Ophthalmology

Question 1

External Anatomy of the Eye

Answer 1

• Average length 24mm; Discrepancies in length lead to Refractory Errors
• Cornea – 78% refractive power; Highly Innervated, Avascular
o Layers of the Cornea – Epithelium, Bowman’s Membrane, Stroma, Descemet’s
Membrane, Endothelium (Responsible for maintaining clarity by continuously
pumping fluid out of tissue; Disruption leads to Corneal Oedema and Blurred vision)
• Sclera – White opaque structure, covers 4/5ths of globe, continuous with Cornea at Limbus;
Attachment of six extraocular muscles and perforation of Optic nerve
• Conjunctiva – Anterior surface of the Sclera; Richly vascularised, innervated mucous
membrane; Stretched from Limbus, over Anterior Sclera (= Bulbar Conjunctiva) and reflected onto undersurface of eyelids (Tarsal Conjunctiva)

Question 2

Internal Anatomy of the Eye

Answer 2

• Anterior Segment comprises Anterior (In front of Iris) and Posterior Chambers (Behind Iris)
• The Uveal Tract comprises Iris anteriorly, Ciliary Body and Choroid
o Aqueous Humour is produced by Ciliary Body at 2Ul/min; ULN pressure 21mmHg
o Aqueous Humour provides nutrients and oxygen for the avascular Cornea
• The Lens – Immediately posterior to pupil; 22% of refractive power; Anterior to Vitreous
humour; Transparent, Biconvex structure; Shape starts to decline by fourth decade, becomes
less transparent and develop cataracts
• Contraction of Ciliary muscles relaxes Suspensory Ligaments, Increasing the Refractive Power
of the Lens (for Accommodation)
• Three Layers – Retinal (Neural), Choroid (Vascular) and Sclera (Fibrous)
• Macula and Fovea Centralis – Recession of Choroid layer and lack of overlying vessels; Point
of highest Visual Acuity and concentration of Cone cells for Colour vision
• Optic Disc – CN II; Accounts for visual blind spot

Question 3

Neurovascular Supply

Answer 3

• Ophthalmic Artery – Divides into Central Retinal Artery to supply inner retinal layers; Venous
return through Central Retinal/Ophthalmic Veins; LN Drainage to Preauricular and Submental
• Sensory innervation through Trigeminal (CN V1) Ophthalmic br

Question 4

Refractive Error

Answer 4

Abnormalities of focusing mechanism of the eye;

Question 5

Myopic or Hyper-metropic

Answer 5

o Myopia is usually inherited, discovered in
childhood; Progresses throughout teenage
years when body is growing
o Hypermetropia also inherited

Question 6

Astigmatism

Answer 6

Refractory error which there is a different degree of refraction in different meridians of curvature (i.e. Defect in another plane)

Question 7

Presbyopia

Answer 7

Normal ageing of the lens resulting in
change in refractory state; Lens less able to alter
curvature, resulting in difficulties in near-vision

Question 8

Keratoconus

Answer 8

Non-inflammatory Degenerative disorder resulting in Cornea thinning and
change into Conical shape; Unknown Aetiology

Question 9

Treatment of Refractory Errors

Answer 9

• Spectacles (Negative Lenses for Myopia, Positive Lenses for Hypermetropia) or Contact lenses
(better quality vision but risk of infection)
• Surgical Techniques – Excimer laser to reprofile Corneal Curvature (e.g. PRK. LASIK, LASEK);
Either removal of Central Corneal tissue to flatten in Myopia, or steepen in Hypermetropia

Question 10

Eyelids

Answer 10

Eyelids protect the eyes and help distribute tear over front surface of globe; Excess tears
drained by Punctae and Lacrimal System

Question 11

Entropion

Answer 11

Lid margin rolls inwards, causing lashes to be against globe, causing irritation
o Can mimic conjunctivitis; Occasionally constant rubbing leads to Corneal Abrasion
o Commonly due to ageing; Surgery is usually required

Question 12

Ectropion

Answer 12

Lid margin rolls outwards, no apposition to globe; Puncta are in poor position to
drain tears, patient complains of watery eye; RF: Age, CN VII Palsy, Skin conditions; Surgery usually required for repair

Question 13

Dacryocystitis

Answer 13

Inflammation of Lacrimal Sac; Tender lump on medial side (Nasal) adjacent to
lower eyelid; Oral Broad-spectrum Abx and watched carefully for signs of Cellulitis
o Referred to Ophthalmology – Mucocoele or dilated sac requiring surgical repair

Question 14

Blepharitis

Answer 14

Inflammation of Lid Margins ± Lashes and Follicles;
Results in Stye (= Hordeolum, Inflammation/Blockage of Meibomian
gland); Itchy, burning eyes (Tear Film instability)
o Commonly due to Meibomian gland dysfunction,
Seborrhoea, S aureus (Frequently responsible for Chronic
Blepharo-conjunctivitis
o Lid Hygiene, Short course Topical Chloramphenicol or
Fusidic acid; If Acne Rosacea suspected, Oral Doxycycline required
o Chalazion – Residual cystic lump; Requires Incision/Curettage for cosmesis

Question 15

Conjunctivitis

Answer 15

• Commonest cause for Red Eye (=Pink Eye); Can arise from Viral, Bacterial and Allergic causes
commonly; Soreness, Redness, Discharge without disruption to Visual Acuity
• Hx – Speed of onset, Colour and Consistency of discharge, Recent Hx Cold or Sore Throat; In
Neonate important to exclude Gonococcal or Chlamydial conjunctivitis

Question 16

Conjunctivitis Red Flags

Answer 16

Severe pain, Photophobia, Sudden Visual Acuity loss, Coloured Halos, Proptosis,
Smaller Pupil in affected eye, High IOP, Keratitis, Shallow Anterior Chamber depth

Question 17

Bacterial Conjunctivitis

Answer 17

• 5% of cases; Sore and Gritty eye in presence of good vision; Invariably bilateral, suspected
with purulent discharge
o Gonococcal – Rapid onset, copious discharge, ocular inflammation includes
Conjunctival Oedema (Chemosis) and Lid Oedema; Palpable preauricular LN
▪ Gram Stain of Conjunctival Swab – Presence of Gram -ve Diplococci
o Less acute Purulent Conjunctivitis with moderate discharge – HiB, S pneumo
• Chronic Conjunctivitis – Mild injection with scanty discharge; S aureus and Moraxella
• Oral and Topical Penicillin for Gonococcal to reduce rate of Corneal Perforation
• Topic Broad-Spectrum (E.g. Chloramphenicol) for other causes

Question 18

Chlamydial Conjunctivitis

Answer 18

• C trachomatis; Direct or indirect contact with genital secretions; Shared eye cosmetics
o Trachoma – Same organism but usually not sexually transmitted; Tropics and Middle
East; Common cause of blindness in the world; Chronic inflammation leads to
Progressive Scarring, Trichiasis, Entropion and Corneal Scarring; Blindness from
Opacification or Ulceration

• Slow onset; Scanty mucopurulent discharge in some; Preauricular LN
o In Neonates – 2/52 onset (C/f Gonococcal, which occurs within days); Swabs taken
and NAAT performed to confirm before starting treatment

• Topical Erythromycin BD; Referral to GUM; Neonates referred to Paediatrician; Assoc with
Otitis Media or Pneumonitis

Question 19

Viral Conjunctivitis: Adenovirus

Answer 19

Highly Contagious, Epidemics; Direct or Indirect contact; May have prodromal
symptoms; Inflammation associated with Chemosis, Lid Oedema and Palpable Preauricular LN
o Some develop membrane on Tarsal conjunctiva, and Haemorrhage on Bulbar
o Can cause deterioration in visual acuity due to focal Corneal Inflammation
o Self-limiting, Eye Lubricants, Cold Compress, Strict Hygiene; Topical steroids for
Inflammation or Corneal Involvement

Question 20

Viral Conjunctivitis: HSV

Answer 20

Typically unilateral; Palpable Preauricular LN, Cutaneous Eyelid Vesicles; 50% develop
Dendritic Corneal Ulcers; Typically, self-limiting; Topical Aciclovir to reduce risk of Corneal
Epithelial involvement

Question 21

Phthiriasis Palpebrarum

Answer 21

Infestation with Phthirus pubis (crab lice); Leads to Blepharitis with marked Conjunctival
Inflammation, Preauricular LN, and rarely secondary infections
• Mechanical removal with fine forceps, Physostigmine 1.25%, and Pilocarpine 4% gel

Question 22

Allergic Conjunctivitis

Answer 22

• Itching, Pink-to-reddish Eyes; Seasonal and Perennial Conjunctivitis mediated by Mast cells;
easily treated with cold compress, eye-wash and allergen avoidance
• Affects 20% of UK populace; Reaction to grass, pollen, fungal spores or HDM
• Reduce allergen load, Antihistamine Eye Drops and Topical Mast-cell Stabilising agents; Oral
Antihistamines reduce itching; Avoid Corticosteroids

Question 23

Traumatic Injury to the Cornea: Corneal Abrasion

Answer 23

Removal of focal area of Corneal Epithelium; Usually occurs due to finger
poking, brushing or foreign body
o Severe pain (Cornea is richly innervated), Lacrimation, Inability to open eye (Blepharospasm); Visual acuity usually reduced
o Topical Anaesthetics (e.g. Oxybuprocaine, Tetracaine) for examination
o Cornea inspected under blue light after instillation of Fluorescein drops
o Broad-spectrum Topical Abx QDS for 5/7; Common practice of padding

Question 24

Traumatic Injury to the Cornea: Corneal Foreign Body

Answer 24

Associated with Lacrimation and Photophobia; EUA, should include
eversion of Eye Lid
o Removal of foreign body and Topical Abx

Question 25

KERATITIS

Answer 25

=Corneal Inflammation; Commonly due to HSV, Contact lens infection and Blepharitis; Sensation of foreign body or pain (depending on size and ulcer depth), Photophobia and Lacrimation; Vision might be reduced

Question 26

Keratitis: HSV

Answer 26

Causes Epithelial Lysis and forming Dendritic Ulcer (50%); Stains Green under Blue light with Fluorescein dye ▪ Topical Steroids or Systemic Immunosuppression can lead to centrifugal spread =Geographic Ulcer ▪ HSV dormant infection can be triggered by UV light, stress or menstruation ▪ Ointment Aciclovir five times daily for 2/52

Question 27

Keratitis: Bacterial Causes

Answer 27

S aureus, or P aeruginosa in contact lens wearers | o Potentially sight threatening in Contact-lens wearers; Referral to Ophthalmology

Question 28

Fuch’s Corneal Dystrophy

Answer 28

Genetically associated Degeneration leading to Corneal Oedema and Vision Loss; Bilateral, more common in females, Gradual onset to blindness in 40-60s o Accumulation of corneal deposits; Thickening of Descemet’s membrane o Treatment with Corneal Transplantation

Question 29

Glaucoma

Answer 29

Raised IOP causing Optic Nerve damage resulting in Visual Field Defects Normal 10-21mmHg; Second commonest cause of blindness worldwide, third most common in UK

Question 30

Primary Open-Angle Glaucoma (POAG)

Answer 30

• Commonest form of Glaucoma; High IOP due to reduced Aqueous Humour outflow through trabecular meshwork; RF: Age, Race (Black), Positive FMHx, Myopia • Gradual, Insidious, Painless loss of peripheral visual field; Initially asymptomatic, central vision remains good till end-stage; Typically, identified on routine Ophthalmic examination (Enlarged cup with thin Neuro-retinal Rim) • Diagnosis only made if IOP measured (by e.g. Tonometry)

Question 31

Primary Open-Angle Glaucoma (POAG) Treatment

Answer 31

Treatment reduces IOP either through reducing Aqueous Humour production, or Increasing Aqueous Drainage o Topical Beta-blockers (Timolol, Carteolol, Levobunolol) reduce Aqueous production; CI in COPD, Asthma, and Heart Block o Prostaglandin Analogues (Latanoprost, Travoprost) increased Outflow; Reduces IOP up to 30% o Carbonic Anhydrase Inhibitors (Acetazolamide) reduce production; Oral or Topical; CI in Sulfonamide Allergy

Question 32

Acute Angle-Closure Glaucoma

Answer 32

• Ophthalmic Emergency; Sudden rise in IOP >50mmHg due to reduced Aqueous drainage due to Lens pushing Iris forward against Trabecular Meshwork; More likely to occur in reduced light conditions in pupil dilation o RF: Shallow Anterior Chamber (Hypermetropia, Women)

Question 33

Acute Angle-Closure Glaucoma Presentation

Answer 33

Presents with sudden onset, painful red eye and blurred vision; Unwell with N+V, complains of Headache and Severe Ocular Pain o Hazy Cornea, Semi-dilated Pupil, Conjunctival injections and Tenderness

Question 34

Acute Angle-Closure Glaucoma Treatment

Answer 34

Prompt treatment to preserve sight o IV Acetazolamide 500mg to reduce IOP, Pilocarpine 4% (Pupil Constrictor) to improve Aqueous Outflow and reduce Iris adhesion to Trabecular meshwork o Topical Beta blockers, Prostaglandin analogues, Analgesia, Antiemetics o Oral Glycerol and IV Mannitol for non-responding patients under Ophthalmologist care; Definitive management through laser or surgical incision of Peripheral Iris

Question 35

Uveitis

Answer 35

• Inflammation of Iris, Ciliary Body and Choroid; If confined to Anterior Segment = Anterior Uveitis (=Iritis); If Ciliary Body involved = Intermediate, and if Choroid Involved = Posterior o If all three regions involved = Pan-uveitis; Posterior involvement – Ophthalmology r/v • Most commonly Blurred vision, Pain, Redness, Photophobia and Floaters • Associated with Ank Spond (HLA-B27 pos), Arthritis, IBD, Sarcoidosis, TB, Syphilis, Toxoplasmosis, Behçet’s syndrome, Lymphoma and Viral Infections

Question 36

Anterior Uveitis

Answer 36

• Triad of Redness (General or Limbus Injection), Pain and Photophobia; Keratic precipitates, Pus and cellular debris within Anterior Chamber; Pupil might have adhered to lens (Posterior Synechiae) • IOP may be raised due to either debris clogging, or Posterior Synechiae, with the aqueous build-up forcing the Iris against the trabecular meshwork • Reduction of Inflammation with Topic Steroids (Dexamethasone), Pupil Dilation to prevent Posterior Synechiae (Cyclopentolate); Examination of Posterior Segment o If IOP raised – Topic Beta Blockage, Prostaglandin Analogues or Acetazolamide

Question 37

Cataracts

Answer 37

• By far, commonest cause of Preventable Blindness in the world with effective surgical treatment; 250,000 Cataract operations per year in the UK = Commonest Surgery • Age-related Opacification; 30% over 65yrs having Snellen <6/12 (Below safe for driving) o Other Aetiologies include Congenital (Maternal Infection, Familial), Metabolic (Diabetes, Hypocalcaemia, Wilson’s Disease), Drug Induced, Traumatic, Inflammatory (Uveitis), or Disease Associated (E.g. Down Syndrome) o Cataract in Infants demand urgent referral to Ophthalmology to minimise subsequent development of Amblyopia • Gradual, Painless deterioration of vision; Early changes correctable by spectacles, but eventually opacification requires surgery • Investigations – Glucose for DM, Ca, LFTs to diagnose metabolic disorders • Surgical Management – Small incision extracapsular, or Phacoemulsification with insertion of Intraocular lens

Question 38

Age Related Macular Degeneration

Answer 38

Commonest cause of Visual Impairment >50yrs in developed nations, and blind registration; 10% of >65yrs, 30% of >80yrs; Unknown cause but RF include Age, Smoking, HTN, Hypercholesterolaemia and UV Exposure

Question 39

Non-exudative (Dry) Macular Degeneration

Answer 39

``` Painless, Progressive loss of Central Vision o Lipofuscin (=Drusen) deposits between Retinal Pigment Epithelium and Bruch’s Membrane; Might cause focal RPE detachment o Not all affected visually; Some might develop distortion and blurring of central vision o Extensive Atrophy can occur (Geographic Atrophy) ```

Question 40

Exudative Macular Degeneration | 10%

Answer 40

Development of abnormal Subfoveal Choroidal Neovascularisation in Macula; Causes severe central visual loss

Question 41

Management of Macular Degeneration

Answer 41

``` • Patients with Central Distortion or Frank Macular Pathology for urgent Ophthalmology R/v • Anti-VEGF (E.g. Ranibizumab, Bevacizumab) by Intravitreal injections; Vision maintained in 95%, improves in about 1/3 of patients • Monthly OCT monitoring recommended • Severe visual loss if possible; Low vision aids, such as Magnifiers, may help ```

Question 42

Acute Visual Loss

Answer 42

• Crucial Hx includes Onset, Progression, Redness, Unilateral or Bilateral, Field Visual Defect, Relative Afferent Pupillary Defects • Acute causes include Uveitis, Acute Glaucoma, Keratitis (Corneal Ulcer), Retinal Detachment, Vascular Occlusion (CRA, CRV, etc), Acute Optic Neuropathy and other Macular or Retinal Diseases

Question 43

Central Retinal Vein Occlusion

Answer 43

• Profound, sudden, painless loss of vision with Thrombosis of CRV at or posterior to where optic nerve exits globe; Obstruction leads to raised intravascular pressure, causing vein dilation, Retinal Haemorrhage, Cotton-Wool spots and Retinal Oedema o In severe cases, RAPD might be present, especially in Ischaemia • RF: Age, HTN, CVS disease, DM, Glaucoma; Blood dyscrasias and Vasculitides in the young • Ophthalmology R/v – Neovascularisation as a result from retinal ischaemia; Intravitreal Anti- VEGF therapy or steroids

Question 44

Central Retinal Artery Occlusion

Answer 44

• Painless severe loss of vision; Infarction of inner 2/3rds of Retina; Arterial stenosis and Retina becomes Opaque and Oedematous o Cherry red spot on Fovea – Neovascularisation appears on thinnest part of retina o RAPD is usually present • Arteriosclerosis-related Thrombosis is the most common cause of CRAO; Emboli from Atheroma and Vulvar disease possible • Need to rule out Giant Cell Arteritis (Temporal Arteritis) • Ophthalmic Emergency; Irreversible Retinal damage occurs after 90 mins; Ocular Massage, IV Acetazolamide to reduce IOP, which might dislodge emboli o Breathing into paper bag – CO2 retention can act as a vasodilator o Thorough medical review for aetiology of emboli/thrombus o Should start on Aspirin as secondary prevention

Question 45

Vitreous Haemorrhage

Answer 45

• Extravasation of blood into or around Vitreous Humour; Most commonly due to Diabetic Retinopathy (Neovascularisation leads to weaker blood vessels), Trauma, Retinal Detachment • Blurry vision, Floaters, Reddish tint to vision and Photopsia (Flashes) • Management involves Head Elevation and limiting eye movement to allow blood to settle and discontinuing Antiplatelets/anticoagulants; Repair of Retinal Tear o Vitrectomy may be necessary to remove for longstanding haemorrhage, or evidence of rubeosis (Neovascularisation of the Iris)

Question 46

Retinal Detachment

Answer 46

• Painless, Progressive Visual Field Loss; Shadow corresponds to area of detachment; If macular affected, central vision lost • Following tear, Fluid collects in space between Sensory Retina and RPE o Tear can occur from Posterior Vitreous Detachment, Injury or Inflammation; • RF includes Myopia and Previous Cataract Surgery • Patients report sudden onset of floaters, often associated with Photopsia (Flashes) • For urgent Ophthalmology referral; Management involves isolating the defect and preventing the detachment from spreading; Either Cryotherapy, Laser Photocoagulation; Pneumatic Retinopexy or Vitrectomy

Question 47

Diabetic Eye Disease

Answer 47

• 90% of young patients T1DM develop retinal changes, but only few progress to sight- threatening retinopathy; 30-50% require Laser Photocoagulation to limit Proliferative Retinopathy; Diabetes is the most common cause of blindness <65yrs • Cataracts – Develop earlier in people with DM; Very poor diabetic control plus ketosis can lead to rapid, acute Snowflake Cataracts o Fluctuations in Blood Glucose can lead to osmotic changes in the lens, leading to refractive variability (Temporary Hypermetropia) • Extraocular Palsies – VI and III most commonly; III not associated with pain; May recover spontaneously in 3 – 6/12

Question 48

Diabetic Retinopathy

Answer 48

• Most commonly diagnosed DM complication; Increasing prevalence with duration of DM; Intramural Pericyte death with Thickening of Basement Membrane; Incompetence and increased Vascular Permeability, leading to occlusion • Damage to small vessels leads to Microaneurysms in retina; when breached, Blot Haemorrhages occur, with leakages into Retina; Deposition of protein and lipids known as hard exudates • Microinfarctions of occluded vessels leads to cotton wool spots (Accumulation of axoplasmic debris; White spot can occur after clearance by macrophages) • Venous damage leads to variance in diameter (Beading) and Elongation (Loops); Blockage leads to capillary non-perfusion, leading to release of neovascularisation factors causing new intraretinal vessel growth (Intraretinal Microvascular Abnormalities) • Bleeding of new, weak vessels results in Pre-Retinal Haemorrhages (Boat-shaped) and Vitreous Haemorrhage, which threatens vision; Collagen growth leads to fibrotic band formation, which may contract and cause Retinal Detachment • Neovascularisation of Pupil Margin (Rubeosis) can lead to rapid rise in IOP (Rubeotic Glaucoma)

Question 49

Maculopathy

Answer 49

• Fluid leaking is cleared poorly; Macular Oedema forms; Distortion and Thickening of the Macula can lead to loss of central vision; Not visible on Ophthalmoscopy; Capillary occlusion can lead to loss of central vision as well

Question 50

Assessment of Diabetic Retinopathy

Answer 50

* Visual Acuity (Pinhole and Spectacles), Ocular Movements; Iris examined for Rubeosis * Dilation with 1% Tropicamide; Examination for Cataract and Retinal Quadrants * Screening – All diabetics >12yrs Annual Acuity measurement and Retinal Photography

Question 51

Management of Diabetic Eye Disease

Answer 51

• Cataracts – Extraction and IOL implantation if causing Visual Disability; Pre-existing Retinopathy might worsen after extraction • Reduce Risk of Eye Disease through good metabolic control of DM and HTN • Fluorescein Angiography to define extent of potentially sight-threatening Retinopathy, OCT to image content of layers of Retina at the Macula; Detect Oedema • Neovascularisation is an indication for Laser Photocoagulation; New vessels on disc have poor prognosis requiring urgent therapy o Laser ablation of new vessels and area of Ischaemia • Pan-Retinal Photocoagulation – Proliferative Retinopathy progressing to new vessels on disc; Also used in Rubeosis • Vitreoretinal Surgery for Recurrent bleeds; Also used to reduce Vitreous Haemorrhage; Also, to treat Fibrotic Traction Retinal Detachment • Treatment for Maculopathy – Laser Photocoagulation for encroaching Foveal Exudates; If centre of Macula affected, Grid Photocoagulation is used; Also, Anti-VEGF Drugs

Question 52

Thyroid Eye Disease

Answer 52

• Due to Immune Response that causes Retro-Orbital Inflammation; Swelling and Oedema of Extraocular Muscles, Proptosis, Increased pressure on Optic nerve leading to Atrophy o Likely due to Antigen in Retro-Orbital tissue with similar immunoreactivity to TSH o Can occur regardless to Thyroid status of patients in Grave Disease; Typically occurs within 2yrs of each other; TSHR Auto Antibodies invariably • Soreness, Painful Watering and Eye Prominence, Lid Retraction; Severe Proptosis in minority of cases; Limitation in Eye Movement and Visual Impairment (CN II compression) o Corneal Damage, Periorbital Oedema, Conjunctival Oedema and Inflammation • Few investigations required if appearance characteristic and bilateral; Serum TSH, T3 and T4 • Hx – Eye Movements, Degree of Oedema and Inflammation; MRI and CT Orbit to exclude Retro-orbital SOL, Reveal Oedema and Muscle damage

Question 53

Treatment of Thyroid Eye Disease

Answer 53

• Lubricant Eyedrops – Methylcellulose, Hypromellose • Eyelids can be taped shut to ensure closure at night • Systemic Steroids (Prednisolone 30 -120mg OD) reduces inflammation if more severe symptoms present; Pulse IV Methylpred may be more effective in severe cases • Surgical Decompression – If pressure threatens vision; Also for Cosmesis • Lid Surgery – Protect cornea if lids are unable to close; Also for Cosmesis • Corrective Eye Muscle Surgery – Deferred until stable for 6/12 • Currently under investigation – Irradiation of the Orbits, Immunomodulatory agents