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Opthalmology > Progressive visual loss > Flashcards

Progressive visual loss Flashcards

1
Q

What is glaucoma

A
  • optic nerve damage that is caused by a significant rise in intraocular pressure.
  • raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.
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2
Q

What happens in open angle glaucoma

A
  • gradual increase in resistance through the trabecular meshwork.
  • This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye.
  • Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.
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3
Q

What happens in acute closed angle glaucoma

A
  • the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away.
  • This leads to a continual build up of pressure.
  • This is an ophthalmology emergency.
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4
Q

What are the risk factors for open angle glaucoma

A

Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)

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5
Q

What is the presentation of open angle glaucoma

A
  • usually asymptomatic and diagnosed on routine screening
  • Gradual progressive loss of peripheral vision
  • gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.
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6
Q

How do you measure intraocular pressure

A

Non-contact tonometry

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7
Q

What is Non-contact tonometry

A
  • commonly used machine for estimating intraocular pressure by opticians.
  • shooting a “puff of air” at the cornea and measuring the corneal response to that air.
  • less accurate but gives a helpful estimate for general screening purposes.
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8
Q

What is Goldmann applanation tonometry

A
  • gold standard way to measure intraocular pressure.
    • special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the front of the cornea to get an accurate measurement of what the intraocular pressure is.
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9
Q

How do you diagnose open angle glaucoma

A
  • Goldmann applanation tonometry
  • Fundoscopy
  • Visual field assessment
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10
Q

What might you see on fundoscopy in a patient with open angle glaucoma

A
  • cupping of the optic disc

- optic cup greater than 0.5 the size of the optic disc is abnormal.

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11
Q

What is normal intraocular pressure

A

10-21 mmHg

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12
Q

What is the management of intraocular pressure

A
  • reduce intraocular pressure
  • Prostaglandin analogue eyedrops: latanoprost
  • Betablockers (e.g. timolol)
  • Carbonic anhydrase inhibitors (e.g. dorzolamide)
  • Trabeculectomy
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13
Q

What are side effect of latanoprost

A

eyelash growth
eyelid pigmentation
iris pigmentation (browning).

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14
Q

When do you begin treating patients with open angle glaucoma

A

> 24mmHG

close monitoring prior to this

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15
Q

How to prostaglandin analogue treat open angle glaucome

A

increase uveoscleral outflow

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16
Q

How do Betablockers treat open angle glaucoma

A

reduce the production of aqueous humour

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17
Q

How do carbonic anhydrase inibitors treat open angle glaucoma

A

reduce the production of aqueous humour

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18
Q

What is trabeculectomy

A
  • involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva
  • causes a “bleb” under the conjunctiva where the aqueous humour drains.
  • It is then reabsorbed from this bleb in to the general circulation.
  • For when drops are not maintaining intraocular pressure
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19
Q

What are the risk factors for acute angle closure

A
  • Increasing age
  • Females: males 4:1
  • Family history
  • Chinese and East Asian ethnic origin. Unlike open angle glaucoma it is rare in people of black ethnic origin.
  • Shallow anterior chamber
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20
Q

What medications can precipitate angle closure

A
  • Adrenergic medications such as noradrenalin
  • Anticholinergic medications such as oxybutynin and solifenacin
  • Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
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21
Q

What is the presentation of acute angle closure

A

Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

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22
Q

What will you see on examination of a patient with acute angle closure

A 
Red eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation
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23
Q

What is the management of acute angle closure

A

Emergency opthalmology appointment, if waiting for an ambulance:

  • Lie patient on their back without a pillow
  • Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
  • Give acetazolamide 500 mg orally
  • Given analgesia and an antiemetic if required
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24
Q

How does pilocarpine work

A
  • acts on the muscarinic receptors in the sphincter muscles in the iris
  • causes constriction of the pupil: miotic agent.
  • ciliary muscle contraction.
  • These two effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up
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25
Q

How does Acetazolamide work

A

carbonic anhydrase inhibitor. This reduces the production of aqueous humour.

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26
Q

What is laser iridotomy

A
  • definitive treatment
  • laser makes a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber.
  • This relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
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27
Q

What is age related macular disease

A
  • degeneration in the macular that cause a progressive deterioration in vision.
  • most common cause of blindness in the UK.
  • drusen seen during fundoscopy.
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28
Q

What are the 4 layers of the macular

A
  • choroid layer: blood vessels that provide the blood supply to the macula.
  • Bruch’s membrane.
  • Retinal pigment epithelium
  • photoreceptors. (top layer)
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29
Q

What is drusen

A
  • yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane.
  • Some drusen can be normal.
  • Normal drusen are small (< 63 micrometres) and hard.
  • Larger and greater numbers of drusen can be an early sign of macular degeneration.
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30
Q

What features are common to both wet and dry AMD

A
  • Drusen
  • Atrophy of the retinal pigment epithelium
  • Degeneration of the photoreceptors
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31
Q

What features are common to both wet and dry AMD

A
  • Drusen
  • Atrophy of the retinal pigment epithelium
  • Degeneration of the photoreceptors
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32
Q

What happens in Wet AMD

A
  • development of new vessels growing from the choroid layer into the retina.
  • These vessels can leak fluid or blood and cause oedema and more rapid loss of vision.
  • A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF)
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33
Q

What are the risk factors of AMD

A 
Age
Smoking
White or Chinese ethnic origin
Family history
Cardiovascular disease
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34
Q

What is the presentation of AMD

A
  • Gradual worsening central visual field loss (more acute if wet)
  • Reduced visual acuity
  • Crooked or wavy appearance to straight lines
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35
Q

What may you find on examination in a patient with AMD

A
  • Reduced acuity using a Snellen chart
  • Scotoma (a central patch of vision loss)
  • Amsler grid test can be used to assess distortion of straight lines
  • Fundoscopy. Drusen are the key finding.
36
Q

What investigations may you complete in a patient with suspected AMD

A
  • Acuity
  • Amsler Grid
  • Fundoscopy
  • Slit-lamp biomicroscopic fundus examination
  • Optical coherence tomography
  • Fluorescein angiography
37
Q

What is Fluorescein angiography

A
  • involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. - Shows up oedema and neovascularisation
  • used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.
38
Q

What is the management of dry AMD

A
  • opthalmology referral
  • Avoid smoking
  • Control blood pressure
  • Vitamin supplementation has some evidence in slowing progression
39
Q

What is the management of wet AMD

A
  • Anti-VEGF injections into the vitreous chamber of the eye
  • Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels.
  • slow and even reverse the progression of the disease.
  • typically need to be started within 3 months to be beneficial.
40
Q

What is the management of diabetic retinopathy

A
  • Laser photocoagulation
  • Anti-VEGF medications such as ranibizumab and bevacizumab
  • Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
41
Q

What are the complications of diabetic retinopathy

A
  • Retinal detachment
  • Vitreous haemorrhage
  • Rebeosis iridis (new blood vessel formation in the iris)
  • Optic neuropathy
    Cataracts
42
Q

What is a vitreous haemorrhage

A

bleeding in to the vitreous humour

43
Q

What is diabetic maculopathy

A
  • Macular oedema

- Ischaemic maculopathy

44
Q

What is Proliferative Diabetic Retinopathy

A

Neovascularisation

Vitreous haemorrhage

45
Q

What may you see on severe Non-proliferative Diabetic Retinopathy

A
  • blot haemorrhages plus microaneurysms in 4 quadrants
  • venous beating in 2 quadrates
  • intraretinal microvascular abnormality (IMRA) in any quadrant
46
Q

What may you see on moderate Non-proliferative Diabetic Retinopathy

A
  • microaneurysms
  • blot haemorhages
  • hard exudates
  • cotton wool spots
  • venous beading
47
Q

What are the different types of classification of diabetic retinopathy

A
  • Proliferative
  • Non-proliferative: often called background or pre-proliferative retinopathy as it can develop in to proliferative retinopathy
  • Diabetic maculopathy
48
Q

What are the two types of classification of diabetic retinopathy

A
  • Proliferative
  • Non-proliferative: often called background or pre-proliferative retinopathy as it can develop in to proliferative retinopathy
49
Q

What is neovascularisation

A

when growth factors are released in the retina causing the development of new blood vessels.

50
Q

How do cotton wool spots form

A

Damage to nerve fibres in the retina due to ischaemia and infarcts cause fluffy white patches to form on the retina

51
Q

How do cotton wool spots form

A

Damage to nerve fibres in the retina causes fluffy white patches to form on the retina

52
Q

What does damage to the blood vessel walls in the retina lead to

A
  • Microaneurysms: weakness in the wall causes small bulges.
  • Venous beading: walls of the veins are no longer straight and parallel and look more like a string of beads or sausages.
53
Q

What are hard exudates

A

yellow/white deposits of lipids in the retina

caused by damaged vessels leaking lipids into the retina.

54
Q

What are hard exudates

A

yellow/white deposits of lipids in the retina

55
Q

How does hyperglycaemia lead to diabetic retinopathy

A

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 the formation of hard exudate

56
Q

What is hypertensive retinopathy

A
  • Damage to the small blood vessels in the retina relating to systemic hypertension
  • Can be due to chronic hypertension or can develop quickly in response to malignant hypertension.
57
Q

What signs are associated with hypertensive retinopathy

A
  • Silver wiring or copper wiring
  • Arteriovenous nipping
  • Cotton wool spots
  • Hard exudates
  • Retinal haemorrhages
  • Papilloedema
58
Q

What is silver wiring/copper wiring

A

where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.

59
Q

What is Arteriovenous nipping

A

the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.

60
Q

What are retinal haemorrhages

A

caused by damaged vessels rupturing and releasing blood into the retina.

61
Q

What is papilloedema

A

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

62
Q

What is the management of hypertensive retinopathy

A
  • controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
63
Q

What are cataracts

A
  • lens in the eye becomes cloudy and opaque.
  • this reduces visual acuity by reducing the light that enters the eye.
  • Develop slowly over years
  • Caution: may conceal other pathology e.g. AMD
64
Q

What are cataracts

A
  • lens in the eye becomes cloudy and opaque.
  • this reduces visual acuity by reducing the light that enters the eye.
  • Develop slowly over years
65
Q

What are the risk factors for cataracts

A
  • Increasing age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypocalcaemia
66
Q

What is the presentation of cataracts

A
  • Usually asymmetrical
  • Very slow reduction in vision
  • Progressive blurring of vision
  • Change of colour of vision with colours becoming more brown or yellow
  • “Starbursts” can appear around lights, particularly at night time
67
Q

What is the main sign for cataracts

A
  • Loss of red reflex: appear grey or white

- Can be seen in congenital cataracts too

68
Q

What is the management of cataracts

A
  • If symptoms manageable, nil

- cataract surgery

69
Q

What does cataract surgery entail

A
  • drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens into the eye.
  • This is usually done as a day case under local anaesthetic. It usually gives good results.
70
Q

What is Endophthalmitis

A
  • inflammation of the inner contents of the eye, usually caused by infection.
  • can be treated with intravitreal antibiotics injected into the eye.
  • can lead to loss of vision and loss of the eye itself.
71
Q

What is Retinitis pigmentosa

A
  • congenital inherited condition where there is degeneration of the rods and cones in the retina
  • Can cause isolated retinitis pigmentosa or systemic diseases
  • Generally, rods degenerate more than cones, leading to night blindness.
  • They get decreased central and peripheral vision.
72
Q

What is the presentaiton of Retinitis Pigmentosa

A
  • Night blindness is often the first symptom
  • Peripheral vision is lost before the central vision
  • Most symptoms start in childhood
73
Q

What systemic disease are associated with retinitis Pigmentosa

A

Usher’s Syndrome
Bassen-Kornzweig Syndrome
Refsum’s Disease

74
Q

What systemic disease are associated with retinitis Pigmentosa

A

Usher’s Syndrome
Bassen-Kornzweig Syndrome
Refsum’s Disease

75
Q

What is Usher’s Syndrome

A

causes hearing loss plus retinitis pigmentosa

76
Q

What is Bassen-Kornzweig Syndrome

A

is a disorder of fat absorption and metabolism causing progressive neurological symptoms and retinitis pigmentosa

77
Q

What is Refsum’s Disease

A

metabolic disorder of phytanic acid causing neurological, hearing and skin symptoms and retinitis pigmentosa

78
Q

What treatment may be potentially initiated by a specialist to manage retinitis pigmentosa (lacks evidence)

A 
Vitamin and antioxidant supplements
Oral acetazolamide
Topical dorzolamide
Steroid injections
Anti-VEGF injections
(gene therapy)
79
Q

What treatment may be potentially initiated by a specialist to manage retinitis pigmentosa

A 
Vitamin and antioxidant supplements
Oral acetazolamide
Topical dorzolamide
Steroid injections
Anti-VEGF injections
80
Q

What is posterior vitreous detachment

A
  • the vitreous gel comes away from the retina.
  • It is very common, particularly in older patients as the vitreous body becomes less firm and less able to maintain its shape
81
Q

What is posterior vitreous detachement

A
  • the vitreous gel comes away from the retina.
  • It is very common, particularly in older patients as the vitreous body becomes less firm and less able to maintain its shape
82
Q

What is the presentation of posterior vitreous detachment

A 
Asymptomatic
Painless
Spots of vision loss
Floaters
Flashing lights
83
Q

What is the management of posterior vitreous detachment

A
  • No treatment, overtime the brain adjusts
84
Q

What does posterior vitreous detachment predispose you to

A
  • retinal tears and detachment

- EXCLUDE

85
Q

Causes of tunnel vision

A 
Papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
86
Q

What type of screening should be done for patients with a strong FH of glaucoma

A

annual screening from 40yo

Opthalmology (4 decks)

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