centre of retina, responsible for HD colour vision in central visual field

Drusen = yellow protein deposits, frequent + large indicates macular degeneration

In wet AMD, new vessels grow from choroid layer into retina > oedema and faster visiion loss

Question 19

Risk factors and presentation of AMD

Answer 19

Risk factors:

• ↑age, smoking, FHx, CVD, obesity, poor diet (low vitamin, high fat)

Features

• Gradual loss of central vision
• Reduced visual acuity
• Crooked or wavy looking straight lines (metamorphopsia)
• Gradually worsening ability to read small text
• Wet AMD more acute than dry (vision loss in days, complete in 2 - 3 years) > often becomes bilateral

Question 20

Diagnosis of AMD

Answer 20

Key findings on examination help with diagnosis

• Reduced visual acuity on Snellen chart
• Scotoma (enlarged central area of vision loss)
• Amsler grid test
• Drusen on fundoscopy

Question 21

Management of AMD

Answer 21

• Specialist ophthalmology assessment and management
• Dry AMD: monitoring and reduce progression by stop smoking, control BP
• Wet AMD: anti-VEGF+ (e.g., ranibizumab, aflibercept and bevacizumab) injected intravitreally monthly

+Vascular endothelial growth factor

Question 22

Retinal detachment

Answer 22

• Neurosensory layer of retina (photoreceptors and nerves) seperating from retinal pigment epithelium (base layer attached to choroid)
• Often due to retinal tear, vitreous fluid leaks into space between the two layers
• Neurosensory layer rely on blood supply from choroid > detachment = permanent damage to photoreceptors = sight-threatening

Risk factors: lattice degeneration (retinal thinning), trauma, diabetic retinopathy, retinal malignancy, FHx

Question 23

Presentation and management of retinal detachment

Answer 23

• Painless, peripheral vision loss, sudden “shadow” across vision
• Blurred vision
• Flashes and floaters

Management

• Immediate ophthalmology referral
• Tears repaired by adhesion between retina and choroid e.g. laser or cryotherapy

Detachment:

• Virectomy: remove vitreous fluid, fix tear, insert oil/gas to hold retina
• Scleral buckling: silicone buckle to squeeze eye content together
• Pneumatic retinopexy: inject gas bubble into vitreous body and it presses seperated layer back together

Question 24

Scleritis

Answer 24

• Inflammation of sclera, outer layer of connective tissue surrounding the eye (white part)
• Most are idiopathic or associated with systemic inflammatory condition e.g. rheumatoid arthritis, vasculitis (particularly granulomatosis with polyangiitis)

Presentation

• Red, inflamed sclera
• Severe pain
• Pain on eye movement
• Photophobia
• Epiphora (excessive tears)
• Reduced visual acuity
• Tenderness to palpation of eye

Management

• Urgent referral to ophthalmologist
• Assess for underlying systemic condition (RA, vasculitis)
• NSAIDs PO, topical/systemic steroids, meds for underlying disease e.g. methorexate in RA

Sclera similar to connective tissue in joint, so can be affected in RA

Question 25

Visual field defect

Answer 25

- Fibres from nasal aspects of right and left retina cross (temporal visual field) over at the optic chasm to the contralateral optic tract, while fibres from temporal retina stays ipsilateral - So left-side post-chiasmal fibres responsible for right side of visual field and vice versa - Pre-chiasmal lesion = ipsilateral monocular visual field defect - Post-chiasmal lesion = homonymous visual field defects of contralateral side