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Year 4 - Neurology + Special Senses > Opthal - Gradual loss of vision > Flashcards

Opthal - Gradual loss of vision Flashcards

1
Q

What are cataracts?

A

Cataracts = Common eye condition where the lens of the eye progressively opacifies

Epidemiology:

  • Women > men
  • Incidence ↑ with age

Features:

  • ↓ visual acuity
  • faded colour vision (difficult to distinguish colours)
  • glare - lights appear brighter than normal
  • halos around lights
  • defect in red-reflex - cataract prevents light getting to retina thus preventing the red reflection of light off the retina

Investigations:

  • Opthalmoscopy w/ pupil dilation - normal fundus + optic nerve
  • Slit lamp exam - visibile cataracts
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2
Q

What is the most common cause of cataracts?

What other causes of cataracts are there?

A

Normal ageing process (commonest cause)

Other causes:

  • Smoking
  • High alcohol consumption
  • Diabetes
  • Long-term corticosteroids
  • Myotonic dystrophy
    • genetic muscular disorder, muscles contract and unable to relax - thus progressive atrophy + weakness
  • Radiation exposure
  • Trauma
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3
Q

How are cataracts managed?

A
  1. Non-surgical - stronger glasses / lenses, use brighter lighting (nothing can slow down the progression of cataracts)
  2. Surgery:
    1. commonest operation in the UK
    2. decision depends on; impact on QoL, degree of visual impairment
    3. remove cloudly lens + replace with artificial lens
    4. high success rate = 85-90% of pts achieve 6/12 post op
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4
Q

What are the complications of cataract surgery?

A

Complications are rare!

  • Bleeding - choroidal haemorrhage
  • Posterior capsule:
    • opacification (thickening of posterior lens capsule)
    • rupture
  • Endophthalmitis - inflammation of aqueous and/or vitreous humour
  • Retinal detatchment
  • Glaucoma
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5
Q

What is the difference between open-angle and closed-angle glaucoma?

A

Open-angle:

  • Iris IS NOT occluding trabecular network i.e. angle between cornea and iris is ‘open’
  • ↑ IOP is due to ↓ functional clearance of aqueous humour by the trabecular network –> build up of aqueous humour in the anterior chamber
  • Chronic, progressive condition

Closed-angle:

  • Iris IS occluding the trabecular network i.e. angle between cornea and iris is ‘closed’
  • ↑ IOP is due to blockage of trabecular network –> causing build up of aqueous humour in the anterior chamber
  • Acute, eye emergency!
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6
Q

What are the risk factors for primary open-angle glaucoma (POAG)?

A

Risk factors:

  • Genetics - 1st degree relatives of POAG pt have ~16% of POAG
  • Old age
  • Black pts
  • Myopia (short-sighted)
  • HTN
  • Diabetes
  • Corticosteroids
  • Thin cornea
  • Wearing tight collar and tie
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7
Q

What are the features of POAG?

A

Symptomless for a long period

Features of POAG:

  • progressive peripheral field loss - often nasal scotomas –> then ‘tunnel vision’ (see image for visual field loss)
  • ↓ visual acuity
  • Painless
  • Fundoscopy:
    • optic disc cupping (cup:disc ratio ↑ e.g. > 0.7)
    • pale optic disc
    • ‘bayonetting of vessels’ - vessels have kinks as they cross into the cup
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8
Q

How is POAG investigated?

A
  • Applanation tonometry e.g. Goldmann tonometer - to measure IOP ( 10-20 mmHg = normal)
    • involves flat-tipped cone coming into contact with cornea to measure pressure required to flatten
  • Central corneal thickness measurement
  • Gonioscopy
    • ​to assess anterior chamber depth and iridocorneal angle (between iris and cornea)
  • Slit lamp exam - may see optic nerve head damage e.g. cup:disc ratio > 0.7
  • Automated perimetry - assess visual fields
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9
Q

How is POAG managed?

A

Mainly with eye-drops!

  • 1st line = Prostaglandin analogue (PGA) eyedrop e.g. Latanoprost once daily
    • ​↑ uveoscleral outflow
    • Adverse effects: brown pigmentation of iris, ↑ eyelash length
  • 2nd line:
    • Beta-blocker
      • e.g. timolol, betaxolol
      • ↓ aqueous production
      • avoid in asthma + heart-block
    • Carbonic anhydrase inhibitor
      • e.g. dorzolamide
      • ↓ aqueous production
      • can cause Stevens–Johnson syndrome, toxic epidermal necrolysis
    • sympathomimetic eyedrop
      • e.g. brimonidine (alpha-2 adrenoreceptor agonist)
      • ↓ aqueous production + ↑ outflow
      • avoid if on MAO-inhibitors or TCAs
      • Adverse effects: hyperaemia
  • 3rd line = surgery / laser treatment
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10
Q

How is aqueous humour drained?

A

Drained via 2 mechanisms:

  1. Trabecular meshwork
    • located between iris and cornea
    • drains aqueous humour into Schlemm’s canal
    • drains ~90% of aqueous humour
    • is IOP dependent
  2. Uveoscleral drainage
    • drains ~10% of aqueous humour
    • is IOP independent
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11
Q

What are the risk factors for Acute close-angle glaucoma (AACG)?

A

Risk factors for AACG:

  • women
  • hypermetropia (long-sightedness)
  • pupillary dilatation
  • age - lens growth association with age
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12
Q

What are the features of AACG?

A

Features of AACG:

  • Unilateral Pain (can be severe) - may be ocular or progressive headache
  • ↓ visual acuity
  • symptoms worse with mydriasis (e.g. pupil dilation when watching TV in a dark room)
  • Red-eye + hard
  • Haloes around lights
  • ↑ IOP - typically > 40 mmHG
  • Semi-dilated, non-reacting pupil - iris ischaemia due to ↑ IOP can cause this
  • Dull / hazy cornea - due to corneal oedema
  • systemic upset may be seen:
    • nausea & vomiting
    • abdominal pain
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13
Q

How is AACG managed?

A
  • Urgent referral to opthalmologist
  • 1st line:
    • carbonic anhydrase inhibitors e.g. dorzolamide (eyedrop) or acetazolamide (oral)
      • ↓ aqueous secretions
      • topical > oral
    • beta-blockers e.g. timolol or betaxolol (eyedrops)
    • Alpha2 adrenergic agonist e.g. bromonidine (eyedrops)
  • Adjunct:
    • Pilocarpine - if AACG is 2ndary to pupillary block
      • muscarinic ACh receptor agonist
      • pupillary contriction –> increases space for flow of aqueous humour
    • Mannitol - osmotic agent, draws fluid into vasculare compartment
      • ↓ IOP + ↓ intracranial pressure
      • ↓ blood viscosity –> ↑ cerebral blood flow –> autoregulatory vasocontriction which may ↓ ICP
  • 2nd line:
    • Laser peripheral iridotomy - laser hole in iris to equalise pressure between posterior + anterior chamber (relieves pupillary block)
      • This is also done prophylactically in the other eye if it has signs of ↑ IOP
    • Anterior chamber paracentesis
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14
Q

What is the commonest cause of blindness in the UK?

A

Age-realted macular degeneration

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15
Q

What is age-related macular degeneration (ARMD)?

A

Degeneration of the central retina (macula), usually bilaterally

  • Characterised by degeneration of retinal photoreceptors that results in the formation of drusen (seen on fundoscopy)
    • Drusen = yellow lipid deposits under the retina (see image)
  • Avg age on onset > 70yrs
  • Women > men
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16
Q

What are the risk factors for ARMD?

A

Risk factors:

  • AGE!! (biggest factor)
  • Smoking
  • 1st degree relatives with ARMD
  • cataract surgery
  • Risk factors for ischaemic heart disease:
    • HTN
    • Dyslipidaemia
    • Diabetes
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17
Q

What are the features of macular degeneration?

A

Features:

  • Progressive loss of vision in 1 or both eyes
  • Subacute blurring or distortion of vision (indicates ‘wet’ form)
  • ↓ visual acuity (particularly for close objects)
  • ↓ night vision and ability to adapt to dark
  • fluctuations in visual disturbance (varies day-to-day)
  • may experience photopsia (perception of flickering or flashing lights) + glare around objects

Signs:

  • Distortion of lines on Amsler grid testing (see image)
  • Drusen on fundoscopy
  • Demarcated red patches (intra-retinal or sub-retinal haemorrhage or fluid leak - seen in ‘wet’ ARMD)
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18
Q

How do you investigate macular degeneration?

A
  • Slit lamp exam + colour fundus photography
    • Identify exudative or haemorrhagic changes (‘wet’ ARMD)
  • Fluorescein angiography
    • Identify neovascular ARMD (used to be called ‘wet’) - neovascularisation can indicate anti-VEGF therapy
  • Ocular coherence tomography
    • Provides 3D image of retina to identify pathology not seen with microscopy alone
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19
Q

What are the types of ARMD?

A
  1. Early age-related macular degeneration (dry / non-exudative):
    • Drusen present
    • Alterations to retinal pigment epithelium
    • 90% of cases
  2. Late age-related macular degeneration (wet / exudative):
    • Choroidal neovascularisation
    • Leakage of serous fluid / haemorrhages
    • 10% of cases
    • Worse prognosis
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20
Q

How is ARMD managed?

A
  • Refer to retinal specialist opthalmologist
  • Risk factor modification:
    • smoking cessation
    • low glycaemic index diet (avoid diabetes)
    • ↓ cholesterol
    • managed HTN
  • Zinc, anti-oxidant vitamins A, C + E, copper:
    • For moderate ‘dry’ ARMD - shows some benefit in reducing progression
  • anti-VEGF:
    • can limit progression in ‘wet’ AMRD
    • administer in < 2 months of diagnosis
    • given as 4-weekly injection
    • e.g. ranibizumab, bevacizumab and pegaptanib
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21
Q

Who must pts diagnosed with POAG inform of their diagnosis?

A
  1. Family - there is a genetic risk component for glaucoma
  2. DVLA
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22
Q

What sign does this image show?

A

Cherry Red spot

(sign of central retinal artery occlusion)

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23
Q

What are the most common causes of sudden, painless loss of vision?

A
  • Ichaemic / vascular e.g. occlusion of central retinal artery / vein
    • large artery disease e.g.
      • atherothrombosis
      • embolus
      • dissection
    • small artery occlusive disease e.g.
      • anterior ischemic optic neuropathy - occlusion of short posterior ciliary arteries –> causing dmg to optic nerve
      • vasculitis (e.g.) temporal arteritis
    • venous disease
    • hypoperfusion
  • vitreous haemorrhage
  • retinal detachment
  • retinal migraine - aura of only one eye (can include temporary blindness)
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24
Q

What is the medical term for sudden, painless, loss of vision?

A

Amaurosis fugax

Define: painless, temporary loss of vision in one or both eyes

  • N.B. a minority of pts describe this as the classic “black curtain descending”
25
Q

What are the causes and features of central retinal artery occlusion?

A

Cause:

  • thromboembolism (due to atherosclerosis)
  • arteritis (e.g. temporal arteritis / giant cell)

Features:

  • sudden, painless loss of vision
  • RAPD
  • fundoscopy - ‘cherry red’ spot on pale retina
26
Q

What are the causes and features of vitreous haemorrhage?

A

Causes:

  • diabetes
  • bleeding disorders
  • anticoagulants

Features:

  • sudden, painless loss of vision
  • dark spots or floaters
27
Q

What are the causes and features of retinal detachment?

A

N.B. retinal detachment has different forms which can present acutely or chronically

Causes:

  • posterior vitreous detachment
  • choroidal tumours
  • trauma
  • myopia (risk factor)

Features:

  • dense shadow
    • starts peripherally and progresses toward central vision
    • feels like ‘veil or curtain’ over field of vision
  • straight lines appear curved
  • central vision loss
  • photopsia - i.e. flashes of light (often seen in temporal visual field)
  • floaters
28
Q

What are the causes and features of central retinal vein occlusion?

A

N.B. central retinal vein occlusion is more common than central retinal artery occlusion

Causes:

  • glaucoma
  • polycythaemia
  • HTN

Features:

  • sudden, painless loss of vision
  • fundoscopy - severe retinal haemorrhages
29
Q

What does the central retinal artery supply?

What do the posterior ciliary arteries supply?

A
  • Central retinal artery = retina
  • Posterior ciliary arteries:
    • short posterior ciliary artieries (6-12 per eye) = choroid up to equator + ciliary processes
    • long posterior ciliary artieries (2 per eye) = iris, ciliary body and choroid
30
Q

What is orbital cellulitis?

A

Infection affecting the fat + muscles posterior to the orbital septum, within the orbit but not the globe

  • Cause - often caused by spreading URTI from sinuses
  • HIGH mortality = EMERGENCY!!
  • Periorbital cellulitis = superficial infection anterior to orbital septum (less serious but can progress to orbital cellulitis)
  • Avg age of hospitalisation = 7-12yrs
31
Q

What are the risk factors for orbital cellulitis?

A

Risk factors:

  • Childhood
  • Previous sinus infection
  • Lack of Haemophilus influenzae type b vaccination
  • Recent infections:
    • eyelid infection / insect bite on eyelid (peri-orbital cellulitis)
    • ear infection
    • facial infection
32
Q

What are the features of orbital cellulitis?

*

A

Features:

  • Red eye + swelling around the eye
  • Eyelid oedema and ptosis
  • Proptosis (i.e. protrusion of eyeball)
  • Severe ocular pain
  • Visual disturbance (↓ visual acuity + RAPD)
  • Ophthalmoplegia / pain with eye movements
  • Drowsiness
  • Nausea / vomiting in meningeal involvement (Rare)
33
Q

What symptoms differentiate orbital cellulitis from periorbital / preseptal cellulits?

A

The following are NOT consistent with periorbital / preseptal cellulits:

  1. ↓ visual acuity
  2. proptosis
  3. ophthalmoplegia / pain with eye movements
34
Q

What do you see in this image?

A

Endophthalmitis (rare)

(i.e. infection of intraocular fluids i.e. vitreous and/or aqueous)

  1. Injected conjunctiva (red + bloodshot)
  2. Pus in anterior chamber
    1. Hypopyon = inflammatory accumulation of WBC (leukocytic exudate) seen as white ‘fluid level’ in anterior chamber + redness of conjunctiva
  3. Corneal sutures (top left)

Risk factors associated with endophthalmitis:

  • Poorly controlled diabetes (↑ infection risk)
  • Painful sudden visual loss (is their eye at risk?)
  • Hx of recent ocular surgery (surgery caused infection)
  • ITU / HDU admission
  • IV lines / catheters
35
Q

What are the features of anterior uveitis?

A

Features:

  • acute onset
  • red-eye
  • eye pain
  • blurred vision
  • photophobia (often intense)
  • hypopyon
  • small, fixed, oval pupil
  • ciliary flush - ring of red or violet spread out from around cornea
36
Q

What conditions is anterior uveitis associated with?

(5 listed)

A
  • ankylosing spondylitis
  • reactive arthritis
  • IBD i.e. ulcerative colitis & Crohn’s disease
  • Behcet’s disease (autoimmune vasculitis, triad: oral ulcers, genital ulcers and anterior uveitis)
  • sarcoidosis: bilateral disease may be seen
37
Q

What structures does uveitis affect?

A

Anterior:

  • Iris
  • Ciliary body

Posterior:

  • Choroid
38
Q

What are the features of conjunctivitis?

A

Features:

  • Red-eye
  • Recent exposure to others with infected eye
  • Recent URTI (more likely viral)
  • Allergen exposure (allergic conjunctivitis)
  • Discharge
    • watery = viral
    • mucoid = allergic
    • purulent = bacterial
  • Itchy (allergic)
  • Eyes stuck together in morning
  • Pre-auricular lymphadenopathy (viral)
  • Normal; visual acuity, reactive pupils
39
Q

What are the risk factors for conjunctivitis?

A

Risk factors:

  • Exposure to infected person
  • Infection in one eye (can spread to other)
  • Atopy
  • Contact lens use
  • Topical eye medication
  • Hx of rheumatological disease
40
Q

What investigations might you do for conjunctivitis?

A
  1. Chlamydial swabs - chlamydia can cause a reactive arthritis which has a triad of:
    • urethritis
    • conjunctivitis
    • arthritis
  2. Bacterial swabs
  3. Viral swabs
41
Q

What test can be used to investigate the condition of the cornea?

A

Fluorescein

  • Is an orange-water soluable dye, used IV (angiogram) and topically for cornea examination
  • Fluorescein - can be used to identify regions of corneal epithelium loss:
    • Intact corneal epithelium = not stained
    • Deeper corneal stroma = stained
  • Image shows dendritic ulcer in corneal stroma highlighted by fluorescein
42
Q

For a dendritic ulcer - what is the likely pathogen?

A

Herpes simplex virus (HSV)

  • HSV is enveloped with a cuboidal capsule and has a linear double-stranded DNA genome
  • HSV resides in almost all neuronal ganglia
  • Sub-types:
    • HSV 1 - causes infection above the waist (principally the face, lips and eyes)
    • HSV 2 - causes venereally-acquired infection (genital herpes)
43
Q

What medication can be used in the management of HSV?

A

Aciclovir - (antiviral)

44
Q

Which organisms commonly cause bacterial conjunctivitis?

A
  • Streptococcus. pneumoniae
  • S. aureus,
  • Haemophilus. influenzae
  • Moraxella catarrhalis
45
Q

What might be involved in the management of conjunctivitis?

A

Most (~60%) cases resolve without treatment in 1-2 weeks

  • Chloramphenicol (topical Abx):
    • Eye drops - 1 drop 3-4 times per day and for 48hrs after healing
    • Ointment - apply QDS
  • Topical lubricants
  • Cool compress
  • DON’T wear contact lenses until 48hrs after complete resolution
  • Avoid sharing towels
46
Q

What does this image show?

A

Bacterial keratitis causing a corneal ulcer (white circle)

  • Keratitis = red eye, pain, ↓ eye-sight, photophobia, ‘gritty’ sensation
  • Avoid contact lens wear
  • Treatment = frequent topical broad-spectrum Abx
  • Contraindicated: steroid eye drops, oral abx
47
Q

What is not included in the management of severe contact lens related keratitis?

  • Oral antibiotics
  • Daily review
  • Corneal Scrape
  • Frequent topical broad-spectrum antibiotics
  • requent Chloramphenicol drops
A

Frequent Chloramphenicol drops

  • Pseudomonas Aeruginosa is the most frequent bacteria associated with contact lens wear and it’s not sensitive to Chloramphenicol
48
Q

What can cause a 6th CN palsy?

A
  • Microvascular:
    • Diabetes
    • Atherosclerosis
    • Smoking
  • Trauma
  • Idiopathic
  • ↑ ICP
  • GCA
  • Cavernous sinus mass
  • MS
  • Sarcoidosis
  • LP
  • Hydrocephalus
  • Idiopathic intracranial hypertension
49
Q

What are the features of a 6th CN palsy?

A
  • Sudden onset, Horizontal Diplopia - worse when looking toward the affected side
    • Pts often turn hear to affected side to compensate by maintaing binocular vision
  • Esotropia (i.e. convergent squint) - during distance fixation the affected eye om directed medially
  • Lateral rectus palsy on affected side
50
Q

Is a 6th CN palsy an indication for urgent neuro-imaging?

A

NO!!

Commonly caused by microvascular pathologies e.g. diabetes, atherosclerosis etc.

51
Q

Is a 3rd CN palsy an indication for urgent neuro-imaging?

A

Yes!!

Especially if w/ sudden pain as it can be a sinister cause e.g.

aneurysm

52
Q

What are the features of a 3rd CN palsy?

A
  • Affected eye = deviated laterally + inferiorly i.e. ‘down and out’
  • Ptosis (CN III innervates levator palpebrae superioris)
  • Dilated pupil (CN III caries parasympathetic fibres for pupil constriction)
53
Q

What can cause a 3rd CN palsy?

A
  • Diabetes
  • Vasculitis e.g. temporal arteritis
  • Posterior communicating artery aneurysm
    • Pupil dilated
    • Often painful
  • Cavernous sinus thrombosis
  • Weber’s syndrome = ipsilateral 3rd nerve palsy + contralateral hemiplegia (midbrain stroke)
  • MS
  • Amyloidosis
54
Q

What are the features of a 4th CN palsy?

A
  • Vertical diplopia
  • Torsional diplopia - subjective tilting of objects
  • Eye - deviates superiorly + rotated laterally
  • May have head tilt (might not be aware)
  • classically noticed when reading a book or going downstairs
55
Q

Can pts with double vision drive?

A

No!!

  • Group 1 licence (cars):
    • Pts can return to driving after a period of adaptation or if double revision resolves
    • Pt can drive is double vision is controlled with prisms or occlude (patch) one eye (assuming vision is remaining eye is 6/12 and good fields)
  • Group 2 licence (HGV /buses) = never!
56
Q

What does Leukocoria mean?

A

Leukocoria = ‘White Pupil’

  • Is a concerning sign (especially in children)
  • It indicates absence of the red-reflex = opacity of optical media (anterior chamber, humour, lens, vitrous chamber)
  • It can be a sign of Retinoblastoma - needs to be exluded URGENTLY!
57
Q

What is a Retinablastoma + what are it’s features?

A

Retinablastoma = most common ocular malignancy in children (still rare)

  • Avg age of diagnosis = 18 months
  • ~ 40% are hereditary - autosomal dominant - LoF of retinoblastoma tumour supressor gene on chromosome 13

Features:

  • Leukocoria (white pupil) - absence of red-reflex (commonest symptom)
  • Strabismus - eyes don’t align with each other
  • Visual problems
58
Q

What is retinopathy of prematurity (ROP)?

A

ROP - is a proliferative retinopathy affecting premature infants of low birth weight, who have often been exposed to high ambient O2 concs.

Risk factors:

  • Either of the following = screen at 4-7 weeks posnatally for ROP:
    • born at or before 31 weeks
    • born 1500g or less
  • ~8% of babies screened require treatment (laser photocoagulation - successful in ~ 80% of cases)

​Mechanism:

  • Retina doesn’t start being vascularised until 4/12 gestation
  • Retinal nasal periphery is vascularised at 8/12 gestation
  • Retinal temporal periphery is vascularised at ~ 1 mo after delivery
  • Incompletely vascularized retina = susceptible to O2 dmg in premature infant
  • Normally - avascular retina produces VEGF –> stims vessel migration/growth
  • But if born premature + O2 therapy –> the VEGF is down-regulated as retina experiences hyperoxia –> then as the infant grows at home the metabolic demand of the eye ↑ –> causing excessive VEGF production –> neovascular proliferative retinopathy
59
Q

Congenital cateracts are rare (3 in 10,000 birth) + take many forms

e.g. dense large areas to fine blue dots.

Name 5 syndromes / microorganisms associated with congenital cataract formation.

A
  1. Rubella
  2. Varicella
  3. Cytomegalovirus
  4. Edward syndrome
  5. Down syndrome

Year 4 - Neurology + Special Senses (12 decks)

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