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Ophthalmology Flashcards

1
Q

What are 4 signs on examination of uveitis?

A
  • ciliary (circumcorneal) injection
  • aqueous flare - leakage of protein + leukocytes into anterior chamber
  • keratic precipitates - on posterior surface of cornea
  • posterior synechiae
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2
Q

What is Talbot’s test?

A

pain on pupil constriction when tested with convergence - moving finger closer to eyes

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3
Q

What is the commonest cause of orbital cellulitis in children and why?

A

Ethmoidal sinusitis - relatively thin medial wall of the orbit

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4
Q

What are 5 risk factors for orbital cellulitis?

A
  1. childhood - mean age of hospitalisation 7-12 years
  2. previous sinus infection
  3. lack of haemophilus influenzae type b (Hib) vaccination
  4. recent eyelid infection / insect bite on eyelid (periorbital celllulitis)
  5. ear or facial infection
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5
Q

What are 4 things that differentiate orbital from preseptal cellulitis?

A
  1. reduced VA
  2. propotosis
  3. ophthalmoplegia / pain with eye movements
  4. RAPD
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6
Q

How much does family history increase the risk of age-related macular degeneration?

A

first degree relatives 4x more likely to inherit

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7
Q

What is the normal optic disc to cup ratio?

A

0.4 - 0.7

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8
Q

What are 6 risk factors for age-related macular degeneration?

A
  • advancing age, particularly >75y
  • smoking
  • family history
  • factors increasing risk of ischaemic heart disease - hypertension, dyslipidaemia, diabetes mellitus
  • female gender
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9
Q

What proportion of cases of AMD are dry?

A

90%

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10
Q

What investigations are indicated for wet AMD and why?

A

fluorescein angiography (+- indocyanine green angiography to visualise choroidal circulation) - can guide intervention with anti-VEGF therapy

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11
Q

What treatment option is there for dry AMD?

A

zinc and anti-oxidant vitamins A + C + E (best in patients with extensive drusen, at least moderate category)

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12
Q

What is the treatment of a corneal abrasion?

A

topical chloramphenicol to prevent infection

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13
Q

What are 2 options for treatment of wet ARMD and what is the drawback of the less preferred option?

A
  • anti VEGF e.g. ranibizumab, bevacizumab, pegaptanib
  • laser photocoagulation - risk of acute visual loss after treatment (especially sub-foveal ARMD)
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14
Q

What are the criteria for someone to be registered as severely sight impaired?

A

Visual acuity <3/60 with full visual field wearing glasses as prescribed - in better eye

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15
Q

How can you distinguish between causes of Horner’s syndrome clinically?

A
  • central: anhidrosis down one side of face, arm and trunk
  • preganglionic: anhidrosis of face
  • postganglionic: no anhidrosis
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16
Q

What characterises mild/moderate/severe non-proliferative retinopathy?

A
  • mild: 1 or more micro aneurysm
  • moderate: microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading, IRMA
  • severe: blot haemorrhages and microaneurysms in 4 quadrants, venous beading in at least 2 quadrants, IRMA in at least 1 quadrant
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17
Q

What characterises diabetic maculopathy?

A

Hard exudates and other background changes on macula

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18
Q

In which diabetes type is maculopathy more commonly seen?

A

T2DM

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19
Q

In which diabetes type is proliferative retinopathy more commonly seen?

A

T1DM

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20
Q

What are the treatment options for diabetic:
- maculopathy
- non-proliferative retinopathy
- proliferative retinopathy

A
  • anti-VEGF
  • PRP if severe
  • anti-VEGF, PRP, vitreoretinal surgery
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21
Q

What are 2 complications of PRP?

A
  • reduction in peripheral vision
  • poor night vision (more rods in peripheral retina)
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22
Q

Why is diabetes a risk factor for developing cataract? Give the 3 explanations

A
  1. increased intracellular accumulation of sorbitol (from glucose metabolism) leads to hyperosmotic effect, resulting in hydropic lens fibres that degenerate and form cataract
  2. osmotic stress due to swelling of cortical lens fibres (esp T1DM)
  3. autoimmune hypothesis in bilateral T1DM cataracts
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23
Q

What are the 2 commonest aetiologies for rubeosis iridis?

A
  1. central retinal venous occlusion
  2. diabetic retinopathy
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24
Q

What type of glaucoma can develop due to rubeosis iridis?

A

initially secondary open angle glaucoma - vessels impair aqueous humour outflow; can progress to secondary closed angle glaucoma as fibrotic membranes develop and contract

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25
Q

What is the gold-standard treatment for rubeosis iridis?

A

pan-retinal photocoagulation (PRP) to reduce neovascularisation
[recently anti-VEGF also shown to have benefit]

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26
Q

What are treatment options are there for CRVO/BRVA?

A
  1. anti-VEGF (macular oedema)
  2. intravitreal steroids
  3. laser photocoagulation (retinal neovascularisation)
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27
Q

What causes ocular ischaemic syndrome?

A

ocular hypoperfusion due to stenosis or occlusion of the common or internal carotif arteries (atherosclerosis = major cause)

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28
Q

What is asteroid hyalosis?

A

form of vitreous degeneration in which calcium aggregates in the vitreous body (see little white flecks in vitreous) - rarely affects visual acuity, no treatment required

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29
Q

What are 5 risk factors for developing diabetic retinopathy?

A
  1. severity of hyperglycaemia (no specific threshold)
  2. duration of hyperglycaemia
  3. hypertension + other cardiovascular risk factors
  4. renal disease
  5. pregnancy (rapid progression)
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30
Q

What is non-high risk proliferative diabetic retinopathy vs. high risk proliferative DR?

A
  • non-high risk: NVD or within 1 disc diameter of it, or NVE
  • high risk: large NVD or NVE, or presence of pre-retinal haemorrhage
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31
Q

What are 3 types of diabetic maculopathy?

A
  1. focal or diffuse macular oedema
  2. ischaemic maculopathy
  3. clinical significant macular oedema (CSMO) - thickening of retina + hard exudates withi a specific distance of the fovea OR of a certain size
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32
Q

What is the screening process for diabetic eye disease in T1 and T2DM?

A
  • T1DM - children 12y and over - annual monitoring
  • T2DM - all patients should be referred for monitoring
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33
Q

What are 4 elements of the treatment of diabetic eye disease?

A
  1. Laser (PRP)
  2. Anti-VEGF intravitreal injection
  3. Intravitreal steroids - CSMO
  4. Surgery - vitrectomy if vitreal haemorrhage
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34
Q

What are 5 investigations that can be performed in suspected chronic glaucoma?

A
  1. automated perimetry (visual field)
  2. slit lamp + mydriasis
  3. applanation tonometry
  4. central corneal thickness
  5. gonioscopy
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35
Q

What are 4 facotrs that influence risk of future visual impairment in glaucoma?

A
  1. IOP
  2. central corneal thickness (CCT)
  3. family history
  4. life expectancy
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36
Q

What is the most commonly associated condition with scleritis?

A

rheumatoid arthritis

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37
Q

What are 4 conditions associated with scleritis?

A
  1. RA
  2. SLE
  3. sarcoidosis
  4. GPA
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38
Q

What are 4 aspects of the management of scleritis?

A
  1. same day ophthal assessment
  2. NSAIDs first line
  3. steroids if severe
  4. imunosuppressive drugs if resistant / for underlying disease
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39
Q

Per NICE guidelines what’s the first line for primary open angle glaucoma?

A

360° selective laser trabeculoplasty (SLT)

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40
Q

What are second and third line treatments for POAG per NICE?

A

after SLT:
* prostaglandin analogue (PGA)
* next line: beta blocker drops, carbonic anhydrase inhibitor drops, sympathomimetic drops

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41
Q

What surgery can be considered in refractive cases of POAG?

A

trabeculectomy

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42
Q

What is the mechanism of action of prostaglandin analogues (e.g. latanoprost)?

A

increase uveoscleral outflow

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43
Q

What are 2 adverse effects of PGA eyedrops?

A
  • brown pigmentation of iris
  • increased eyelash length
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44
Q

What is the mechanism of action of beta blocker eye drops e.g. timolol?

A

reduce aqueous production

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45
Q

What are 2 contraindications to beta blocker eye drops?

A
  1. asthma
  2. heart block
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46
Q

What is the mechanism of action of sympathomimetic eye drops e.g. alpha-1 adrenoceptor agonists such as birmonidine?

A

reduce aqueous production AND increase aqueous outflow

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47
Q

What is an adverse effect of alpha-2-adrenceptor agonist drops e.g. brimonidine?

A

hyperaemia

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48
Q

What is a key drug interaction of alpha-2 adrenoceptor agonists e.g. brimonidine?

A

MAOI or tricyclic antidepressants

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49
Q

What is the mechanism of action of carbonic anhydrase inhibitors e.g. dorzolamide?

A

reduces aqueous production

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50
Q

What is an adverse effect of carbonic anhydrase inhibitors?

A

may cause sulphonamide like reactions

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51
Q

What is the mechanism of action of miotics e.g. pilocarpine for POAG?

A

muscarinic receptor agonist - increases uveoscleral outflow

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52
Q

What are 3 side effects of miotics e.g. pilocarpine?

A
  1. constricted pupil
  2. headache
  3. blurred vision
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53
Q

What is the typical presentation of conjunctivitis?

A

sore, red eyes, sticky discharge (purulent if bacteria, serous if viral)

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54
Q

What is the management of infective conjunctivitis?

A
  • normally self-limited, settles without treatment within 1-2 weeks
  • topic abx often offered e.g. chloramphenicol
  • chloramphenicol drops 2-3 hourly initially; ointment QDS initially
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55
Q

When should chloramphenicol drops be avoided and what is an alternative?

A

pregnant women - topical fusidic acid (BD)

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56
Q

What is the management of infective conjunctivitis in contact lens users?

A

topical fluoresceins should be used to identify corneal staining; treat as usual, but do not wear CL during episode of conjunctivitis

57
Q

Should school exclusion be advised for conjunctivitis?

A

no

58
Q

What is the management of molluscum contagiosum with eyelid/ocular involvement and red eye?

A

urgent ophthalmology review

59
Q

What is the most common ocular manifestation of rheumatoid arthritis?

A

ketaoconjunctivitis sicca

60
Q

What type of cause of anterior uveitis should be suspected in bilateral eye disease?

A

sarcoidosis

61
Q

What happens to visual acuity in anterior uveitis?

A

usually initiall normal, later becomes impaired

62
Q

What are 5 conditions associated with anterior uveitis?

A
  1. ankylosing spondylitis
  2. reactive arthritis
  3. ulcerative colitis, crohn’s
  4. Behcet’s disease
  5. sarcoidosis: bilateral disease
63
Q

What are 3 aspects of the management of anterior uveitis?

A
  1. urgent ophthalmology review
  2. cycloplegics (dilates pupu, helps relieve pain and photophobia) e.g. atropine, cyclopentolate
  3. steroid eye drops
64
Q

What is the average age of diagnosis of retinoblastoma?

A

18 months

65
Q

What is the inheritance pattern of hereditary cases of retinoblastoma?

A

autosomal dominant

66
Q

What proportion of cases of retinoblastoma are hereditary?

A

10%

67
Q

What is the genetic abnormality in retinoblastoma?

A

loss of function of retinoblastoma tumour suppressor gene on chromosome 13

68
Q

What are 3 possible features on presentation of retinoblastoma?

A
  1. absence of red-reflex (leukocoria)
  2. strabismus
  3. visual problems
69
Q

What are the management options for retinoblastoma?

A
  • enucleation (not only option)
  • external beam radiation therapy
  • chemotherapy
  • photocoagulation
70
Q

What is the prognosis of retinoblastoma?

A

good - >90% survive to adulthood

71
Q

How can episcleritis be differentiated from scleritis on the basis of pressing on the eye?

A

injected vessels are mobile when gentle pressure applied to sclera in episcleritis; in scleritis, vessels deeper + don’t move

72
Q

What medication can be used to differentiate episcleritis + scleritis?

A

phenylephrine drops - phenylephrine blanches conjunctival and episcleral vessels but NOT scleral vessels, so if eye redness improves with drops, can diagnose episcleritis

73
Q

What is the management of episcleritis?

A

conservative - can use artificial tears

74
Q

What are 2 types of drugs which can cause corneal opacities?

A
  1. amiodarone
  2. indomethacin
75
Q

What are 3 drugs which can cause optic neuritis?

A
  1. ethambutol
  2. amiodarone
  3. metronidazole
76
Q

What are 2 key drugs which can cause retinopathy?

A

hydroxchloroquine/chloroquine, quinine

77
Q

What are 2 ocular side effects of sildenafil?

A
  1. blue discolouration
  2. non-arteritic anterior ischaemic neuropathy
78
Q

Is the Holmes-Adie pupil a benign condition?

A

yes - benign

79
Q

Which gender is the Holmes-Adie pupil more often seen in?

A

women

80
Q

What is the presentation of Holmes-Adie pupil?

A
  • dilated pupil
  • slowly reaction to accommodation
  • poorly (if at all) reactive to light
  • once pupil constricts, remains small for abnormally long time
81
Q

In what proportion of cases is the Holmes-Adie pupil unilateral?

A

80%

82
Q

What is Holmes-Adie syndrome?

A

Holmes-Adie pupil with absent ankle/knee reflexes

83
Q

What condition is the Argyll-Robertson pupil associated with?

A

neurosyphilis

also diabetes mellitus

84
Q

What is the presentation of the Argyll-Robertson pupil?

A
  • small, irregular pupils
  • accomodation reflex present (ARP)
  • pupillary light reflex absent (no response to light)
85
Q

What causes inferior vs superior homonymous hemianopia?

A

PITS
* contralateral parietal lobe lesion - inferior
* contralateral temporal lobe lesion - superior

86
Q

What causes incongruous visual field defects vs. congruous defects?

A
  • incongruous: optic tract lesion
  • congruous: optic radiation lesion or occipital cortex
87
Q

Which part of the visual field pathway travels through the temporal lobe?

A

inferior portion of optic radiations - Meyer’s loop

88
Q

Which part of the visual field pathway travels through the parietal lobe?

A

superior portion of optic radiations

89
Q

What is the difference in superior vs inferior bitemopral hemianopia lesions?

A
  • upper defect = inferior chiasmal compression = pituitary tumour
  • lower defect = superior chiasmal compression = craniopharyngioma
90
Q

What type of visual field loss is seen with POAG?

A

unilateral peripheral visual field loss

91
Q

In which gender is cataract more common?

A

female

92
Q

What can cause dot-opacity type cataracts?

A

common in normal lenses, also in diabetes and myotonic dystrophy

93
Q

What type of cataract is caused by steroid use?

A

subcapsular

94
Q

What is often the cause of polar cataracts?

A

inherited causes

95
Q

When should anti-VEGF treatment in wet AMD be ideally started?

A

within first 2 months of diagnosis if possible

96
Q

What are 3 examples of anti-VEGF agents?

A
  1. ranibizumab
  2. bevacizumab
  3. pegaptanib
97
Q

How often are anti-VEGF injections usually given?

A

4-weekly

98
Q

What are the recommendations regarding prescribing topical anaesthetic eyedrops for patient analgesia at home?

A
  • should not be used - can have toxic effects on cornea and decrease corneal re-epithelialisation, prolonging healing time e.g. in corneal ulcer
  • use oral analgesics for pain relief instead
99
Q

What are the 2 treatment options for wet AMD?

A
  1. anti-VEGF injections
  2. laser photocoagulation
100
Q

What is the risk of laser photocoagulation in wet AMD?

A

acute visual loss - increased in patients with sub-foveal AMD

101
Q

What are 4 investigations in AMD?

A
  1. slit lamp microscopy
  2. fundus photography
  3. FFA / IGA
  4. OCT
102
Q

What is the most effective intervention to slow dry AMD?

A

stop smoking

103
Q

What are the symptoms of retinal detachment?

A
  • dense shadow that starts peripherally then progresses towards central vision / veil or curtain
  • straight lines appear curved
  • can get central vision loss
  • may be preceded by flashes / floaters (due to vitreous detachment which can cause tear)
104
Q

What should form part of the treatment of amaurosis fugax?

A

should be treated as form of TIA with 300mg aspirin

105
Q

What causes ischaemic optic neuropathy (a differential for amaurosis fugax)?

A

occlusion of short posterior ciliary arteries - e.g. vasculitis, venous disease / hypoperfusion

106
Q

What are 3 causes of central retinal vein occlusion?

A
  1. glaucoma
  2. polycythaemia
  3. hypertension
107
Q

What is more common, CRVO or CRAO?

A

CRVO

108
Q

What are 2 broad causes of CRAO?

A
  1. thromboembolism e.g. atherosclerosis
  2. arteritis e.g. temporal arteritis
109
Q

What is the typical presentation of vitreous haemorrhage?

A

sudden visual loss, dark spots

110
Q

What are 3 factors that can predispose to vitreous haemorrhage?

A
  1. diabetes
  2. bleeding disorders
  3. anticoagulants
111
Q

What is the presentation of posterior vitreous detachment?

A
  • Flashes of light (photopsia) - in the peripheral field of vision
  • Floaters, often on the temporal side of the central vision
112
Q

What are first and second line treatments for allergic conjunctivitis?

A
  • 1st: topical or systemic antihistamines
  • 2nd: topical mast-cell stabilisers e.g. sodium cromoglicate and nedocromil
113
Q

What are 5 causes of chorioretinitis?

A
  1. syphilis
  2. CMV (must perform HIV test)
  3. toxoplasmosis
  4. sarcoidosis
  5. tuberculosis
114
Q

Where is the lesion likely to be to cause a left homonymous hemianopia with some macula sparing?

A

occipital sparing

115
Q

What is seen on fundoscopy in retinitis pigmentosa?

A

black bone spicule-shaped pigmentation in the peripheral retina, mottling of retinal pigment epithelium

116
Q

What are 6 diseases associated with retinitis pigmentosa?

A
  1. Refsum - cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
  2. Usher syndrome
  3. abetalipoproteinaemia
  4. Lawrence-Moon-Biedl syndrome
  5. Kearns-Sayre syndrome
  6. Alport’s syndrome
117
Q

What type of fluorescein staining will be seen in dry eye e.g. due to Bells palsy?

A

punctate staining

118
Q

What is the cause of dendritic corneal ulcer?

A

herpes simplex keratitis

119
Q

What is the first line treatment of herpes simplex keratitis?

A

immediate referral to ophthal; topical aciclovir

120
Q

What 2 bacteria typically cause keratitis?

A
  1. Staphylococcus aureus
  2. Pseudomonas (contact lens wearers)
121
Q

Which organism causing keratitis causes pain out of proportion to the findings?

A

acanthamoebic keratitis

122
Q

What are 3 aspects of the management of contact lens associated keratitis?

A
  1. stop using CLs until symptoms fully resolved
  2. topical abx - quinolones e.g. ciprofloxacin
  3. cycloplegic for pain relief
123
Q

What are 4 complications of keratitis?

A
  1. corneal scarring
  2. perforation
  3. endophthalmitis
  4. visual loss
124
Q

What are 5 risk factors for CRVO?

A
  1. increasing age
  2. hypetension
  3. cardiovascular disease
  4. glaucoma
  5. polycythaemia
125
Q

What will be seen on fundoscopy in CRVO?

A

widespread hyperaemia, severe retinal haemorrhages - stormy sunset

126
Q

What is thought to cause BRVO?

A

branch retinal vein occlusion

127
Q

What are 2 options for treatment in CRVO and what are the 2 indications?

A
  • conservative (majority)
  • indications for treatment: macular oedema (anti-VEGF), retinal neovascularisation (laser photocoagulation)
128
Q

What is the first investigation to perform in someone presenting with an atraumatic subconjunctival haemorrhage?

A

check BP (if on warfarin, check INR)

129
Q

What should be done if you cannot see the whole border of the subconjunctival haemorrhage?

A

may be associated with intracranial bleed or orbital roof fracture - should do full cranial nerve exam + CTH

130
Q

How long does it take subconjunctival haemorrhage to resolve?

A

2-3 weeks (may go yellow/green then brown as clears)

131
Q

What is the treatment for herpes zoster ophthalmicus?

A
  • oral aciclovir 7 - 10 days
  • sometimes topical steroid used for inflammation
  • urgent ophthalmology review

IV antivirals if infection very severe

132
Q

What is the main risk to sight in ocular trauma?

A

raised intraocular pressure - due to angle blockage with erythrocytes

133
Q

Why is strict bed rest required after ocular trauma?

A

excessive movement can redisperse blood that had previously settled - blocked angle, raised IOP - sight threatening

134
Q

What are 4 features of orbital compartment syndrome?

A
  1. eye pain / swelling
  2. proptosis
  3. rock hard eyelids
  4. RAPD
135
Q

What is the management of orbital compartment syndrome?

A

urgent lateral canthotomy (before diagnostic imaging) - to decompress orbit

136
Q

What is the management of dry AMD if detected in primary care?

A

referral to ophthalmology to be seen within 1 week

137
Q

What is the earliest sign of diabetic retinopathy?

A

microaneurysms

138
Q

What type of retinal changes are seen in wet AMD?

A

choroidal neovascularisation

DrFeelGood Stuffs (27 decks)

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