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Ophthalmology > Opthamology fifth yr > Flashcards

Opthamology fifth yr Flashcards

1
Q

Summary of cataracts?

A

lens of the eye gradually opacifies i.e. becomes cloudy

Difficult for light to reach the retina, causing reduced/blurred vision

leading cause of curable blindness

F>M, increases with age

causes - normal ageing process

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2
Q

RF for cataracts?

A

Increasing age
Smoking
Increased alcohol consumption
Trauma
DM
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders - hypocalcaemia

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3
Q

Features of cataracts?

A

Sx - gradual onset
Reduced visual acuity
Faded colour vision
Glare - lights brighter than usual - “starbursts”
Halos
Asymmetrical

Signs
Defect in red reflex

Ix
Opthalmoscopy - after pupil dilation - normal fundus and optic nerve
Slit-lamp examination - visible cataract

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4
Q

Classification of cataracts?

A

Nuclear: change lens refractive index, common in old age

Polar: localized, commonly inherited, lie in the visual axis

Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis

Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy

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5
Q

Tx of cataracts?

A

Non-surgical - stronger glasses/contact lens, brighter lighting

Surgery - removing cloudy lens and replacing this with an artificial one.

NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice.

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6
Q

Complications following cataract surgery?

A

Posterior capsule opacification: thickening of the lens capsule

Retinal detachment

Posterior capsule rupture

Endophthalmitis: inflammation of aqueous and/or vitreous humour - treat with intravitreal antibiotics

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7
Q

Summary of open angle glaucoma?

A

Glaucoma refers to optic nerve damage due to significant rise in intraocular pressure

This is caused by a block in aqueous humour trying to escape the eye

2 types - open-angle and closed-angle

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8
Q

Normal intraocular pressure?

A

10-21 mmHg - caused by resistance to flow through the trabecular meshwork into the canal of Schlemm

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9
Q

Pathophysiology of open-angle glaucoma?

A

Gradual increase in resistance through trabecular meshwork.

More difficult for aqueous humour to flow through meshwork and exit eye. Pressure SLOWLY builds - slow and chronic onset of glaucoma

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10
Q

Pathophysiology of acute angle-closure glaucoma?

A

Iris bulges forward and seals off the trabecular meshwork from the anterior chamber - preventing aqueous humour from being able to drain away

Leads to a continual build-up of pressure - opthalmology emergency

Increased pressure = cupping of optic disc. Indent in optic disc (optic cup) larger - ‘cupping’

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11
Q

RFs for open angle glaucoma?

A

Increasing age
FHx
Black ethnic origin
Myopia

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12
Q

Presentation of open angle glaucoma?

A

Rise in IOP for long time

It is diagnosed by routine screening when attending optometry for an eye check.

Peripheral vision loss - closes in to cause tunnel vision

It can present with gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.

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13
Q

Ix for open angle glaucoma?

A

Non-contact tonometry - via opticians

Goldmann applanation tonometry - gold standard way

Visual field assessment - check for peripheral vision loss

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14
Q

Management of open-angle glaucoma?

A

Aims to reduce intraocular pressure - start at pressure of 24 mmHg or above

Prostaglandin analogue eye drops (e.g. latanoprost) are first line. Increase uveoscleral outflow. SE = eyelash, eyelid pigmentation, iris pigmentation (browning)

BB - timolol - reduce the production of aqueous humour

Carbonic anhydrase inhibitors - dorzolamide - reduce the production of aqueous humour

Sympathomimetics - brimonidine - reduce production of aqueous fluid and increase uveoscleral outflow

Trabeculoectomy surgery - required where eye drops are ineffective. Creates new channel from anterior chamber, through the sclera to a location under the conjunctiva. Causes a bleb

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14
Q

Management of open-angle glaucoma?

A

Aims to reduce intraocular pressure - start at pressure of 24 mmHg or above

Prostaglandin analogue eye drops (e.g. latanoprost) are first line. Increase uveoscleral outflow. SE = eyelash, eyelid pigmentation, iris pigmentation (browning)

BB - timolol - reduce the production of aqueous humour

Carbonic anhydrase inhibitors - dorzolamide - reduce the production of aqueous humour

Sympathomimetics - brimonidine - reduce production of aqueous fluid and increase uveoscleral outflow

Trabeculoectomy surgery - required where eye drops are ineffective. Creates new channel from anterior chamber, through the sclera to a location under the conjunctiva. Causes a bleb

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15
Q

Pathophysiology of diabetic retinopathy?

A

Condition where blood vessels in retina are damaged by prolonged exposure to hyperglycaemia

Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells.

Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages, and formation of hard exudates. Hard exudates are yellow/white deposits of lipids in the retina

Damage to blood vessels lead to micro aneurysms and venous beading.

Damage to nerve fibres in retina - cotton wool spots

Intraretinal microvascular abnormalities (IMRA) - dilated and tortuous capillaries in the retina. Shunt between arterial and venous vessels in the retina.

Neovascularisation - growth factors released in the retina causing the development of new blood vessels

16
Q

Findings of diabetic retinopathy?

A

Cotton wool spots
Neovascularisation
Microaneurysms
Venous beading
Hard exudates
Blot haemorrhages

17
Q

Staging of diabetic retinopathy?

A

Non-proliferative and proliferative
Diabetic maculopathy

Non-proliferative
Mild - microaneurysms
Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading
Severe - blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants, intreretinal microvascular abnormality (IMRA) in any quadrant

Proliferative
Neovascularisation
Vitreous haemorrhage

Diabetic maculopathy
Macular oedema
Ischaemic maculopathy

18
Q

Complications of diabetic retinopathy?

A

Retinal detachment

Vitreous haemorrhage (bleeding in to the vitreous humour)

Rebeosis iridis (new blood vessel formation in the iris)

Optic neuropathy

Cataracts

19
Q

Management of diabetic retinopathy?

A

Optimise glycemic control, BP and hyperlipidaemia

Regular opthalmology review

Maculopathy - VEGF inhibitors

Non-proliferative retinopathy - regular observation, severe/very severe consider panretinal laser photocoagulation

Proliferative retinopathy
- panretinal laser photocoagulation - SE - reduction in visual fields
- intravitreal VEGF inhibitors - combination with panretinal laser photocoagulation, e.g., ranibizumab
- severe or vitreous haemorrhage - vitreoretinal surgery

20
Q

Signs in retina due to hypertensive retinopathy?

A

As a result of chronic HTN or rapidly due to malignant HTN

Silver wiring or copper wiring - where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light

AV nipping - arterioles cause compression of veins where they cross - due to sclerosis and hardening of the arterioles

Cotton wool spots - caused by ischaemia and infarction in the retina causing damage to nerve fibres

Hard exudates - due to lipids leaking from damaged vessels

Retinal haemorrhages - damaged vessels rupturing and releasing blood into the retina

Papilloedema - by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins

21
Q

Classification of hypertensive retinopathy?

A

Stage 1: Mild narrowing of the arterioles

Stage 2: Focal constriction of blood vessels and AV nicking

Stage 3: Cotton-wool patches, exudates and haemorrhages

Stage 4: Papilloedema

22
Q

Management of hypertensive retinopathy?

A

controlling the blood pressure and other risk factors such as smoking and blood lipid levels.

23
Q

Management of hypertensive retinopathy?

A

controlling the blood pressure and other risk factors such as smoking and blood lipid levels.

24
Q

What is glaucoma?

A

refers to the optic nerve damage that is caused by a significant rise in intraocular pressure

The raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.

25
Q

What is acute angle-closure glaucoma?

A

The raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.

Causes build up of pressure in eye - pressure builds in posterior chamber and behind iris, worsening closure of angle

Ophthalmology emergency!

26
Q

RFs for acute angle-closure glaucoma?

A

Increasing age - ^ lens growth

Females are affected around 4 times more often than males

Family history

Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.

Shallow anterior chamber

Hypermetropia

Pupillary dilatation

Certain medications:

Adrenergic - noradrenaline

Anticholinergic - oxybutynin, solifenacin

TCAs - amitriptyline

27
Q

Features of acute angle-closure glaucoma?

A

Severely painful red eye

Blurred vision

Halos around lights

Associated headache, nausea and vomiting

O/E:
red eye
teary
hazy cornea
decreased visual acuity
dilatation of affected pupil
fixed pupil size
firm eyeball on palpation

28
Q

Initial management of acute angle-closure glaucoma?

A

Same day ophthalmology referral

If delay:
Lie patient on back
Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
Give acetazolamide 500mg orally
Give analgesia and antiemetic if required

29
Q

MOA of pilocarpine?

A

acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil. Therefore it is a miotic agent.

It also causes ciliary muscle contraction

30
Q

MOA of acetazolamide?

A

carbonic anhydrase inhibitor.

This reduces the production of aqueous humour.

31
Q

Secondary care management of acute angle-closure glaucoma?

A

Pilocarpine

Acetazolamide (oral or IV)

Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye

Timolol is a beta-blocker that reduces the production of aqueous humour

Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour

Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow

Laser iridotomy is definitive Tx. This involves using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber.

32
Q

What is age-related macular degeneration?

A

Most common cause of blindness in the UK

Degeneration of the central retina (macula) is the key feature with changes usually bilateral. Degeneration of retinal photoreceptors that results in the formation of drusen which are seen on fundoscopy and retinal photography.

More common with advancing age and in females

Drusen, atrophy of retinal pigment epithelium, degeneration of photoreceptors

33
Q

RFs for age-related macular degeneration?

A

Advancing age

Smoking

FHx

Ischaemic CVD - HTN, dyslipidaemia, DM

34
Q

Classification of macular degeneration?

A

Dry - also known as atrophic, drusen, 90% of cases

Wet - also known as exudative or neovascularisation, characterised by choroidal neovascularisation, leakage of serous fluid and blood can cause rapid loss of vision, worst prognosis

35
Q

Features of age-related macular degeneration?

A

Subacute onset of visual loss - central visual field loss

Reduction in visual acuity - particularly near field objects - gradual in dry ARMD, subacute in wet ARMD

Difficulties in dark adaptation - deterioration in vision at night

Visual disturbance may vary day to day

Photopsia (flickering or flashing lights)

Glare around objects

Visual hallucinations - Charles-Bonnet syndrome

Distortion of line perception - Amsler grid testing

Fundoscopy - drusen

Wet ARMD - well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage

36
Q

Ix of age-related macular degeneration?

A

Snellen chart - reduced acuity

Scotoma - central patch of vision loss

Slit-lamp microscopy - identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD

Fluorescein angiography - if neovascular ARMD is suspected - can guide anti-VEGF therapy

Ocular coherence tomography is used to visualise the retina in three dimensions

37
Q

Management of age-related macular degeneration?

A

Dry - combination of zinc with anti-oxidant vitamins A,C and E

Wet - vascular endothelial growth factor (VEGF) - increased vascular permeability

Also laser photocoagulation - but VEGF preferred

Ophthalmology (2 decks)

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