Important eye presentations Flashcards

1
Q

Painful loss of vision

A
Trauma: corneal foreign body, corneal abrasion, traumatic hyphaema, penetrating injury, globe rupture.
Corneal ulcer.
Herpes simplex keratitis.
Anterior uveitis.
Endophthalmitis.
Scleritis.
Giant cell arteritis.
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2
Q

Acute painless loss of vision

A

Vitreous haemorrhage.
Wet age-related macular degeneration.
Central or branch retinal vein occlusion.
Central or branch retinal artery occlusion.
Anterior ischaemic optic neuropathy.
Temporal arteritis or giant cell arteritis.
Retinal detachment

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3
Q

Acute painless loss of vision: vitreous haemorrhage

A

Impaired or no fundal view, ± reduced red reflex.

Causes: retinal detachment, diabetic retinopathy.

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4
Q

Acute painless loss of vision: central or branch retinal vein occlusion

A

Widespread or hemispheric retinal haemorrhages, ± cotton wool spots, exudates, disc swelling, macular oedema.
Common causes: hypertension, diabetes, hyperlipidaemia.
Other causes: vasculitis (e.g. Behçet’s, sarcoidosis, SLE), clotting disorders (e.g. protein S or C deficiency, antiphospholipid syndrome) multiple myeloma, glaucoma.

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5
Q

Acute painless loss of vision: central or branch retinal artery occlusion

A

Sudden loss of vision, may have symptoms of GCA, 10% of patients have preceding amaurosis fugax.
Pale retina, cherry red spot, retinal vessel emboli.
Causes: atherosclerotic (hypertension, diabetes, smoking, hyperlipidaemia), embolic (carotid/aortic artery disease, cardiac valve disease), haematological (protein C deficiency, antiphospholipid syndrome, lymphoma, leukaemia), inflammatory (GCA, SLE, polyarteritis nodes, Wegener’s granulomatosis), other (oral contraceptive, trauma, migraine).

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6
Q

Acute painless loss of vision: anterior ischaemic optic neuropathy

A

May be arteritic (temporal arteritis or GCA) or non-arteritic (hypertension, diabetes, anaemia, smoking, hyperlipidaemia).

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7
Q

Acute painless loss of vision: temporal arteritis or giant cell arteritis

A

Headache, scalp tenderness, jaw claudication, neck pain, fever, malaise, joint pains.
Tender, non-pulsatile temporal artery, relative afferent pupillary defect, swollen optic disc, ± central retinal arterial occlusion, ± cranial nerve palsies.

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8
Q

Acute painless loss of vision: retinal detachment

A

Floaters, flashing lights, loss of vision/visual field defect.
Ocular risk factors: history of trauma, cataract surgery, myopia.
Systemic risk factors: Stickler syndrome, Marfan’s syndrome, Ehlers-Danlos syndrome.

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9
Q

Hypertensive retinopathy

A

Findings depend on classification grade of retinopathy.
Focal/generalised arteriolar constriction and straightening.
Arteriosclerosis leading to changes at arteriovenous crossing points: AV nipping or nicking and silver-wiring of retinal arterioles.
Microaneurysms.
Cotton wool spots indicating ischaemia.
Retinal haemorrhages, usually flame shaped.
Exudate, often in macular star pattern.
Arterial macroaneurysms.
Disc oedema.
Tortuous vessels in malignant hypertension.

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10
Q

Diabetic retinopathy: pathogenesis

A

Microangiopathy primarily affecting pre-capillary arterioles, capillaries, and post-capillary venules.
There is loss of pericytes, damage to the vascular endothelial cells, deformation of red blood cells with increased aggregation leading to microvascular occlusion and leakage.

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11
Q

Diabetic retinopathy: clinical features

A

Fundus findings are usually bilateral and broadly symmetrical.
Abnormalities depend on the severity of the disease.
Microaneurysms.
Dot and blot haemorrhages.
Lipid exudates.
Venous beading.
Intraretinal microvascular abnormalities.
Cotton wool spots.
New vessels at the disc or elsewhere.
Tractional retinal detachment.
Macular oedema and thickening (diabetic maculopathy).

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12
Q

Glaucoma: overview

A

Glaucoma is an optic neuropathy associated with raised intraocular pressures leading to irreversible optic nerve damage.
It is usually asymptomatic and is often detected incidentally, but can lead to blindness.

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13
Q

Glaucoma: applied physiology

A

Aqueous humour is produced by the ciliary body and mainly drained through the trabecular meshwork but there is also drainage through uveoscleral routes.
Normal intraocular pressure = 8-21mmHg.

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14
Q

Glaucoma: primary angle closure

A

Narrowing of the anterior chamber drainage angle prevents aqueous fluid outflow resulting in increased intraocular pressure.
Acute: classically a red, painful eye, hazy cornea due to oedema, fixed mid-dilated oval pupil, reduced vision, headache, nausea and vomiting.
Chronic/subacute: may give a history of haloes around lights at night.

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15
Q

Glaucoma: primary open angle

A

Aqueous fluid outflow is reduced despite anterior chamber angle remaining open.
Most common form of glaucoma in patients >50 years.
Risk factors: increased IOP, reduced central corneal thickness, Afro-Caribbean origin, increased age, affects 1st degree relative, hypertension, diabetes, myopia.

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16
Q

Glaucoma: secondary glaucoma

A

Angle may be open or closed but the pathology results from a separate ocular condition or its treatment.

17
Q

Glaucoma: normal tension/pressure glaucoma

A

Open angle and glaucomatous field loss and disc changes despite and IOP falling within the ‘normal’ range.

18
Q

Glaucoma: conditions leading to secondary glaucoma

A

Uveitis: trabeculitis (chronic inflammation of the trabecular meshwork resulting in reduced aqueous outflow) or iris bombé (iris adhesions to the anterior capsule of the lens through 360 degrees following anterior uveitis can result in bowing forward of the iris, from trapped aqueous, closing the drainage angle).
Rubeosis: ischaemic insults to the eye (retinal vein/artery occlusions, diabetes) can lead to new blood vessel growth/bleeding in the anterior chamber angle obstructing aqueous flow.
Trauma: damage to the drainage angle from blunt trauma can lead to scarring of the trabecular meshwork.

19
Q

Age-related macular degeneration: overview

A

AMD is the leading cause of blindness registration in the western world.
There are 2 main types: wet and dry.
The common dry form is associated with gradual visual loss, while the much less common wet or neovascular AMD is associated with rapid and more severe visual loss.

20
Q

Age-related macular degeneration: dry

A

Progressive atrophic changes of the macula characterised by the presence of drusen, extracellular material deposited between the retinal pigment epithelium and the underlying Bruch’s membrane.
There is resulting loss of the RPE and photoreceptor layers of the retina.

21
Q

Age-related macular degeneration: wet

A

Accounts for 10% of cases of AMD and is the most common cause of blindness in the Western world.
New vessels grow from the choroidal vasculature and enter the retina forming a choroidal neovascular membrane, which can leak fluid or blood at the macula leading to scarring and visual loss.

22
Q

Age-related macular degeneration: symptoms

A

Central visual loss (gradual or sudden).
Distortion (metamorphopsia: straight lines look wavy and distorted).
Scotoma.

23
Q

Age-related macular degeneration: signs

A

Hard drusen (well demarcated yellow lesions).
Soft drusen (ill-defined paler lesions which may become confluent).
Pigmentation.
Subretinal or intraretinal haemorrhage.
Exudate.

24
Q

Age-related macular degeneration: risk factors

A
Age
Family history
Female sex
Caucasian
Smoking
Hypertension
Cardiovascular disease
Hypercholesterolaemia
25
Q

Cataract: overview

A

The lens is a biconvex, transparent, avascular structure enclosed by a capsule.
Lens fibres are continually laid down throughout life so the lens is the only eye structure that continues to grow.
With time the lens loses its transparency leading to cataract formation, which is universal with increasing age.

26
Q

Cataract: common symptoms

A

Gradual deterioration of vision, difficulty reading.

Glare from oncoming car headlights.

27
Q

Cataract: risk factors

A
Majority are senile.
Diabetes mellitus.
Disorders of calcium homeostasis.
Uveitis.
Intraocular tumours.
Angle closure glaucoma.
Wilson's disease.