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Neurology and Special Senses > Ophthalmology Conditions > Flashcards

Ophthalmology Conditions Flashcards

1
Q

What is blepharitis?

A

Range of conditions causing eyelid inflammation

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2
Q

What is the difference between anterior and posterior blepharitis?

A

Anterior - involve the lashes

Posterior - involve meibomian glands

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3
Q

What complications are associated with blepharitis?

A

Dry eye
Conjunctivitis
Keratitis

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4
Q

What is the pathophysiology of blepharitis?

A

Build up of bacteria on lash follicle or gland orifice

Immune response to this causes collateral damage and further inflammation

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5
Q

How does blepharitis present?

A 
Bilateral
Burning watery eyes (with foreign body sensation if cornea involved)
Worse in morning - eyes may stick
Red inflamed eyelid
Crusts/scales along eyelashes
Tear film deficiency
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6
Q

How is blepharitis managed?

A

Lid hygiene and topical chloramphenicol

+Stop mascara use, remove crusts, warm compress, tear supplements

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7
Q

What makes up the uvea/vascular layer of the eye?

A

Iris
Choroid
Ciliary body

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8
Q

What is the difference between causes of unilateral and bilateral uveitis

A

Unilateral - infectious, acute cause

Bilateral - chronic systemic cause

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9
Q

How can anterior uveitis be further categorised?

A

Iritis - just iris

Iridocyclitis - iris and ciliary body

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10
Q

When do most patients present with anterior uveitis?

A

Between 20-50yo

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11
Q

What can cause anterior uveitis?

A

Idiopathic - 50%
Inflammatory - ank spond. sarcoidosis, Behcet’s, IBD, Kawasaki, SLE
Infectious - Lyme disease, herpes
Trauma

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12
Q

Where does the most severe injections in anterior uveitis occur?

A

At the limbus - opposite to conjunctivitis (further away from limbus)

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13
Q

What is the pathogenesis of uveitis?

A

Antigen thought to provoke inflammatory response that breaks down eye-blood barrier. This enables WBC and proteins to enter anterior chamber

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14
Q

How does uveitis present?

A 
Symptoms occur over hours-days
Painful - worse pain on eye movement
Red
Photophobia
Blurred vision
Watery eye - may overflow
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15
Q

What signs are seen on examination in a patient with uveitis?

A 
Reduced visual acuity
Perilimbal injection
Direct photophobia
Keratic precipitates - WBC visible as little white spots
Small fixed oval pupil
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16
Q

How is uveitis managed?

A

Refer to ophthalmology within 24hrs

Cycloplegic dilating agents
Corticosteroids

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17
Q

Why and what are cycloplegia dilating agents used for uveitis?

A

Relieve pain
Prevent adhesions

Atropine and Cyclopentolate

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18
Q

Why are corticosteroids used for uveitis?

A

Reduce inflammation

Prevent adhesions

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19
Q

What complications are associated with uveitis?

A

Relapse
Posterior synechiae (adhesions from lens to iris)
Cataract
Glaucoma (due to steroids)

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20
Q

What are posterior synechiae?

A

Inflammatory adhesions between lens and iris

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21
Q

What must you examine for if a patient has uveitis?

A 
Back pain - ank spond
Rash/bite - lyme
Resp. Symptoms - Sarcoidosis
GI symptoms - IBD
Cold sore - herpes
Oral/genital ulcers - Behcet's
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22
Q

What is affected in intermediate uveitis?

A

Posterior ciliary body
Peripheral retina
Choroid

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23
Q

What features are associated with intermediate uveitis?

A

Painless floaters
Decreased vision
Minimal redness and pain

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24
Q

What is affected in posterior uveitis?

A

Retina and choroid

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25
Q

What features are associated with posterior uveitis?

A

Bilateral
Painless floaters
Gradual visual loss
Absence of redness, pain and photophobia

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26
Q

What is infectious keratitis and what is it also known as?

A

Infection of the cornea

Corneal ulcer

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27
Q

What causes infectious keratitis?

A

Microorganisms getting in via defect in corneal epithelium

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28
Q

What must be done if a patient has a corneal ulcer?

A

Take swab under topical anaesthesia

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29
Q

What risk factors are associated with corneal ulcers?

A

Wearing contact lenses
Dry eyes and blepharitis
Diabetes and immunosuppression
Topical corticosteroid use

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30
Q

How do corneal ulcers present?

A

Severe pain
Photophobia
FB sensation
Reduced vision

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31
Q

How are corneal ulcers managed?

A

Topical broad spectrum quinolone

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32
Q

What can be seen on examination of a corneal ulcer?

A

Hypopyon - white fluid in anterior chamber

White lesions on cornea - infiltrate

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33
Q

What is the prognosis of corneal ulcers?

A

Good prognosis

Increased risk of long term visual disability in:
Elderly, Contact lens wearers, Fungal disease

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34
Q

What causes herpetic keratitis?

A

HSV1

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35
Q

What happens in herpetic keratitis?

What is the hallmark feature on examination?

A

Virus travel along trigeminal nerve to ophthalmic division to corneal nerve

Dendritic ulcer pattern seen

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36
Q

How is herpetic keratitis treated?

A

Topical aciclovir

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37
Q

What is an acanthamoeba? Who does it most often affect?

A

Rare sight threatening protozoal infection

Seen in contact lens wearers

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38
Q

How does acathamoeba present?

A

Pain out of proportion to clinical signs

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39
Q

How is acanthamoeba treated?

A

Propamidine
Chlorhexadine

Several months

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40
Q

What risk factors are associated with corneal abrasion?

A

Inability to close eyes

Wearing contact lenses

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41
Q

How does corneal abrasion present?

A 
Watery red eye
Unable to keep open/repeated blinking
Photophobia
Decreased visual acuity
FB sensation
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42
Q

What investigations would you request for someone with a corneal abrasion?

A

None normally needed
CT = 1st choice
X-ray if metallic FB
MRI contraindicated for metallic FB

Fluorescein examination

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43
Q

What would you see on fluorescein examination of a corneal abrasion?

A

Yellow stained abrasion

Usually visible to naked eye

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44
Q

How is corneal abrasion managed?

A

Topical NSAID’s
Topical Chloramphenicol - prevent bacterial infection
Tetanus prophylaxis
Follow up and review

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45
Q

How are corneal foreign bodies managed?

A

Remove (IF EXPERIENCED)
Topical anaesthetic
Irrigate eye or remove with cotton wool bud

Then treat as abrasion (NSAIDs, chloramphenicol, tetanus prophylaxis)

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46
Q

How are contact lens wearers who have a corneal abrasion managed?

A

Topical anti-pseudomonas antibiotics

No contact lens for 2 weeks

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47
Q

What is the prognosis for a corneal abrasion on the visual axis?

A

Potential for loss of visual acuity - scarring

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48
Q

What must you exclude with penetrating corneal injury?

A

Full thickness injury - this means ruptured globe

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49
Q

What mustn’t you do if a patient has a penetrating corneal injury?

A

Apply pressure to the globe

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50
Q

What is Seidel’s test (ophthalmology)?

A

Used to assess leakage from cornea, sclera or conjunctiva

If see paler fluid within pool or dye leaks then injury has penetrated anterior chamber

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51
Q

What are the red flags associated with penetrating corneal injury?

A

Obvious deep laceration
Subconjunctival haemorrhage
Pupil or iris deformity

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52
Q

How would you manage a patient with penetrating corneal injury?

A

Urgent referral to ophthalmologist
Eye shield
Advise not to cough, blow nose or strain

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53
Q

What is glaucoma?

A

Damage to the optic nerve head with progressive loss of retinal ganglion cells and their axons

Associated with raised IOP

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54
Q

How does aqueous humour normally drain in the eye?

A

Ciliary epithelium secrete aqueous humour

Pass through trabecular meshwork at the iridocorneal angle

Pass through canal of scheme

Into aqueous veins and episcleral venous system

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55
Q

Where is flow reduced in open angle primary glaucoma?

A

Trabecular meshwork

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56
Q

What IOP is seen in open angle primary glaucoma?

A

> 21mmHg

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57
Q

What risk factors are associated with open angle primary glaucoma?

A 
Age
Afro-caribbean
Myopia
Retinal disease
Family history
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58
Q

How can primary open angle glaucoma be managed?

A

Topical drops
Laser trabeculoplasty
Surgical trabeculectomy

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59
Q

What is the pathophysiology of primary open angle glaucoma?

A 
Poorly understood
Could be:
Raised IOP reduce blood flow to nerve head leading to vascular perfusion problem
or
Autoimmune damage of the nerve head
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60
Q

What examinations would you carry out if you suspect primary open angle glaucoma?

A 
Goldman tonometry - IOP measurement
Corneal thickness
Gonloscopy - measure iris-corneal angle
Visual field assessment
Optic disk examination
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61
Q

What signs could be seen on optic disk examination in a patient with primary open angle glaucoma?

A 
Cupping
Pallor
Bayoneting of vessels
Cup notching
Disc haemorrhage
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62
Q

How common is primary open angle glaucoma?

A

10% of >75yo

63
Q

How does primary open angle glaucoma present?

A

Initial visual field loss peripheral - asymptomatic for long time

Usually picked up on routine optician appointment

By checking Visual Fields and Intra Ocular pressure of relatives

64
Q

What conditions does the open angle glaucoma spectrum include?

A

Ocular hypertension - IOP>21 but nerve and VF normal

Normal tension glaucoma - IOP<21 but cupping optic disc and visual field defect

65
Q

What is the prognosis for open angle glaucoma?

A

Treatment stall progression but doesn’t stop or reverse it

Good compliance normally means vision retained for lifetime

66
Q

What is secondary open angle glaucoma?

A

A primary disease causes raised IOP and optic neuropathy

67
Q

What are the causes of secondary open angle glaucoma?

A

Neurovascular
Corticosteroid induced
Pseudoexfoliative - deposits in drainage angle
Pigment dispersion - pigment deposit block drainage angle

68
Q

What is the pathophysiology of neurovascular caused open angle glaucoma?

A

Ischaemia of the eye leads to new vessels growing and fibrosing in the drainage angle

69
Q

How is secondary open angle glaucoma treated?

A

Neurovascular cause - laser treatment and anti-VEGF injections

Others - stop corticosteroids and drops

70
Q

What happens in acute closed angle glaucoma?

A

Acutely raised IOP
Obstructed irido-corneal angle
Lens pushed against iris

71
Q

What risk factors are associated with closed angle glaucoma?

A

Age
Chinese
Women
Hypermetropes

72
Q

What are the possible complications of closed angle glaucoma?

A

Loss of vision

Central retinal artery/vein occlusion

73
Q

What are the causes of closed angle glaucoma?

A

Severe hypermetropes - narrow angle so vulnerable to blocking off
Lens grow as we age - narrow angle
Short axial length
Thick lens
Thin iris
Pupil dilation - push iris into angle
Alpha-adrenergic agonists and other systemic drugs
Lens dislocation
Diabetes and Uveitis - meshwork blocked by vasculature and proteins

74
Q

How does closed angle glaucoma present?

A

Severe acute pain
Blurred vision –> vision loss
Coloured haloes around lights
N&V

75
Q

What can be seen on examination of a patient with closed angle glaucoma?

A 
Red eye
Hazy cornea
Mid-dilated and non-reactive pupil
Globe feels hard
Shallow anterior chamber
Closed irido-corneal angle
RIOP (40-70)
76
Q

What is the immediate management for acute closed angle glaucoma?

A 
Immediate referral
Topical drops
IV acetazolamide - carbonic anhydrase inhibitor
IV mannitol
Analgesia and anti-emetics
77
Q

What is the definitive closed angle glaucoma management?

A

Laser iridotomy

78
Q

What is age related macular degeneration?

A

Central retina changes without obvious precipitating cause occurring in >55yo

79
Q

What are the types of macular degeneration? How common are they?

A

Dry - geographic atrophy - 90%

Wet - neovascularisation - 10%

80
Q

What is the most common cause of UK blindness?

A

Age related macular degeneration

25% develop in other eye within 4 years

81
Q

What are the risk factors for age related macular degeneration?

A 
Age
Smoking
Family Hx
Diet and Obesity
Caucasian
CVS risk factors
82
Q

How does age related macular degeneration present?

A 
Painless loss of central vision
Near vision affected most
Can't discern between different shades of colour
Difficulty adapting from light to dim
Photopsia
Visual hallucinations
83
Q

What is the main differential for age related macular degeneration?

A

Diabetic maculopathy

84
Q

How is age related macular degeneration diagnosed?

A

Slit lamp
OCT
Fundus fuorescein angiography

85
Q

How does dry macular degeneration appear?

A

Soft druse
Changes in pigmentation of retinal epithelium
Atrophy

86
Q

How does wet macular degeneration appear?

A

New vessel growth seen
Leakage from vessels - esp in periphery
Red patches - haemorrhages

87
Q

How do symptoms of wet and dry macular degeneration vary?

A

Dry - gradual vision loss, partial vision loss

Wet - sudden symptom, straight lines appear wavy

88
Q

How is age related macular degeneration managed?

A

Dry

  • no treatment
  • Vision rehab, smoking cessation help, vitamin supplements

Wet
- Intravitreal anti-VEGF injections (ranibizumab)

89
Q

What are the ADR’s associated with anti-VEGF injections?

A

Retinal detachment
Endophthalmitis
Allergic reaction

90
Q

What is retinitis pigmentosa?

A

Inherited eye disease that is characterised by black pigmentation and gradual degeneration of the retina

91
Q

How does retinitis pigmentosa present?

A

Night blindness
Ring scotoma - loss of all peripheral vision –> tunnel vision –> blindness
Black bone spicule pigmentation of the peripheral retina
Mottling of retinal pigmented epithelium
Waxy looking disc

92
Q

What is the pathogenesis of retinitis pigmentosa?

A

Photoreceptor death - rods first

Cell death lead to inflammation of vitreous humour

93
Q

What is the epidemiology of retinitis pigmentosa?

A

Some cases X linked - more men

Peak ages - 7.5, 17 and >50yo

94
Q

Why do you not get a relative afferent pupillary defect in Retinitis Pigmentosa?

A

It is bilateral and symmetrical

95
Q

What is the prognosis for Retinitis pigmentosa?

A

Most legally blind by 40yo

96
Q

How is Retinitis pigmentosa managed?

A

Visual rehab
Counselling

No way to stop disease progression

97
Q

What is retinoblastoma?

A

Most common childhood ocular cancer originating from primitive retinal cells

98
Q

Describe the epidemiology of retinoblastomas

A

Autosomal dominant
Average age of diagnosis - 18 months
10% of cases hereditary

99
Q

What is the pathophysiology of retinoblastoma?

A

Mutation in retinoblastoma tumour suppressor gene on chromosome 13

Follow 2 hit model:
Sporadic - both mutations at fertilisation
Inherited - one mutation inherited, other occur after birth

100
Q

How does retinoblastoma present?

A

Absence of red-reflex - Leukocoria (white pupil)
Strabismus - squint
Varied ocular symptoms as disease progress - red eye, nystagmus, vision loss

101
Q

How are retinoblastoma managed?

A 
Range of options:
Enucleation
External beam radiation therapy
Chemo
Photocoagulation
102
Q

How is retinoblastoma diagnosed?

A

Examination under general anaesthesia with fully dilated pupil

MRI

103
Q

What is the prognosis of retinoblastoma?

A

Excellent - >90% survive
Increased risk of other malignancy - Ewing’s sarcoma, osteosarcoma, neuroblastoma
Metastasis to bone and brain rare
Long term decrease in visual acuity and visual fields

104
Q

What do the central retinal and posterior ciliary arteries supply?

A

Central - optic disc and central retina
Posterior - Outer retina

Both must function to maintain retinal function

105
Q

What causes retinal artery occlusion?

A

Equivalent to cerebral stroke with end organ ischaemia:

Atheroma related thrombus
Emboli
Inflammatory cause - giant cell, SLE, wegener's
Thrombophilic disorder
COCP and cocaine
Vasospasm
106
Q

What is the peak age of retinal artery occlusion?

A

60-80yo

107
Q

Describe the vessels that supply the retina

A

Internal carotid – ophthalmic –> Central retinal and Posterior ciliary arteries

Circle of zinn formed from posterior ciliary arteries

108
Q

How is retinal artery occlusion diagnosed?

A

Clinical diagnosis
ESR, CRP and vasculitis screen req. if suspect giant cell arteritis
Full CVS exam

109
Q

How does retinal artery occlusion present?

A

Sudden unilateral painless loss of vision

Amaurosis fugax history

110
Q

What can be seen on examination of a patient with retinal artery occlusion?

A

Relative afferent pupillary defect
Pale retina with cherry red spot
Centre of macula thin, can see underlying vascular choroid
Oedematous retina

111
Q

How is retinal artery occlusion managed?

A

NEEDS TO BE STARTED WITHIN 100 MINS - still make attempts upto 24hrs after event

Giant cell arteritis suspected - IV steroids
Treatments have very little evidence:
Ocular massage
Inhale high CO2 content
Topical glaucoma drops
Anterior chamber paracentesis
112
Q

What is the long term management of retinal artery occlusion?

A

Reduce CVS and atherosclerotic risk factors

113
Q

What is the prognosis for retinal artery occlusion?

A

Only 1/3 get improved vision even with rapid treatment

114
Q

What causes retinal vein occlusion?

A

Disruption to virchow’s triad:

  • Thrombus
  • Increased viscosity of blood
  • Disease of the vein wall
  • Compression from outside - arterial hypertension
115
Q

What are the key risk factors for retinal vein occlusion?

A 
Advancing age
Hyperlipidaemia
Hypertension
Diabetes
Raised IOP
Inflammatory disease
Hyperviscosity syndromes
Renal disease
116
Q

What are the types of retinal vein occlusion?

A

Branch retinal vein - more common

Central retinal vein - less common

117
Q

How do branch and central retinal vein occlusion vary?

A

Branch - Image distortion, visual field defect
50% get 6/12 vision back

Central - Start on walking
Cotton wool spots, flame haemorrhages and RAPD (if ischaemia) on fundoscopy

118
Q

What signs and symptoms are seen with both branch and central retinal vein occlusion?

A

Unilateral painless loss of vision

Vascular dilatation and Tortuous vessels on fundoscopy

119
Q

How is retinal vein occlusion investigated?

A 
BP
Lipid profile
ESR
Blood glucose
(Thrombophilia screen)
120
Q

How can retinal vein occlusion be managed?

A

Manage CVS risk factors

Laser treatment - if associated macula oedema or neovascularisation

Intravitreal anti-VEGF - neovascularisation

121
Q

What complications are associated with retinal vein occlusion?

A

Macula oedema
Retinal neovascularisation - due to hypoxia
Secondary glaucoma - due to neovascularisation

122
Q

What is the normal sequence of events in retinal detachment?

A

1 Vitreous liquefies and shrinks with age
2 Posterior vitreous detachment
3 Traction on retina lead to tear
4 Vitreous seep underneath causing detachment

123
Q

What are the symptoms of posterior vitreous detachment?

A

Flashing lights

Floaters - often temporal side of central vision

124
Q

How may retinal detachment present?

A

Shadow start peripherally and progress centrally
Begin slowly and progress over hours to weeks

Black curtain come down and obstruct view
Central vision loss - macula involved
Straight lines appear curved

125
Q

What signs would be seen on examination of a patient with retinal detachment?

A 
RAPD if severe
Loss of red reflex
Reduced visual acuity
Shafer's sign - vitreous lined with brown pigmented material
Tears visible
White appearance of detached retina
126
Q

What risk factors are associated with retinal detachment?

A 
Age
Myopes - long eye
Family Hx
Previous tears
Marfan's
127
Q

How is retinal detachment diagnosed?

A

Slit lamp examination

Ultrasound or OCT

128
Q

How is retinal detachment managed?

A

Same day urgent Ophthalmology review

Tear - laser or cryotherapy to make adhesions between neural and pigmented layer

Detachment:

  • Vitrectomy - air/oil injected to push retina back
  • Scleral buckling - silicone placed on sclera to push eye closer to detached retina
  • Pneumatic retinopexy - Gas bubble injected - expand
129
Q

What are the complications associated with retinal detachment?

A 
Vision loss
Scar tissue can fibrose - further detachment
Macula oedema
Infection
Haemorrhage
130
Q

What is the prognosis for retinal detachment?

A

85% successful reattachment
Can take months for vision to improve again
Managing tears stop 95% from detaching

131
Q

What is a squint (strabismus)?

A

Eyes don’t point in the same direction

132
Q

What are the types of squint?

A

Congenital/acquired - onset before/after 6 months
Concomitant/incomitant
Manifest/latent

133
Q

What is a concomitant squint?

A

Angle between eyes remain same through all positions of gaze

134
Q

What is a manifest squint?

A

Present when both eyes are open and being used

135
Q

What is a latent squint?

A

Present only when other eye is shut

136
Q

How can the angle between the eyes in a squint be described?

A

Exo - divergent angle
Eso - convergent angle
Hypo - downward deviation
Hyper - upward deviation

137
Q

What are concomitant squints associated with?

A

Poor fine motor skills
Hypermetropes or Anisometropia (different refraction in each eye)
Opacities

138
Q

What is accommodative esotropia?

A

Excessive inward turning of eye during accommodation

Need drops or patch to correct

139
Q

What tests can be done to examine concomitant squints?

A

Hirschberg’s - hold pen torch at arms length - see where light reflection lies

Cover/uncover - cover one eye and observe open eye while the other one is uncovered

Alternate cover test - focus on object with occluder rapidly switching between eyes

140
Q

When should concomitant squints be examined?

A

2 months of age if constant or progressive

141
Q

How are concomitant squints managed?

A

Correct refractive errors
<8 - correct any amblyopia

If all fails and squint large - surgery

142
Q

What usually causes incomitant strabismus?

A

Extra-ocular muscle or nerve damage

143
Q

How are incomitant squints managed?

A

If due to small vessel disease - conservative with CVS risk factor reduction for 6 months

Prisms can be fitted to glasses
Surgical correction may be needed

144
Q

How would a cranial nerve 3 palsy appear?

A

Eye down and out
Ptosis
Dilated pupil

145
Q

How would a cranial nerve 4 palsy appear?

A

Vertical diplopia

146
Q

How would a cranial nerve 6 palsy appear?

A

Eye in

147
Q

What is a hyphema?

A

Blood in the anterior chamber

148
Q

What can cause a hyphema?

A

Usually trauma
Sickle cell
Haemophilia

149
Q

How would hyphema’s present?

A

Painful

Can cause vision loss

150
Q

How would you manage a hyphema?

A

Steroid drops
Cyclopentolate - dilate pupil
Limited eye movement
Bed rest

151
Q

What is the main complication associated with a hyphema?

A

Raised IOP

152
Q

What is a hypopyon?

A

Pus in the anterior chamber

153
Q

What can cause a hypopyon?

A

Anterior uveitis
Behcet’s
Drug reaction - rifampicin

154
Q

what organism would you expect to be the cause of infectious keratitis in

a) contact lens wearer
b) general population
c) following exposure to dirty water

A

a) pseudomonas
b) staph aureus
c) amoebic

Neurology and Special Senses (28 decks)

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