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Ophthalmology > Common retinal diseases | > Flashcards

Common retinal diseases | Flashcards

1
Q

What age do most people get age-related macular degeneration (AMD)?

A

> 50

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2
Q

What are the 2 forms of AMD?

A
  1. Dry (atrophic)

2. Wet (neovascular) - choroidal neovascularisation (CNV)

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3
Q

What is the pathophysiology of the dry form of AMD (4)?

A
  1. Breakdown of light-sensitive cells in the macula causes one or more sharply demarcated areas of partial or complete depigmentation (atrophy) of the RPE.
  2. The areas of atrophy can enlarge over time.
  3. Atrophy may or may not involve the fovea (the central part of the macula)
  4. There is accumulation of membranous or lipophilic debris between the RPE and the underlying Bruch’s membrane, with amorphous thickening of Bruch’s membrane - these deposits appear as Drusen
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4
Q

What is the pathophysiology of the wet form of AMD (3)?

A
  1. The development of new blood vessels beneath and within the retina, they proliferate and penetrate Bruch’s membrane
  2. The new vessels are unlike normal retinal vessels and easily bleed or leak blood constituents, resulting in distortion and scarring of the retina which leads to distorted vision/LOV
  3. In neovascular AMD, the development of soft, diffuse drusen is associated with breaks in Bruch’s membrane. These breaks may provide sites through which new blood vessels from the underlying choriocapillaris grow and proliferate.
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5
Q

What is the ratio of dry:wet forms of AMD?

A

90:10

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6
Q

What is the clinical picture of dry AMD?

A

As there is slow and gradual loss of the macula, there is the gradual loss of central vision related to difficulty in reading and recognising faces (unless it converts to the wet type)

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7
Q

What is the treatment of dry AMD?

A

No treatment at present - just visual rehabilitation

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8
Q

What is the visual loss in wet AMD (2)?

A
  1. Distortion in vision

2. Sudden loss of central vision

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9
Q

What is the risk factor for AMD (wet and dry) (3)?

A
  1. Smoking
  2. Cardiovascular disease: hypertension, hyperlipidaemia
  3. Low antioxident levels in blood
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10
Q

What disabilities are associated with AMD (8)?

A
  1. Increased risk of falling
  2. Difficulty shopping
  3. Difficulty managing money
  4. Difficulty preparing meals
  5. Difficulty using telephone
  6. Difficulty with housework
  7. Suffer from emotional distress and depression
  8. High users of healthcare and community support services
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11
Q

Where is the RPE located?

A

Between the choroidal layer from the retinal neurons or photoreceptors

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12
Q

What is Bruch’s membrane?

A

Innermost layer of the choroid

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13
Q

What is an Amsler’s grid? What does someone with AMD see?

A

A squared grid with a dot

Someone with AMD experiences distortion in their vision, making the grid distorted

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14
Q

What 4 visual components do you need to evaluate in someone with AMD?

A
  1. VA - distance and near
  2. Reading speed
  3. Contrast sensitivity
  4. Central visual field - Amsler
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15
Q

What 5 investigations would you do in someone with AMD?

A
  1. Fundus photos
  2. Fundus fluorescein angiography
  3. Indocyanine green angiography (ICGA)
  4. Optical coherent tomography (OCT)
  5. US
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16
Q

In wet AMD with choroidal neovascularisation, how is it characterised (2)?

A
  1. Location in relation to foveal centre

2. Fluorescein Angiograph characteristics/leakage type

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17
Q

In the characterisation of CNV, how is it characterised according to location (2)?

A
  1. Extrafoveal (>200u from foveal centre)
  2. Juxtafoveal (1-199u from the foveal centre)
  3. Subfoveal (under foveal centre)
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18
Q

In the characterisation of CNV, how is it characterised according to FFA/leakage type (2)?

What can be used to distinguish them?

A
  1. Classic
  2. Occult

Fluorescein angioraphic features help distinguish classic and occult choroidal neovascularization.

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19
Q

What is the natural history of wet AMD (2)?

A
  1. Variable, dependent on type

2. Occult CNV: 50% develop classic CNV within 1 year, otherwise visual loss is slow

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20
Q

How can you differentiate between classic and occult CNV on fluorescein angiography (2)?

A
  1. Classic’ lesions penetrate the RPE and thus are located in front of the RPE, and ‘occult’ lesions are sub-RPE.
  2. Classic membranes are associated with an early hyperfluorescent area that is well-demarcated, which increases in intensity and extent beyond the early phase boundary by mid- to late-frames. Pooling of fluorescein associated with a concomittant subsensory retinal detachment may also be appreciated.
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21
Q

What are the 5 types of treatment available for wet AMD?

A
  1. Focal laser photocoagulation
  2. Photodynamic therapy (PDT) with visudyne
  3. Pharmacologic agents
  4. Surgery
  5. Combination treatments
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22
Q

What are the aims of treatment for AMD?

A

To reduce spread of neovascularisation

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23
Q

When is laser photocoagulation used?

A

No longer the preferred mode of treatment, but useful in small extrafoveal lesions (less than 5% cases)

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24
Q

How does laser photocoagulation work?

A

It is a non-selective thermal laser

  • destroys choroidal neovascular lesions
  • can also damage the overlying retina
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25
Q

What is the eligibility for laser photocoagulation (3)?

A
  1. Extrafoveal or juxtafoveal lesions
  2. Classic CNV
  3. Well-demarcated lesion boundaries
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26
Q

What are limitations of laser photocoagulation (3)?

A
  1. Only 13-25% of patients with wet AMD are eligible
  2. Laser can cause immediate irreversible retinal damage associated with an absolute scotoma and loss of VA
  3. Leakage persists or recurs in 50% of treated patients
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27
Q

What is photodynamic therapy (PDT) with visudyne (2)?

A

2-step process

  1. Visudyne is injected over 10 min
  2. Non-thermal light via slit lamp activates Visudyne. Localised endothelial cell damage occurs in the CNV resulting in thrombus formation leading to occlusion of abnormal vessels

Needs to be repeated at 3-monthly intervals

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28
Q

What are the aims of pharmacologic agents in the treatment of wet AMD?

A

Interrupting the factors stimulating or maintaining the growth of the endothelial cells in the CNV, especially VEGF
-anti-VEGF agents

29
Q

What anti-VEGF agents are used in the treatment of wet AMD (5)?

A
  1. Pegaptanib sodium - given 6 weekly
  2. Ranibizumab - blocks all isoforms of VEGF
  3. Aflibercept - blocks all isoforms of VEGF
  4. Anecortave acetate
  5. Avastin - used off license
30
Q

What surgery can be done in the treatment of wet AMD (2)?

A

Vitrectomy and submacular excision of CNV and:
1. Replacing ‘sick’ RPE
or
2. Macular rotation required to lie foveal retina on ‘normal’ RPE

31
Q

What other forms of rehabilitation are given to patients with AMD in their management (3)?

A
  1. Registration as visually impaired - may allow access to help from social services
  2. Low vision assessment (LVA) - initial visit and continuing dialogue
  3. Support groups and societies - macular disease society, RNIB
32
Q

What is the pathophysiology of diabetic retinopathy (DR) (3)?

A
  1. Affects retinal precapillary arterioles, capillaries and venules
  2. Resulting retinal disease may be vascular leakage and/or closure (and sequelae)
  3. Sequelae related to VEGF and other factors released in the retina
33
Q

What is the incidence of DR most related to?

A

DM

34
Q

What are risk factors for DR (8)?

A
  1. Duration of dm
  2. Age
  3. Smoking
  4. Hypertension
  5. Poor dm control
  6. Hyperlipidaemia
  7. Renal impairment
  8. Pregnancy
35
Q

What are the 2 types of DR?

A
  1. Non-proliferative DR (NPDR)/’background’ DR

2. Proliferative (PDR)

36
Q

When does diabetic maculopathy occur?

A

Occurs with either NPDR or PDR

37
Q

How long after onset of DM does NPDR usually occur?

A

> 8-10 years

38
Q

What is the usual clinical presentation of NPDR?

A

Usually asymptomatic

39
Q

What are the 3 levels of severity of NPDR?

A

Mild
-Indicated by presence of at least 1 microaneurysm

Moderate
-Includes the presence of haemorrhages, microaneurysms and hard exudates

Severe (4-2-1)
-Characterised by haemorrhages and microaneurysms in 4 quadrants, with venous beading in at least 2 quadrants and intraretinal microvascular abnormalities in at least 1 quadrant

40
Q

What are the 7 clinical manifestations of NPDR on fundoscopy?

A
  1. Microaneurysms
  2. Exudates
  3. Retinal haemorrhages
  4. Cotton wool spots
  5. Vascular dilatations
  6. Calibre variations
  7. Intraretinal microvascular abnormalities (IRMA)
41
Q

What are microaneurysms?

A

Focal dilatations of retinal capillaries

Small red dots in the superficial retinal layers which may leak, usually temp to macula

42
Q

What are the 3 different haemorrhages that can occur in NPDR?

A
  1. Dot (small)
  2. Blot (large) from the venous end of retinal capillaries occur deep in the retinal outer and inner plexiform layers
  3. Flame shaped haemorrhages (located in nerve fibre layer) may occur
43
Q

What are exudates in NPDR and what do they look like (2)?

A
  1. Yellowish-white deposits with well defined edges
  2. Represent leaked lipoproteins from diseased retinal vasculature resulting from breakdown of blood-retina barrier. Deeper to superficial retinal bv
44
Q

What are cotton wool spots (CWS) in NPDR and what do they look like (2)?

A
  1. Greyish white, poorly defined fluffy edged lesions in the nerve fibre layer;
  2. Reflect leakage of axoplasmic fluid: a sign of ischaemia
45
Q

What manifestations of severe NPDR would you find on fundoscopy (4)?

A
  1. Large number of dark haemorrhages
  2. Irregular calibre variation (beading)
  3. Dilatation of retinal veins
  4. Intraretinal microvascular abnormalities (IRMAs)
46
Q

What is the prognosis of severe NPDR?

A

Most will progress to PDR within 12 months

47
Q

What % of people with dm get PDR?

A

5%

48
Q

Patients with which type of DM are more likely to get PDR?

A

Type 1

49
Q

What is the pathophysiology of PDR?

A

Characterised by the development of:
-new vessels on the optic disc (NVD)
or
-new vessels elsewhere e.g. the retina (NVE)

Occurs as a response to significant retinal ischaemia

50
Q

What are the characteristics of new vessels (NV) in PDR (3)?

A

NV appear as small tufts of

  1. Irregularly ramifying vasculature arising from veins
  2. NV are initially flat but enlarge and move forward into the vitreous
  3. The NV are fragile and likely to bleed with slight traction resulting in pre-retinal and/or vitreous haemorrhage
51
Q

What are 4 late changes/complications of PDR?

A
  1. Retinal fibrosis, which can lead to traction retinal detachment
  2. Traction RD (progressive contraction of fibrovascular membrane)
  3. Iris neovascularisation (rubeosis iridis) and neovascular glaucoma
  4. Risk of pre-retinal/vitreous haemorrhage
52
Q

What is diabetic maculopathy?

A

Specific type of DR with macular involvement

53
Q

Does diabetic maculopathy occur more commonly among those with Type 1 or 2 dm?

A

Type 2

54
Q

What is the prognosis of diabetic maculopathy if left untreated?

A

Leads to visual loss

55
Q

What are the 3 types of diabetic maculopathy?

A
  1. Focal
  2. Diffuse
    + (mixed)
  3. Ischaemic
56
Q

What is focal diabetic maculopathy?

A

Focal leakage from microaneurysms or dilated capillaries resulting in focal retinal thickening and surrounding exudates

-Retinal thickening and hard exudates

57
Q

What is diffuse diabetic maculopathy?

A

Diffuse leak from dilated capillaries resulting in diffuse retinal oedema/thickening which may be associated with some retinal haemorrhages but usually no exudates

-Features of ischaemia and exudation

58
Q

What is ischaemic diabetic maculopathy?

A

Due to closure of the perifoveal capillary network; manifests as diffuse oedema plus associated dark haemorrhages. Fluorescein angiography is important in confirming ischaemia

-Normal foveal appearance and reduced vision

59
Q

What are the forms of treatments for:

  1. All DR
  2. PDR
  3. Diabetic maculopathy
A
  1. All
    - Control of diabetes and other risk factors
  2. PDR
    - Pan-retinal photocoagulation
    - Vitrectomy for vitreous haemorrhage, tractional RD
  3. Maculopathy
    - Anti-VEGF agents - intravitreal injection (now mainstay of treatment)
    - Laser photocoagulation for focal/diffuse maculopathy (not for ischaemic)
    - Combination of intravitreal injection and laser
    - Intravitreal steroid injection
60
Q

What 4 types of laser photocoagulation can be used for DR and what for?

A
  1. Focal laser - for stopping focal leaks in focal maculopathy
  2. Grid laser - In diffuse macular oedema
  3. Mixed maculopathies require combined strategies
  4. Pan-retinal photocoagulation (PRP) is recommended treatment for PDR
61
Q

What other 6 diabetic eye diseases are there apart from DR (6)?

A
  1. Increased incidence of eyelid infections
  2. Increased incidence of cataracts
  3. Cranial nerve palsies: III, IV, VI
  4. Delayed healing of corneal abrasions, corneal ulcers
  5. More severe post-op intraocular inflammation e.g. after cataract surgery
  6. Abnormal wound healing
62
Q

What are the first-line management of wet AMD?

A

anti-VEGF agents

63
Q

What are the 2 indications for vitrectomy in DR?

A
  1. No-response or inadequate response to laser photocoagulation for PDR
  2. Clearing persistent vitreous haemorrhage or retinal fibrosis and/or traction retinal detachment which is threatening the macula or causing reduction in vision
64
Q

What is the NSC grading for DR?

A

R0 - No retinopathy
R1 - Background
R2 - Pre-proliferative (beading, IRMA, blots)
R3 - Proliferative (3a - active/3s - stable)

M0 - No maculopathy
M1 = Exudate within 1 disc diameter (DD) of macula, circinate exudates, retinal thickening <1DD, haemorrhage or microaneurysm <1DD with VA<6/12

65
Q

What are IRMAs?

A

Intraretinal microvascular anomalies

  • Dilated, tortous retinal capillaries that act as a shunt between arterioles and venules, that act to supply areas of non-perfusion in DR, frequently seen adjacent to areas of capillary closure
  • Arteriole to venule and do not cross another large vessel
  • Compared to NV, they are larger with more broad arrangement and always contained in the intraretinal layers. They also do not leak, unlike NV.
66
Q

What is venous looping, beading and sausage like segmentation, found in NPDR (2)?

A
  1. Occurs in areas of capillary closure
  2. Frequently occur adjacent to areas of nonperfusion; they reflect increasing retinal ischaemia and their occurence is the most significant predictor of pregression to PDR
67
Q

What are the features of mixed diabetic maculopathy?

A

Features of ischaemia and exudation

68
Q

When is treatment advised for diabetic maculopathy (3)?

A

If there is clinically significant macular oedema (CSMO) comprising at least one of the following:

  1. Thickening of the retina within 500um of the fovea
  2. Hard exudates located within 500um of the fovea with adjacent retinal thickening
  3. Retinal thickening at least one disc area in size, part of which is located within one disc diameter of the fovea
69
Q

What 7 questions in the history should you ask about in a patient with DR?

A
  1. Who looks after your DM and when is your next appt?
  2. How is your DM treated?
  3. What was last HbA1c? (trend)
  4. Age of onset
  5. Duration of diabetes
  6. What was last BP and how often is it checked?
  7. Do you take a statin/fibrate/glitazone/aspirin/warfarin/ACEi

Ophthalmology (12 decks)

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