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Y4 NSS > Ophthalmology - high yield > Flashcards

Ophthalmology - high yield Flashcards

1
Q

What is glaucoma?

A

optic nerve damage caused by a rise in intra-ocular pressure by blockage in aqueous humour trying to escape eye
*peripheral vision loss then total

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2
Q

What is the path of travel for aqueous humour?

A
  • produced by ciliary body
  • flows through posterior chamber and around iris into anterior
  • drain through trabecular meshwork to canal of schlemm
  • eventually entering general circulation
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3
Q

What is the normal intra ocular pressure?

A

10-21 mmHg

*created by resistance to flow through trabecular meshwork

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4
Q

What is the pathophysiology of acute angle-closure glaucoma?

A

iris bulges forward and seals off trabecular meshwork from anterior chamber, preventing aqueous drainage

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5
Q

What is the pathophysiology of open angle glaucoma?

A

gradual increase in resistance to flow through the trabecular meshwork, pressure slowly builds up

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6
Q

What are some risk factors of open angle glaucoma?

A

ncreasing age
family history
black ethnic origin
myopia

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7
Q

What are some risk factors of close-angle glaucoma?

A

increasing age
family history
Chinese and was asian ethnic origin
shallow anterior chambers
female

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8
Q

What medications might precipitate acute angle-closure?

A

adrenergic eg: noradrenaline
anticholinergic eg: oxybutynin and solifenacin
tricyclic eg: amitriptyline

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9
Q

How does closed angle closure present?

A

severely painful red eye
blurred vision
halos around lights
associated headaches, N+V

o/e - red eye, hazy cornea, decreased visual acuity, mid-dilated pupil not reactive to light, hard eye on gentle palpation

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10
Q

How does open angle present?

A

luctuating pain, headaches, blurred vision, halos around lights, particularly at night

*peripheral loss of vision, arcuate scotomoa, nasal step

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11
Q

What are some secondary causes of glaucoma?

A

iatrogenic, lens relates issues like cataracts, medicine related like steroids, neovascular, pigment related

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12
Q

How would you investigate suspected glaucoma?

A

measure intra-ocular pressure with non-contact tonometry or Goldmann
slit lamp for cup-disk ratio and angle
visual field
gonioscopy

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13
Q

How do you manage open-angle glaucoma?

A

360 degree selective laser trabeculoplasty
prostaglandin analogue - latanoprost
beta blocker - timolol
carbonic anhydrase inhibitor - dorzolamide
sympathomimetics
trabeculectomy

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14
Q

How do you manage closed angle glaucoma?

A

*>24 pressure first line laser trabeculoplasty
*second latanoprost, then others as needed

initial - pilocarpine, acetazolamide, other like timolol, latanoprost, analgesia

secondary - pilocarpine, acetazolamide, timolol, brimonidine

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15
Q

What is uveitis?

A

inflammation of uveal tract, comprising iris, ciliary body and choroid
*commonly uveitis

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16
Q

What is anterior uveitis?

A

iritis - which only affects the iris and iridocyclitis affects iris and ciliary body

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17
Q

What are some causes of iritis?

A

HLA-B27 conditions - AS, reactive arthritis, IBD
autoimmune - sarcoidosis, vasculitis
infection - herpes, herpes zoster
traumatic
iatrogenic - surgery, bisphosphonates
cancer - leukaemia, malignant melanoma

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18
Q
A
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19
Q

What is posterior uveitis?

A

inflammation of back of eye - retina or choroid

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20
Q

How does anterior uveitis present?

A

*over few hours or gradually over several

bilateral presentation - systemic conditions
unilateral - idiopathic or herpetic
painful, red eye with blurring of vision
photophobia
tearing
systemic - joint pain, back pain, flare up of IBD, infective sx

*chronic or intermediate and posterior - painless and decreased vision

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21
Q

How is anterior uveitis investigated?

A

general - ciliary injection, irregular pupil, cloudy cornea, hypopyon
slit lamp - ciliary flush, inflammatory cells in anterior chamber, flare, adhesions between lens and pupil
lab - bloods for HLA-B27, ANA, infectious diseases screen
OCT - macular oedema, CXR, spinal XR for AS

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22
Q

How is anterior uveitis managed?

A

*can be self limiting

ophthalmologist referral 24h assessment
aim to control inflammation, prevent visual loss, minimise long term complications
topical steroid drops to reduce inflammation
pupil dilating drops (cyclopentolate) to alleviate sx
treat underlying
systemic in severe - steroids and immunosuppressants

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23
Q

What are the complications of anterior uveitis?

A

severe - vision loss
macular oedema
secondary cataract
rise in intra-ocular pressure by inflammation of trabecular meshwork

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24
Q

What is age related macular degeneration?

A

progressive loss of central vision associated with formation of drusen or angiogenesis and changes in retinal pigmentary epithelium
*dry or wet

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25
Q

What is characteristic of dry macular degeneration?

A

drusen in buch’s membrane - undigested cellular debris from degeneration of RPE (retinal pigment epithelium) cells as a part of normal ageing process

*accumulation leads to atrophy of retinal epithelium

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26
Q

What characterises wet macular age degeneration?

A

characterised by choroidal neovascularisation - VEGF (vascular endothelial growth factor) is a protein molecule that has critical role in angiogenesis so in wet AMD causes abnormal angiogenesis and vessel leakage

*fibrous scar tissue and central vision loss and leads to scotoma

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27
Q

What are some RF for AMD?

A

age
smoking
Caucasian ethnicity
high fat diet
drugs like aspirin
co-morbidities like CVS and HTN
ocular characteristics
light coloured iris
hyperopia
genetics
complement factor H
gene variant Y402H (drusen formation link)

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28
Q

How would you classify AMD?

A

early - few medium sized druse, mild pigmentary abnormalities
intermediate - >1 large drusen
advanced - gradual vision loss or advanced wet is rapid vision loss

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29
Q

How does dry AMD present?

A

visual changes unilateral with
gradual loss of central vision
reduced visual acuity
crooked or wavy appearance to straight lines (metamorphopsia)

gradually worsening ability to read small text

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30
Q

How does wet AMD present?

A

wet AMD - more acutely

visual loss within days and progress to complete within 2-3 years
often progresses to bilateral disease

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31
Q

How is AMD investigated?

A
  • pinhole worsens
  • reduced visual acuity - snellen chart
  • scotoma - enlarged central area of vision loss
  • amsler grid test - assess for distortion of straight lines seen in AMD
  • drusen - fundoscopy
  • slit lamp - detailed view of retina and macula
  • optical coherence tomography
  • cross sectional view of retina
  • fluorescein angiography - fluorescein contrast and photographing the retina to assess the blood supply,
    oedema
    neovascularisation in wet AMD
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32
Q

How is dry AMD managed?

A

no cure, ambler to monitor
vitamin supplements in early disease
registration with national centre for blind
social work involvement, OT, psychology involvement
informing DVLA if visual acuity poor

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33
Q

How is wet AMD managed?

A

*no cure - maintain functional sight, amsler grid to monitor

2w referral for wet AMD
intravitreal anti-VEGF therapy - monthly
registration with national centre for blind
social work involvement, OT, psychology involvement
informing DVLA if visual acuity poor

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34
Q

What may cause gradual vision loss?

A

corneal abrasion
chemical injury
cataracts
diabetic eye disease
presbyopia

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35
Q

What is a cataract?

A

progressively opaque eye lens which reduces light entering eye and visual acuity
*can be congenital or progressive

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36
Q

What are some causes of cataracts?

A

age related

pre-senile
steroids
DM
trauma
uveitis

congenital

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37
Q

What are some risk factors of developing cataracts?

A

increasing age
smoking
alcohol
DM
steroids
hypocalcaemia

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38
Q

How does cataracts present?

A

*asymmetrical
- change in glasses prescription - myopic shift with short sighted first as light converges as cataract hardens
- slow reduction in visual acuity
- progressive blurring of vision
- colours more faded - brown or yellow
- starbursts around lights at night especially
*loss of red reflex

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39
Q

How are cataracts managed?

A

phacoemulsification - if vision 6/12 with sub-tenon block

*important to treat as prevents detection of other pathology like AMD, DM retinopathy etc

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40
Q

What is a complication of cataracts?

A

post-surgery endophthalmitis - inflammation of vitreous and aqeous humour
mx: intravitreal abx

seondary glaucoma

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41
Q

What is the blood supply to the retina?

A

carotid → ophthalmic → central retinal and posterior ciliary artery

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42
Q

What is the pathophysiology of diabetic retinopathy?

A

chronic hypoglycaemia damages retinal small vessels and endothelial cells
increases vascular permeability -> leaks and blot haemorrhages + hard exudates
neovascularisation etc

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43
Q

What are some characteristic features of diabetic retinopathy?

A

hard exudates
micro-aneurysms and venous beading
cotton wool spots
intra-retinal microvascular abnormalities
neovascularisation

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44
Q

What are the stages of diabetic retinopathy?

A

background retinopathy
pre-proliferative
proliferative
diabetic maculopathy
ischaemic diabetic maculopathy

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45
Q

What is background diabetic retinopathy? and what does this mean for management?

A

micro-aneurysms
dot and blot haemorrhages
cotton wool spots
hard exudates

*no tx indicated, annual screening with digital photography

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46
Q

What is pre-proliferative stage and what’s the management?

A

extensive blot haemorrhages and intra-retinal microvascular abnormalities (ischaemia)

*4-6m follow up with digital fundus colour photos + retinal laser tx

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47
Q

what is proliferative stage and what is the management?

A

neovasuclarisation and vitreous haemorrhages

*pan retinal photocoagulation targeting new vessels, retinal laser, anti-VEGF

48
Q

Differentiate between diabetic maculopathy and ischaemic diabetic maculopathy and what is the management?

A

diabetic - exudates within macula and macular oedema!
ischaemic - angio needed to diagnose, occlusions within vessels

*mx - anti-VEGF bevacizumab, ranibizumab, intravitreal dexamethasone implant to reduce macular oedema

49
Q

What are some risk factors for diabetic retinopathy?

A

duration of diabetes - 50% at 7 years duration and 90% at 17-50
poor glycaemic control
hypertension
dyslipidaemia
obesity
pregnancy

50
Q

How might diabetic retinopathy present?

A

asymptomatic and most present with severe disease

floaters
blurred vision and distortion if macula affected
decreased visual acuity - gradual, painless reduction in quality
loss of vision - severe haemorrhage in results in sudden complete and painless vision loss
blindness in untreated and uncontrolled

51
Q

What is the diabetic eye screening programme?

A

for anyone with diabetes
every 1-2 years
depends on previous 2 scans

52
Q

How is diabetic retinopathy investigated?

A

visual acuity - logMAR
gold: fundoscopy with slit lamp or through fundus photography
OCT: non invasive and infrared
Fundus fluorescein angiography
dye into arm to see retinal blood vessels

53
Q

What is the general management options available for non-proliferative diabetic retinopathy?

A

close monitoring and careful diabetic control

pre-proliferative: 4-6m follow up with digital fundus colour photos

retinal laser treatment given if,
only one good eye left
attendance to clinic poor
prior cataract surgery

54
Q

What is the management for proliferative DM retinopathy?

A

Pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels
aim to kill ischaemic retina so hypoxic drive and oxygen demand is lessened and supply focused to central retina
*complications - visual field defects, impaired night vision, accidental macular burn

anti VEGF - medication intravitreal injection
bevacizumab, ranibizumab
surgery - vitrectomy in severe disease
macular oedema
intravitreal implant containing dexamethasone

55
Q

what conditions cause sudden loss of vision?

A

retinal detachment
central retinal artery occlusion
central retinal vein occlusion vitreous haemorrhage (due to diabetic retinopathy)

56
Q

what causes amaurosis fugax?

A

temporary loss of vision caused by a temporary interruption to the blood supply

57
Q

what is the pathophysiology of central retinal artery occlusion?

A

obstruction to blood flow through the central retinal artery, which was a brach of ophthalmic artery which is a brach of ICA

*cause atherosclerosis, GCA, vasculitis hence CVS RF

58
Q

how does central artery occlusion present?

A

sudden painless loss of vision: curtain coming down
RAPD

59
Q

what is relative afferent pupillary defect?

A

pupil in affected eye constricts more when light shone in other eye than when shone in itself, hence appears to dilate when shone on affected when swung from non-affected

input not sensed by ischaemic retina when testing direct but sensed in consensual

60
Q

how is retinal artery occlusion investigated?

A

fundoscopy: pale retina with cherry red spot (fovea) due to lack of perfusion

GCA: ESR, temporal artery biopsy
*refer immediately

61
Q

how is central artery occlusion managed?

A

GCA: potentially reversible so high dose prednisolone +/- IV Methylpred

attempt to dislodge blockage: ocular massage, anterior chamber paracentesis, inhaled carbogen, IV
acetazolamide+mannitol etc

secondary prevention of CVS, treat reversible RF

62
Q

what is the pathophysiology of central vein occlusion?

A

thrombus forms in retinal veins and obstructs the venous drainage from retina

central retinal vein run through the optic nerve - responsible for draining retinal capillaries
atherosclerotic thickening of central retinal artery leading to vein compression
causes retinal tissue ischaemia, infarction, vessel leakage and neovascularisation

63
Q

what are some risk factors for central vein occlusion?

A

age
FHx of vascular
atherosclerosis
open angle glaucoma
inflammatory: sarcoidosis, Lyme
hyper coagulable state
myeloproliferative states

64
Q

what is the presentation of central vein occlusion?

A

sudden, painless unilateral visual loss (more gradual than artery occlusion)
relative afferent pupillary defect - ischaemia
visual field defect

65
Q

what is a differential for CRVO?

A

branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded

66
Q

how is retinal venous occlusion investigated?

A

fundoscopy: widespread hyperaemia, severe retinal haemorrhages, macular oedema, cotton wool spots
BP
FBC, glucose, ESR
fundal photo
fundus fluorescein angio

67
Q

how is CRVO managed?

A

immediate ophthal referral
control BP
treatment aim to control complications
macular oedema: anti-VEGF, intravitreal steroid implant, laser
neovascular complications: pan-retinal photocoagulation

68
Q

what is a complication of CRVO?

A

Ischaemic carries poorer prognosis
retinal non-perfusion, capillary closure, retinal hypoxia which increases neovascularisation risk
may resolve spontaneously, cause vitreous haemorrhages or cystoid macular oedema

69
Q

what is retinal detachment?

A

involves the neurosensory layer of retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (base later attached to choroid)

*resulting in fluid accumulation in between

70
Q

what is the consequence of a retinal detachment?

A

due to retinal tear -> vitreous fluid to get under the neurosensory retina and fill the space

neurosensory retina relies on blood vessels of the choroid for its blood supply
detachment disrupts this causing permanent damage to photoreceptors -> sight threat

71
Q

what are some RF for retinal detachment?

A

lattice degeneration (thinning of retina)
posterior vitreous detachment
trauma
diabetic retinopathy
retinal malignancy
family history

72
Q

how does retinal detachment present?

A

painless
peripheral vision loss - sudden, shadow coming across vision
blurred vision or distorted vision
flashes and floaters
RAPD if optic nerve involved
fundoscopy: red reflex might be lost

73
Q

how is retinal detachment managed?

A

aim to create adhesions between retina and choroid with laser and cryo
aim to reattach retina: vitrectomy, scleral buckle, pneumatic retinoplexy

74
Q

what is optic neuritis?

A

inflammatory condition of the optic nerve that leads to acute, unilateral, central loss of vision (over hours to days)

common in females 20-40

75
Q

what is the pathophysiology of optic neuritis?

A

immune-mediated demyelination of the optic nerve as an isolated incident or part of wider disorder

acute version of MS

also associated with DM, syphillis

76
Q

what is the presentation of optic neuritis?

A

acute, central vision loss - unilateral over hours to days
poor discrimination of colours - red desaturation
pain worse of eye movement
photopsia - flashes of light
relative afferent pupillary defect
visual field defects - central scotoma
optic atrophy - chronic

77
Q

how is optic neuritis investigated?

A

swinging light test: RAPD
visual acuity
ishihara colour test
ophthalmoscopy: mildly swollen disc
MRI brain and orbits with contrast: confirm demyelinating optic neuritis
LP: elevated protein, lymphocytes,oligoclonal bands

78
Q

how is optic neuritis managed?

A

high dose IV steroids - methylprednisolone
disease modifying therapies - MS?
recovery usually 4-6w

79
Q

what is the significance of thyroid diseases in relation to ophthalmology?

A

autoimmune condition resulting in inflammation and swelling of extra-ocular muscle, fatty tissue and connective tissue within orbit

*follows acute phase for 6m to 2y where damage happens, inactive phase when sx remain

80
Q

how might thyroid related eye disease present?

A

excessive watering
‘gritty’ sensation
photophobia
eye pain
ask - red eye, blurred vision, pressure sensation
systemic - pretibial myxoedema, goitre, acropachy

81
Q

what might thyroid eye disease examination show?

A

eye lid retraction
proptosis
lig lag - von Graefe’s sign
lid oedema
diplopia due to restriction of inferior rectus
incomplete eyelid closure
strabismus

82
Q

what investigations are carried out for thyroid related eye disease?

A

measure proptosis
assess optic disc
visual acuity, colour vision, RAPD
TFT
antibody test
anti-thyroid peroxidase, anti-TSH
USS extra-ocular muscles
CT orbit - nerve involvement
MRI orbits

83
Q

how is thyroid related eye disease managed?

A

compressive optic neuropathy - Urgent IV methylprednisolone
Ophthal + endo review
correct thyroid hormone levels
smoking cessation
steroids to reduce swelling

84
Q

what are some complications of thyroid related eye disease?

A

*compressive optic neuropathy - reduced visual acuity, colour vision → sight-threatening

globe subluxation
gaze abnormalities
raised IOP → glaucoma

85
Q

what is the pathophysiology of amaurosis fugax?

A

result of ischaemia to the retina, choroid, or optic nerve from an arterial embolus, usually in the retinal artery (from ipsilateral carotid artery disease)

86
Q

what are some RF for amaurosis fugax?

A

over 50
vascular RF
HTN, HPL, smoking, previous TIA or stroke

87
Q

how does amaurosis fugax present?

A

transient vision loss in one or both eyes
abrupt, maximum severity within seconds lasting to minutes
full recovery
negative visual phenomenon - blackout or ‘greying out’ of vision
normal ophthal exam

88
Q

how is amaurosis fugax investigated?

A

inflammatory markers - rule out GCA
carotid imaging for stenosis
cardiac investigations - AF other stroke RF
neuro-imaging is needed

89
Q

how is amaurosis fugax managed?

A

300mg of aspirin unless contraindicated
urgent TIA referral within 24h
secondary prevention - statin, antiplt, optimising BP etc

90
Q

what is blepharitis?

A

inflammation of the eyelid margins
- due to meibomian gland dysfunction (common, posterior bleph), or seborrhoeic dermatitis/ staphylococcal infection (less common, anterior bleph)

91
Q

how does blepharitis present?

A

bilateral symptoms
grittiness and burning discomfort - around lid margins
eyes sticky in the morning
results in dry eye which could cause redness
foreign body sensation
margins may be red - swollen in staphylococcal blepharitis
styes and chalazions common in these
secondary conjunctivitis

92
Q

what does blepharitis look like on examination?

A

anterior - eyelash deformity and depigmentation and loss
posterior - dilated and obstructed Meibomian glands

93
Q

how is blepharitis managed?

A

diagnosis - history, examination
- slit lamp
- swabs maybe done for cultures

hot compress
lid hygiene
artificial tears
abx
ophthal referral if painful

94
Q

how is lid hygiene done for blepharitis?

A

lid hygiene - mechanical removal of debris from margins
cotton wool buds dipped in mix of cooled boiled water and baby shampoo often used
alternative is sodium bicarb, teaspoonful in cup of cooled water recently boiled

95
Q

what is the pathophysiology of posterior vitreous detachment?

A

vitreous body comes away from retina - common in older age
vitreous humour is gel inside the vitreous chamber of eye, maintain structure of eyeball and keeps retina pressed on choroid
with age, less firm and less able to maintain shape

96
Q

How is posterior vitreous detachment managed?

A

*exclude retinal detachement

brain adjusts overtime
safety net for retinal detachment as predisposes

96
Q

how does posterior vitreous detachment present?

A

painless
can be asymptomatic
floaters
flashing lights
blurred vision

97
Q

How is red eyes assessed?

A

history of symptoms and onset
- pain
- visual loss - serious
- gritty - conjunctivitits, dry eyes, foreign body
- itching - allergic, blepharitis

examination of both eyes
- visual acuity with snellen
- evidence of trauma, discharge, swelling
- pattern on redness
- perform fluorescein examination
- assess pupils, RAPD?
- BP

98
Q

what are some red flags for a red eye?

A

reduced visual acuity
severe pain, headache, photophobia
significant ciliary injection, fluorescein staining
unequal pupils and abnormal reactions
pain on pupillary constriction, loss of red eye, corneal haze, hyphaema or hypopyon (blood and pus in anterior chamber)

99
Q

what are some differentials for a painful red eye?

A

acute angle-closure glaucoma
anterior uveitis
scleritis
corneal ulcerations
keratitis
foreign body
trauma or chemical injury
endophthalmitis

100
Q

what are some differentials for a painless red eye?

A

conjunctivitis
episcleritis
subconjuctival haemorrhage
dry eye
episcleritis

101
Q

what is anisocoria?

A

difference in pupil size

physiological is ≤2mm and difference same in all light levels

102
Q

what is the pupillary light reflex anatomy?

A

light activates retinal ganglion cells → axons through optic nerve → chiasm → optic tract → synapse at EWN → efferent parasympathetic fibres travel with CN3 → cilairy ganglion

iris contains 2 muscles - constricting sphincter innervated by parasympathetic and dilating by sympathetic (which starts at ipsilateral hypothalamus)

103
Q

what is the significance of anisocoria in dark or light?

A

greater anisocoria in dark → impaired dilation in small pupil (sympathetic dysfunction)

greater anisocoria in light → impaired constriction in large pupil (parasympathetic dysfunction)

104
Q

what are some differentials for a large pupil?

A

Adie’s tonic pupil
post viral denervation of the sphincter pupillae and ciliary muscle
dilator drops
3rd nerve palsy
traumatic mydriasis

105
Q

what are some differentials of a small pupil?

A

horners syndrome
pilocarpine drops
uveitis

106
Q

what is your understanding of positive or negative phenomenon in terms of vision loss?

A

positive - brightness, shimmering, hallucinations → migraine aura, seizure

negative - blackness, greyness, shade-obscuring vision → TIA, stroke

107
Q

how do you assess visual loss?

A

visual acuity and colour vision
snellen, pinhole, fingers, movement
ishihara, red saturation
swing test for RAPD
visual fields
ophthalmoscopy

108
Q

what are some differentials for acute loss of vision?

A

amaurosis fugax
central venous occlusion
central arterial occlusion
vitreous haemorrhage
retinal detachment
optic neuritis
GCA

109
Q

what is strabismus?

A

misalignment of the two eyes when focusing on one object which could be persistent (manifest or tropia) or latent (phoria)(discovered with cover test)

110
Q

what could cause strabismus?

A

Primary

  • idiopathic
  • congenital

Secondary

  • cranial nerve palsies of EOM
  • intracranial infection
  • intracranial, intraorbital and intraocular masses
  • orbital # or other trauma
  • myopathies - MG
  • endocrine - DM, graves
  • heavy metals and toxins
111
Q

what are some risk factors for developing strabismus?

A
  • family history
  • low birth weight
  • premature birth
  • maternal smoking
112
Q

what are some red flags associated with strabismus?

A
  • recent trauma
  • symptoms of raised ICP
  • new strabismus in school age child
113
Q

how might strabismus present?

A
  • onset, reduced visual acuity, diplopia, asthenopia, decreased socialisation, behavioural problems, maladjustment at home or school
  • other - developmental history, obstetric, previous medical, previous visual acuity
114
Q

how would you examine strabismus?

A
  • corneal light reflex - Deflection of the corneal light reflex in one eye suggests a misalignment
  • Brüchner test - asymmetry of red reflexes suggest ocular disorder
  • cover test - determine heterotropia (latent stabismus)
  • cover-uncover test - check covered eye for refixation movement, if phoria present eye will shift back to being orthopic or straight
  • prism cover test
115
Q

how would you manage strabismus?

A
  • orthoptics - measure visual acuity, assess eye movement, assess binocular vision, monitors amblyopia with patching to encourage use of amblyopic eye
    • patch unsuccessful after age of 7
  • refraction to correct deviation and improve acuity
  • strabismus surgery - EOM operated on

Y4 NSS (11 decks)

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