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Ophthalmology > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is the most common cause of blindness in the UK?

A

age-related macular degeneration

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2
Q

What are the risk factors for age-related macular degeneration?

A
  • > 75yo
  • smoking
  • family history
  • IHD
  • HTN
  • dyslipidaemia
  • diabetes mellitus
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3
Q

How is age-related macular degeneration classified?

A

Dry macular degeneration:
- 90% of cases
- atrophic
- drusen (in Bruch’s membrane)
- early age related degeneration

Wet macular degeneration:
- 10% of cases
- exudative or neovascular
- choroidal neovascularisation
- leakage of serous fluid and blood causing rapid loss of vision
- worst prognosis
- late age related degeneration

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4
Q

Features of age related macular degeneration:

A
  • reduced acuity
  • overall deterioration of night vision
  • fluctuations day to day
  • photopsia and glare around objects
  • distortion line perception (Amsler grid testing)
  • wet ARMD - red patches
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5
Q

How is age related macular degeneration investigated?

A
  • slit lamp microscopy
  • fluorescein angiography if neovascular to guide intervention
  • ocular coherence tomography
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6
Q

How is age related macular degeneration treated?

A
  • anti-VEGF: inhibits potent mitogen which drives vascular permeability in wet ARMD e.g. ranibizumab, bevacizumab, pegatanib (4 weekly injections)
  • laser photocoagulation to slow progression where new vessels form
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7
Q

What is acute angle closure glaucoma and what are the predisposing factors?

A
  • optic neuropathy due to raised IOP
  • secondary to impairment of aqueous outflow
  • predisposing factors: hypermetropia, pupillary dilatation, lens growth associated with age, mydriatic drops
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8
Q

What are the features of AACG?

A
  • pain
  • reduced acuity
  • worse with mydriasis e.g. watching TV in dark room
  • hard red eye
  • halo around light
  • semi-dilated non-reacting pupil
  • corneal oedema -> dull hazy
  • systemic upset
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9
Q

Management of AACG:

A
  • emergency - urgent referral
  • direct parasympathomimetic e.g. pilocarpine to contract ciliary muscle, open trabecular network and increase aqueous outflow
  • beta blocker e.g. timolol to reduce aqueous production
  • alpha-2 agonist e.g. apraclonidine which does both
  • IV acetazolamide to reduce aqueous secretions
  • definitive: laser peripheral iridotomy
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10
Q

What is anterior uveitis and what are the features?

A
  • inflammation of the iris and ciliary body
  • acute pain
  • small, irregular pupil
  • photophobia
  • blurred vision
  • redness
  • lacrimation
  • ciliary flush
  • hypophon (pus in anterior chamber)
  • impaired acuity
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11
Q

What is anterior uveitis associated with?

A
  • ankylosing spondylitis
  • reactive arthritis
  • IBD
  • Bechet’s
  • sarcoidosis
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12
Q

How do you treat anterior uveitis?

A
  • urgent review by ophthalmologist
  • cycloplegics - to dilate pupil e.g. atropine, cyclopentolate, steroid eye drops
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13
Q

What are some ischaemic/vascular causes of sudden loss of vision and how is it treated?

A
  • large artery disease e.g. atherothrombosis, embolus, dissection
  • small artery disease e.g. temporal arteritis
  • venous disease
  • hypoperfusion
  • ischaemic optic neuropathy
    Treat with: aspirin 300mg
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14
Q

How does sudden loss of vision due to central artery occlusion present?

A
  • afferent pupillary defect
  • cherry red spot on pale retina
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15
Q

How does sudden loss of vision due to vitreous haemorrhage present and some causes?

A
  • one of the most common causes
  • sudden visual loss with dark spots and bleeds, red hue, reduced visual acuity
  • caused by: proliferative diabetic retinopathy, posterior vitreous detachment, bleeding disorders, anticoagulation, ocular trauma
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16
Q

How does sudden loss of vision due to retinal detachment present?

A
  • dense shadow peripherally progressing to central vision (curtain)
  • straight lines look curved
  • pigment in anterior vitreous
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17
Q

How does sudden loss of vision due to posterior vitreous detachment present?

A
  • separation of vitreous membrane from retina
  • painless loss of vision
  • flashes of light (photopsia) in periphery
  • floaters on temporal side of central vision
  • cobweb across vision
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18
Q

What are the different types of blepharitis and features?

A
  • inflammation of eyelid margins
  • meibomian gland dysfunction: posterior blepharitis
  • seborrhoea dermatitis/staph: anterior blepharitis
  • features: bilateral discomfort, grittiness, sticky, red margins, styes and chalazions, secondary conjunctivitis
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19
Q

Management of blepharitis:

A
  • soften using hot compresses twice a day
  • lid hygiene
  • artificial tears for symptom relief with dry eyes
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20
Q

How does diabetic retinopathy come about?

A
  • hyperglycaemia leads to increased retinal blood flow and metabolism of vessel walls
  • increased vascular permeability forms exudates
  • pericyte dysfunction leads to micro aneurysms
  • neovascularisiation due to growth factor response to retinal ischaemia
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21
Q

What is the new classification of diabetic retinopathy?

A

Mild:
- 1 or more microaneurysms

Moderate:
- microaneurysms
- blot haemorrhages
- hard exudates
- CWS, venous beading/looping, IRMA

Severe:
- blot haemorrhages and microaneuryssm in 4 quadrants
- venous beading in at least 2 quadrants
- IRMA in at least 1 quadrant

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22
Q

What is proliferative retinopathy?

A
  • neovascularisation leading to haemorrhage
  • fibrous tissue anterior to retinal disc
  • more common in type 1 diabetes (blindness in 5 years)
  • use pan retinal photocoagulation
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23
Q

What is maculopathy?

A
  • hard exudates on background of change on macula
  • check visual acuity
  • more common in T2DM
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24
Q

What causes optic neuritis and what are the features?

A
  • causes: MS, diabetes, syphilis
  • features: unilateral reduced acuity over hours/days, red desaturation, pain worse on movement, RAPD, central scotoma
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25
Q

How do you treat optic neuritis?

A

high dose steroids - recovery in 4-6 weeks

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26
Q

How does central retinal vein occlusion present and what are some risk factors?

A
  • sudden unilateral painless loss of vision
  • sever retinal haemorrhages on fundoscopy
  • risk factors: age, polycythaemia, glaucoma
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27
Q

What is a stye, different types?

A
  • infection of glands in eyelid
  • external: staph infection of glands of Moll
  • internal: Meibomian glands - may leave residual chalazion
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28
Q

What is a chalazion?

A

retention cyst of Meiboomian gland - firm painless lump in eyelid

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29
Q

What is primary open angle glaucoma?

A
  • optic neuropathy associated with increased IOP due to the peripheral iris covering the trabecular network (where aqueous humour drains from the anterior chamber)
  • risk factors: age >40, genetic, black, myopia, HTN, DM, steroids
  • has hereditary component so screen annually from 40yo
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30
Q

What is seen on investigations for primary open angle glaucoma?

A
  • automated perimetry: peripheral visual field loss (nasal scotoma, tunnel vision)
  • reduced acuity
  • fundoscopy: optic disc cupping (cup:disc >0.7), optic disc pallor (atrophy), bayonetting of vessels, cup notching, disc haemorrhages
  • application tonometry to measure IOP >24mmHg
  • central corneal thickness measurement
  • gonioscopy to assess peripheral anterior chamber
31
Q

1st and 2nd line treatment for POAG:

A

1st: prostaglandin analogues e.g. latanoprost
2nd: beta blockers, carbonic anhydrase inhibitors, sympathomimetic

also surgery/laser treatment

32
Q

How do prostaglandin analogues work?

A
  • e.g. latanoprost
  • increases uveoscleral outflow
  • once a day
  • ADR: brown pigmentation iris, increased lash length
33
Q

How do beta-blocker eye drops work?

A
  • e.g. timolol, betaxolol
  • reduced aqueous production
  • avoid in asthmatics and heart block
34
Q

How do sympathomimetics work?

A
  • e.g. brimonidine alpha-2 adrenoceptor agonist
  • reduces production and increases outflow
  • avoid if taking MAOI or TCA
  • ADR: hyperaemia
35
Q

How do carbonic anhydrase inhibitors work?

A
  • e.g. dorzolamide
  • reduces production
  • systemic absorption may cause sulphonamide like reactions
36
Q

How do miotics work?

A
  • e.g. pilocarpine muscarinic receptor agonist
  • increases uveoscleral outflow
  • ADR: constricted pupil, headache, blurred vision
37
Q

What are the causes of cataracts?

A
  • old age
  • smoking
  • alcohol
  • trauma
  • diabetes
  • long term steroids
  • radiation
  • myotonic dystrophy
  • hypocalcaemia
38
Q

What are the features of cataracts?

A
  • reduced vision, colour vision
  • glare and haloes
  • defect red reflex
  • cataracts visible on ophthalmoscopy (after dilation) and with slit lamp
39
Q

Classification of cataracts:

A
  • nuclear: change in lens refractive index, common in old age
  • polar: localised, inherited, lie in visual axis
  • sub scapular: steroid use, deep to lens capsule, in visual axis
  • dot opacities: common in normal lenses, diabetes and myotonic dystrophy
40
Q

Management of cataracts:

A
  • non surgical: stronger glasses/contact lenses
  • surgical: only effective treatment - replace with artificial lens
41
Q

Surgical complications of cataracts surgery:

A
  • posterior capsule opacification (thickened lens capsule)
  • retinal detachment
  • posterior capsule rupture
  • endophthalmitis
42
Q

What is herpes zoster ophthalmicus?

A
  • reactivation of VZF in the area supplied by the ophthalmic division of trigeminal nerve
  • vesicular rash around the eye area
  • Hutchinson’s sign
43
Q

Treatment and complications of herpes zoster ophthalmicus:

A
  • oral antivirals 7-10 days, start within 72 hours
  • IV Abx if severe or immunocompromised
  • topical steroids for secondary inflammation of eye
  • ocular involvement - urgent ophthalmology review
  • complications: conjunctivitis, keratitis, episcleritis, anterior uveitis, ptosis, post-herpetic neuralgia
44
Q

How does Horner’s syndrome present?

A
  • miosis
  • ptosis
  • enopthlamos
  • anhidrosis
45
Q

Presentation of central lesions of Horner’s syndrome:

A
  • anhidrosis of face, arm and trunk
  • stroke
  • syringomyelia
  • MS
  • tumour
  • encephalitis
46
Q

Presentation of pre-ganglionic lesions of Horner’s syndrome:

A
  • anhidrosis of the face
  • Pancoast tumour
  • thyroidectomy
  • trauma
  • cervical rib
47
Q

Presentation of post-ganglionic lesions of Horner’s syndrome:

A
  • no anhidrosis
  • carotid artery dissection
  • carotid aneurysm
  • cavernous sinus thrombosis
  • cluster headache
48
Q

How is hypertensive retinopathy classified?

A

Keith Wagener classification
I - arteriolar narrowing and tortuosity, increased light reflex, silver wiring
II - arteriovenous nipping
III - cotton wool exudates, flame and blot haemorrhages
IV - papilloedema

49
Q

How does papilloedema appear on fundoscopy?

A
  • venous engorgement
  • loss of venous pulsation
  • blurring optic disc margin
  • elevation of disc
  • loss of optic cup
  • Paton’s lines (concentric retinal lines cascading from disc)
50
Q

Causes of papilloedema:

A
  • SOL
  • malignant HTN
  • idiopathic ICHTN
  • hydrocephalus
  • hypercapnia
51
Q

Investigations to be carried out in vitreous haemorrhage:

A
  • dilated fundoscopy (haemorrhage in vitreous cavity)
  • slit lamp: RBCs in anterior vitreous
  • US: rule of retinal tear/detachment
  • fluorescein angiography: look for neovascularisation
  • orbital CT: if open globe injury
52
Q

How does herpes simplex keratitis presentation and how do you treat?

A
  • dendritic corneal ulcer - shown by fluoroscein staining
  • red, painful, photophobia, epiphora, reduced acuity
  • treatment: immediate referral and topical acyclovir
53
Q

Difference in presentation between bacterial and viral conjunctivitis:

A

Bacterial:
- purulent discharge
- eyes stuck in morning

Viral:
- serous discharge
- recent URTI
- preauricular lymph nodes

54
Q

Treatment of bacterial conjunctivitis:

A
  • normally self-limiting and settles in 1-2 weeks
  • topical Abs e.g. chloramphenicol eye drops 2-3 hourly
  • topical fusidic acid if pregnant
  • no contact lenses or sharing towels
  • not school exclusion
55
Q

What is keratitis and what are some causes?

A
  • inflammation of cornea
  • bacterial: staph aureus, pseudomonas (contact lenses)
  • fungal
  • amoebic: acanthamoebic keratitis (if exposure to soil or contaminated water)
  • parasite: onchocercal keratitis
56
Q

Presentation of keratitis, treatment and complications:

A
  • red eye, pain, photophobia, foreign body, gritty, hypophon
  • contact lens wearers should have same day referral to rule out microbial keratitis
  • treatment: stop contacts, topical quinolone, cycloplegics for pain relief
  • complications: corneal scarring, perforation, endophthalmitis, visual loss
57
Q

What is orbital cellulitis and what is the difference to periorbital cellulitis?

A
  • infection of fat and muscles posterior to orbital septum but not involving globe
  • usually from URTI spreading
  • medical emergency
  • periorbital cellulitis: less serious, superficial infection anterior to orbital septum due to superficial injury
58
Q

Risk factors for orbital cellulitis:

A
  • childhood
  • previous sinus infection
  • lack of Hib vaccination
  • recent eyelid infection
  • ear or facial infection
59
Q

What are the features of orbital cellulitis and how does it differ from preseptal cellulitis:

A

Orbital:
- redness and swelling
- severe ocular pain
- visual disturbance
- proptosis
- ophthalmoplegia
- eyelid oedema and ptosis
- drowsiness

Preseptal:
- no reduced visual acuity
- proptotis

60
Q

Investigations and treatment for orbital cellulitis:

A
  • afferent pupillary defect
  • proptotis
  • dysmotility
  • oedema
  • CT: inflammation of orbital tissues deep to septum, sinusitis
  • blood culture and microbiological swab
  • Treatment: admission for IV Abx
61
Q

What are the ocular complications of RA:

A
  • keratoconjunctivitis sicca (most common)
  • episcleritis
  • scleritis
  • corneal ulceration
  • keratitis
  • iatrogenic: steroid induced cataracts, chloroquine retinopathy
62
Q

What is Argyll Robertson pupil?

A
  • neurosyphilis and diabetes
  • small irregular pupils
  • ARP: accommodation reflex present
  • PRA: pupillary reflex absent
63
Q

What is central retinal occlusion:

A
  • sudden unilateral vision loss due to thromboembolism or arteritis
  • afferent pupillary defect, cherry red spot on pale retina
64
Q

What is episcleritis and treatment:

A
  • red eye
  • not painful
  • watering, mild photophobia
  • injected vessels mobile when gentle pressure applied
  • phenylephrine drops can help to distinguish from slceritis
  • Tx: conservative, artificial tears
65
Q

What are some causes of dilated pupil (mydriasis):

A
  • 3rd nerve palsy
  • Holmes-Adie pupil
  • traumatic iridoplegia
  • topical mydriatics: tropic amide, atropine
  • sympathomimetics: amphetamines, cocaine
  • anticholinergics: TCA
66
Q

What can be seen on investigation of posterior vitreous detachment and what is the treatment?

A
  • ophthalmoscopy: Weiss ring
  • all referred within 24 hours to rule out retinal tears and detachment
  • Tx: symptoms gradually improve over 6 months, surgery if associated tear/detachment
67
Q

What is allergic conjunctivitis and what is the treatment?

A
  • bilateral conjunctival erythema and swelling
  • prominent itch, swollen eyelids
  • history of atopy
  • Tx: first line - topical/systemic antihistamines; second line - topical mast cell stabilisers e.g. sodium cromoglicate
68
Q

What are the risks of ocular trauma?

A
  • hyphema - urgent referral
  • increased IOP due to blockage of angle and trabecular network with erythrocytes
69
Q

Treatment of preseptal cellulitis:

A
  • referral to secondary care
  • oral antibiotics e.g. co-amoxiclav
70
Q

What is RAPD?

A
  • Marcus Gunn pupil
  • swinging light test: affected and normal eye dilated when light shone into affected
  • lesion anterior to optic chiasm so nerve or retina
  • causes: retinal detachment, optic neuritis
  • afferent: retina -> optic nerve -> lateral geniculate body -> midbrain
  • efferent: Edinger-Westphal nucleus -> oculomotor
71
Q

What is retinitis pigmentosa?

A
  • tunnel vision
  • nightblindness
  • black bone spicule shaped pigmentation in peripheral retina on fundoscopy
  • mottling of retinal pigment epithelium
72
Q

How does scleritis present:

A
  • red eye
  • painful compared to episcleritis
  • watering and photophobia
  • gradual decrease in vision
73
Q

What causes tunnel vision:

A
  • papilloedema
  • glaucoma
  • retinitis pigmentosa
  • choroidoretinitis
  • optic atrophy secondary to tabes dorsalis

Ophthalmology (1 decks)

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