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Opthalmology > Summary eye conditions: Retinal > Flashcards

Summary eye conditions: Retinal Flashcards

1
Q

common retinal problems

A
  • Age related macula degeneration (most common cause of sight loss in UK)
  • Diabetic retinopathy
  • Hypertensive retinopathy
  • Retinal artery occlusion
  • Retinal vein occlusion
  • Posterior vitreous detachment
  • Retinal tear/ detachment
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2
Q

diabetic retinopathy background

A

High glucose content over a long period of time can cause damage to the retinal blood vessels, which causes haemorrhage and subsequent ischaemia to the retina.

Pathophysiology

  • Hyperglycaemia causes increased vascular permeability of the blood vessels
  • This causes leakage from the blood vessels including blot haemorrhage and hard exudates (lipids- yellow)
  • Ischaemia to the nerve fibres in the retina due to microaneursyms causes cotton wool spots (fluffy white patches)
  • Overtime due to chronic ischaemia neovasculisation occurs due to release of VEGF by the retina
    • Vitrous Haemorrhage can occur which can cause changes to vision (think blood blocking vision)
  • Over time diabetic retinopathy can lead to retinal detachment due to ischaemia of the retina
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3
Q

classification of diabetic retinopathy

A
  • Background
  • Pre-proliferative
  • Proliferative
  • Advanced
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4
Q

presentation of diabetic retinopathy

A

Asymptomatic

Symptoms
- Floaters -> small haemorhrages obscuring vision
- Blurred vision if maculopathy
- Decreased visual acuity
- Loss of vision
- Blindness

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5
Q

Key findings on fundoscopy: Diabetic retinopathy

A
  • Dot and blot haemorrhages
  • Hard exudates
  • Cotton wool spots
  • Venous beading
  • Microaneurysms
  • Neovascularisation
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6
Q

fundoscopy: background diabetic retinopathy

A

Microanerysms
Dot and blot haemorrhage

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7
Q

fundscopy: Pre-proliferative diabetic retinopathy

A

Cotton wool spots
- Accumulations of dead nerve cells from ischaemic damage

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8
Q

Fundoscopy: proliferative diabetic retinopathy

A

Neovascularisation (due to VEGF)

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9
Q

Advanced diabetic retinopathy can result in

A
  • Recurrent vitreous haemorrhage from bleeding areas of neovascularisation
  • Tractional retinal detachments as areas of neovascularisation grow into the vitreous and form fibrous bands suspending the retina
  • Rubeosis as neovascularisation occurs at the iris and drainage angle resulting in increased intraocular pressure and progressive glaucoma
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10
Q

management of diabetic retinopathy

A
  • Pan-retinal photocoagulation
  • Anti-VEGF medications such as ranibizumab and bevacizumab
  • Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
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11
Q

Pan-retinal photocoagulation

A

is the primary treatment for proliferative diabetic retinopathy.

The rationale behind the treatment is to reduce the production of VEGF by reducing the oxygen demand from the peripheral retina.

Clinically it is seen as clusters of burn marks on the retina which have been created by the laser used in the treatment process.

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12
Q

hypertensive retinopathy background

A

Damage to retinal vessels caused by systemic hypertension
- Chronic hypertension
- Malignant hypertension (acute)

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13
Q

Hypertensive retinopathy is graded as follows:

A

Keith-Wagner Classification

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 (similar to diabetic)
Stage 4: Papilloedema (malignant hypertension)

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14
Q

Key findings on fundoscopy: Hypertensive retinopathy

A
  • Silver/copper wiring (arterioles thickeed and sclerosed)
  • Arteriovenous nipping
  • Cotton wool spots (ischaemia to nerve fibres)
  • Hard exudates (damaged vessels leaking lipids into retina)
  • Retinal haemorrhage (damaged vessels rupture)
  • Papilloedema - ischameia to optic nerve leading to oedema
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15
Q

Malignant hypertension

A

Ggrade 4 hypertensive eye disease
- Which includes all the features of grade 3, with the addition of optic disc swelling.
- Other features include headaches, eye pain, reduced visual acuity and focal neurological deficits.

**Initial management **typically involves antihypertensives and emergency hospital admission.

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16
Q

general management of hypertensive retinopathy

A

Management is focused on controlling the blood pressure and other risk factors such as smoking and blood lipid levels.

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17
Q

age related macular degeneration background

A

Most common cause of vision loss in UK

Two types
- Wet (more acute and worse prognosis)
- Dry (90%) - no exudation or neovascularisation

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18
Q

pathophysiology of ARMD

A

Disease starting with the choroid layer (blood vessels), which affects all layers above: Bruchs membrane, retinal pigement epithleium and photoreceptors

Due to disrutpion of these layers Drusen form between the retinal pigment layer and Brich membrane
- found in both wet and dry AMD

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19
Q

Key findings on fundoscopy: both wet and dry

A
  • Drusen (yellow depsotis of protein and lipids)
  • Atrophy of the retinal epithelium
  • Degeneration of photoreceptors
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20
Q

Wet AMD pathophysiology

A
  • 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.
  • Fluid can be seen on OCT
  • A key chemical that stimulates the development of new vessels is **vascular endothelial growth factor (VEGF) **and this is the target of medications to treat wet AMD.
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21
Q

risk factors ARMD

A
  • Age
  • Smoking
  • White or Chinese ethnic origin
  • Family history
  • Cardiovascular disease
22
Q

presentation of ARMD

A
  • Gradual central visual field loss (scotoma)
  • Reduced visual acuity
  • Crooked or wavy appearance to straight lines

Wet age- much more acute

23
Q

investigation for wet ARMD

A

Optical coherence tomography

  • oedema caused by fluid leakage may be seen between layers
  • as well as drusen
24
Q

drusen on OCT

A
25
Q

management of Dry AMD

A

there is no specific treatment for dry age-related macular degeneration. Management focuses on lifestyle measure that may slow the progression:

  • Avoid smoking
  • Control blood pressure
26
Q

Wet AMD management

A

Anti-VEGF medications are used to treat wet age-related macular degeneration.
- Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels.
- They are injected directly into the vitreous chamber of the eye once a month.
- They slow and even reverse the progression of the disease.
- They typically need to be started within 3 months to be beneficial.

27
Q

Retinal artery occlusion

A

retinal artery is branch of ophthalmic artery, branch of internal carotid - think carotid stenosis

Can be:
- Central retinal artery
- Branch retinal artery

Cause:
- atheroscleorsis
- emboli e.g. from carotid
- Giant cell arteritis (polymyalgia rheumatica)

28
Q

presentation of central retinal artery occlusion

A

sudden, profound loss of vision
- painless
- relative afferent pupillary defect

29
Q

relative afferent pupillary defect

A

This is where the pupil in the affected eye constricts more when light is shone in the other eye compared when it is shone in the affected eye. This occurs because the input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex.

30
Q

key fundoscopy findings central retinal artery occlusion

A
  • Pale retina- due to lack of perfusion
  • Cherry-red spot - due to macula having a thinner surface
31
Q

management of central retinal artery occlusion

A

If GCA (high ESR and temporal artery biopsy)
- High dose prednisolone

If stroke
- ocular massage (if soon after)
- 300mg aspirin for 14 days

Long term
- statins
- management of hypertension and diabetes
- carotid endarectomy if required

32
Q

retinal vein occlusion background

A

when a thrombus forms in the retinal veins and blocks drainage of the eye

Types
- Central -> whole retina affected
- Branch (x4 branches) -> problem in area drained by that branch

33
Q

pathophysiology of central retinal vein occlusion

A
  • Occurs secodnary to atheroscleortic thickening of the central retinal artery compressing rhe central retinal vein at a common crossing poiint
  • Blockage of a retinal vein causes pooling of blood in the retina.
  • Central retinal veins runs through the optic nerve and is responsible for draining blood from the retina
  • This results in leakage of fluid and blood causing macular oedema and retinal haemorrhages.
  • This results in damage to the tissue in the retina and loss of vision.
  • It also leads to the release of VEGF, which stimulates the development of new blood vessels (neovascularisation).
34
Q

presentation of Central retinal vein occlusion

A
  • Sudden painless loss of vision
  • Relative afferent pupillary defect
35
Q

key fundoscopy findings: central retinal vein occlusion

A

Stormy sunset appearance
* Flame and blot haemorrhages
* Optic disc oedema
* Macula oedema
* Cotton wool spots

36
Q

management of retinal vein occlusion

A

Management in secondary care aims to treat macular oedema and prevent complications such as neovascularisation of the retina and iris and glaucoma. The options for this are:

  • Laser photocoagulation
  • Intravitreal steroids (e.g. a dexamethasone intravitreal implant)
  • Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)
37
Q

posterior vitreous detachment

A

the precursor to retinal tears and detachment
- very common as we get older due to the vitreous becoming more liquid and less able to hold shape (made up of collagen and water)
- PVD is where the vitreous gel comes away from the retina

38
Q

presentation of posterior vitreous detachment

A
  • Painless
  • Spots of vision loss
  • Floaters
  • Flashing lights
39
Q

OCT and posterior vitreous detachment

A
40
Q

Management of posterior vitreous detachment

A

No treatment is necessary. Over time the symptoms will improve as the brain adjusts.

41
Q

posterior vitreous detachment relationship to retinal tear and detachement

A
  • Can predispose patients to developing retinal tears and retinal detachment (1in 10)
  • They can also present very similarly.

It is essential to exclude and assess the risk of a retinal tear or detachment with a thorough assessment of the retina.

42
Q

Retinal detachment background

A

Retinal detachment is where the retina separates from the choroid underneath.

Cause
- This is usually due to a retinal tear that allows vitreous fluid to get under the retina and fill the space between the retina and the choroid.
- Outer retina relies on blood vessels of the choroid for its blood supply -> therefor sight threaning emergency unless treated quickly

43
Q

RF retinal detachment

A

Risk Factors

  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Trauma to the eye
  • Retinal malignancy
  • Older age
  • Family history
44
Q

presentation of retinal detachment

A

Sudden painless loss of vision described as a dark curtain or shadow
- Flashes and floaters (black dots)
- Peripheral vision loss

Visual acuity
Functions as a crude guide to determine if there is any macular involvement. The visual acuity is normal if the macula is still attached (macula on) and severely impaired if the macula is detached (macula off). It is important to perform crude confrontational visual fields assessment as this could pick up a peripheral retinal detachment.

45
Q

management of retinal tear

A

If a retinal tear is found, this can be treated with laser photocoagulation in the clinic and to reduce the risk of a detachment occurring.

46
Q

Surgical management of retinal detachment

A

Vitrectomy
- where vitreous and subretinal fluid are drained, allowing the retina to lie flat
- cryotherapy or laser therapy is then used to seal the retinal tear
- eye is then filled with absorbing gas, air or silicone oil to keep it from collapsing

after the surgery
- maintain head position e.g. on lateral side
- do not fly for 3-6 mkonths post surgery
- no anaesthetics involving NO

47
Q

imaging for retinal detachment

A
48
Q

Retinitis Pigmentosa background

A

congenital inherited condition where there is degeneration of the rods and cones in the retina
- normally rods degenerate more than cones (night blindness)

49
Q

Presentation of retinitis pigmentosa

A

The presentation can vary between different underlying causes. Family history is very important. In most causes the symptoms start in childhood.

  • Night blindness is often the first symptom
  • Peripheral vision is lost before the central vision.
50
Q

key fundoscopy findings: retinitis pigmentosa

A

Fundoscopy will show pigmentation. This is described as “bone-spicule” pigmentation. Spicule refers to sharp, pointed objects. Bone-spicule is used to refer to the similarity to the networking appearance of bone matrix.

The pigmentation is most concentrated around the mid-peripheral area of the retina.

51
Q

retinitis pigmentosa management

A

General management involves:

  • Referral to an ophthalmologist for assessment and diagnosis
  • Genetic counselling
  • Vision aids
  • Sunglasses to protect the retina from accelerated damage
  • Driving limitations and informing the DVLA
  • Regular follow up to assess vision and check for other potentially reversible conditions that may worsen the vision such as cataracts

Opthalmology (16 decks)

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