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Year 4k: Neuro and Special Senses > Inner Eye: Optic Nerve, Retina, Vitreous Humour > Flashcards

Inner Eye: Optic Nerve, Retina, Vitreous Humour Flashcards

1
Q

What causes Diabetic Retinopathy?

A
  • Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls.
  • This precipitates damage to endothelial cells and pericytes

Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old.

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2
Q

What are examination signs of Diabetic Retinopathy?

A

Fundoscopy:

  • ​Exudates present due to endothelial dysfunction leading to increased vascular permeability
  • Microaneurysms formed predispoing from pericyte dysfunction
  • Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia
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3
Q

How is diabetic retinopathy classified?

A
  • Non-proliferative diabetic retinopathy (NPDR)
  • Proliferative retinopathy (PDR)
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4
Q

What are the traditional classifications for Diabetic Retinopathy?

A
  1. Background retinopathy
    • Microaneurysms (dots)
    • Blot haemorrhages (<=3)
    • Hard exudates
  2. Pre-proliferative retinopathy
    • Cotton wool spots (soft exudates; ischaemic nerve fibres)
    • > 3 blot haemorrhages
    • Venous beading/looping
    • Deep/dark cluster haemorrhages
    • More common in Type I DM, treat with laser photocoagulation
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5
Q

What are the new classifications for Diabetic Retinopathy?

A
  • Mild NPDR
    • 1 or more microaneurysm
  • Moderate NPDR
    • Microaneurysms
    • Blot haemorrhages
    • Hard exudates
    • Cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
  • Severe NPDR
    • Blot haemorrhages and microaneurysms in 4 quadrants
    • Venous beading in at least 2 quadrants
    • IRMA in at least 1 quadrant
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6
Q

What is Proliferative Retinopathy?

A
  • Retinal neovascularisation - may lead to vitrous haemorrhage
  • Fibrous tissue forming anterior to retinal disc

More common in Type I DM, 50% blind in 5 years

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7
Q

What is Maculopathy?

A
  • Based on location rather than severity, anything is potentially serious
  • Hard exudates and other ‘background’ changes on macula
  • Check visual acuity

More common in Type II DM

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8
Q

What are causes of Optic Neuritis?

A
  • Multiple sclerosis
  • Diabetes
  • Syphilis
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9
Q

What are features of Optic Neuritis?

A
  • Unilateral decrease in visual acuity over hours or days
  • Poor discrimination of colours, ‘red desaturation’
  • Pain worse on eye movement
  • Relative afferent pupillary defect
  • Central scotoma
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10
Q

What is the management of Optic Neuritis?

A
  • High-dose steroids
  • Recovery usually takes 4-6 weeks
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11
Q

What is the prognosis of Optic Neuritis?

A
  • MRI: if > 3 white-matter lesions
  • 5-year risk of developing multiple sclerosis is c. 50%
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12
Q

What is the classification of Hypertensive Retinopathy?

A

Keith-Wagener classification

  • Stage 1:
    • Arteriolar narrowing and tortuosity
    • Increased light reflex (silver wiring)
  • Stage 2
    • Arteriovenous nipping
  • Stage 3
    • Cotton-wool exudates
    • Flame and blot haemorrhages
  • Stage 4
    • Papilloedema
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13
Q

What is Papilloedema?

A

Papilloedema describes optic disc swelling that is caused by increased intracranial pressure. It is almost always bilateral.

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14
Q

What is observed on fundoscopy on Papilloedema?

A
  • Venous engorgement: usually the first sign
  • Loss of venous pulsation: although many normal patients do not have normal pulsation
  • Blurring of the optic disc margin
  • Elevation of optic disc
  • Loss of the optic cup
  • Paton’s lines: concentric/radial retinal lines cascading from the optic disc
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15
Q

What are causes of Papilloedema?

A
  • Space-occupying lesion: neoplastic, vascular
  • Malignant hypertension
  • Idiopathic intracranial hypertension
  • Hydrocephalus
  • Hypercapnia
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16
Q

What are rarer causes of Papilloedema?

A
  • Hypoparathyroidism and Hypocalcaemia
  • Vitamin A toxicity
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17
Q

What are features of Central Retinal Artery Occlusion?

A
  • Causes sudden unilateral visual loss due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
  • Features include afferent pupillary defect, ‘cherry red’ spot on a pale retina
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18
Q

What are risk factors for central vein occlusion?

A
  • Increasing age
  • Glaucoma
  • Polycythaemia
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19
Q

What are features of Central Retinal Vein Occlusion?

A
  • Sudden, painless reduction or loss of visual acuity, usually unilaterally
  • Severe retinal haemorrhages are usually seen on fundoscopy
  • Differential for sudden painless loss of vision
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20
Q

What are causes of Central Retinal Vein Occlusion?

A
  • Glaucoma
  • Polycythaemia
  • Hypertension
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21
Q

What are the most common causes of sudden painless loss of vision?

A
  • Ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
  • Vitreous haemorrhage
  • Retinal detachment
  • Retinal migraine
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22
Q

What are signs of Retinitis Pigmentosa?

A
  • Night blindness is often the initial sign
  • Tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
  • Fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
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23
Q

What is an Argyll-Robertson pupil?

A
  • Classic pupillary syndrome sometimes seen in neurosyphilis.
  • A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
  • Features
    • small, irregular pupils
    • no response to light but there is a response to accommodate
24
Q

What are causes of Argyll-Robertson pupil?

A
  • Diabetes mellitus
  • Syphilis
25
Q

What are associated diseases of Retinitis Pigmentosa?

A
  • Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
  • Usher syndrome
  • Abetalipoproteinemia
  • Lawrence-Moon-Biedl syndrome
  • Kearns-Sayre syndrome
  • Alport’s syndrome

Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision

26
Q

What is Holmes-Adie Pupil?

A
  • Holmes-Adie pupil is a benign condition most commonly seen in women.
  • Caused by damage to parasympathetic innervation (hence damage to the right ciliary ganglion) due to viral or bacterial infection.
27
Q

What are the signs of Holmes-Adie Pupil?

A

unilateral in 80% of cases

  • Dilated pupil
  • Once the pupil has constricted it remains small for an abnormally long time
  • Slowly reactive to accommodation but very poorly (if at all) to light
  • Association of Holmes-Adie pupil with absent ankle/knee reflexes
28
Q

What causes Marcus-Gunn pupil?

A
  • Relative afferent pupillary defect is found by the ‘swinging light test’.
  • Caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina
29
Q

How does a Marcus-Gunn pupil present on examination?

A

Relative afferent pupillary defect is found by the ‘swinging light test’.

  • the affected and normal eye appears to dilate when light is shone on the affected
30
Q

What causes Marcus-Gunn pupil?

A
  • Retinal detachment
  • Optic neuritis e.g. multiple sclerosis
31
Q

What are the afferent and efferent pathways in the pupillary light reflex?

A
  • Afferent: retina → optic nerve → lateral geniculate body → midbrain
  • Efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
32
Q

How is macular degeneration traditionally classified?

A

Dry (90% of cases, geographic atrophy) macular degeneration:

  • Characterised by drusen - yellow round spots in Bruch’s membrane

Wet (10% of cases, exudative, neovascular) macular degeneration:

  • characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis
33
Q

What is the new classification for age related macular degenerated?

A
  • Early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
  • Late age-related macular degeneration (neovascularisation, exudative)
34
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.
  • ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography.
  • Commonest cause of visual loss in elderly persons in the developed world. It affects 30-50 million people worldwide. The average age of presentation is greater than 70 years of age
35
Q
A
36
Q

What are risk factors of Age related macular degeneration?

A
  • Advancing age itself is the greatest risk factor for ARMD. The risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.
  • Smoking is another key risk factor in the development of ARMD, current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
  • Family history is also a strong risk factor for developing ARMD. First degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.
  • Other risk factors for developing the condition include those associated with increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.
37
Q

How does Age Related Macular degeneration present?

A

Typically present with a subacute onset of visual loss

  • Reduction in visual acuity, particularly for near field objects
  • Difficulties in dark adaptation with an overall deterioration in vision at night
  • Fluctuations in visual disturbance which may vary significantly from day to day
  • May also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
38
Q

What are signs on examination for Age Related Macular Degeneration?

A
  • Amsler grid testing
    • ​Distortion of line perception may be noted
  • Fundoscopy
    • Presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
    • In wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
39
Q

What are investigations for Age Related Macular Degeneration?

A
  • Slit-lamp microscopy is the initial investigation of choice
    • identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. Usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
  • Fluorescein angiography
    • Utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. May be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
  • Ocular coherence tomography
    • Used to visualise the retina in three dimensions, because it can reveal areas of disease which aren’t visible using microscopy alone.
40
Q

What is the treatment for Age Related Macular Degeneration?

A
  • AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that a combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
  • Vascular endothelial growth factor, (VEGF) is a potent mitogen and drives increased vascular permeability in patients with wet ARMD. A number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss. Evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible. Examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
  • Laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.
41
Q

What is Posterior Vitreous Detachment?

A
  • Occurs due to natural changes to vitreous fluid with ageing.
  • Common condition that does not cause any pain or loss of vision.
  • Can also lead to tears and detachment of the retina. Important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment as may result in permanent loss of vision
42
Q

What are risk factors for Posterior Vitrous Detachment?

A
  • Age of the individual
    • vitreous fluid becomes less vicous and pulls vitreous membrane away from retina towards centre of the eye
  • Highly myopic patients
    • due to longer axial length
43
Q

What are symptoms of Posterior Vitreous Detachment?

A
  • Sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
  • Flashes of light in vision (photopsia_
  • Blurred vision
  • Cobweb across vision
  • The appearance of a dark curtain descending down vision (means that there is also retinal detachment)
44
Q

What are signs of Posterior Vitrous Detachment?

A
  • Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
45
Q

What are investigations for Posterior Vitreous Detachment?

A
  • All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.
46
Q

How is Posterior Vitreous Detachment managed?

A
  • Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
  • If there is an associated retinal tear or detachment the patient will require surgery to fix this.
47
Q

What is a Vitreous Haemorrhage?

A
  • Vitreous haemorrhage is bleeding into the vitreous humour
  • One of the most common causes of sudden painless loss of vision.
  • Causes disruption to vision to a variable degree, ranging from floaters to complete visual loss. The source of bleeding can be from disruption of any vessel in the retina as well as the extension through the retina from other areas.
  • Once the bleeding stops, the blood is typically cleared from the retina at an approximate rate of 1% per day1.
48
Q

What are common causes of Vitreous Haemorrhage?

A
  • Proliferative diabetic retinopathy (over 50%)
  • Posterior vitreous detachment
  • Ocular trauma: the most common cause in children and young adults
  • Bleeding disorders
  • anticoagulants
49
Q

How does a Vitreous Haemorrhage present?

A
  • Painless visual loss or haze (commonest)
  • Red hue in the vision
  • Floaters or shadows/dark spots in the vision
50
Q

What are signs of Vitreous Haemorrhage?

A
  • Decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage
  • Visual field defect if severe haemorrhage
51
Q

What are investigations for Vitreous Haemorrhage?

A
  • Dilated fundoscopy: may show haemorrhage in the vitreous cavity
  • Slit-lamp examination: red blood cells in the anterior vitreous
  • Ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
  • Fluorescein angiography: to identify neovascularization
  • Orbital CT: used if open globe injury
52
Q

What are the most common causes of sudden painless loss of vision?

A
  • Ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
  • Vitreous haemorrhage
  • Retinal detachment
  • Retinal migraine
53
Q

How does Retinal Detachment present?

A
  • Dense shadow that starts peripherally progresses towards the central vision
  • A veil or curtain over the field of vision. Central visual loss
  • Straight lines appear curved
  • Features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters (see below)
54
Q

What are the differential of Ischaemia/vascular sudden visual loss (amaurosis fugax)?

A
  • Large artery disease (atherothrombosis, embolus, dissection)
  • Small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis)
  • Venous disease and hypoperfusion
55
Q

How can Ischaemic/Vascular sudden vision loss occur?

A
  • May represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
  • Ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
  • Altitudinal field defects are often seen: ‘curtain coming down’

Year 4k: Neuro and Special Senses (14 decks)

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