9. OPTHALMOLOGY Flashcards
There are 6 extraocular muscles. Describe their innervation.
SO4LR6!
Superior Oblique = CN IV
Lateral Rectus = CN VI
Inferior oblique, sup, med, inf rectus = CN III
Describe the path of the optic nerve to the visual cortex.
Optic nerve
Optic chiasm
Lateral geniculate nucleus
Optic radiation
Visual cortex
How do you remember where the lesion is of a homonymous quadrantanopia?
PITS
Parietal lobe, Inferior optic radiations = inf.
Temporal lobe, Superior optic radiations = sup.
Which visual field defect does an optic chiasm lesion cause?
Bitemporal hemianopia
Upper quadrant defect > lower = inferior chiasm compression, commonly pituitary tumour
Lower > upper = superior chiasm compression e.g. craniopharyngioma
Someone is found to have an incongruous left homonymous hemianopia. Where is the lesion likely to be?
Right optic tract
Incongruous = incomplete or asymmetric
Someone is found to have a congruous right homonymous hemianopia. Where is the lesion likely to be?
Left optic radiation or occipital cortex.
Congruous = complete / symmetrical field loss
Someone has a homonymous hemianopia with macula sparing. Where is the lesion likely to be?
Occipital cortex
What range of acuity does the human eye have, both vertically and horizontally?
60* up
75* down
100* lateral
60* medial
Does the optic nerve sit nasally or temporally?
NASAL
Describe the path of the central retinal artery.
Internal carotid > Ophthalmic > Central Retinal
2 causes of CRAO:
Atherosclerosis
Giant cell arteritis
Risk factors for CV disease increase the risk of CRAO. What risk factors exist for GCA to be aware of?
White ethnicity
Older
Female
Polymyalgia rheumatica
Give 4 differentials for sudden painless loss of vision:
CRAO
CRVO
Retinal detachment
Vitreous haemorrhage
Clinical features of CRAO:
Sudden, painless, unilateral loss of vision.
RAPD
Pale fundus. Cherry red spot on fundoscopy: fovea. Macular has different blood supply to rest of retina?
CRAO can cause permanent visual loss, and is essentially a stroke event. What medication should patients be given, and where should they be referred / investigated?
300 mg aspirin
Stroke / TIA clinic
CPR/ESR bloods important as GCA is a potentially reversible cause - IV methylpred may be indicated.
Vitreous haemorrhage is one of the most common causes of PAINLESS loss of vision. Give 3 causes of a vitreous haemorrhage.
Diabetic retinopathy
Posterior vitreous detachment / Retinal detachment
Ocular trauma (most common in children and young people)
Posterior vitreous detachment is a painless condition. usually occuring due to natural changes with age. Give 3 key features a patient may present with, and discuss managment.
Floaters
Flashing lights
Blurred vision
Dark curtain coming down; this would indicate retinal detachment.
No management often, symptoms improve over a period of 6 months.
BUT if an associated retinal tear, then surgery will be required to fix this.
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24 hours to exclude:
Retinal tear or detachment
2 risk factors for vitreous detachment:
Aging - vitreous fluid does not hold it’s shape as well as it becomes less viscous.
Near-sightedness / myopia - longer axial length
Age-related macular degeneration is the most common cause of blindness in the UK. What is the % prevalence of the 2 types?
Dry 90%
Wet 10%
More often unilateral
Describe the pathology in wet AMD.
New blood vessels develop from the choroid layer and grow into the retina (neovascularisation). These vessels are new and weak and can leak fluid or blood, causing oedema and faster rate of decline if VA.
4 layers of the macula, which generates high -definition colour vision in the central visual field, from base to surface.
Choroid
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors
Yellowish deposits are seen in a older patient. What do these indicate, and give 2 other features that are common to both wet and dry AMD.
Drusen - protein and lipid deposition between the retinal pigment epithelium and Bruch’s membrane.
Atrophy of retinal pigment epithelium
Degeneration of photoreceptors
Describe how AMD can present, and highlight the differences between wet and dry.
Gradual loss of central vision (DRY), but wet can develop within days and progress very quickly.
Reduced VA
Metamorphopsia
Gradually worsening ability to read small text
Key differences between glaucoma and AMD:
Glaucoma = halos around lights and PERIPHERAL loss
AMD = wavy appearance to straight lines and CENTRAL loss
4 examination findings in AMD:
Scotoma (enlarged central vision loss)
Snellen chart reduced VA
Amsler grid test - distortion of straight lines
Drusen on fundoscopy
OCT - xsection of layers of the retina - used for Dx and monitoring
Initial investigation of choice for AMD:
Slit-lamp microscopy
What therapy can be used in wet AMD and how is it administered?
Anti-VEGF agents e.g. bevacizumab
Injection into eye, regular
Fluroscein angiography used to guide
Management of dry AMD:
Avoid smoking
Control BP
Vitamin supplementation growing evidence?
The majority of patients with CRVO are managed conservatively. Give 2 indications for treatment.
Macular oedema; anti-VEGF agents, ?dexamethasone
Retinal neovascularization; laser photocoagulation of the new vessels
Clinical and fundoscopy features of CRVO:
Sudden, painless loss of vision
Reduced VA / blurred vision
Tortuous, dilated retinal veins
Flame and blot haemorrhage s
Retinal oedema
Cotton wool spots
Hard exudates
RFs for CRVO:
CV risk factors
Age
Hypertension
Polycythaemia / viscosity e.g myeloma.
Glaucoma
Describe the blood supply and drainage to the retina.
Branch retinal veins > central retinal vein > drains into superior ophthalmic vein or cavernous sinus.
Blockage of the branch retinal veins can lead to a more limited area of the fundus being affected by the occlusion. Where are these blockages most likely to occur in these branch veins?
Arteriovenous crossings - compression of the veins causing occlusion is more likely.
The neurosensory layer of the retina can become detached from the underlying pigment epithelium, and is known as retinal detachment. It can be reversed, but if left untreated can progress to permanent visual loss. Give 5 risk factors.
Often due to tears that allow the vitreous fluid to get under the neurosensory layer and fill the space.
Diabetes
Myopia
Age
Previous cataract surgery
Eye trauma e.g. boxing
Clinical features of retinal detachment:
New onset flashes and floaters
Sudden onset, painless, progressive visual loss
‘Curtain’ coming down, peripheral progressing to central
RAPD if optic nerve involved
Red reflex lost
Suspicion of retinal detachment requires immediate ophthalmology referral to assess for tears or detachment. What are the options for each respectively?
Tears:
Laser therapy
Cryotherapy
Detachment:
Vitrectomy
Scleral buckling
Pneumatic retinopexy
5 clinical features of optic neuritis:
Pain, worse on eye movement
Scotoma
Unilateral decrease in VA / blurred vision over hours to days
RAPD
Red desaturation / poor discrimination of colours
MS is obviously associated with optic neuritis (inflammation of the optic nerve), but which 2 other conditions are associated as well?
Diabetes
Syphilis
Investigation and management of optic neuritis episode?
MRI brain + orbit with gadolinium contrast
High dose steroids, recovery usually takes 4-6 weeks
Keratitis describes inflammation of what?
Cornea
Potentially sight threatening
2 typical organisms in bacterial keratitis?
Staph aureus
Pseudomonas in contact lenses
A person presents with keratitis with a history of eye exposure to soil and contaminated water, in pain out of proportion to clinical examination. What is the most likely causative organism?
Acanthamoebic keratitis
Accounts for 5% of cases
4 clinical features of keratitis:
Red eye, pain, erythema
Photophobia
Foreign body / gritty sensation
Hypopyon
What is the most common cause of keratitis?
HSV
HSV keratitis can be primary or recurrent, caused by the virus travelling to the trigeminal ganglion and becoming latent. Which layer of the cornea does HSV affect?
Epithelial
Slit lamp examination is required to diagnose keratitis. What is used to visualise the eye properly and what might be seen in HSV keratitis?
Fluroscein stain
Dendritic corneal ulcer - branching appearance
Treatment for HSV keratitis?
Topical +/- oral aciclovir
Clinical features of AACG:
severe pain; ocular or headache
decreased VA
symptoms worsen with mydriasis (watching tv in a dark room)
hard, red eye
non-reacting pupil
dull/hazy cornea?
halos around lights
AACG is a medical emergency where treatment is required to lower the IOP, and then surgery. Patients should be lain on their back without a pillow. Give 3 examples of eye drops and their mechanism for reducing IOP.
Pilocarpine, direct parasympathomimetic - contraction of ciliary muscle, increasing outflow of the aqueous humour
BB e.g. timolol - decreases aqueous humour production
Apraclonidine e, alpha-2 agonist - decreases humour production and increases outflow
Which IV drug is often given in AACG and what is the action?
IV acetazolamide (carbonic anhydrase inhibitor)
Reduces aqueous secretions
Tonometry is used to assess for elevated IOP and gonioscopy is used to visualise the angle in AACG. What is the definitive management of AACG?
Laser peripheral iridotomy - tiny hole in the peripheral iris so aqueous humour can flow into the angle
Risk factors for AACG:
Increased age
Family history
Female
Chinese and East Asian ethnicity
Shallow anterior chamber / Hypermetropia (long sighted)
Cataracts
Give 3 medication classes that can precipitate AACG:
Adrenergic e.g. noradrenaline
Anticholinergic e.g. oxybutynin, solfenacin
Tricyclic antidepressants e.g. amitriptyline (has anti-Ach effects)
Provisional diagnosis is done by an optometrist, and the patient is then referred to the ophthalmologist by the GP. What investigations can be done to confirm the diagnosis of open-angle glaucoma?
Visual field assessment
Slit lamp with pupil dilatation
Applnation tonometry to assess IOP
Gonioscopy
What is normal intraocular pressure?
10-21 mmHg
Created by resistance to flow through the trabecular meshwork
When is 360 degree selective laser trabeculoplasty (SLT) offered first line to people with glaucoma?
IOP >=24 mmHg
Second and third line options for open angle glaucoma:
2) Prostaglandin analogue eyedrops e.g. latanoprost
3) BB, carbonic anhydrase and sympathomimetic eye drops (timolol, dorzolamide, brimonidine respectively)
Risk factors for open-angle glaucoma:
Black ethnic origin
Increased age
First degree relatives
Myopia
HTN
DM
Corticosteroid use
Panretinal laser photocoagulation is used in proliferative diabetic retinopathy. Give 2 complications / side effects of this treatment and explain them.
Noticeable reduction in visual fields.
Decreases in night vision.
Peripheral fields are targeted in PRP to reduce / halt neovascularisation.
They usually target the periphery.
Rods are most abundant in the periphery and they are predominantly responsible for night vision, therefore there is a decrease in night vision.
Causes of mydriasis:
CN III palsy
Holmes-Adie pupil
Traumatic iridoplegia
Phaeochromocytoma
Congenital
Drugs: tropicamide, atropine, amphetamines, cocaine, tricyclics
What is an Argyll-Robertson pupil?
Small, irregular pupil
Don’t respond to light but do accommodate
Causes e.g. neurosyphilis, DM
Anything above ? on an audiogram is normal.
20 decibels
How to read an audiogram:
Sensorineural hearing loss; both air and bone conduction are impaired
Conductive hearing loss; only air conduction is impaired
Presenting symptoms of vitreous haemorrhage:
Dark floaters
Red hue to vision
Painless loss of vision or haze
Which electrolyte abnormality predisposes to cataracts?
Hypocalcaemia
3 features that distinguish pre-septal cellulitis from orbital cellulitis.
Ophthalmoplegia / pain on eye movements
Reduced VA
Proptosis
There is an associated systemic inflammatory condition in 50% of patients presenting with scleritis. Give the 4 of the most common:
RA - scleral tissue is similar to connective tissue in joints
Vasculitis esp GPA
SLE
Sarcoidosis
What are the classic associations with anterior uveitis?
HLA-B27
Seronegative spondyloarthropathies:
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteropathic arthritis (associated with IBD)
ALSO,
Sarcoidosis; bilateral disease
Behcet’s disease - oral ulcers, genital ulcers and anterior uveitis
Symptoms of anterior uveitis:
Inflammation of the anterior uvea - ciliary body and the iris.
Acute onset ocular discomfort and pain
Small / irregular pupil
Intense photophobia
Blurred vision
Red eye
Lacrimation
VA initially normal, then impaired
Hypopyon = very bad
Management of anterior uveitis:
Urgent ophthalmology review
Cycloplegics - dilate pupil to relieve pain and photophobia e.g. atropine, cyclopentolate
Steroid eye drops
Diabetic retinopathy is often split into NPDR, PDR and maculopathy. Which is more common in T1DM, and describe the pathophysiology?
Proliferative retinopathy
Retinal neovascularisation occurs, thought to be due to production of VEGF in response to the retinal ischaemia caused by endothelial dysfunction.
May lead to vitreous haemorrhage, fibrous tissue forming anterior to retinal disc.
50% have profound visual impairment within 5 years.
NPDR describes the presence of microaneurysms, plus or minus blot haemorrhages, hard exudates and cotton wool spots. Describe the categorisation of mild, moderate and severe NPDR.
Mild = 1 or more microaneurysm.
Moderate = microaneurysm, blot haemorrhage, hard exudates, cotton wool spots. Venous beading and intraretinal microvascular abnormalities (IRMA), but less than severe.
Severe = blot haemorrhages and microaneurysms in 4 quadrants. Venous beading in 2 quadrants. IRMA in at least 1 quadrant.
Maculopathy describes any changes on the macula area e.g. hard exudates. If there is a change in visual acuity, what treatment can be initiated?
Anti-VEGF
What is the treatment for proliferative diabetic retinopathy?
Panretinal laser photocoagulation (PRP)
Differences between bacterial and viral conjunctivitis:
Bacterial = purulent discharge, ‘stuck together’ eyes in the morning
Viral = serous discharge, recent URTI, pre-auricular lymph nodes
A pregnant woman presents with bacterial conjunctivitis. What should her management be?
Topical fusidic acid
(NOT chloramphenicol)
Management of allergic conjunctivitis:
Topical / systemic antihistamines for symptom control
Topical mast-cell stabilisers e.g. sodium cromoglicate / nedocromil
Cataracts are the leading cause of curable visual impairment. Give some causes / risk factors.
Age
Smoking
Long term steroids
Alcohol
Radiation
DM
Hypocalcaemia
Trauma
Myotonic dystrophy
Give 4 symptoms and 1 sign of a cataract:
Reduced VA and blurring
Faded colour vision / brown / yellow
Glare, lights appearing brighter than normal
Haloes around lights
All gradual onset ^
Defect in red reflex
Findings on ophthalmoscopy of a cataract:
Normal fundus and optic nerve
4 classifications of cataract:
Nuclear; changes lens refractive index, age related
Polar; localised, ?inherited
Subcapsular; steroid use
Dot opacities; common in normal lenses, also DM and myotonic dystrophy
3 complications of cataract surgery:
Endophthalmitis = inflammation of the vitreous humour
Retinal detachment
Posterior capsule rupture / opacification
Describe the role and control of the lens.
To focus light onto the retina.
It is held in place by suspensory ligaments that are attached to the ciliary body which contracts and relaxes to change the shape of the lens.
Ciliary body relaxes, suspensory ligaments tense and the lens narrows.
Ciliary body contracts, suspensory ligaments loosen and lens thickens.
Blepharitis is the inflammation of …
Eyelid margins
There are two types of blepharitis; discuss them.
Most common = posterior blepharitis. Meibomian gland dysfunction.
Less common = anterior blepharitis. Seborrhoiec dermatitis / staph infection.
Blepharitis is more common in patients with rosacea, regardless of type.
What is the function of meibomian glands ? Give presenting features of blepharitis.
They secrete oil onto the eye surface to prevent rapid evaporation of tear film. Problems with these can cause dry eyes and therefore irritation.
Features of blepharitis:
Gritty eyes
Bilateral
?Sticky eyes in the morning
Swollen eyelids in staph infection
Stye
Secondary conjunctivitis
Management of blepharitis:
Hot compresses BD to soften lid margins
Lid hygiene - cleaning debris from lid margins, baby shampoo or sodium bicarb
Artificial tears for dry eyes
What is a chalazion?
Meibomian gland cyst - firm painless lump in the eyelid.
Spontaneous resolvement usually, but maybe drainage.
Management of scleritis:
Same day ophthalmologist assessment, and review for underlying systemic conditions.
Oral NSAIDs first line
Severe = oral steroids
Immunosuppression appropriate to the underlying systemic conditions if applicable e.g. MTX in RA.
Most common complication of thyroid eye disease?
Exposure keratopathy
Eyelid retraction and exopthalmos causing proptosis - cornea is excessively exposed disrupting the normal tear film - dryness, irritation and corneal ulceration.
Foreign body sensation, pain, photophobia.
Features of thyroid eye disease:
Exophthalmos
Conjunctival oedema
Failure to close eyelids fully
Optic disc swelling
Ophthalmoplegia
Pathophysiology of thyroid eye disease:
Autoimmune response to an autoantigen of the ?TSHr.
Lead to retro-orbital inflammation.
Inflammation results in glycosaminoglycan and collagen deposition in the muscles, causing the classic appearance of thyroid eye disease.
Prevention of thyroid eye disease:
STOP SMOKING
If taking radio-iodine treatment, 15% of patients developed or had worsening of their eye disease. Prednisolone could be protective for this.
Most serious complication of thyroid eye disease, and when does it occur?
Optic neuropathy
Enlarged extraocular muscles compress the optic nerve at the apex of the orbit.
Results in reduction of VA, colour vision deficits and visual field defect.
URGENT INTERVENTION to prevent permanent visual loss.
How does thyroid eye disease cause strabismus?
Fibrosis and enlargement of the extra-ocular muscles can result in restrictive strabismus (misalignment of the eyes) and therefore double vision.
For patients with established thyroid eye disease what should indicate an urgent ophthalmology review?
Unexplained vision deterioration
Colour vision change
Globe subluxation
Obvious corneal opacity
Cornea visible when eyes are closed
Disc swelling
