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Y4 special senses, neurology & dermatology > Ophthalmology conditions > Flashcards

Ophthalmology conditions Flashcards

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1
Q

AMD

A

Progressive disease affecting the macula classified by a number of physical characteristics, in particular the number and consistency of drusen

Most common cause of blindness in the UK

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2
Q

AMD risk factors

A

Age - AMD increases with age

Smoking

Caucasian

Concomitant diseases - CVD, HTN

Ocular characteristics - light iris, hyperopia

Genetics - complement factor H, gene variant Y402H

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3
Q

Dry AMD

A

Less aggressive form, accounts for between 80-90% of all AMD

Initially no apparent symptoms but drusen present

Visual loss caused by atrophy or conversion to wet AMD

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4
Q

Wet AMD

A

New vessels develop from the choroid layer and grow into the retina (neovascularisation)

Vessels can leak fluid or blood, causing oedema and faster vision loss

VEGF stimulates the development of new vessels

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5
Q

AMD vs glaucoma

A

Glaucoma - associated with peripheral vision loss and halos around lights

AMD - associated with central vision loss and a wavy appearance to straight lines

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6
Q

AMD presentation

A

Unilateral

Gradual loss of central vision

Reduced visual acuity

Crooked or wavy appearance to straight lines (metamorphopsia)

Gradually worsening ability to read small text

Wet AMD presents more acutely than dry AMD → can progress to complete vision loss within 2-3 years & bilateral disease

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7
Q

AMD examination

A

Reduced visual acuity using a Snellen chart

Scotoma (enlarged central area of vision loss)

Amsler grid test - used to assess for the distortion of straight lines seen in AMD

Drusen may be seen in fundoscopy

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8
Q

AMD Ix

A

Slit lamp examination - detailed view of the retina and macula

Optical CT - used to diagnose and monitor AMD

Fluorescein angiography - assess retina blood supply → shows oedema & neovascularisation in wet AMD

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9
Q

AMD management

A

Require specialist ophthalmology assessment and management

No specific treatment for dry AMD, reducing risk of progression:

  • avoiding smoking
  • controlling BP
  • vitamin supplementation has some evidence in slowing progression

Wet AMD - anti-VEGF medications (eg. ranibizumab) block VEGF & slow the development of new vessels

  • injected directly into the vitreous chamber of the eye, usually about once a month
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10
Q

Charles Bonnet syndrome

A

Causes a person whose vision has started to deteriorate to see things that aren’t real

Brain doesn’t receive as much information as it used to and responds by filling in the gaps with fantasy patterns or images that it’s stored

Reassuring patients is essential to help them cope with hallucinations

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11
Q

Uveitis classification

A

Anatomical location - anterior (iris), intermediate (ciliary body), posterior (choroid)

Granulomatous vs non-granulomatous

Acute, recurrent or chronic

  • recurrent - more than 3 months
  • chronic - less than 3 months
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12
Q

Uveitis aetiology

A

Autoimmune - sarcoid, SLE, MS, Behcets, seronegative spondyloarthropathies, IBD

Infectious - CMV, HSV, HZV, candida, toxoplasma

Drug induced - bisphosphonates

Traumatic

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13
Q

Anterior uveitis clinical features

A

Symptoms - blurring of vision, pain, photophobia, redness of eye, floaters

Signs - keratic precipitates, cells in anterior chamber, fibrin in anterior chamber, flare in anterior chamber, posterior synechae (posterior part of the iris can get stuck to the lens during inflammation), cells in vitreous, choroiditis lesions, macular oedema

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14
Q

Uveitis investigations

A

Infectious vs non infectious

FBC, U&Es, LFT, Q Gold (TB), treponemal antibody (syphilis)

Other investigations dependent on suspected cause

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15
Q

Uveitis management

A

Anterior uveitis - topical steroids/subconjunctival steroids, cycloplegics

  • cycloplegics - dilate the pupil & reduce pain associated with ciliary spasm
  • topical steroids SE: ocular hypertension → glaucoma, posterior subcapsular cataract

Intermediate and posterior uveitis

  • local treatment: periocular steroids, intravitreal steroid implants
  • systemic treatment: pulse therapy, oral steroids, immunosuppression, aetiology specific antibiotic/antifungal/antiviral
    • SE of steroids: insomnia, weight gain, osteoporosis, hyperglycaemia, immunosuppression, hypertension
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16
Q

Anterior uveitis complications

A

Posterior synechiae

Pupillary membrane

Ocular hypertension/glaucoma

Hypotony → no treatment so will lead to blindness

Cataract

Cystoid macular oedema

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17
Q

Glaucoma

A

Glaucoma - refers to optic nerve damage (characteristic optic head changes), associated with corresponding visual field defects, with or without raised intraocular pressure

Raised pressure caused by a blockage in aqueous humour trying to escape the eye

Main cause of irreversible blindness in the world

Two types: open-angle glaucoma, acute angle-closure glaucoma

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18
Q

Open-angle glaucoma pathophysiology

A

Gradual increase in resistance to flow through the trabecular meshwork

Pressure slowly builds within the eye

Raised intraocular pressure causes cupping of the optic disc → cup-disk ratio > 0.5 is abnormal

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19
Q

Open-angle glaucoma risk factors

A

Increasing age

Family history

Black ethnic origin

Myopia (nearsightedness)

Eye injuries/eye operations

Ocular hypertension

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20
Q

Open-angle glaucoma presentation

A

Rise in intraocular pressure may be asymptomatic for a long time & diagnosed by routine eye testing

Glaucoma affects the peripheral vision first → gradual onset of peripheral vision loss (tunnel vision)

Fluctuating pain

Headaches

Blurred vision

Halos around lights, particularly at night

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21
Q

Measuring intraocular pressure

A

Non-contact tonometry: estimates intraocular pressure by opticians; involves shooting a ‘puff of air’ at the cornea

Goldmann applanation tonometry - gold-standard to measure intraocular pressure → involves a device mounted on a slip lamp that makes contact with the cornea & applies various pressures

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22
Q

Open-angle glaucoma diagnosis

A

Goldmann applanation tonometry

Slit lamp

Visual field assessment

Gonioscopy

Central corneal thickness

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23
Q

Open-angle glaucoma management

A

360 degrees selective laser trabeculoplasty → laser directed at the trabecular meshwork, improving drainage

  • may delay/prevent the need for eye drops

Next line: prostaglandin analogue eye drops (latanoprost) - increase uveoscleral outflow

  • SE: eyelash growth, eyelid pigmentation, iris pigmentation

Other eye drop options: beta-blockers, carbonic anhydrase inhibitors, sympathomimetics

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24
Q

Open-angle glaucoma surgery

A

360 degree selective laser trabeculoplasty (SLT) first line to people with an IOP > 24mmHg

Trabeculectomy may be considered in refractory cases

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25
Q

Acute angle closure glaucoma

A

Iris bulges forward and seals off the trabecular meshwork from the anterior chamber → prevents aqueous humour from draining & leads to continual increase in intraocular pressure

The pressure builds in the posterior chamber, pushing the iris forward & exacerbating angle closure

Ophthalmological emergency

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26
Q

Acute angle closure glaucoma risk factors

A

Long-sightedness

Increasing age

Family history

Female

Chinese and east asian ethnic origin

Shallow anterior chamber

Certain medications - adrenergic medication, anticholinergic medications, tricyclic antidepressants

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27
Q

Acute angle-closure glaucoma presentation

A

Appears generally unwell

Severely painful red eye

Blurred vision

Halos around lights

Associated headache, nausea & vomiting

Signs: red eye, hazy cornea, decreased visual acuity, mid-dilated pupil, fixed size pupil, hard eyeball on gentle palpation

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28
Q

Acute-angle closure glaucoma initial management

A

Immediate admission

Lie patient flat without a pillow

Pilocarpine eye drops

Acetazolamide 500mg orally

Analgesia & anti-emetic

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29
Q

Acute-angle closure secondary care management

A

Specialist medical options - pilocarpine eye drops, acetazolamide IV, timolol, brimonidine

Laser iridotomy = definitive treatment

  • relieves pressure pushing iris forward against the cornea & opens the pathway for the aqueous humour to drain
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30
Q

Central retinal artery occlusion

A

Sudden, painless loss of vision caused by occlusion of the central retinal artery

Less common than retinal vein occlusion

More proximal an occlusion is, the worse effect on vision

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31
Q

CRAO aetiology

A

Atherosclerosis

Embolism

Inflammatory

Thrombophilia

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32
Q

CRAO clinical features

A

Sudden-onset painless loss of vision typically occurring over seconds

History of amaurosis fugax (transient loss of vision)

O/E - pale retina with a ‘cherry red spot’ at the macula, may also have a RAPD

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33
Q

CRAO investigations

A

Fundoscopy & thorough H&E

Imaging - OCT & fluorescein angiography may also be utilised

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34
Q

CRAO management

A

Vision unlikely to improve with treatment beyond 90-100 minutes - only 30% of patients will have any improvement in vision after presentation

Aim is to reperfuse the ischaemic retina as quickly as possible:

  • ocular massage - aiming to dislodge the embolus
  • vasodilation with isosorbide dinitrate
  • anterior chamber paracentesis - reduce IOP to help dislodge the embolus
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35
Q

CRVO

A

Central retinal vein (or one of its branches) is occluded by a thrombus

More common than central retinal artery occlusion

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36
Q

CRVO risk factors

A

Atherosclerotic - age, smoking, obesity, hypertension, diabetes

Haematological - protein S, protein C or antithrombin deficiency, factor V Leiden, multiple myeloma, glaucoma, antiphospholipid syndrome

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37
Q

CRVO clinical features

A

Sudden, painless loss of vision/visual field defects

Ischaemic CRVO → must worse reduced visual acuity (6/60 or worse)

O/E - classic fundoscopy description is ‘stormy sunset’ with findings that include:

  • numerous flame haemorrhages
  • dot & blot haemorrhages
  • cotton wool spots
  • retinal oedema
  • dilated/tortuous retinal veins
  • visual field defects
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38
Q

CRVO investigations

A

Bloods - FBC, ESR, CRP, U&Es, LFTs, lipid profile, clotting screen

Further screening for thrombophilia if pt has a family history of clotting disorders

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39
Q

CRVO management

A

Immediate referral to ophthalmology

Conservative management

Retinal neovascularisation - laser photocoagulation

Macular oedema - intravitreal anti-VEGF injections

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40
Q

CRVO complications

A

Neovascularisation

Vitreous haemorrhage - new vessels are fragile and can bleed

Hyphaema - neovascularisation in the iris can lead to bleeding in the anterior chamber

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41
Q

Episcleritis

A

Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera

Relatively common in young & middle-aged adults, often associated with inflammatory disorders

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42
Q

Episcleritis clinical features

A

Localised/diffuse redness (often a patch of redness in the lateral sclera

No pain

Dilated episcleral vessels

No photophobia/discharge

Normal visual acuity

Applying phenylephrine eye drops → causes blanching episcleral vessels → causes redness to disappear

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43
Q

Episcleritis management

A

Self-limiting & will resolve in 1-2 weeks

Symptoms may be relieved with analgesia & lubricating eye drops

More severe cases → steroid eye drops

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44
Q

Scleritis

A

Inflammation of the sclera

Most severe type = necrotising scleritis → lead to perforation of the sclera

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45
Q

Scleritis aetiology

A

Idiopathic

Underlying systemic inflammatory condition - RA, vasculitis

Infection - pseudomonas or staph aureus

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46
Q

Scleritis clinical features

A

Gradual onset, can be unilateral or bilateral

Red, inflamed sclera

Congested vessels

Severe pain

Pain with eye movement

Photophobia

Epiphora (excessive tear production)

Reduced visual acuity

Tenderness to palpation of the eye

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47
Q

Scleritis management

A

Urgent assessment and management by an ophthalmologist

Oral NSAIDs

Steroids - topical or systemic

Immunosuppression appropriate to underlying systemic condition

Antimicrobials for infectious scleritis

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48
Q

Diabetic retinopathy

A

Involves damage to the retinal blood vessels due to prolonged high blood sugar levels

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49
Q

Diabetic retinopathy pathophysiology

A

Hyperglycaemia damages the retinal small vessels & endothelial cells

Increased vascular permeability → leading blood vessels, blot haemorrhages & hard exudates (deposits of lipids & proteins)

Damage to the blood vessel walls leads to microaneurysms and venous beading

Damage to nerve fibres → cotton wool spots

Intraretinal microvascular abnormalities (IRMA) refer to dilated and tortuous capillaries in the retina

Neovascularisation

50
Q

Diabetic retinopathy clinical features

A

Early stages may be asymptomatic

Floaters/dark spots in the vision

Blurred or distorted vision

Difficulty seeing at night

Sudden loss of vision

51
Q

Diabetic retinopathy grading

A

Background - microaneurysms, retinal haemorrhages, hard exudates & cotton wool spots

Pre-proliferative - venous beading, multiple blot haemorrhages, intraretinal microvascular abnormality (IMRA)

Proliferative - neovascularisation and vitreous haemorrhage

52
Q

Diabetic maculopathy

A

Exudates within the macula

Macular oedema

53
Q

Diabetic retinopathy complications

A

Vision loss

Retinal detachment

Vitreous haemorrhage

Rubeosis iridis (new blood vessel formation in the iris)

Optic neuropathy

Cataracts

54
Q

Diabetic retinopathy management

A

Non-proliferative diabetic retinopathy = close monitoring and careful diabetic control

Treatment options:

  • pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels
  • anti-VEGF injections
  • surgery (eg. vitrectomy) may be required in severe disease

Intravitreal implant containing dexamethasone → option for macular oedema

55
Q

Hypertensive retinopathy

A

Damage to the small blood vessels in the retina relating to hypertension

56
Q

Hypertensive retinopathy features

A

Silver wiring/copper wiring - walls of the arterioles become thickened & sclerosed

AV nipping - arterioles cause compression of the veins

Cotton wool spots

Hard exudates

Retinal haemorrhages

Papilloedema due to ischaemia to the optic nerve, resulting in the optic nerve swelling

57
Q

Hypertensive retinopathy mx

A

Focused on controlling BP & managing risk factors

58
Q

Conjunctivitis

A

Inflammation of the conjunctiva

May be bacterial, viral or allergic

59
Q

Conjunctivitis aetiology

A

Allergic conjunctivitis - type I hypersensitivity reaction to allergens in the environment (eg. pollen, dust mites, pet dander)

Viral conjunctivitis - adenoviruses, can also be herpes simplex

Bacterial conjunctivitis - staph aureus, strep pneumoniae, H, influenzae, Moraxella catarrhalis, STIs

60
Q

Conjunctivitis clinical features

A

Red, bloodshot eye

Itchy or gritty sensation

Discharge

  • bacterial: purulent, typically worse in the morning & eyes may be stuck together
  • viral: serous discharge
  • allergic: serous discharge

No pain, photophobia or reduced visual acuity

61
Q

Conjunctivitis management

A

Allergic - avoid allergens, antihistamines, topical mast-cell stabilisers

Viral - self-limiting, symptom relief & good hygiene practice

Bacterial - generally self-limiting, topical abx if severe

Patients should be advised to seek medical attention if condition worsens/fails to improve after a week of treatment

62
Q

Optic neuritis

A

Inflammation of the optic nerve, often resulting in visual impairment and ocular discomfort

63
Q

Optic neuritis aetiology

A

Demyelinating lesions - MS

Autoimmune disorders

Infectious conditions - particularly those affecting the CNS

64
Q

Optic neuritis clinical features

A

Visual loss

Periocular pain - pain around the eye, often aggravated by eye movement

Dyschromatopsia - impaired colour discrimination, especially involving red-green spectrum

65
Q

Optic neuritis ix

A

Visual function tests - visual acuity, colour vision, visual field

MRI head and spine

66
Q

Optic neuritis mx

A

IV methylprednisolone

67
Q

Cataracts

A

Characterised by an opacity in the lens, which is typically caused by denaturation of lens proteins

68
Q

Cataracts risk factors

A

Age

Smoking

Diabetes mellitus

Systemic corticosteroid use

Others: alcohol consumption, UV exposure, trauma, previous eye surgery, radiation exposure

69
Q

Cataracts clinical features

A

Gradual painless loss of vision

Difficulty reading/watching television

Difficulty recognising faces

Haloes around lights, particularly at night

Children → can present as a squint

Signs - loss of red reflex, brown/white appearance of lens on slit-lamp

70
Q

Cataracts ix

A

Slit-lamp biomicroscopy

71
Q

Cataracts mx

A

Surgical intervention → pseudophakia

  • removal of the lens affected by the cataract & its replacement with an artificial lens
  • most common surgical technique is phacoemulsification
72
Q

Complications of cataract surgery

A

Endophthalmitis - severe pain, loss of vision, hyperaemia, presenting within days of surgery. Immediate ophthalmological intervention is required

Posterior lens capsule opacification - few weeks post-surgery, characterised by blurry vision & visible white opacity. Can be easily treated with outpatient laser procedure

Rare → retinal detachment, macular oedema, glaucoma & corneal oedema

73
Q

Blepharitis

A

Various conditions which cause chronic inflammation of the eyelid margins

74
Q

Blepharitis aetiology

A

Staphylococcus infection

HSV or VZV infection

Meibomian gland dysfunction

Seborrheic dermatitis

Rosacea

75
Q

Blepharitis clinical features

A

Painful, gritty, itchy eyes

Eyelids sticking together upon waking

Dry eye symptoms

Erythema, crusting or scaling at eyelid margins

Visibly blocked Meibomian gland orifices

76
Q

Blepharitis management

A

Lid hygiene - at least twice a day

Avoidance of contact lens use during flare-ups

77
Q

Stye

A

Hordeolum externum - abscess at an eyelash follicle, commonly caused by staphylococcus

Hordeolum internum - abscess of the Meibomian gland

  • can lead to a chalazion if the gland becomes blocked
78
Q

Stye clinical features

A

Painful, red hot lump that points outwards causing localised inflammation

79
Q

Stye management

A

Warm compresses

OTC pain relief

Topical antibiotic ointments

Persistent cases → surgical intervention may be required to drain the abscess

80
Q

Chalazion

A

Occurs when a Meibomian gland becomes blocked and swells, often called a Meibomian cyst

81
Q

Chalazion clinical features

A

Swelling in the eyelid

Initially painful, but evolves into a non-tender swelling that points inwards

82
Q

Chalazion management

A

Warm compresses

Gentle massage towards the eyelashes (encourage drainage)

Rarely → surgical drainage

83
Q

Thyroid eye disease

A

Complication of Grave’s disease, which is an autoimmune hyperthyroidism

Inflammatory process results in swelling of the extraocular muscles and orbital fat, which leads to multiple ocular complications

84
Q

Thyroid eye disease pathophysiology

A

Evidence suggests an autoimmune reaction to TSH receptors results in lymphocyte infiltration into orbital tissues → initiates an inflammatory process

Inflammatory phase of TED typically lasts 6-24 months & results in the swelling of extraocular muscles & orbital fat

  • TED only responsive to medical management

After the inflammatory phase → inactive fibrotic phase

  • nonresponsive to medical therapy
85
Q

TED RFs

A

Smoking

Family history of Grave’s disease & other autoimmune disease

Female sex

Poor thyroid control

86
Q

TED clinical features

A

Ocular pain - often worse on movement

Dry, red eyes

‘bulging eyes’

Painful eyelids

Proptosis/exophthalmos

Lid retraction & lid lag

Chemosis

Orbital fat prolapse

Exposure keratopathy

87
Q

TED mx

A

Good control of thyrotoxicosis & other medical therapies, such as steroids or other immunosuppressants

Sight-threatening TED → urgent surgical orbital decompression may be required, followed IV corticosteroids

Conservative therapy → artificial tears, ointments & prisms

88
Q

TED complications

A

Exposure keratopathy - where corneal damage & infection occur as the patient is unable to close their eyes

Compressive optic neuropathy - retro-orbital swelling begins to compress on the optic nerve

Diplopia

89
Q

Preseptal cellulitis

A

Infection of tissue anterior to the orbital septum

Much more common than orbital cellulitis & 80% of cases occur in children < 10 years

90
Q

Preseptal cellulitis clinical features

A

Erythematous swollen eyelid

Mild fever

Erythema surrounding the orbit

Normal eye movements

Normal optic nerve function

91
Q

Preseptal cellulitis ix

A

Blood tests - FBC, CRP

Swabs - sent for M, C & S

CT orbit is the gold standard investigation to differentiate from orbital cellulitis

92
Q

Preseptal cellulitis mx

A

Young or systemically unwell children should be admitted for IV antibiotics

Otherwise, treatment is with oral antibiotics & daily outpatient review

93
Q

Orbital cellulitis

A

Sight and life threatening emergency

Describes infection of the structures behind the orbital septum

94
Q

Orbital cellulitis risk factors

A

Trauma

Surgical - ocular, adnexal or sinus

Sinus disease - ethmoidal sinusitis is most common site of infection that spreads to the orbit

Other facial infections - preseptal, dental abscess or dacryocystitis

95
Q

Orbital cellulitis clinical features

A

Periocular pain and swelling

Fever

Malaise

Erythematous, swollen and tender eyelid

Chemosis

Proptosis

Restricted eye movements +/- diplopia

96
Q

Orbital cellulitis ix

A

Blood tests - FBC, CRP

Swabs sent for M, C & S

CT orbit

97
Q

Orbital cellulitis mx

A

Admission for IV antibiotics

Close monitoring with input from the ophthalmology, ear, nose and throat & medical teams

98
Q

Infective keratitis

A

Inflammation of the cornea

99
Q

Infective keratitis aetiology

A

Viral - herpes simplex → most common cause of keratitis

Bacterial - Pseudomonas or Staphylococcus

Fungal - candida or aspergillus

Contact lens-induced acute red eye (CLARE)

Exposure keratitis (caused by inadequate eyelid coverage)

100
Q

HSV keratitis

A

Can cause inflammation in any part of the eye but most commonly affects the epithelial layer of the cornea

Primary or recurrent

  • recurrent = virus travelling to the trigeminal ganglion, where it becomes latent & can reactivate later

Inflammation of stroma (layer between the epithelium and endothelium) = stromal keratitis → associated with stromal necrosis, vascularisation & scarring

101
Q

HSV keratitis clinical features

A

Red, painful eye

Photophobia

Epiphora

Visual acuity may be decreased

Fluorescein staining -> epithelial ulcer

102
Q

HSV keratitis ix

A

Slit lamp examination

Fluorescein staining shows a dendritic corneal ulcer

Corneal scrapings can be used for viral testing

103
Q

HSV keratitis mx

A

Urgent assessment & management by an ophthalmologist

Topical/oral antivirals

Corneal transplant is an option to treat permanent scarring & vision loss after keratitis

104
Q

Retinal detachment

A

Neurosensory layer of the retina separates from the retinal pigment epithelium, usually due to retinal tear

Allows vitreous fluid to get into the neurosensory retina & fill the space between the layers

105
Q

Retinal detachment risk factors

A

Lattice degeneration (thinning of the retina)

Posterior vitreous detachment

Trauma

Diabetic retinopathy

Retinal malignancy

Family history

106
Q

Retinal detachment clinical features

A

Painless

Peripheral vision loss - sudden & shadow coming across the vision

Blurred or distorted vision

Flashes and floaters

107
Q

Retinal detachment mx

A

Detailed assessment to detect retinal tears & retinal detachment → immediate ophthalmology

Management of retinal tears aims to create adhesions between the retina & choroid:

  • laser therapy
  • cryotherapy

Management of retinal detachment aims to reattach the retina & reduce traction/pressure that may cause it to detach again:

  • vitrectomy - removing the vitreous fluid, fixing the tear & inserting gas/oil into the eye to hold the retina in place
  • scleral buckling - silicone ‘buckle’ to put pressure on the sclera from outside the eye, squashing the eye inwards to reconnect the layers of the retina
  • pneumatic retinopexy - injecting a gas bubble into the vitreous body & positioning patient so the gas bubble presses the separated layer back into place
108
Q

Pre-chiasmal field defects

A

Occur due to a lesion anterior to the optic chiasm

Unilateral & commonly occur due to damage of the retina/optic nerve → typically present with a scotoma/unilateral anopia

109
Q

Scotoma

A

Area of reduced vision in an otherwise normal visual field

Physiological scotoma = blind spot due to the optic nerve

Central scotoma = involves the macula leading to a defect in central vision

Abnormalities of the peripheral retina (retinal detachment) can lead to a peripheral enlarging scotoma

110
Q

Anopia

A

Absence of sight

One-half of vision = hemianopia

Complete anopia refers to the complete absence of vision

Pre-chiasmal field defects = anopia is unilateral (damage to optic nerve)

111
Q

Optic chiasm field defects

A

Characterised by bitemporal hemianopia

Loss of vision in both temporal fields (outer half of the visual field)

Pituitary tumour most common cause due to close proximity & subsequent compression

112
Q

Post-chiasmal field defects

A

May occur from a lesion anywhere along the visual pathway from the optic chiasm to the visual cortex in the occipital lobe

Bilateral

Commonly associated with stroke due to disruption of blood supply to the optic radiations/occipital cortex

113
Q

Homonymous hemianopia

A

Visual field defect involving either the two right or the two left halves of the visual fields of both eyes

Vascular causes - cerebral infarction or cerebral haemorrhage

Children - most common cause is a tumour

Right is due to lesion on left and vice versa

114
Q

Superior homonymous quadrantanopia

A

Visual field defect involving the two right/two left upper quadrants of the visual fields in both eyes

Lesion involving the temporal lobe optic radiations → stroke, tumour or demyelination

Accompanying features - aphasia, memory deficits, complex seizures, auditory & visual hallucinations

115
Q

Inferior homonymous quadrantanopia

A

Visual field defect involving the two right or two left lower quadrants of the visual fields in both eyes

Causes may include stroke, tumour or demyelination

Accompanying features: finger agnosia, acalculia, right-left disorientation, neglect & inattention

116
Q

Macular sparing

A

Refers to the preservation of central vision

Lesion of the occipital lobe causes isolated homonymous hemianopia with macular sparing

  • reason for this is due to bilateral representation of the macula in the occipital cortex (receives input from both the right and left occipital lobes)
117
Q

Abnormal pupil shape

A

Trauma to sphincter muscles in the iris (eg. during surgery)

Anterior uveitis can cause adhesions in the iris → irregular pupil shape

Acute angle-closure glaucoma → vertical oval pupil shape

Rubeosis iridis (neovascularisation in the iris) can distort shape of iris & pupil → associated with diabetic retinopathy

118
Q

Mydriasis (dilated pupil) causes

A

Congenital

Stimulants - cocaine

Anticholinergics - oxybutynin

Trauma

Third nerve palsy

Holmes-Adie syndrome

Raised IP

Acute angle-closure glaucoma

119
Q

Miosis (constricted pupil)

A

Horner syndrome

Cluster headaches

Argyll-Robertson pupil (neurosyphilis)

Opiates

Nicotine

Pilocarpine

120
Q

3rd nerve palsy (eye findings)

A

Ptosis

Dilated non-reactive pupil - 3rd nerve carries parasympathetic fibres that innervate the circular muscles of the iris

Divergent strabismus in the affected eye, with a ‘down and out’ position of the affected eye

Can be idiopathic

3rd nerve palsy that does not affect the pupil suggests a microvascular cause:

  • diabetes
  • hypertension
  • ischaemia

Full 3rd nerve palsy is caused by compression of the nerve:

  • trauma
  • tumour
  • cavernous sinus thrombosis
  • PCA aneurysm
  • raised IP
121
Q

Horner syndrome

A

Triad of ptosis, miosis & anhidrosis (loss of sweating)

Caused by damage to the sympathetic nervous system supplying the face

Location of Horner syndrome can be determined by the anhidrosis:

  • central lesions - anhidrosis of the arm, trunk & face
    • stroke, MS, swelling (tumours), syringomyelia
  • pre-ganglionic lesions - anhidrosis of the face
    • Pancoast tumour, trauma, thyroidectomy, top rib (cervical rib)
  • post-ganglionic lesions - no anhidrosis
    • carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache

Cocaine eye drops can be used to test for Horner - no pupil reaction seen

Low-adrenalin eye drops will dilate the pupil in Horner

122
Q

Argyll-Robertson pupil

A

Specific finding in neurosyphilis

Constricted pupil that accommodates when focusing on a near object but does not react to light

‘Prostitute’s pupil’

Y4 special senses, neurology & dermatology (7 decks)

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