Ophthalmology Flashcards
State some risk factors for age-related macular degeneration (non-modifiable and modifiable)
Non-modifiable:
- Older age
- Ethnicity
- Ocular characteristics (light coloured iris, hyperopia)
- Genetics (complement factor H)
Modifiable:
- Smoking
- Cardiovascular disease (CVS & HTN)
Outline the main causes of blindness worldwide
Most common in those ages > 50
Distance vision issues:
- Refractive errors
- Cataract
- Glaucoma
- AMD (age-related macular degeneration)
- Diabetic retinopathy
Near vision issues:
- Presbyopia
Outline the 2 muscles responsible for moving the eyelids and what nerves they are innervated by
- Levator palpebrae superioris = open eyelids
- Oculomotor nerve (CN3) - Orbicularis oculi = close eyelids
- Facial nerve (CN7)
Outline the 3 main layers of the eyeball
Outer:
- Sclera
- Cornea
Middle:
- Choroid
- Ciliary body
- Iris
Inner:
- Retina
State the 2 compartments of the eyeball and which areas they sit between
- Anterior chamber
- Between cornea and iris - Posterior chamber
- Between iris and ciliary body + lens
Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline what drusen is (in age-related macular degeneration) and the 2 main types
- 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)
- Soft drusen - larger, soft deposits
- Hard drusen - small, hard, solid deposits
State the way in which soft drusen can contribute to age-related macular degeneration
Lift the retinal pigment epithelium away from the underlying membrane
1. Hypoxia
2. Inflammation
State the 2 main types of age-related macular degeneration and relative frequency
Dry (non-neovascular) = 90% cases
Wet (neovascular) = 10% cases
State 2 findings common to both dry and wet AMD
- Atrophy of the retinal pigment epithelium
- Degeneration of photoreceptors
Age-related macular degeneration - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline which bones make up the superior, medial, lateral and floor of the orbital cavity
Superior = frontal bone + lesser wing of sphenoid
Medial = ethmoid bone + maxilla + lacrimal + sphenoid
Lateral = zygomatic + greater wing of sphenoid
Floor = maxilla + palatine + zygomatic
Outline what nerve and muscle causes eyelid opening and eyelid closing
Eyelid opening:
- Levator palpebrae superioris
- Oculomotor nerve (CN3)
Eyelid closing:
- Orbicularis oculi
- Facial nerve (CN7)
Outline the 3 layers of the globe of the eye
Retina (innermost)
Choroid
Sclera (outermost)
Outline the difference between rods and cones
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
Outline some differentials for someone presenting with ocular discomfort (organise by structure)
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
Outline some differentials for someone presenting with acute loss of vision
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
Outline some differentials for someone presenting with gradual loss of vision
- Age-related macular degeneration
- Presbyopia
- Cataracts
- Chronic open-angle glaucoma
- Diabetic retinopathy
Concerning:
- Vitreous haemorrhage
- Giant cell arteritis
- Chronic optic nerve compression
Outline some differentials for someone presenting with transient visual loss (lasts <24hrs)
- Amaurosis fugax
- Migraine
- Papilloedema
Outline some differentials for someone presenting with sudden (painless) loss of vision
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)
Outline some differentials for someone presenting with gradual (painless) loss of vision
- Cataracts
- Refractive errors / presbyopia
- Cataracts
- Dry age-related macular degeneration (AMD)
- Open-angle glaucoma
- Tumours affecting visual pathway
Outline some differentials for someone presenting with painful loss of vision
- Acute closed-angle glaucoma
- Optic neuritis
- Uveitis
- Keratitis / corneal ulcer
- Endophthalmitis
- Orbital cellulitis
+ GCA (headache)
Outline some differentials for someone presenting with diplopia (double vision)
- Monocular
- Binocular
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
Outline some differentials for someone presenting with red eye
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
Outline some differentials for someone presenting with ocular discharge (separate into purulent and wartery causes)
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)
Outline some differentials for someone presenting with abnormal pupil shape
- 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
Outline some differentials for someone presenting with mydriasis (dilated pupil)
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
Outline some differentials for someone presenting with miosis (constricted pupil)
Medication:
- Opiates
- Nicotine
- Pilocarpine
Other:
- Horner syndrome
- Cluster headaches
- Advanced syphilis (Argyll-Robertson pupil)
Outline some differentials for someone presenting with loss of red reflex
- Corneal scars
- Cataracts
- Vitreous hemorrhage
- Retinal detachment
- Refractive error
- Strabismus
- Coloboma
- Retinoblastoma
Outline some differentials for someone presenting with visual hallucinations
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
Outline 3 roles of the cornea
- Protection of the eye (including corneal reflex)
- Allow transmission of light (transparent)
- Refraction of light
Keratitis (infection of cornea) - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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
Outline some triggers/risk factors for infective keratitis (infection of cornea)
- Trauma
- Contact lenses
- Dry eyes
- Pre-existing corneal disease e.g. ulcers
Immunocompromised will make infection more likely
State what is used to measure IOP and the value at which above is considered raised IOP
Tono-meter
- Measures force needed to flatten cornea
> 21 considered to be ocular hypertension (11-21 considered normal)
Outline some classes of medications that can reduce aqueous production (and reduce IOP)
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
Cataracts - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
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)
