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Ophthalmology Flashcards

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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
How do you treat optic neuritis?
high dose steroids - recovery in 4-6 weeks
26
How does central retinal vein occlusion present and what are some risk factors?
- sudden unilateral painless loss of vision - sever retinal haemorrhages on fundoscopy - risk factors: age, polycythaemia, glaucoma
27
What is a stye, different types?
- infection of glands in eyelid - external: staph infection of glands of Moll - internal: Meibomian glands - may leave residual chalazion
28
What is a chalazion?
retention cyst of Meiboomian gland - firm painless lump in eyelid
29
What is primary open angle glaucoma?
- 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
30
What is seen on investigations for primary open angle glaucoma?
- 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
1st and 2nd line treatment for POAG:
1st: prostaglandin analogues e.g. latanoprost 2nd: beta blockers, carbonic anhydrase inhibitors, sympathomimetic also surgery/laser treatment
32
How do prostaglandin analogues work?
- e.g. latanoprost - increases uveoscleral outflow - once a day - ADR: brown pigmentation iris, increased lash length
33
How do beta-blocker eye drops work?
- e.g. timolol, betaxolol - reduced aqueous production - avoid in asthmatics and heart block
34
How do sympathomimetics work?
- e.g. brimonidine alpha-2 adrenoceptor agonist - reduces production and increases outflow - avoid if taking MAOI or TCA - ADR: hyperaemia
35
How do carbonic anhydrase inhibitors work?
- e.g. dorzolamide - reduces production - systemic absorption may cause sulphonamide like reactions
36
How do miotics work?
- e.g. pilocarpine muscarinic receptor agonist - increases uveoscleral outflow - ADR: constricted pupil, headache, blurred vision
37
What are the causes of cataracts?
- old age - smoking - alcohol - trauma - diabetes - long term steroids - radiation - myotonic dystrophy - hypocalcaemia
38
What are the features of cataracts?
- reduced vision, colour vision - glare and haloes - defect red reflex - cataracts visible on ophthalmoscopy (after dilation) and with slit lamp
39
Classification of cataracts:
- 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
Management of cataracts:
- non surgical: stronger glasses/contact lenses - surgical: only effective treatment - replace with artificial lens
41
Surgical complications of cataracts surgery:
- posterior capsule opacification (thickened lens capsule) - retinal detachment - posterior capsule rupture - endophthalmitis
42
What is herpes zoster ophthalmicus?
- reactivation of VZF in the area supplied by the ophthalmic division of trigeminal nerve - vesicular rash around the eye area - Hutchinson's sign
43
Treatment and complications of herpes zoster ophthalmicus:
- 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
How does Horner's syndrome present?
- miosis - ptosis - enopthlamos - anhidrosis
45
Presentation of central lesions of Horner's syndrome:
- anhidrosis of face, arm and trunk - stroke - syringomyelia - MS - tumour - encephalitis
46
Presentation of pre-ganglionic lesions of Horner's syndrome:
- anhidrosis of the face - Pancoast tumour - thyroidectomy - trauma - cervical rib
47
Presentation of post-ganglionic lesions of Horner's syndrome:
- no anhidrosis - carotid artery dissection - carotid aneurysm - cavernous sinus thrombosis - cluster headache
48
How is hypertensive retinopathy classified?
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
How does papilloedema appear on fundoscopy?
- 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
Causes of papilloedema:
- SOL - malignant HTN - idiopathic ICHTN - hydrocephalus - hypercapnia
51
Investigations to be carried out in vitreous haemorrhage:
- 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
How does herpes simplex keratitis presentation and how do you treat?
- dendritic corneal ulcer - shown by fluoroscein staining - red, painful, photophobia, epiphora, reduced acuity - treatment: immediate referral and topical acyclovir
53
Difference in presentation between bacterial and viral conjunctivitis:
Bacterial: - purulent discharge - eyes stuck in morning Viral: - serous discharge - recent URTI - preauricular lymph nodes
54
Treatment of bacterial conjunctivitis:
- 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
What is keratitis and what are some causes?
- inflammation of cornea - bacterial: staph aureus, pseudomonas (contact lenses) - fungal - amoebic: acanthamoebic keratitis (if exposure to soil or contaminated water) - parasite: onchocercal keratitis
56
Presentation of keratitis, treatment and complications:
- 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
What is orbital cellulitis and what is the difference to periorbital cellulitis?
- 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
Risk factors for orbital cellulitis:
- childhood - previous sinus infection - lack of Hib vaccination - recent eyelid infection - ear or facial infection
59
What are the features of orbital cellulitis and how does it differ from preseptal cellulitis:
Orbital: - redness and swelling - severe ocular pain - visual disturbance - proptosis - ophthalmoplegia - eyelid oedema and ptosis - drowsiness Preseptal: - no reduced visual acuity - proptotis
60
Investigations and treatment for orbital cellulitis:
- 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
What are the ocular complications of RA:
- keratoconjunctivitis sicca (most common) - episcleritis - scleritis - corneal ulceration - keratitis - iatrogenic: steroid induced cataracts, chloroquine retinopathy
62
What is Argyll Robertson pupil?
- neurosyphilis and diabetes - small irregular pupils - ARP: accommodation reflex present - PRA: pupillary reflex absent
63
What is central retinal occlusion:
- sudden unilateral vision loss due to thromboembolism or arteritis - afferent pupillary defect, cherry red spot on pale retina
64
What is episcleritis and treatment:
- 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
What are some causes of dilated pupil (mydriasis):
- 3rd nerve palsy - Holmes-Adie pupil - traumatic iridoplegia - topical mydriatics: tropic amide, atropine - sympathomimetics: amphetamines, cocaine - anticholinergics: TCA
66
What can be seen on investigation of posterior vitreous detachment and what is the treatment?
- 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
What is allergic conjunctivitis and what is the treatment?
- 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
What are the risks of ocular trauma?
- hyphema - urgent referral - increased IOP due to blockage of angle and trabecular network with erythrocytes
69
Treatment of preseptal cellulitis:
- referral to secondary care - oral antibiotics e.g. co-amoxiclav
70
What is RAPD?
- 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
What is retinitis pigmentosa?
- tunnel vision - nightblindness - black bone spicule shaped pigmentation in peripheral retina on fundoscopy - mottling of retinal pigment epithelium
72
How does scleritis present:
- red eye - painful compared to episcleritis - watering and photophobia - gradual decrease in vision
73
What causes tunnel vision:
- papilloedema - glaucoma - retinitis pigmentosa - choroidoretinitis - optic atrophy secondary to tabes dorsalis

Ophthalmology (1 decks)

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