Ophthalmology Flashcards

1
Q

Myopia

Pathology (2)

A

Eyeball too long (short sight)

Only close objects focus on retina unless concave glasses used

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2
Q

Myopia

Glasses (2)

A

Myopia worsens but changes stop below 6 dioptres in most, so must have regular checks as expect prescription changes every 6 months
Avoid over-correction as can make it worse

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3
Q

Hypermetropia

Pathology (4)

A

Eyeball too short (long sight)
Distant objects focused behind retina
The ciliary muscles contract and the lens gets more convex to focus the object on the retina
Can produce tiredness of gaze and sometimes a convergent squint in children

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4
Q

Hypermetropia

Glasses (1)

A

Convex lenses to bring the image forward to focus on the retina

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5
Q

Presbyopia

Pathology (3)

A

The ciliary muscle reduces tension in the lens, allowing it to get more convex, for close focusing
With age, the lens stiffens (presbyopia), hence the need for glasses for reading
Changes start in the lens at 40 and are complete by 60

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6
Q

Presbyopia

Management (2)

A

Laser surgery to correct refraction

Process of ageing means that glasses may still be required as ageing continues

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7
Q

Astigmatism

Pathology (3)

A

Cornea doesn’t have the same degree of curvature and becomes an irregular surface (usually one half is flatter/steeper than the other half)
When light rays strike the cornea, they don’t focus together in one point, and produce a blurred image either longitudinally or vertically
Can occur alone or be associated with myopia/hypermetropia

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8
Q

Astigmatism

Glasses (1)

A

Correcting lens to compensate

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9
Q
Visual Field Defects 
Optic nerve (4)
A

Having a complete lesion on the optic nerve causes total blindness of that eye
Absent direct pupillary reflex
Intact indirect pupillary reflex
Acuity affected

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10
Q
Visual Field Defects 
Optic chiasm (3)
A

Lesions cause bitemporal hemianopia
Due to the fibres coming from the nasal halves of both retinas are involved
Normal direct, consensual and accommodative light reflexes

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11
Q
Visual Field Defects 
Optic tracts (3)
A

Causes contralateral homonymous hemianopia
Eg. right sided optic tract lesion causes a left temporal hemianopia
Normal direct light reflexes

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12
Q

Visual Field Defects

Causes (4)

A

Ischaemia (TIA, migraine, stroke)
Glioma
Meningioma
Abscess

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13
Q

Episcleritis

Definition (1)

A

Inflammation below the conjunctiva in the episclera, often seen with an inflammatory nodule

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14
Q
Episcleritis
Risk factors (3)
A

Female
SLE
Rheumatic fever

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15
Q

Episcleritis

Signs + symptoms (5)

A

Acute onset
Sclera looks blue below a focal cone-shaped wedge of enlarged vessels that can be moved over the area
Dull eye ache
Tender, eye, especially over inflamed area
Acuity usually fine

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16
Q

Episcleritis

Treatment (1)

A

Symptomatic relief with artificial tears and topical/systemic NSAIDs

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17
Q

Scleritis

Definition (2)

A

Generalised inflammation of the sclera with oedema of the conjunctiva, scleral thinning and vasculitic changes
50% of patients have associated systemic disease (typically rheumatoid arthritis or granulomatosis with polyangitis)

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18
Q

Scleritis

Signs + symptoms (6)

A

Constant severe dull ache
Ocular movements painful since the muscles insert into the sclera
Headache
Photophobia
Reduced acuity suggests dangerous pathology
Red eye

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19
Q

Scleritis

Treatment (3)

A

Urgent referral
NSAIDs
Prednisolone

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20
Q

Uveitis

Aetiology (3)

A

Anterior: ankylosing spondylitis, Still’s disease, IBDM, reactive arthritis, TB, syphilis, HIV, sarcoidosis
Intermediate: MS, lymphoma, sarciodosis
Posterior and panuveitis: HSV, TB, lymphoma, sarcoidosis

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21
Q

Uveitis

Pathology (3)

A

Anterior: inflammation of iris (most common)
Intermediate: inflammation of vitreous
Posterior: inflammation of choroid

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22
Q

Uveitis

Signs + symptoms (6)

A

Pain
Blurred vision
Photophobia
Increased lacrimation (but NO sticky discharge, unlike conjunctivitis)
Pupil may be small, initially from iris spasm, later it may be irregular/dilate irregularly due to adhesions between lens and iris
Red eye

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23
Q

Uveitis

Investigations (2)

A

Slit lamp to visualise inflammatory cells location (leucocytes in the anterior uveitis, think posterior uveitis if not seen)
Ocular imaging eg. fundus fluorescein to examine for retinal and choroidal disease

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24
Q

Uveitis

Treatment (2)

A

0.5-1% prednisolone drops to reduce inflammation

1% cyclopentolate to relieve spasm of ciliary body and adhesions between lens and iris to keep pupil dilated

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25
Q

Uveitis

Complications (3)

A

Prolonged visual loss in 2/3
22% meet criteria for blindness
Cystoid macular oedema and cataracts

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26
Q

Acute Closed-Angle Glaucoma

Aetiology (2)

A

Primary: anatomical predisposition
Secondary: arises from pathological processes eg. traumatic haemorrhage pushing the posterior chamber forwards

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27
Q

Acute Closed-Angle Glaucoma

Pathology (2)

A

Normally, aqueous humour is produced by the ciliary body and flows through the pupil and empties out at the drainage angle through the canal of Schlemm
Any structural change to this angle will block the flow and raise intra-ocular pressure (normal is 15-20)

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28
Q
Acute Closed-Angle Glaucoma
Predisposing factors (4)
A

Shallow anterior chamber
Thick lens
Thin iris
Hypermetropic eye

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29
Q

Acute Closed-Angle Glaucoma

Signs + symptoms (3)

A

Generally unwell with nausea and vomiting
Uniocular attack of headache and painful red eye
Often preceded by blurred vision or haloes around lights at night

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30
Q

Acute Closed-Angle Glaucoma

Investigations (1)

A

Urgent gonioscopy (must avoid eye patches or dark rooms which will worsen the angle closure by pupillary dilatation)

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31
Q

Acute Closed-Angle Glaucoma

Treatment (6)

A

Triad of B-blockers + pilocarpine + acetazolamide
B-blocker: timolol to suppress aqueous humour production (drops)
Pilocarpine: to induce miosis and open blocked, closed drainage angle (drops)
Acetazolamide: reduce aqueous formation (oral/IV)
Analgesia + anti-emetics
Laser/surgical peripheral iridectomy: do once IOP is controlled, a piece of iris is removed at 12 o’clock in both eyes to allow aqueous flow

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32
Q

Acute Closed-Angle Glaucoma

Complications (3)

A

Visual loss
Central retinal artery/vein occlusion
Repeated episodes in either eye

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33
Q

Conjunctivitis

Non-infectious causes (2)

A

Allergic conjunctivitis most frequent

Contact lens wearers may develop reaction

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34
Q
Conjunctivitis
Infectious causes (2)
A

Non-herpetic viral (serous discharge), most common, 80% are adenoviruses
Bacterial (purulent discharge)

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35
Q

Conjunctivitis

Signs + symptoms (6)

A
Conjnctiva red and inflamed
Hyperaemic vessels may be moved over the sclera by gentle pressure on the globe 
Acuity, pupillary responses unaffected 
Eyes, itch, burn and lacrimate 
Often bilateral 
Discharge sticks lids together
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36
Q

Conjunctivitis

Investigations (1)

A

Conjunctival cultures only needed if suspect gonococcal/chlamydial infection, neonatal conjunctivitis or recurrent disease not responding to therapy

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37
Q

Conjunctivitis

Treatment (3)

A

Most cases are viral and only need symptomatic relief with artificial tears and topical antihistamines, viral conjunctivitis is highly contagious
Bacterial tends to be self-limiting but topical antibiotics reduce duration and transmission (chloramphenicol)
For allergic, try antihistamine drops

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38
Q

Corneal Abrasion

Aetiology (3)

A

Trauma
Contact lenses
Previous corneal disease

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39
Q

Corneal Abrasion

Signs + symptoms (4)

A

Pain
Photophobia
May have reduced visual acuity
Lacrimation

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40
Q

Corneal Abrasion

Investigations (2)

A

Fluorescein drops and blue light- abrasions stain green

Check for foreign bodies

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41
Q

Corneal Abrasion

Treatment (2)

A

Local anaesthetic drops eg/ tetracaine

Send home with analgesics, chloramphenicol ointment for lubrication and compression pads

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42
Q

Corneal Ulcer

Aetiology (4)

A

Bacterial
Herpetic
Fungal
Vasculitic eg. in RA

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43
Q

Corneal Ulcer

Signs + symptoms (3)

A

Eye pain
Photophobia
Eye watering

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44
Q

Corneal Ulcer

Treatment (1)

A

Antibiotic drops

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45
Q
Sudden Painless Loss of Vision
Differential diagnoses (8)
A

Optic neuropathies (usually monocular vision loss with a central scotoma and afferent defect)
Anterior ischaemic optic neuropathy (optic nerve damage when posterior vascular supply to it is blocked by inflammation/atheroma)
Giant cell arteritis (may be transient- amaurosis fugax, before permanent)
Optic neuritis (affects colour vision, afferent defect, often a precursor to MS)
Central retinal artery occlusion (uncommon, dramatic loss within seconds, type of stroke, retina white with cherry red spot at macula)
Retinal vein occlusion (central or branch)
Vitreous haemorrhage
Retinal detachment

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46
Q

Retinal Vein Occlusion

Definition (1)

A

2nd most common cause of blindness from retinal vascular disease (diabetic neuropathy is 1st)

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47
Q

Retinal Vein Occlusion

Aetiology (4)

A

Arteriosclerosis
High BP
Diabetes
Glaucoma

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48
Q

Retinal Vein Occlusion

Pathology (3)

A

If the whole central retinal vein is thrombosed, there is visual loss
Less sudden than central retinal artery occlusion
Visual loss may be perceived as sudden by patient but the mechanism of visual loss is due to the development of ischaemia and macular oedema

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49
Q

Retinal Vein Occlusion

Investigations (1)

A

Fundus fluorescein angiogram determines the degree of ischaemia and to give pan-retinal photcoagulation is given to prevent/treat neovascularisation

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50
Q

Retinal Vein Occlusion

Treatment (3)

A

1st anti-VEGF
2nd dexamethasone implant or intravitreal triamcinolone acetonide
Photocoagulation if retinal neovascularisation has started to develop

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51
Q

Central Retinal Vein Occlusion

Pathology (1)

A

Occurs at level of optic nerve and will present with sudden onset painless blurred vision in one eye (never asymptomatic)

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52
Q

Central Retinal Vein Occlusion

Classification (2)

A

Non-ischaemic: more common, better acuity and prognosis but 30% convert to ischaemic
Ischaemic: with cotton wool spots, swollen optic nerve, macular oedema and risk of neovascularisation

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53
Q

Branch Retinal Vein Occlusion

Pathology (1)

A

Can be asymptomatic if the macula isn’t affected, but most complain of visual deficits corresponding to the area of occlusion

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54
Q

Vitreous Haemorrhage

Pathology (2)

A

Arise from neovascularisation (DM, branch retinal/central retinal vein occlusion), retinal tears, retinal detachment or trauma
Small extravasations of blood produce vitreous floaters

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55
Q

Vitreous Haemorrhage

Signs + symptoms (4)

A

Sudden, painless loss of vision or haze
Floaters
Shadows/dark spots in vision
Decreased visual acuity depending on size, location and degree

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56
Q

Vitreous Haemorrhage

Treatment (2)

A

Usually spontaneously absorbs

If dense, vitrectomy to remove blood if retinal tear or detachment

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57
Q

Gradual Loss of Vision

Differentials (6)

A
Cataract 
Macular degeneration 
Glaucoma (primary open angle) 
Diabetic retinopathy 
Optic atrophy 
Slow retinal detachment
58
Q

Macular Degeneration

Pathology (2)

A
Pigment drusen (signifies optic nerve-head axonal degeneration and calcium deposits) and sometimes bleeding at the macula 
Over time it progresses to retinal atrophy and central retinal degeneration which causes a loss of central vision
59
Q
Macular Degeneration
Risk factors (5)
A
Age
Smoking 
Cardiovascular disease 
Family history 
Cataract surgery
60
Q

Macular Degeneration

Signs + symptoms (5)

A

Initially there is no deterioration in visual acuity but difficulty making out images due to failing contrast
Difficulty with reading and making out faces
Difficulty with night vision and changing light conditions
Visual fluctuation (some days it is ok)
Metamorphosia (distortion of visual images)

61
Q

Macular Degeneration
Wet age related macular degeneration (exudative)
(4)

A

Pathological choroidal neovasular membranes develop under the retina, they can leak fluid and blood causing a central disciform scar
Vision deteriorates rapidly and distortion is a key feature (over months)
Ophthalmoscopy shows fluid exudation, localised detachment of the pigment
Treat with anti-VEGF, laser photocoagulation, intravitreal steroids

62
Q

Macular Degeneration
Dry age related macular degeneration (non-exudative)
(3)

A

Much slower, progressive visual loss (over decades)
Ophthalmoscopy shows mainly drusen and changes at the macula
Treatment: preventive and mineral supplements

63
Q

Optic Atrophy

Ophthalmoscopy (1)

A

Pale discs

64
Q

Optic Atrophy

Causes (3)

A
Increased intraocular pressure (glaucoma) 
Retinal damage (choroiditis, retinitis pigmentosa) 
Ischaemia (retinal artery occlusion)
65
Q
Chronic Simple (Open-Angle) Glaucoma
Aetiology (1)
A

Optic neuropathy with death of many retinal ganglion cells and their optic nerve axons, often with a raised IOP

66
Q
Chronic Simple (Open-Angle) Glaucoma
Pathology (3)
A

Loss of disc substance which makes the cup look larger
As damage progresses, the disc pales (atrophies) and the cup widens and deepens, so vessels emerge from the disc appear to have breaks as they disappear into the cup and are then seen at the base again
As cupping develops, the disc vessels are displaced nasally so nasal + superior fields are lost first (temporal last) and central vision is maintained

67
Q
Chronic Simple (Open-Angle) Glaucoma
Risk factors (6)
A
>35 (typical patient is 60) 
\+ve family history 
Afro-Caribbean 
Myopia 
Diabetic/thyroid eye disease 
Screening for high risk groups
68
Q
Chronic Simple (Open-Angle) Glaucoma
Signs + symptoms (5)
A

Asymptomatic until visual fields impaired
High IOP
Slowly progressive, usually bilateral, peripheral visual field impairment (tunnel vision)
Optic disc paleness
Cupping and haemorrhage

69
Q
Chronic Simple (Open-Angle) Glaucoma
Investigations (5)
A

IOP measurement using tonometry
Central corneal thickness measurement
Peripheral anterior chamber configuration and depth assessments using gonioscopy
Visual field measurement
Optic nerve assessment with slit lamp + cup:disc ratio (shows high C:D ratio, disc haemorrhages, nasal displacement of vessels, disc pallor)

70
Q
Chronic Simple (Open-Angle) Glaucoma
Treatment (5)
A

Prostaglandin analogues to increase uveoscleral outflow
B-blockers reduce aqueous production to reduce IOP
A-adrenergic agonists to reduce production of aqueous and increase uveoscleral outflow
Laser therapy (trabeculoplasty) increases aqueous outflow so reduces IOP
Surgery (trabeculectomy)

71
Q

Cataracts

Definition (2)

A

Any opacity in the lens

Leading cause of blindness

72
Q
Cataracts
Risk factors (8)
A
Age (75% of >65s) 
Genetics 
Diabetes 
Smoking 
Alcohol excess 
Sunlight exposure 
Trauma 
Radiotherapy
73
Q

Cataracts

Classification (5)

A

Immature cataracts- red reflex occurs
Dense cataracts- no red reflex, or visible fundus
Nuclear cataracts- change the lens refractive index and dulls colours, common in old age
Cortical cataracts- spoke-like wedge-shaped opacities, milder effects on vision
Posterior subcapsular cataracts- progresses faster, cause the classic glare from bright sunlight and lights whilst driving at night, even if little effect on visual acuity

74
Q

Cataracts

Signs + symptoms (4)

A

Blurred vision- gradual painless loss of vision
Dazzle (especially in sunlight)
Monocular diplopia
Haloes

75
Q

Cataracts

Treatment (4)

A

Mydriatic drops
Sunglasses
Surgery: phacoemulsion and intraocular lens (IOL) implant (ocular biometry done pre op to measure for suitable implant)
Post-op capsule thickening is common

76
Q

Retinal Detachment

Pathology (1)

A

Holes/tears in the retina allow fluid to separate the sensory retina from the retinal pigment epithelium

77
Q

Retinal Detachment

Classification (3)

A

Rhegmatogenous retinal detachment: tear in retina causes fluid to pass from the vitreous space into the subretinal space between the sensory retina and the retinal pigment epithelium, typically caused by trauma
Exudative retinal detachmentL the retina detaches without a tear eg. hypertension, vasculitis, macular degeneration
Tractional retinal detachment: pulling on the retina eg. proliferative retinopathy, more common in myopic eyes

78
Q

Retinal Detachment

Signs + symptoms (5)

A

Floaters
Flashes
Field loss
Fall in acuity (painless and may be as a curtain falling over the vision-field defects indicate position and extent of the detachment ie. superior detachment = inferior field loss)
Ophthalmoscopy: grey opalescent retina, ballooning forward

79
Q

Retinal Detachment

Treatment (3)

A

Rest: if superior detachment lie flat, if inferior detachment lie 30 degrees head up
Laser photocoagulation
Surgery: vitrectomy + gas tamponade, scleral silicone implants, cryotherapy/laser to secure retina

80
Q

Macular Hole

Anatomy (2)

A

The macula is an area 5.5mm across, just lateral to the optic disc
In the middle of the macula is a 1.5mm pit, the fovea (fovea centralis- no ganglion cells)

81
Q

Macular Hole

Definition (1)

A

A small break in the macular region of the retinal tissue, it involves the fovea therefore affecting the visual acuity causing blurred + distorted central vision

82
Q

Macular Hole

Pathology (1)

A

With ageing, the vitreous starts to lose some of the 80% water content, which causes it to shrink causing traction on the retinal tissue

83
Q

Macular Hole

Signs + symptoms (3)

A

Distorted vision with visual loss
Tiny punched-out area in the centre of the macula, there may be yellow-white deposits at the base
Hole typically surrounded by a grey halo of detached retina

84
Q

Macular Hole

Treatment (2)

A

Some will spontaneously resolve (if impending hole seen as a yellow spot on the fovea)
Vitrectomy

85
Q

Vascular Retinopathy

Pathology (2)

A

Arteriopathic: arteries nip veins where they cross-share the same connective tissue sheath
Hypertensive: arteriolar vasoconstriction and leakage producing hard exudates, macular oedema, haemorrhages and rarely papilloedema

86
Q

Vascular Retinopathy

Ophthalmoscopy (3)

A

Thick, shiny arterial walls appear like wiring
Narrowing of arterioles leads to infarction of the superficial retina seen as cotton wool spots and flame haemorrhages
Leaks from these appear as hard exudates /- macular oedema or papilloedema

87
Q

Keratoconjunctivitis Sicca

Pathology (3)

A

There is reduced tear formation, producing a gritty feeling in the eyes
Decreased salivation also gives a dry mouth (xerostomia)
Occurs in association with collagen diseases

88
Q

Keratoconjunctivitis Sicca

Treatment (2)

A

Pilocarpine and cevimeline help features

Topical ciclosporin helps moderate/severe dry eye

89
Q

Eye in Diabetes Mellitus

Epidemiology (1)

A

30% of adults have ocular problems when diabetes presents but vast majority remain asymptomatic until advanced disease takes hold

90
Q
Eye in Diabetes Mellitus
Structural changes (2)
A

DM causes ocular ischaemia, which can cause new blood vessel forming on the iris (rubeosis) and if these block the drainage of aqueous fluid, glaucoma may result
Formation of age-related cataract is accelerated in DM

91
Q

Eye in Diabetes Mellitus

Pathology-Vascular Occlusion (3)

A

Causes ischaemia +/- new vessel formation (ie. proliferative retinopathy) which bleed (vitreous haemorrhage)
Causes cotton wool spots (ischaemic nerve fibres)
Causes retraction of fibrous tissue running with new vessels heightens risk of retinal detachment

92
Q

Eye in Diabetes Mellitus

Pathology- Vascular Leakage (2)

A
Capillaries bulge (microaneurysms) and there is oedema and hard exudates 
Rupture of microaneurysms at nerve fibre level causes flame-shaped haemorrhages, and when deep in the retina they form blot haemorrhages
93
Q

Eye in Diabetes Mellitus

Classification (3)

A

Non-proliferative: microaneurysms (dots), haemorrhages (flame-shaped or blots), hard exudates (yellow patches), engorged tortuous veins, cotton wool spots and large blot haemorrhages = ischaemia
Proliferative: fine new vessels appear on the optic disc, retina and can cause vitreous haemorrhage
Maculopathy: leakage from the vessels close to the macula cause oedema and can significantly threaten vision

94
Q
Eye in Diabetes Mellitus
Presymptomatic screening (4)
A

At the time of diagnosis and at least 1x/year thereafter
Dilated fundus retinopathy
Lesions mostly at posterior pole
Referral for laser photocoagulation if maculopathy, pre-proliferative retinopathy (venous bleeding/loops, blot haemorrhages) or proliferative retinopathy

95
Q

Eye in Diabetes Mellitus

Treatment (4)

A

Target BP <140/80 (<130/80 if end-organ damage)
Don’t correct refractive errors until controlled diabetes because diabetes causes relative myopia which improves on treatment
Laser photocoagulation for maculopathy + proliferative retinopathy
Add on anti-VEGF if macular oedema

96
Q

Papilloedema

Definition (1)

A

Swelling of the optic disc caused by raised intracranial pressure, always bilateral but may not be symmetrical

97
Q

Papilloedema

Signs + symptoms (4)

A

N+V
Headache worse in mornings, centred in frontal region + worsened by bending
CN XI palsy
Transient visual obscurations

98
Q

Papilloedema

Investigations (2)

A

MRI to rule out SOL

BP to check for malignant hypertension

99
Q

Styes

Definition (1)

A

Inflammatory lid swellings

100
Q
Styes
Hordeolum externum (4)
A

Abscess/infection (usually Staph) in a lash follicle
Can affect glands of Moll (sweat glands) and of Zeis (sebum-producing gland attached directly to lash follicles)
Point outwards
Treat with warm compress

101
Q
Styes
Hordeolum internum (5)
A

Abscesses of Meibomian glands
Point inwards
Opening to conjunctiva
Cause less local reaction but leave a residual swelling called a chalazion or a Meibomian cyst when they subside
Residual swellings treated with incision + curettage

102
Q

Blepharitis

Definition (1)

A

Lid inflammation eg. from staphs, seborrhoeic dermatitis or rosacea

103
Q

Blepharitis

Signs + symptoms (2)

A

Burning, itching red margins

Scales on the lashes

104
Q

Blepharitis

Treatment (3)

A

Good eyelid hygiene
Baby shampoo diluted 1:10 with warm water
In children consider oral erythromycin

105
Q

Entropion

Signs + symptoms (2)

A
Lid inturning (typically due to degeneration of lower lid fascial attachments and their muscles) 
The inturned eyelashes irritate cornea
106
Q

Entropion

Treatment (3)

A

Taping lower eyelids to cheek
Botox to lower lid
Surgery

107
Q

Ectropion

Signs + symptoms (3)

A

Lower lid eversion
Eye irritation
Watering

108
Q

Ectropion

Associations (2)

A

Old age

Facial palsy

109
Q

Ectropion

Treatment (2)

A

Plastic surgery

If facial palsy, consider surgical correction with an implant in upper lid to aid closure

110
Q

Retinoblastoma

Associations (2)

A

Hereditary (autosomal dominant mutation of RB gene located at 13q14)
Pineal/other tumour

111
Q

Retinoblastoma

Signs + symptoms (3)

A

Strabismus (squint)
Leukoconia (white pupil)
Absent red reflex

112
Q

Retinoblastoma

Treatment (3)

A

Chemotherapy
Enucleation (eye removal) if large or complicated
External beam radiotherapy

113
Q

Ophthalmic Shingles

Aetiology (1)

A

Herpes zoster ophthalmicus

114
Q
Ophthalmic Shingles
Shingles sites (2)
A
Most common (55%) is the thoracic nerves 
Second is the ophthalmic branch of trigeminal nerve (20%)
115
Q
Ophthalmic Shingles
Risk factors (3)
A

Increasing age
Trauma to the area
Immunocompromised patients

116
Q

Ophthalmic Shingles

Signs + symptoms (6)

A
Pain and neuralgia in distribution of cranial nerve V1 dermatome precedes a blistering inflamed rash 
Purulent conjunctivitis 
Visual loss 
Episcleritis/scleritis
Cranial nerve palsy 
Iritis
117
Q

Ophthalmic Shingles

Predictors of ocular involvement (2)

A

Globe is affected in 50% of those with HZO (corneal signs +/- iritis)
Nose-tip involvement (Hutchinson’s sign) makes it likely the eye will be affected

118
Q

Ophthalmic Shingles

Treatment (2)

A

Oral antivirals

Steroid eye drops

119
Q

Ophthalmic Shingles

Ramsay Hunt Syndrome (4)

A

Aetiology: herpes zoster oticus
Definition: herpes zoster infection of facial nerve
Signs + symptoms: severe otalgia precedes VII cranial nerve palsy (then spreads to other cranial nerves in ascending order), zoster vesicles appear around ear in the deep meatus, may have vertigo/tinnitus/deaf
Treatment: aciclovir + prednisolone

120
Q

Orbital Cellulitis

Pathology (2)

A

Infection of soft tissues posterior to the orbital septum

Spread typically via paranasal sinus infection (typically in a child)

121
Q

Orbital Cellulitis

Signs + symptoms (5)

A
Orbital inflammation 
Fever
Lid swelling 
Reduced eye mobility and painful eye movement 
Conjunctival swelling
122
Q

Orbital Cellulitis

Complications (4)

A

Subperiosteal and orbital abscesses
Optic neuritis
Central retinal vein or artery occlusion
Intracranial involvement can result in meningitis, brain abscesses and thrombosis in the dural or cavernous sinuses

123
Q

Orbital Cellulitis

Treatment (2)

A

Antibiotics

Drain abscesses

124
Q

Periorbital Cellulitis

Pathology (2)

A

Infection of soft tissues anterior to the orbital septum

Commonly caused by sinusitis or facial skin lesions

125
Q

Periorbital Cellulitis

Signs + symptoms (2)

A

Acute erythematous swelling of the eyelid

Distinguishing from orbital cellulitis: absence of painful eye movements, diplopia and visual impairment

126
Q

Periorbital Cellulitis

Treatment (1)

A

Amoxicillin

127
Q
Squints (Strabismus) 
Convergent squint (esotropia) (3)
A

Commonest type in children
May be no cause or due to hypermetropia
In strabismic amblyopia the brain suppresses the deviated image, the visual pathway doesn’t develop normally

128
Q
Squints (Strabismus) 
Divergent squint (exotropia) (2)
A

Occur in older children

Often intermittent

129
Q

Squints (Strabismus)

Non-paralytic squints (4)

A

Usually start in childhood
May be constant or not
Corneal reflection: reflection from a bright light falls centrally and symmetrically on each cornea if no squint, asymmetrically if squint present
Cover test: movement of the uncovered eye to take up fixation as the other eye is covered demonstrates manifest squint; latent squint is revealed by movement of the covered eye as the cover is removed

130
Q

Squints (Strabismus)

Treatment (3)

A

Optical: assess refractive state after cyclopentolate drops and exclude structural abnormality
Orthoptic: patching the good eye encourages use of the one which quints
Operations: resection and recession of rectus muscles, help alignment and gives good cosmetic results, botulinum toxin is sometimes good enough

131
Q
Squints (Strabismus) 
Paralytic squints (2)
A

Diplopia is most on looking in the direction of pull of the paralysed muscle
When the separation between the 2 images is greatest, the image from the paralysed eye is furthest from the midline and faintest

132
Q

Squints (Strabismus)

Third nerve palsy (oculomotor) (4)

A

Ptosis
Proptosis (as recti tone decreases)
Fixed pupil dilatation
Eye looking down and out

133
Q

Squints (Strabismus)

Fourth nerve palsy (trochlear) (2)

A

Diplopia

Eye looking upward, in adduction and cannot look down and in (superior oblique paralysed)

134
Q

Squints (Strabismus)

Sixth nerve palsy (abducens) (2)

A

Diplopia

Eye medially deviated and cannot move laterally from the midline, as the lateral rectus is paralysed

135
Q
Squints (Strabismus) 
Eye muscles (6)
A

Superior rectus: elevation (adduction and medial rotation)- oculomotor
Inferior rectus: depression (adduction and lateral rotation)- oculomotor
Medial rectus: adduction- oculomotor
Lateral rectus: abduction- abducens
Superior oblique: depression, abduction and medial rotation- trochlear
Inferior oblique: elevation, abduction + lateral rotation- oculomotor

136
Q
Afferent Defects
Afferent pathway (1)
A

Nerve impulse from pupil to brain along the optic nerve when a light is shone in that eye

137
Q

Afferent Defects

Causes (3)

A

Optic neuritis
Optic atrophy
Retinal disease

138
Q

Afferent Defects

Signs + symptoms (3)

A

Absent direct response- pupil won’t respond to light, but constricts to a beam in the other eye (consensual response)
Swinging light test: on beaming light to normal eye, both pupils constrict, if on swining the light to the affected eye the pupil dilates it is a relative afferent pupillary defect
Pupils same size

139
Q
Efferent Defects
Efferent pathway (1)
A

The impulse sent from the midbrain back to both pupils via ciliary ganglion and CNIII causing both pupils to constrict, even though only one eye is being stimulated by the eye

140
Q

Efferent Defects

Causes (2)

A

Diabetes, hypertension (pupil often spared in vascular causes)
Tumour, aneurysm (pupillary fibres are peripheral and are the first affected by compressive lesions)

141
Q

Efferent Defects

Signs + symptoms (3)

A

Complete ptosis
Fixed, dilated pupil
Eye looks down and out