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Zero to Finals: Medicine A.S. > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

causes of optic neuritis?

A
  • MS (most common)
  • DM
  • syphilis
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2
Q

features of optic neuritis?

A
  • unilateral reduction in visual acuity
  • relative afferent pupillary defect
  • loss of colour discrimination
  • “red desaturation”
  • central scotoma
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3
Q

management of optic neuritis? how long does it take to fully recover?

A
  • high-dose steroids

- 4-6 weeks

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4
Q

prognosis of optic neuritis?

A

if >3 white matter lesions seen on MRI, very high risk of developing MS

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5
Q

describe the pathophysiology of (all types of) glaucoma

A
  • blockage in aqueous humour drainage from eye
  • causes rise in intraocular pressure
  • this raised pressure damages the optic nerve (CN2)
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6
Q

which fluid fills the anterior chamber? vitreous chamber?

A
  • aqueous humour

- vitreous humour

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7
Q

which structure produces aqueous humour?

A

ciliary body

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8
Q

what is normal intraocular pressure?

A

10-21 mmHg

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9
Q

pathophysiology of open-angle glaucoma?

A
  • gradual increase in resistance through trabecular meshwork
  • pressure slowly builds in eye
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10
Q

pathophysiology in acute angle-closure glaucoma?

A
  • iris bulges forward
  • completely seals off trabecular meshwork
  • continual build up of pressure
  • emergency
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11
Q

how does increased intraocular pressure affect the optic disc?

A
  • causes “cupping”

- optic cup in centre of disc gets wider and deeper

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12
Q

risk factors for open angle glaucoma?

A
  • ageing
  • FHx
  • Black ethnic origin
  • myopia (short-sightedness)
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13
Q

presentation of open angle glaucoma?

A
  • often asymptomatic, picked up on screening
  • loss of peripheral vision first
  • eventually gives “tunnel vision”
  • gradual onset
  • fluctuating pain
  • headaches
  • blurred vision
  • halos around light, esp at night
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14
Q

how can intraocular pressure be measured in suspected glaucoma?

A
  • non-contact tonometry (puff of air, useful for screening)

- goldmann applanation tonometry (gold standard)

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15
Q

investigations and findings in open angle glaucoma?

A
  • goldmann applanation tonometry (high intraocular pressure)
  • fundoscopy (disc cupping)
  • visual field assessment (peripheral vision loss)
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16
Q

at what intraocular pressure should treatment be started in open angle glaucoma?

A

24mmHg or above

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17
Q

management of open angle glaucoma?

A
  • 1st: latanoprost (prostaglandin analogue) eye drops
  • timelol (BB)
  • dorzolamide (carbonic anhydrase inhibitor)
  • brimonidine (sympathomimetic)
  • trabeculectomy surgery if eye drops fail
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18
Q

notable SEs of latanoprost?

A
  • eyelash growth
  • eyelid pigmentation
  • iris browning
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19
Q

risk factors for acute angle closure glaucoma?

A
  • ageing
  • being female
  • FHx
  • Chinese / East Asian ethnic origin
  • drugs
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20
Q

which drugs can precipitate acute angle closure glaucoma?

A
  • noradrenaline
  • oxybutynin / solifenacin
  • amitriptyline
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21
Q

presentation of acute angle closure glaucoma?

A
  • pt feels generally unwell
  • severely painful, red eye
  • blurred vision
  • halos around lights
  • headache
  • N+V
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22
Q

findings O/E of acute angle closure glaucoma?

A
  • red-eye
  • teary eye
  • hazy cornea
  • decreased visual acuity
  • affected pupil is dilated and fixed in size
  • eyeball is firm on palpation
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23
Q

initial management of acute angle closure glaucoma?

A
  • same day ophthalmology assessment
  • lay on back w/ pillow
  • pilocarpine eye drops
  • PO acetazolamide 500mg
  • analgesia / antiemetics if needed
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24
Q

drug class of acetazolamide?

A

carbonic anhydrase inhibitor

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25
Q

secondary care management of acute angle closure glaucoma? hint: similar to open angle

A
  • pilocarpine
  • PO / IV acetazolamide
  • glycerol / mannitol
  • timolol
  • dorzolamide
  • brimonidine
  • laser iridotomy
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26
Q

definitive treatment of acute angle closure glaucoma?

A

laser iridotomy

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27
Q

most common cause of blindness in the UK?

A

age-related macular degeneration (ARMD)

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28
Q

key finding on fundoscopy in ARMD?

A

drusen

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29
Q

how can ARMD be classified? which type is most common?

A
  • dry (90%)

- wet (10%)

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30
Q

which type of ARMD carries a worse prognosis?

A

wet

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31
Q

feature common to both dry and wet ARMD?

A

drusen on fundoscopy

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32
Q

risk factors for ARMD?

A
  • ageing
  • smoking
  • White / Chinese ethnic origin
  • FHx
  • CVD
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33
Q

presentation of ARMD?

A
  • gradually worsening central visual field loss
  • reduced visual acuity
  • straight lines look crooked / wavy
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34
Q

how might wet ARMD present slightly differently to dry ARMD?

A
  • more acute
  • vision is lost over days
  • full blindness after 2-3 years
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35
Q

findings O/E of ARMD?

A
  • reduced acuity
  • scotoma on visual fields test
  • distorted straight lines on amsler grid test
  • drusen on fundoscopy
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36
Q

what is a scotoma?

A

a central patch of vision loss

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37
Q

specialist investigations used in ARMD?

A
  • slit-lamp biomicroscopic fundus exam
  • optical coherence tomography
  • fluoroscein angiography
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38
Q

management of dry ARMD?

A
  • refer to ophthalmology
  • stop smoking
  • control BP
  • vitamin supplements
39
Q

management of wet ARMD?

A
  • refer to ophthalmology

- anti-VEGFs (ranibizumab, bevacizumab, pegaptanib)

40
Q

describe the pathophysiology and examination findings in diabetic retinopathy

A
  • repeated exposure to hyperglycaemia causes increased vascular permeability of retina, causing:
  • blot haemorrhages
  • hard exudates
  • microaneurysms
  • venous beading
  • “cotton wool spots”
  • neovascularisation
41
Q

how can diabetic retinopathy be classified?

A

based on fundoscopy findings:

  • proliferative
  • non-proliferative
42
Q

signs on fundoscopy in mild / moderate non-proliferative diabetic neuropathy?

A
  • mild: microaneurysms

- moderate: microaneurysms, blot haemorrhages, hard exudates, cotton wool spots and venous beading

43
Q

signs on fundoscopy in severe non-proliferative diabetic retinopathy?

A
  • blot haemorrhages
  • microaneurysms in 4 quadrants
  • venous beading in 2 quadrants
  • IRMA in any quadrant (intraretinal microvascular abnormality)
44
Q

signs on fundoscopy in proliferative diabetic retinopathy?

A
  • neovascularisation

- vitreous haemorrhage

45
Q

signs on fundoscopy in diabetic maculopathy?

A
  • macular oedema

- ischaemic maculopathy

46
Q

complications of diabetic retinopathy?

A
  • retinal detachment
  • vitreous haemorrhage
  • rebeosis iridis (new blood vessels in iris)
  • optic neuropathy
  • cataracts
47
Q

management of diabetic retinopathy?

A
  • laser photocoagulation
  • anti-VEGF (ranibizumab, bevacizumab)
  • vitreoretinal surgery (keyhole in eye)
48
Q

how could hypertensive retinopathy develop?

A

2 ways:

  • very slowly from chronic HTN
  • quickly in malignant HTN
49
Q

signs on retina on fundoscopy in hypertensive retinopathy?

A
  • silver / copper wiring (arterioles compressing veins)
  • AV nicking
  • cotton wool spots
  • hard exudates
  • retinal haemorrhages
  • papilloedema (end stage sign)
50
Q

how can hypertensive retinopathy be classified?

A

keith-wagener classification

51
Q

management of hypertensive retinopathy?

A
  • control BP
  • stop smoking
  • control lipids
52
Q

what is a cataract?

A
  • when the lens becomes cloudy and opaque

- causes loss of visual acuity

53
Q

how are congenital cataracts picked up?

A

screened for using red reflex in NIPE

54
Q

risk factors for cataracts?

A
  • ageing
  • smoking
  • alcohol
  • DM
  • steroids
  • hypocalcaemia
55
Q

presentation of cataracts?

A
  • asymmetrical
  • very slow vision loss
  • progressive blurring
  • change of colour vision (more yellow / brown)
  • “starbursts” in light, esp at night
56
Q

finding O/E of cataracts?

A
  • loss of red reflex

- might be picked up in flash pics

57
Q

management of cataracts?

A
  • if asymptomatic, nothing

- surgically breaking less and replacing with artificial lens

58
Q

why might someone get cataract surgery and still have poor visual acuity afterwards?

A

cataracts can mask other eye conditions (e.g. macular degeneration, DM retinopathy)

59
Q

important complication of cataract surgery?

A

endophthalmitis, secondary to infection

60
Q

management of endophthalmitis?

A

intravitreal ABx

61
Q

causes of abnormal pupil shape?

A
  • trauma from cataract surgery
  • anterior uveitis
  • acute angle closure glaucoma
  • rubeosis iridis
  • coloboma
  • tadpole pupil
62
Q

what is the difference between rubeosis iridis and coloboma?

A
  • RI is caused by neovascularisation secondary to DM (retinopathy)
  • coloboma is congenital
63
Q

key associated condition of tadpole pupil?

A

migraines

64
Q

causes of mydriasis (dilated pupil)?

A
  • CN3 palsy
  • holmes-adie syndrome
  • RICP
  • congenital
  • trauma
  • stimulants (e.g. cocaine)
  • anticholinergics
65
Q

causes of miosis (constricted pupil)?

A
  • horner syndrome
  • cluster headaches
  • argyll-robertson pupil (neurosyph)
  • opiates
  • nicotine
  • pilocarpine
66
Q

how does CN3 palsy affect the eye?

A
  • ptosis
  • dilated, non-reactive (mydriasis) pupil
  • divergent squint
  • “down and out” position
67
Q

which unique feature is found in congenital horner syndrome?

A

heterochromia (different coloured irises)

68
Q

how can you test for horner syndrome?

A
  • cocaine eye drops
  • normal eye will dilate but not in horner syndrome
  • alt: adrenalin eye drops (opposite results)
69
Q

describe the holmes-adie pupil

A
  • unilateral dilated pupil
  • slow light responses
  • pupil gets smaller over time
70
Q

features of holmes-adie syndrome?

A
  • HA pupil
  • absent ankle reflexes
  • absent knee reflexes
71
Q

describe the argyll-robertson pupil

A
  • “prostitute’s pupil”
  • constricted
  • accommodates when focussing on object
  • does not react to light
72
Q

what is blepharitis? what does it predispose to?

A
  • inflammation of eyelid margins
  • styes
  • chalazions
73
Q

management of blepharitis?

A
  • hot compresses
  • gentle cleaning with cotton wool
  • hypromellose drops
  • polyvinyl alcohol drops
  • carbomer drops
74
Q

what is a stye?

A

infection of the sebaceous / sweat glands at base of eyelashes

75
Q

management of a stye?

A
  • hot compress
  • analgesia
  • topical chloramphenicol if conjunctivitis present / persistent
76
Q

what is a chalazion? how does it present?

A
  • blocked meibomian gland

- non-tender swelling

77
Q

management of chalazion?

A
  • hot compress
  • analgesia
  • consider chloramphenicol
  • surgery (last line)
78
Q

what is an entropion? does it hurt?

A
  • eyelid turns in on itself and eyelashes touch the eyeball

- painful

79
Q

complications arising from entropion?

A
  • corneal damage

- ulceration

80
Q

management of entropion?

A
  • taping eyelid down to prevent it turning in on itself
  • lubricating eye drops (to stop dryness)
  • same-day referral if risk to sight
81
Q

what is an ectropion?

A
  • eyelid turning outwards, exposing inner eyelid mucosa

- usually bottom lid affected

82
Q

complication of ectropion?

A

exposure keratopathy, due to dryness

83
Q

management of ectropion?

A
  • mild cases may need nothing
  • regular lubricating eye drops
  • same-day referral if risk to sight
84
Q

what is trichiasis?

A
  • inward growth of eyelashes

- causes pain

85
Q

complications of trichiasis?

A
  • corneal damage

- ulceration

86
Q

management of trichiasis?

A
  • specialist epilation of lashes
  • electrolysis if recurrent cases
  • crytherapy
  • laser treatment
  • same-day referral if risk to sight
87
Q

what is periorbital cellulitis?

A

infection of eyelid and skin in front of eye

88
Q

presentation of periorbital cellulitis?

A
  • swelling around eye
  • redness
  • skin hot to touch
89
Q

key differential of periorbital cellulitis? how can these be distinguished?

A
  • orbital cellulitis

- CT

90
Q

management of periorbital cellulitis?

A
  • PO / IV systemic ABx

- admit and observe if severe

91
Q

what is orbital cellulitis?

A

infection around eyeball involving tissue behind orbital septum

92
Q

features of orbital cellulitis NOT found in peri-orbital cellulitis?

A
  • pain on movement
  • reduced eye movement
  • changes in vision
  • abnormal pupil reactions
  • proptosis
93
Q

management of orbital cellulitis?

A
  • emergency!
  • admit
  • IV ABx
  • surgical drainage if abscess present

Zero to Finals: Medicine A.S. (11 decks)

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