Ophthalmology Flashcards

1
Q

State some risk factors for age-related macular degeneration (non-modifiable and modifiable)

A

Non-modifiable:
- Older age
- Ethnicity
- Ocular characteristics (light coloured iris, hyperopia)
- Genetics (complement factor H)

Modifiable:
- Smoking
- Cardiovascular disease (CVS & HTN)

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2
Q

Outline the main causes of blindness worldwide

A

Most common in those ages > 50

Distance vision issues:
- Refractive errors
- Cataract
- Glaucoma
- AMD (age-related macular degeneration)
- Diabetic retinopathy

Near vision issues:
- Presbyopia

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3
Q

Outline the 2 muscles responsible for moving the eyelids and what nerves they are innervated by

A
  1. Levator palpebrae superioris = open eyelids
    - Oculomotor nerve (CN3)
  2. Orbicularis oculi = close eyelids
    - Facial nerve (CN7)
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4
Q

Outline the 3 main layers of the eyeball

A

Outer:
- Sclera
- Cornea

Middle:
- Choroid
- Ciliary body
- Iris

Inner:
- Retina

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5
Q

State the 2 compartments of the eyeball and which areas they sit between

A
  1. Anterior chamber
    - Between cornea and iris
  2. Posterior chamber
    - Between iris and ciliary body + lens
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6
Q

Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
Most common cause of blindness in the UK
- Progressive condition affecting the macula, with drusen deposits (proteins and lipids) between the retinal pigment epithelium and Bruch’s membrane
- 2 main types = dry (90%) and wet (10%)

Presentation:
Often unilateral, but can be bilateral
- Gradual loss of central vision
- Reduced visual acuity (variable, vision worse close up e.g. seeing faces)
- Straight lines appear wavy (metamorphopsia)
*Wet AMD presents more acutely than dry AMD, with vision loss developing within days

Investigations:
- Snellen chart (reduced visual acuity)
- Fundoscopy (drusen)
- Amsler grid test (metamorphopsia)
- Slit lamp examination
- OCT (optical coherence tomography)
- Fluorescein angiography

Management:
- NO specific treatment for dry AMD = reduce risk of progression e.g. smoking cessation, BP control. Some suggestion of Zinc and Vitamin A, C, E
- If wet AMD = Anti-VEGF as monthly injections

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7
Q

Outline what drusen is (in age-related macular degeneration) and the 2 main types

A
  • Occurs due to retinal pigment epithelium degeneration
  • Undigested cellular debris, deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane (white/yellow colour)
  • Drusen may remain unchanged for years without causing vision loss (small drusen are present in up to 95% of elderly patients)
  1. Soft drusen - larger, soft deposits
  2. Hard drusen - small, hard, solid deposits
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8
Q

State the way in which soft drusen can contribute to age-related macular degeneration

A

Lift the retinal pigment epithelium away from the underlying membrane
1. Hypoxia
2. Inflammation

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9
Q

State the 2 main types of age-related macular degeneration and relative frequency

A

Dry (non-neovascular) = 90% cases
Wet (neovascular) = 10% cases

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10
Q

State 2 findings common to both dry and wet AMD

A
  • Atrophy of the retinal pigment epithelium
  • Degeneration of photoreceptors
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11
Q

Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Abnormal cellular deposits of proteins and fats in the layer between retinal pigment epithelium and Bruch’s membrane
- Leads to progressive central vision loss
- 2 main types of dry (non-neovascular) and wet (neovascular)
- Usually first affects people in their 50s and 60s and often unilateral but may be bilateral

Presentation:
- Gradual loss of central vision
- Reduced visual acuity e.g. difficulty in reading small text
- Crooked or wavy appearance to straight lines (metamorphopsia)
- Drusen may be seen during fundoscopy
*Wet AMD progresses presents more acutely than dry AMD (vision loss within days)

Investigations:
- Amsler grid test = assess for the distortion of straight lines
- Fundoscopy = drusen may be seen
- Slit lamp examination
- Optical coherence tomography = can help diagnose + monitor AMD
- Fluorescein angiography for suspected wet AMD

Management - depends on type:
No specific treatment for dry AMD
- Monitoring and reducing the risk of progression by avoiding smoking, controlling blood pressure
Wet AMD
- Anti-VEGF as monthly injections directly into the vitreous chamber of the eye

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12
Q

Outline which bones make up the superior, medial, lateral and floor of the orbital cavity

A

Superior = frontal bone + lesser wing of sphenoid
Medial = ethmoid bone + maxilla + lacrimal + sphenoid
Lateral = zygomatic + greater wing of sphenoid
Floor = maxilla + palatine + zygomatic

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13
Q

Outline what nerve and muscle causes eyelid opening and eyelid closing

A

Eyelid opening:
- Levator palpebrae superioris
- Oculomotor nerve (CN3)

Eyelid closing:
- Orbicularis oculi
- Facial nerve (CN7)

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14
Q

Outline the 3 layers of the globe of the eye

A

Retina (innermost)
Choroid
Sclera (outermost)

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15
Q

Outline the difference between rods and cones

A

Cones:
- Colour vision
- Active at high light levels
- High definition
- High density in fovea / macula

Rods:
- Non-colour vision
- Active at low light levels
- Low definition
- High density in peripheral retina

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16
Q

Outline some differentials for someone presenting with ocular discomfort (organise by structure)

A

Cornea:
- Trauma (corneal abrasion)
- Dry eyes
- Keratitis (viral, bacterial, parasite)

Conjunctiva:
- Conjunctivitis (viral, bacterial or allergic)

Sclera:
- Scleritis

Anterior chamber:
- Acute closed-angle glaucoma

Uvea:
- Anterior uveitis

Optic nerve:
- Optic neuritis

Other:
- Orbital cellulitis
- Cluster headaches

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17
Q

Outline some differentials for someone presenting with acute loss of vision

A

Ophthalmology:
- Vascular occlusion e.g. amaurosis fugax, central retinal artery occlusion
- Haemorrhage (diabetes or trauma)
- Retinal detachment
- Acute closed-angle glaucoma (PAIN)
- Uveitis (anterior or pan) (PAIN)
- Corneal ulcer (PAIN)
- Optic neuritis (PAIN)

Other
- Stroke / TIA
- Migraine
- Giant cell arteritis

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18
Q

Outline some differentials for someone presenting with gradual loss of vision

A
  • Age-related macular degeneration
  • Presbyopia
  • Cataracts
  • Chronic open-angle glaucoma
  • Diabetic retinopathy

Concerning:
- Vitreous haemorrhage
- Giant cell arteritis
- Chronic optic nerve compression

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19
Q

Outline some differentials for someone presenting with transient visual loss (lasts <24hrs)

A
  • Amaurosis fugax
  • Migraine
  • Papilloedema
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20
Q

Outline some differentials for someone presenting with sudden (painless) loss of vision

A

Mainly vascular:
- Vitreous haemorrhage
- Retinal detachment
- Wet age-related macular degeneration
- Retinal vein or artery occlusion
- Stroke affecting the visual pathways
- Giant cell arteritis (ischaemia)

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21
Q

Outline some differentials for someone presenting with gradual (painless) loss of vision

A
  • Cataracts
  • Refractive errors / presbyopia
  • Cataracts
  • Dry age-related macular degeneration (AMD)
  • Open-angle glaucoma
  • Tumours affecting visual pathway
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22
Q

Outline some differentials for someone presenting with painful loss of vision

A
  • Acute closed-angle glaucoma
  • Optic neuritis
  • Uveitis
  • Keratitis / corneal ulcer
  • Endophthalmitis
  • Orbital cellulitis
    + GCA (headache)
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23
Q

Outline some differentials for someone presenting with diplopia (double vision)
- Monocular
- Binocular

A

Monocular differentials - suggests distortion of light transmission through the eye:
- Cataracts
- Irregular corneal shape e.g. scarring
- Astigmatism
- Dislocated lens

Binocular differentials - suggests misalignment of the eyes:
- Cranial nerve palsy (3rd, 4th, or 6th) e.g. intracranial lesion, aneurysm
- Myasthenia gravis / MS
- Graves’ ophthalmopathy
- Trauma / damage to extraocular eye muscles
- Ocular myositis

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24
Q

Outline some differentials for someone presenting with red eye

A

Conjunctival / sclera:
- Conjunctivitis (viral, bacterial, allergic)
- Subconjunctival haemorrhage
- Episcleritis / scleritis

Cornea:
- Corneal abrasion e.g. foreign body
- Corneal ulcer

Other:
- Anterior uveitis
- Acute angle-closure glaucoma
- Herpes simplex keratitis or herpes simplex keratitis

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25
Q

Outline some differentials for someone presenting with ocular discharge (separate into purulent and wartery causes)

A

Purulent:
- Conjunctivitis (bacterial)
- Ophthalmia neonatorum (neonatal conjunctivitis)
- Blepharitis
- Corneal ulcer
- Bacterial Keratitis (infection of cornea)

Watery:
- Conjunctivitis (allergic or viral)
- Blocked tear duct / system
- Endophthalmitis
- URTI
- Dry eyes
- Trichiasis
- Dacryocystitis (infection lacrimal sac)

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26
Q

Outline some differentials for someone presenting with abnormal pupil shape

A
  • Trauma (to iris sphincter muscles) e.g. cataract surgery
  • Anterior uveitis can cause adhesions (scar tissue)
  • Acute angle-closure glaucoma (ischaemic damage to the muscles of the iris)
  • Rubeosis iridis (neovascularisation in the iris)
  • Coloboma (congenital malformation)
  • Tadpole pupil (muscle spasm in part of dilator muscle of the iris) = may be associated with migraines and Horner syndrome
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27
Q

Outline some differentials for someone presenting with mydriasis (dilated pupil)

A

Medications:
- Dilating drops used
- Stimulants e.g. Cocaine
- Anticholinergics e.g. oxybutynin

Cranial nerves:
- Trauma
- Raised intracranial pressure
- Third nerve palsy

Other:
- Congenital
- Acute angle-closure glaucoma
- Holmes-Adie syndrome

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28
Q

Outline some differentials for someone presenting with miosis (constricted pupil)

A

Medication:
- Opiates
- Nicotine
- Pilocarpine

Other:
- Horner syndrome
- Cluster headaches
- Advanced syphilis (Argyll-Robertson pupil)

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29
Q

Outline some differentials for someone presenting with loss of red reflex

A
  • Corneal scars
  • Cataracts
  • Vitreous hemorrhage
  • Retinal detachment
  • Refractive error
  • Strabismus
  • Coloboma
  • Retinoblastoma
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30
Q

Outline some differentials for someone presenting with visual hallucinations

A

Charles-Bonnet syndrome

Psychiatry:
- Schizophrenia
- Mood disorders / mania
- Dementia esp. Lewy Body dementia
- Delirium
- Parkinson’s disease
- PTSD

Medications:
- Substance misuse / alcohol
- Prescribed e.g. opioids, anticholinergics, anti-Parkinsonians

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31
Q

Outline 3 roles of the cornea

A
  1. Protection of the eye (including corneal reflex)
  2. Allow transmission of light (transparent)
  3. Refraction of light
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32
Q

Keratitis (infection of cornea) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Infection of cornea (non-infectious keratitis is rare)
- Causes inflammation and damage to the corneal layers
- Usually occurs secondary to damage/disruption of epithelial surface

Presentation:
Usually unilateral
- Severe pain (exposed free nerve endings from loss of epithelium)
- Red eye
- Discharge (watery or purulent)
- Reduced visual acuity
- Photophobia
- May have corneal ulcer

Investigations:
- Ophthalmoscope (may show corneal infiltrate and hypopyon)
- Corneal scraping (histology and MC&S)

Management:
- Stop contact lens use
- Analgesia
(Cycloplegic drops if photophobia e.g. Atropine)
Bacterial suspected = immediate empirical fortified eye drops e.g. Tobramycin (high risk) or Fluoroquinolone (moderate risk)
Viral suspected = antivirals

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33
Q

Outline some triggers/risk factors for infective keratitis (infection of cornea)

A
  • Trauma
  • Contact lenses
  • Dry eyes
  • Pre-existing corneal disease e.g. ulcers

Immunocompromised will make infection more likely

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34
Q

State what is used to measure IOP and the value at which above is considered raised IOP

A

Tono-meter
- Measures force needed to flatten cornea

> 21 considered to be ocular hypertension (11-21 considered normal)

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35
Q

Outline some classes of medications that can reduce aqueous production (and reduce IOP)

A

Reduce aqueous production (ABC):
Alpha agonists e.g. Apraclonidine (a receptors normally suppress)
Beta blockers e.g. Timolol (b receptors normally stimulate)
Carbonic Anhydrase inhibitor e.g. Dorzolamide

Improve outflow:
Prostaglandins e.g. Latanoprost
Parasympathomimetic e.g. Pilocarpine

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36
Q

Cataracts - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Cloudy lens = lens of the eye becomes progressively opaque, due to denaturation of lens proteins
- Reduces light entering the eye = reduced visual acuity
- Usually seen in the elderly (present in ~75% of individuals aged over 65), but can be congenital

Presentation:
Usually asymmetrical
- Gradual reduction in visual acuity
- Gradual blurring of the vision
- Faded colour vision
- Glare around lights (esp. driving at night)
- Loss of red reflex (grey or white)

Investigations:
- Ophthalmoscope (loss of red reflex)
- Slit lamp examination of the anterior chamber (brown/white appearance of the lens)

Management:
- May not need intervention if symptoms are manageable
- Surgery phacoemulsification (break down with ultrasound, then implant artificial lens)

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37
Q

List some risk factors for cataracts

A
  • Increasing age!!
  • Smoking
  • Systemic steroids
  • Diabetes
  • Alcohol
  • Hypocalcaemia
38
Q

List some causes of cataracts in younger patients

A
  • Trauma e.g. direct, electric shock
  • Drugs e.g. systemic steroids, Amiodarone
  • Systemic disease e.g. diabetes, neurofibromatosis type 2
39
Q

List 2 main complications of cataract surgery

A
  • 1 in 1000 risk of infection (endophthalmitis)
  • 1 in 100 risk of failure to complete the procedure
    + lens capsule opacification
40
Q

State the technical names for pupil dilation and contristriction and which muscles and nerves are responsible for each

A

Pupil dilation = mydriasis
- Dilator pupillae
- Sympathetic nerves

Pupil constriction = miosis
- Sphincter pupillae
- Parasympathetic nerves (CN3)

41
Q

List the 3 structures of the uveal tract

A
  • Iris
  • Ciliary body
  • Choroid
42
Q

Outline the different types of uveitis

A

Anterior uveitis - inflammation of:
- Iris
- Ciliary body

Intermediate uveitis - inflammation of:
- Posterior ciliary body
- Peripheral retina
- Choroid

Posterior uveitis - inflammation of:
- Retina
- Choroid

Panuveitis - inflammation of:
- Whole uveal tract!

43
Q

Anterior uveitis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Most common type of uveitis (75% cases)
- Inflammation of the iris and ciliary body (anterior chamber)
- Usually autoimmune cause but can be infection, trauma, ischaemia or malignancy
- Can be acute, recurrent, or chronic
- All types of uveitis are potentially blinding conditions

Presentation:
Unilateral
- Painful red eye
- Photophobia
- Reduced visual acuity
- Watery eye
- On examination: ciliary red ring, miosis, abnormally shaped pupil, hypopyon

Investigations:
Mainly clinical diagnosis
- Ophthalmoscope (keratic precipitates or synechia)

Management:
- Steroids (eye drops, oral or intravenous)
- Cycloplegics e.g. atropine eye drops

44
Q

Suggest some indications for mydriatic / cyclopaedic drops

A
  • Dilate pupil to better visualise the retina
  • Children and amblyopia
  • Refraction of children for prescription of glasses
45
Q

Give the difference between mydriatic and cyclopaedic drops and give some examples

A

Mydriatic drops:
Medications that make pupils dilate

Cyclopaedic drops:
Paralysis of the muscles that are responsible for accommodation

Examples:
- Atropine (anticholinergic)
- Cyclopentolate (anticholinergic)
- Tropicamide (anticholinergic)
- Phenylephrine (sympathetic)

46
Q

List contraindications for the following mydriatic and cyclopaedic drops:
- Atropine, Cyclopentolate, Tropicamide (anticholinergics)
- Phenylephrine (sympathetic)

A

Atropine, Cyclopentolate and Tropicamide (anticholinergics)
- Allergy
- Acute closed-angle glaucoma
- HTN for Atropine

Phenylephrine (sympathetic)
- Allergy
- Children
- Acute closed-angle glaucoma

47
Q

List some side effects of mydriatic and cyclopaedic drops

A
  • Temporary stinging (few seconds)
  • Temporary blurring of vision
  • Whitening of eyelids (temporary)
  • Atropine = red / warm face
    CAN’T DRIVE UNTIL BLURRING WORN OFF
48
Q

Suggest some indications for Fluorescein eye drops

A

Diagnostic:
- Identify defects in corneal epithelium
- Assess tear drainage in children with congenital nasolacrimal duct obstruction
- Part of measuring intraocular pressure (tonometry)

+ combined with local anaesthetic

*Warn patients about staining (clothes and contact lenses)

49
Q

Outline the general pathophysiology of glaucoma and describe the pattern of vision loss experienced initially then in later disease

A

Neurodegenerative condition primarily due to dysfunction in outflow of aqueous humour (produced by ciliary bodies)
- Either acute (sudden narrowing of iridocorneal angle) or chronic (wide iridocorneal angle)
- Causes build-up of intraocular pressure
- Leads to damage of optic nerve and retinal ganglion cells

Vision loss:
Early disease = peripheral vision loss
Later disease = central vision loss

50
Q

Chronic (open-angle) glaucoma - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Gradual increase in resistance to flow of aqueous humour through the trabecular meshwork
- Slow increase in intraocular pressure

Presentation:
Usually asymptomatic
- Gradual peripheral vision loss (tunnel vision)
- Fluctuating pain
- Headaches
- Blurred vision
- Halos around lights (particularly at night)

Investigations:
- Slit lamp = cupping (optic cup 50% bigger than optic disc)
- Non-contact tonometry (screening)
- Contact Goldmann applanation tonometry (gold-standard)
- Visual field assessment (peripheral vision loss)
- Gonioscopy (assess angle between the iris and cornea)
- Central corneal thickness assessment

Management - when pressure > 24mmHg:
- Prostaglandin eye drops e.g. Latanoprost (improve drainage)
- Topical beta blockers e.g. Timolol
- Topical Carbonic Anhydrase inhibitor e.g. Dorzolamide
- Parasympathomimetic e.g. Pilocarpine
- Surgical: 360° selective laser trabeculoplasty

51
Q

List some risk factors for chronic (open-angle) glaucoma

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Myopia (nearsightedness)
52
Q

List some risk factors for acute (closed-angle) glaucoma

A
  • Increasing age
  • Family history
  • Female (4 times more likely)
  • Chinese and East Asian ethnic origin
  • Shallow anterior chamber

Medications:
- Adrenergic medications e.g., noradrenaline
- Anticholinergics
- Tricyclic antidepressants (anticholinergic effects)

53
Q

Acute (closed-angle) glaucoma - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
Ophthalmological emergency
- Iris bulges forward, which seals off the trabecular meshwork
- This prevents aqueous humour from draining, leading to a continual increase in intraocular pressure
- Pressure builds in the posterior chamber, pushing the iris forward and further exacerbating angle closure

Presentation:
- Severely painful red eye
- Associated headache, N&V
- Decreased visual acuity
- Fixed, mid-dilated pupil
- Hazy cornea
- Halos around lights
- Hard eyeball on gentle palpation

Management:
- Lying flat on back
- Analgesia and antiemetics
- Pilocarpine eye drops (improve drainage)
- IV Acetazolamide, Timolol, Dorzolamide or Brimonidine (reduce production of aqueous humour)
- Hyperosmotic agents e.g. IV mannitol if no improvement
- Laser iridotomy to BOTH eyes = definitive treatment

54
Q

List some common eyelid disorders (differentials)

A
  • Blepharitis
  • Chalazion
  • Stye
  • Entropion / ectropion
  • Trichiasis
  • Periorbital cellulitis / orbital cellulitis
55
Q

Blepharitis - state the following:
- Pathophysiology
- Presentation
- Management

A

Inflammation of the eyelid margins

Presentation:
Typically bilateral
- Crusting around eyelashes
- Surrounding erythema
- Gritty sensation
- Itchy eyelids
- Dry sensation

Management:
- Warm compresses
- Gentle cleaning of the eyelid margins

56
Q

Chalazion (Meibomian cyst) - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Non-infectious inflammatory granuloma
- Caused by sebaceous gland blockage

Presentation:
Usually single lesions, sometimes multiple lesions
- Painless lid lump (usually upper lid)

Management:
Usually self-limiting
- Warm compress for 5–10 minutes 2–4 times daily until resolved

57
Q

Stye - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Also known as a hordeolum
- Infection of either sweat or sebaceous glands at the base of upper or lower eyelid, leading to local abscess

Presentation:
Unilateral, usually solitary lesion
- Eyelid pain
- Pustule at eyelid margin

Management:
- Warm compress for 5–10 minutes 2–4 times daily until resolved

58
Q

Entropion - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Inward rotation of the eyelid margin (usually lower lid)
- Causes eyelashes to come into contact with the surface of the eye
- Can result in corneal damage and ulceration

Presentation:
- Visible inturning of eyelid
- Pain
- Foreign body sensation
- Red, watery eye
- Blurring of vision

Management:
- Taping affected eyelid away from eye with supplementary lubricating eye drops
- Definitive management with surgery

59
Q

Ectropion - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Outward rotation of the eyelid margin (usually lower lid)

Presentation:
Symptoms variable depending on severity
- Lower lid visibly away from eyelid
- Painful / sore
- Red
- Watery eye

Management:
Mild cases require no treatment
- Lubricating eye drops
- Definitive management with surgery

60
Q

Trichiasis - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Inward growth of the eyelashes, can be secondary to a number of conditions
- Can cause corneal damage and ulceration

Presentation:
Unilateral or bilateral
- Foreign body sensation
- Red eye
- Watery eye

Management:
- Lubricating eye drops
- Epilation of eyelashes with forcep (likely to grow back)
- Definitive management with medical management e.g. electrolysis of hair follicle, cryotherapy, laser treatment

61
Q

Periorbital cellulitis - state the following:
- Pathophysiology
- Presentation
- Investigation (help differentiate from orbital cellulitis)
- Management

A

Pathophysiology:
- Infection of tissues lying anterior to the orbital septum (orbit not involved)
- Usually mild, except in young children

Presentation:
- Acute onset of swelling, redness and tenderness of lid(s)
- Fever
- Malaise / irritability in children

Investigation (help differentiate from orbital cellulitis):
- CT scan (orbits and sinuses)

Management:
- Systemic antibiotics (oral or IV)

62
Q

Orbital cellulitis - state the following:
- Pathophysiology
- Presentation
- Investigation
- Management

A

Pathophysiology:
- Infection of tissues lying posterior to the orbital septum (orbit involved)
- Severe sight and life-threatening emergency

Presentation:
- Unilateral swelling of conjunctiva and lids +/- pain
- Pain on ocular movement / restricted eye movements
- Blurred vision
- Diplopia
- Proptosis
- Fever
- Severe malaise

Investigation:
- CT scan (orbits and sinuses)
- Blood tests (CRP, ESR)

Management:
- IV antibiotics
- Possible drainage of orbital abscess + culture

63
Q

Central retinal artery occlusion - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
Ophthalmic emergency
- Obstruction to blood flow through the central retinal artery (branch of ophthalmic artery)
- Most common cause is atherosclerosis, but can be caused by GCA

Presentation:
- Sudden painless loss of vision = ‘curtain coming down’
- Relative afferent pupillary defect (RAPD)

Investigations:
- Fundoscopy (pale retina with a cherry red spot)
- Try to rule out GCA as a cause (ESR blood test and temporal artery biopsy)

Management:
Aim to resolve blockage (no consensus on treatment)
- Massage eye
- Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure)
- Methods to dilate artery e.g. inhaled high % oxygen, sublingual isosorbide dinitrate, oral pentoxifylline
- Methods to reduce intraocular pressure e.g. IV Mannitol or Acetazolamide, topical Timolol
(immediate systemic steroids if GCA suspected cause)
Importance on secondary prevention!

64
Q

Conjunctivitis - state the following:
- Pathophysiology
- Presentation
- Management

A

Pathophysiology:
- Inflammation of conjunctiva
- Bacterial, viral or allergic
= Highly contagious

Presentation:
Unilateral or bilateral
- Red eye
- Itchy or gritty sensation
- Discharge (watery or purulent)
Bacterial = purulent discharge, starting in one eye and spreading to other
Viral = watery discharge, associated with UTRI symptoms e.g. cough, runny nose

Management:
Conjunctivitis usually resolves in 1-2 weeks without needing treatment (even bacterial cases)
- Hygiene measures and clean eye to remove discharge
- If bacterial, can use: topical Chloramphenicol drops or fusidic acid eye drops
- If allergic, antihistamines (oral or topical)

**Neonates under one month with conjunctivitis need urgent ophthalmology assessment = can cause permanent vision loss

65
Q

Diabetic retinopathy - outline the pathophysiology and the 3 main stages

A

Caused by chronic hyperglycaemia

Damages endothelium of retinal capillaries, leading to:
- Microaneurysms
- Haemorrhage
- Mini-infarctions

Risk of oxidative stress and increased VEGF production

3 main stages:
1. Background
2. Preproliferative
3. Proliferative

66
Q

Outline some investigations to consider for suspected diabetic retinopathy

A

Investigations:
- OCT
- Fundus Fluorescein angiography

67
Q

Outline some features seen on:
- Background diabetic retinopathy
- Pre-proliferative diabetic retinopathy
- Proliferative diabetic retinopathy

A

Background diabetic retinopathy:
- Haemorrhages
- Microaneurysms
- Cotton wool spots
- Hard exudates

Pre-proliferative diabetic retinopathy:
- Larger haemorrhages
- Venous beading / loops
- Microvascular abnormalities

Proliferative diabetic retinopathy:
- New vessel formation (disc, iris or everywhere)

68
Q

Outline how the following stages of diabetic retinopathy are managed:
- Background diabetic retinopathy
- Pre-proliferative diabetic retinopathy
- Proliferative diabetic retinopathy

A

At every stage - improve diabetes control

Background diabetic retinopathy:
- No action required
- Annual monitoring

Pre-proliferative diabetic retinopathy:
- Closer follow up (4-6 monthly)
- Consider retinal laser treatment

Proliferative diabetic retinopathy:
- Photocoagulation of all layers of retina within 2 weeks of diagnosis

69
Q

Outline how diabetic maculopathy is different from diabetic retinopathy and how it is generally managed

A

Diabetic maculopathy is a type of diabetic retinopathy
- Blood vessels to the macula can become blocked
- Other blood vessels enlarge to compensate but are leaky and bleed into macular
- Causes loss of central vision (peripheral vision usually okay)

Management:
- Anti-VEGFs e.g. Bevacizumab
- Intravitreal Dexamethasone implant
- Intravitreal Flucinolone implant

70
Q

List some complications of diabetic retinopathy

A
  • Retinal detachment / vitreous haemorrhage
  • Cataracts
  • Secondary glaucoma
  • Retinal vein occlusion
  • Optic neuropathy
71
Q

Optic neuritis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Inflammation of the optic nerve
- Primary demyelinating disease occurring in isolation (idiopathic) or as part of MS

Presentation:
Usually unilateral
- Eye pain (worse with eye movements)
- Loss of colour vision
- Loss of vision (central)
- Relative afferent pupillary defect (RAPD)

Investigations:
Generally clinical diagnosis
- Fundoscopy (swollen optic disc)
- Testing of visual acuity, contrast and colour vision, visual field testing
- MRI optic nerve if suspecting MS

Management:
- Consider Methylprednisolone for acute symptoms (doesn’t impact level of final vision)

72
Q

Retinal detachment - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Seperation of the neurosensory layer (rods and cones) of the retina from the retinal pigment epithelium (RPE)
- Usually secondary to a retinal tear, allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
- Neurosensory layer relies on the choroid for blood supply therefore detachment can disrupt blood supply = permanent damage to the photoreceptors, making it sight-threatening

Presentation:
**painless
- Peripheral vision loss (often sudden and described as a shadow coming across the vision)
- Blurred vision
- Flashes and floaters

Investigations:
- Red reflex (may be absent)
- Dilated fundal examination / slit lamp examination (visualise tears)
- Ultrasound or OCT (optical coherence tomography)

Management:
- Vitrectomy (keyhole eye surgery to remove vitreous fluid and repair tear)
- Scleral buckle (silicone “buckle” to squish retina to choroid layer again)
- Pneumatic retinopexy (inject gas bubble to squish retina to choroid layer again)

73
Q

List some risk factors for retinal detachment

A
  • Trauma
  • Thinning of the retina
  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Family history
  • Retinal malignancy
74
Q

State 2 methods that can be used to manage retinal tears (to reduce likelihood of retinal detachment occuring)

A
  • Laser therapy
  • Cryotherapy

Creates adhesions between retina and choroid layers

75
Q

Outline the key differences between episcleritis and scleritis including:
- Anatomical structures involved
- Pain
- Associated ocular symptoms
- Blood vessels

A

Episcleritis = inflammation of the superficial, episcleral layer of the eye
- Relatively common
- Benign and self-limiting
**Episcleritis does not progress to scleritis

Scleritis = inflammation involving the sclera
- Severe inflammation
- Often causes complications, nearly always requires systemic treatment

Pain: mild (episcleritis) severe (scleritis)
Associated ocular symptoms: none (episcleritis) diplopia, vision loss (scleritis)
Blood vessels: superficially inflamed and mobile (episcleritis) severely inflamed and immobile (scleritis)

76
Q

Scleritis - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Inflammation of full thickness of the sclera (outer layer of connective tissue surrounding most of the eye)
- Most cases are idiopathic or associated with inflammatory conditions (although can be associated with infection)
- Severe type of scleritis = necrotising scleritis

Presentation:
Usually unilateral, more common in women 40-60 years
- Red, inflamed sclera (localised or diffuse)
- Severe pain (typically a boring pain), worse on eye movement
- Photophobia
- Watery eyes
- Reduced visual acuity
- Tenderness to palpation of the eye

Investigations:
- Slit-lamp examination (detect intraocular inflammation)

Management:
- NSAIDs (oral)
- Steroids (topical or systemic)
- Immunosuppression of underlying systemic condition if present
Assessment for underlying inflammatory conditions if not already diagnosed

77
Q

List some inflammatory conditions associated with anterior uveitis and scleritis (seperate)

A

Anterior uveitis:
Seronegative spondyloarthropathies e.g.
- Ankylosing spondylitis
- Psoriatic arthritis
- Reactive arthritis
IBD
Sarcoidosis
Behçet’s disease

Scleritis:
- Rheumatoid arthritis
- Vasculitis (esp. granulomatosis with polyangiitis)

78
Q

Thyroid eye disease (Graves’ ophthalmology) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Most common extra-thyroidal manifestation of Graves’ (90% patients with TED have Graves)
- Autoimmune reaction to TSH causes infiltration of T lymphocytes into orbital tissue stimulates the release of cytokines
- Leads to oedema of extraocular muscles and orbital fat
- Usually develops within 2 years of hyperthyroidism
- Initial inflammatory phase lasting 6-24 months
- Followed by inactive fibrotic phase, where further changes are unlikely

Presentation:
Mostly bilateral, females 30-50 years
- Proptosis +/- lid lag (together = exophthalmos)
- Aching eyes (worse in the mornings, worse on movement)
- Diplopia
- Puffy eyelids
- Red eyes
- Discomfort / pressure
- Gritty / watery eyes
+ concurrent symptoms of hyperthyroidism

Investigations:
ADVISE ABOUT DRIVING
- Thyroid function tests and thyroid autoantibodies
- Exophthalmometry (quantify eye protrusion)
- MRI (or CT) of orbits

Management:
Generally should resolve after inflammatory phase (6-12 months)
Optimise thyroid levels + smoking cessation
- Mild = lubricating eye drops + Selenium
- Moderate = steroids (oral or IV)
If left with residual issues - surgical interventions e.g. decompression surgery or radiotherapy

79
Q

Name some conditions that Graves’ disease is associated with

A
  • T1DM
  • Vitiligo
  • Myasthenia gravis
  • Sjogren’s syndrome
  • RA
  • SLE
80
Q

List some complications from thyroid eye disease

A
  • Corneal ulceration
  • Superficial keratitis (inflammation of cornea)
  • Diplopia/ strabismus = eye misalignment
  • Optic nerve compression
  • Glaucoma (increased intraocular pressure)
81
Q

State some signs of optic neuropathy in thyroid eye disease

A

Mourits score of 4 or more (benefit from immunosuppression)
- Decreased vision
- Decreased colour vision
- RAPD
- Visual field defects
- Optic nerve compression / swelling on MRI scan

82
Q

Retinitis Pigmentosa - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Genetic condition causing degeneration of the photoreceptors in the retina, particularly the rods
- Many different genetic causes, some associated with systemic conditions

Presentation:
Mostly symptoms start in childhood
- Night blindness (often the first symptom)
- Peripheral vision loss (before the central vision)

Investigations:
- Fundoscopy (pigmentations in spiky appearance, nearer edges of periphery)
- Narrowing of the arterioles
- Pale appearance of optic disc

Management:
Difficult to slow disease progression
- Vision aids
- Sunglasses (protect the retina)
- Driving limitations and informing the DVLA
- Genetic counselling

83
Q

Retinoblastoma - state the following:
- Pathophysiology
- Most common age affected
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Cancer of the retina
- Intraocular (within eyeball) or extraocular (spread outside eyeball)
- Best outcome for childhood cancer 99% survival rate

Most common age affected:
- Children under 5

Presentation:
- White reflex (leukocoria), instead of red
- Squint
- Poor visual acuity
- Erythema eye
- Nystagmus

Investigations:
- Ophthalmoscopy
- Ultrasound
- MRI scan
- Genetic testing

Management:
- Cryotherapy or laser therapy
- Chemotherapy / radiotherapy
- Surgery

84
Q

Amaurosis fugax - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Retinal TIA (transient ischaemic attack) caused by an emboli
- Leads to temporary blockage of either internal carotid artery or central retinal artery
- Other causes include giant cell arteritis or optic neuritis

Presentation:
- Sudden unilateral painless vision loss ‘curtain coming across eye’
Typically self-resolving after a few minutes

Investigations:
- Angiography
- Doppler ultrasound neck (carotid atherosclerosis)

Management:
Aimed at treating the underlying vascular risk factors e.g. hypercholesterolaemia, HTN
- Anticoagulants e.g. Aspirin or Clopidogrel

85
Q

Squint (strabismus) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Misalignment of the eyes
- Poor direction of light onto retina, therefore experience double vision
- In childhood, brain ‘tunes out’ weaker eye and can lead to amblyopia (‘lazy eye’)

Presentation:
- Misalignment of eye at rest (esotropia, exotropia, hypertropia, hypotropia)
- Double vision

Investigations:
- Cover test
- Hirschberg’s test (shine light directly at both corneas)

Management:
Treatment needs to begin before 8 years old (whilst still developing)
- Patch covering good eye
- Atropine drops in good eye (makes good eye blurry)

86
Q

Amblyopia (‘lazy eye’) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management

A

Pathophysiology:
- Poor vision from one eye (can be bilateral)
- Caused by the brain ‘tuning out’ weaker eye
- May be caused by refractive errors, strabismus or cataract

Presentation:
Often picked up on routine eyesight tests aged 3-5
- Poor depth perception
- Squinting
- Shutting 1 eye
- Tilting their head

Investigations:
- Routine eyesight test at 3-5 years

Management:
Treatment needs to begin before 8 years old (whilst still developing)
- Patch covering good eye
- Atropine drops in good eye (makes good eye blurry)

87
Q

Other than being idiopathic (most common), list some other acquired causes of a squint

A
  • Cranial nerve palsy
  • Trauma
  • Raised ICP e.g. space occupying lesions or hydrocephalus
  • Cerebral palsy
88
Q

List some risk factors for development of amblyopia (‘lazy eye’)

A
  • Family history of amblyopia or other eye conditions
  • Premature / low birth weight
  • Developmental disabilities
89
Q

Suggest how you could differentiate between episcleritis and scleritis with medication

A

Use topical adrenaline drops

Episcleritis = blanching of blood vessels
Scleritis = no blanching of blood vessels (as the vessels are too deep)

90
Q

List some differentials for ptosis

A
  • Oculomotor CN3 palsy
  • Horners syndrome
  • Myasthenia gravis / Lambert-Eaton syndrome
  • Age
91
Q

List some complications of herpes zoster ophthalmicus

A
  • Cranial nerve 3, 5, 6 palsy
  • Keratitis
  • Uveitis
  • Conjunctivitis
92
Q

List some causes of optic disc swelling

A
  • Raised intracranial pressure (papilloedema)
  • Severely raised blood pressure
  • Optic neuritis e.g. in MS
  • Anterior ischaemic optic neuropathy