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OPTOM 450 > Posterior > Flashcards

Posterior Flashcards

1
Q

What is the pathogenesis of retinal vein occlusion

A

compression at AV crossings –> degenerative venous changes –> hypercoagubility

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2
Q

What are the risk factors of retinal vein occlusion? (9)

A 
hypertension
hyperlipidemia
diabetes
CVD
increased IOP/glaucoma
smoking
high BMI
CT disorders/sarcoidosis/lupus
vasculitis
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3
Q

Symptoms of BRVO? (5)

A 
may be asymptomatic
onset often in morning
transient vision loss
metamorphopsia
VF defects
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4
Q

Signs of acute BRVO (6)

A 
located in one quadrant
flame/dot-blot haemorrhages
CW spots
dilated, tortuous veins
oedema
ON swelling/hyperaemia
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5
Q

Signs of chronic BRVO (2)

A

venous collateral formation

vascular sheathing

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6
Q

What modalities should you use to investigate BRVO? (2)

A

Fluorescein angiography

OCT

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7
Q

BRVO complications (2)

A

macula oedema

vitreous haemorrhage

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8
Q

BRVO are urgently referred if acute and semi-urgently if chronic for a systemic work-up and consideration of what types of treatment? (3)

A

laser
intravitreal steroid
anti-VEGF Tx

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9
Q

What is the optometrists role in managing BRVO other than referral?

A

monitoring for signs of NV and assoc complications

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10
Q

What are the clinical features of CRVO? (7)

A 
intra-retinal haemorrhage (all quadrants)
venous engorgement and tortuosity
optic disc swelling
CW spots
CMO
sudden painless loss of vision
presenting VA reduced
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11
Q

Pathogenesis of CRVO?

A

Compression of CRV at lamina cribosa either by thrombus or CRA

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12
Q

Ischaemic vs non-ischaemic CRVO

A

Ischaemic

  • VA <6/60
  • marked RAPD
  • optic nerve swelling
  • severe venous tortuosity
  • risk of developing retinal and iris NV

Non-ischaemic

  • more common
  • VA >6/60
  • minimal RAPD
  • may convert to ischaemic
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13
Q

CRVO management? (4)

A

monitoring monthly for 1 year
thrombolytics
Laser chorioretinal anastomosis (L-CRA)
pan retinal photocoagulation

*possibly intra-vitreal anti-VEGFs

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14
Q

A person with CRVO has a better outcome when

A

present early and treated early

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15
Q

CRAO symptoms (3)

A
  • painless vision loss over several seconds
  • possible Hx of amaurosis fugax
  • vision significantly reduced (<6/120) unless cilioretinal artery present
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16
Q

CRAO signs (4)

A
  • VA <6/120 and RAPD in affected eye
  • Within first few minutes retina may look normal
  • ischaemic whitening of retina resulting in cherry-red spot at macula
  • retinal arteriole thinning and attenuation with possible segmentation of blood flow
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17
Q

What is the level of urgency for CRAO?

A

ophthalmic emergency - urgent referral

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18
Q

Management for CRAO? (7)

A
  • emergency referral
  • digital ocular massage or with gonio
  • reduction of IOP by paracentesis or pharmaceutically
  • assessment of risk of GCA
  • control of systemic disease (HT, diabetes, hyperchol)
  • assessment of carotid and cardiac disease as source of emboli
  • use of aspirin or warfarin
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19
Q

BRAO can occur secondary to what two things?

A

emboli

inflammation

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20
Q

Over 90% of BRAOs involve arteries in which area?

A

temporal retinal arteries

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21
Q

BRAO symptoms (2)

A
  • acute, unilateral, painless loss of vision over several seconds
  • visual field defect may be noticed
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22
Q

BRAO signs (4)

A
  • VA <6/12 affected eye
  • initially fundus looks normal within first few mins
  • localised ishaemic whitening of retina in area fed by arteriole
  • retinal arteriole thinning and attenuation with possible segmentation of blood flow
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23
Q

Management of BRAO (4)

A
  • referral for assessment of systemic associations
  • control of systemic disease as for CRAO
  • assessment for carotid and cardiac disease as for CRAO
  • majority of Px achieve 6/12 or better with conservative Tx
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24
Q

Which is more common: BRVO or CRVO?

A

BRVO

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25
Q

BRAO level of urgency?

A

urgent referral

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26
Q

Optic disc drusen is believed to be buried or superficial _______ material as a biproduct from which cells?

A

hyaline-like astrocyte

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27
Q

Optic disc drusen can often cause what two signs?

A

field defects

choroidal neovascular membranes

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28
Q

What tests are done for a definitive Dx of optic disc drusen? (2)

A

B-scan and FA

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29
Q

Optic disc drusen are associated with what condition?

A

Pseudoxanthoma elasticum

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30
Q

The most important thing with optic disc drusen is?

A

to rule out other conditions which involve the disc

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31
Q

Optic disc colobomas are typically located where and accompanies a field defect located where?

A

inferior nasal

superior

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32
Q

Optic disc and chorioretinal colobomas can develop into what?

A

serous macular detachment

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33
Q

Morning glory anomaly is what?

A

variant of ONH coloboma

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34
Q

With morning glory anomaly the disc is deeply escavated with what sort of tissue at the base?

A

glial

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35
Q

Optic disc pits are what?

A

atypical coloboma of ONH

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36
Q

What is management of Px with optic disc pit?

A

monitor carefully including home Amsler

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37
Q

With posterior coloboma conditions we need to be aware that these can develop what?

A

serous maculopathy

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38
Q

Which condition demonstrates the “double ring sign”

A

optic nerve head hypoplasia

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39
Q

Optic nerve head hypoplasia results in?

A

loss of NFL with variable VF defects

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40
Q

Which condition is associated with maternal infection or drug abuse, fetal alcohol syndrome, gestational diabetes and brain malformations?

A

optic nerve head hypoplasia

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41
Q

What condition can make the disc look raised with indistinct margins and have anomalous vascular branching patterns (not papilloedema, papillitis)

A

small optic disc

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42
Q

Which condition is characterised by an enlarged ONH with large cupping with the lamina often visible (DDx with glaucomatous cupping)

A

megalopapilla

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43
Q

High survival rates of retinoblastoma are associated with?

A

early detection

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44
Q

Retinoblastoma signs? (5)

A
  • White mass projecting forwards or backwards from retina
  • leukocoria
  • strabismus
  • intraocular inflammation
  • increased IOP
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45
Q

Tx of retinoblastoma? (4)

A
  • cryotherapy
  • thermotherapy
  • radiation therapy
  • enucleation
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46
Q

What condition is characterised by a retrolental mass of persistent embryonic hyaloid system and primary vitreous?

A

persistent hyperplastic primary vitreous

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47
Q

Retinopathy of prematurity is characterised by?

A

abnormal retinal vasculature in premature infants and/or low birth wt

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48
Q

ROP can be associated with?

A

supplemental oxygen

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49
Q

What are the five stages of ROP?

A

Stage 1 - white line at demarcation of avascular zone
Stage 2 - development of ridge and abnormal vessels
Stage 3 - fibrovascular proliferation
Stage 4 - contraction of fibrovascular tissue and RD
Stage 5 - complete RD

WARP CD

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50
Q

What is this condition?

  • single or grouped usually unilateral
  • flat, well demarcated, dark
  • tend to depigment over time
  • can be grouped (bear tracks)
  • can be atypical and associated with colon polyps
A

congenital hypertrophy of the RPE

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51
Q

When there are multiple, large, bilateral CHRPEs affecting several quadrants, what other condition needs to be considered?

A

familial adenomatous polyposis

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52
Q

What are myelinated nerve fibres?

A

persistent myelination of axons anterior to lamina cribosa

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53
Q

Which condition causes the fundus to later develop granularity pigmentary changes and vessel attenuation with other signs: sluggish pupils, nystagmus, strabismus, cataract, KC, abnormal ERG?

A

leber’s congenital amaurosis

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54
Q

Splitting of the NFL from retina in periphery is called?

A

retinoschisis

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55
Q

What condition has hypoplasia of ONH and/or fovea with varying levels of reduced VA?

A

albinism

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56
Q

varying degrees of amelanosis is due to varying levels of what?

A

tyrosinase

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57
Q

What is management of albinism? (2)

A
  • control glare and photophobia

- low vision aids

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58
Q

When examining a Px with albinism what should you keep in mind?

A

don’t prolong fundoscopy

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59
Q

What is the condition when you are born with no fovea?

A

hypoplastic fovea

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60
Q

What is tilted disc syndrome?

A

ONH appears rotated about its axis

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61
Q

Tilted disc syndrome signs? (4)

A
  • oval shape disc
  • scleral crescent
  • myopic astigmatism common
  • bi-temporal VF defects possible
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62
Q

What is obliquely inserted disc?

A

ONH inserts through scleral canal at an oblique angle

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63
Q

Obliquely inserted disc signs (4)

A
  • elevated nasally, buried temporally
  • function normal (usually)
  • often hyperopic
  • usually bilateral
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64
Q

Glial remnants are common in premature babies and protrude into the vitreal cavity and they are remnants of what?

A

embryonic hyaloid artery and related glial tissue

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65
Q

Toxoplasmosis scars are _________ in location, focal, with pigmented borders and can re-activate causing _____

A

chorio-retinal

retinitis

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66
Q

Risk factors for ARMD (3)

A
  • Age
  • Smoking
  • Race - higher incidence in Caucasians
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67
Q

Classification of ARMD including proportion of cases

A

atrophic - dry - 80-90%

exudative - wet - 10-20%

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68
Q

In atrophic AMD, atrophy of what three cell types occurs?

A

photoreceptors
RPE
choriocapillaris

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69
Q

What test is essential for diagnosis of ARMD?

A

OCT

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70
Q

Hard drusen are _____ in size (___um), discrete and usually does not necessarily signify ARMD

A

small

<50-60um

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71
Q

Soft drusen are _____ in size (___)um, have indistinct margins and is more associated with ARMD

A

larger

=/>60 microns

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72
Q

Soft drusen can develop and become two things which are?

A

confluent drusen

calcified

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73
Q

Drusen are accummulation of waste products from which layer of the PRs and are found in between what layers?

A

Outer segment

Bruch’s and RPE

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74
Q

Generally it is agreed that a Px has AMD after what is compromised? This occurs due to the ___ no longer being intact and causing damage to the PRs at the macula

A

BCVA

Inner segment

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75
Q

reflective deposits between RPE and retina found in the peripheral retina often seen in association with drusen and a risk factor for ARMD are called?

A

reticular pseudodrusen

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76
Q

Symptoms of atrophic ARMD? (4)

A
  • slowly decreasing BCVA
  • deepening central scotoma
  • usually bilateral but asymptomatic
  • positive Amsler grid findings
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77
Q

Signs of atrophic ARMD (4)

A
  • RPE atrophy and hyperpigmentation
  • broadening of atrophy with progression
  • visible choroidal vessels
  • drusen and mottling
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78
Q

Use of fluorescein angiography with atrophic AMD shows what two things?

A

hyperfluorescence in areas of RPE atrophy

hyper or hypo fluorescence of drusen

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79
Q

Tx of atrophic ARMD? (3) ish

A
  • none effective
  • nutritional supplements may slow progression
  • low vision aids when BCVA severely affected
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80
Q

Exudative ARMD signs? (4)

A
  • often soft, confluent drusen
  • serous maculopathy (sometimes with hard exudates)
  • Sub-RPE or sub-retinal CNV
  • Sub-retinal haemorrhage
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81
Q

Exudative ARMD symptoms (3)

A
  • increased blurred vision
  • metamorphopsia
  • vision loss can be sudden due to sub-macular haemorrhage
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82
Q

Suspected cases of exudative ARMD should be urgently referred for what test which determines the exact location in relation to the retina?

A

FA

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83
Q

Exudative ARMD Tx starting from historical to current main Tx (3)

A
  • Photodynamic therapy - inject VISUDYNE and laser applied to CNV
  • Argon laser photocoagulation - destroys CNV however cannot be undertaken if CNV near or under macula. 50% recurrence rate.
  • VEGF blockers
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84
Q

What are the 3 current VEGF blockers used to treat exudative ARMD?

A

1) bevacizumab (Avastin) - funded
2) ranibizumab (Lucentis) - restricted funding
3) aflibercept (Eylea) - better binding - not funded

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85
Q

Tx with anti VEGF usually starts with what regime? What else is also sometimes used in conjunction with anti-VEGFs?

A

monthly injections for 3 months then monitor for stability.

Intra-vitreal steroids

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86
Q

What conclusions came about from the AREDS studies?

A
  • zinc and antioxidants modestly effective in slowing progression of some AMD
  • adding lutein + zeaxanthin, DHA + EPA or both did not further reduce risk of progression
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87
Q

What sort of nutritional advice could you give to Px to reduce risk of ARMD?

A
  • increase intake antioxidants - colored veges, omega 3 (fish), vitamin supplements
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88
Q

What other advice could you tell patients to reduce risk of ARMD (4)

A
  • avoid smoking
  • improve lifestyle
  • home amsler grid
  • UV eye protection
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89
Q

Compare and contrast type 1 and 2 diabetes

A 
Type 1
- rapid onset in youth
- dependent on insulin
- 10% of diabetes
Type 2
- progressive
- variable dependence on insulin 
- can be treated with diet, exercise, weight control, oral agents and insulin
- 90% diabetes
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90
Q

Factors that determine presence of DR

A
  • duration of disease
  • level of blood glucose (HbA1c)
  • poor metabolic control
  • HT
  • pregnancy
  • nephropathy
  • elevated blood lipids
  • smoking
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91
Q

HbA1c levels have been classified as a percentage and categorise people as not diabetic or at risk. What are the values?

A

Not diabetic <6%

At risk 6-7%

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92
Q

Diabetes can cause what changes to the cornea? (4)

A
  • epithelial changes
  • reduced sensation and tear production
  • possibly thicken stroma
  • early aging signs at endothelium
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93
Q

Diabetes can cause what changes to iris and ciliary body? (3)

A
  • vacuoles of pigment epithelium
  • pinhole trans-illumination defects
  • rubeosis irides
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94
Q

Diabetes can cause what changes to lens? (4)

A
  • snowflake cataract
  • increased risk of age-related cataracts
  • varying of refractive power
  • more post op complications after cataract surgery
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95
Q

Diabetes can cause what changes to the vitreous? (2)

A
  • haemorrhage

- possibly early PVD

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96
Q

Diabetes can also cause diplopia, ptosis and anisocoria through complications of which cranial nerves?

A

III
IV
VI

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97
Q

Non-proliferative signs of DR are related to loss of which type of cells?

A

pericytes

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98
Q

Signs of NPDR (8)

A
  • microaneurysms
  • macular oedema
  • dot, blot, flame haemorrhages
  • hard exudates
  • intraretinal oedema
  • CW spots
  • IRMAs
  • venous beading
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99
Q

PDR is associated with retinal _____ causing the formation of ________ and involves ______ growth factors

A

hypoxia
new vessels
vascular endothelial

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100
Q

Signs of PDR (4)

A
  • NV
  • fibrous tissue
  • pre-retinal or vitreous haemorrhages
  • tractional RD
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101
Q

Clinically significant macular oedema (CSMO) is defined as oedema within how many DD?

A

1/3

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102
Q

Macular oedema is defined as within?

A

2DD of centre of macula

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103
Q

Assessment of macular oedema requires _______ ______ and diagnosis requires _____

A

stereoscopic examination

OCT

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104
Q

CSMO is treated with? (2)

A

Anti-VEGFs

laser

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105
Q

What sort of examination is required for every diabetic Px?

A

DFE

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106
Q

What two tests are needed for detecting DR?

A

FA

OCT

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107
Q

Grade R0 (No DR) - clinical signs and outcome?

A

No abnormalities
For type 1 - re-screen at 2 years, adjusting for clinical modifiers
For type 2 - re-screen at 2-3 years, adjusting for clinical modifiers

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108
Q

Grade R1 (Minimal) - clinical signs and outcome?

A

<5 microaneurysms or dot haemorrhages

Re-screen at 2 years depending on clinical modifiers

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109
Q

Grade R2 (mild) - clinical signs and outcome?

A

> 4 microaneurysms or dot haemorrhages
Exudates >2DD from fovea
Some blot and larger haemorrhages acceptable
If more than 20 microaneurysms or haemorrhages per photographic field, upgrade to R3
Outcome - Re-screen after 12 months

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110
Q

Grade R3 (moderate) - clinical signs and outcome?

A

Any features of mild
Blot or larger haemorrhages
Up to one quadrant of venous beading
Outcome - re-screen 6 months

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111
Q

Grade R4 (severe) - clinical signs and outcome?

A

One or more of:

  • definite IRMA
  • two quadrants or more of venous beading
  • four quadrants of blot or larger haemorrhages

Outcome - review by ophthal within 6 weeks

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112
Q

Grade R5 (proliferative) - clinical signs and outcome?

A

One or more of:

  • NV
  • sub-hyaloid or vitreous haemorrhage
  • traction RD or retinal gliosis

Outcome - urgent referral to ophthal

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113
Q

Adequate quality of photos for grading require a minimum field size of? When is it required to take a superior and inferior image also?

A

two 45 degree fields

type 1 diabetes or R3 and higher

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114
Q

Taking a quality diabetic photo should produce an overlap of at least how many degrees horizontally and vertically?

A

75 horizontally

45 vertically

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115
Q

Which form of treatment for DR reduces risk of VA loss and is more effective if undertaken before high risk features are present?

A

photocoagulation

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116
Q

Symptoms of vitreous inflammation (4)

A
  • Floaters
  • Ache ?
  • Decreased VA (depending on maculopathy)
  • Red eye (depending on location)
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117
Q

Signs of vitreous inflammation (7)

A
  • vitritis
  • vitreous opacities
  • PVD
  • retinitis/scarring
  • CMO
  • cataract
  • RD
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118
Q

What in particular causes vitreous inflammation?

A

intermediate and posterior uveitis

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119
Q

Which vitreous opacity are calcium soaps suspended in the vitreous that do not usually affect vision, usually do not move and is associated with diabetes and vascular disease?

A

asteroid hyalosis

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120
Q

Which vitreous opacity is any part of the hyaloid system that can remain and can cause floaters. They are also known as Mittendorf’s dot and Bergmeister’s papilla

A

hyaloid remnants

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121
Q

Which vitreous opacity often results from NV or retinal tears?

A

intra-vitreal haemorrhage

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122
Q 
Which vitreous opacity can result from:
trauma
intraocular surgery
intraocular inflammation
RD
A

pigment particles

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123
Q

Which vitreous opacity are cholesterol crystals which:

  • tend to form and settle in liquefied vitreous
  • can be stirred up with movement
  • tend to occur following vitreal inflammation and haemorrhage
A

synchysis scintillans

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124
Q

Persistent hyperplastic primary vitreous is what?

A

failure of regression of embryonic hyaloid vascular system

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125
Q

PHPV is usually unilateral/bilateral, common/rare, causes __________ and often associated with what (4) conditions?

A

unilateral
rare
leukocoria
microphthalmia, cataract, glaucoma, RD (+ others)

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126
Q

Retinoblastoma originates from where?

A

any layer of the retina

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127
Q

There are two types of retinoblastomas which are?

A

endophytic - grows inwards towards vitreous

exophytic - grows outwards into subretinal space –> RD + haem

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128
Q

Retinoblastomas can cause? (4)

A
  • leukocoria
  • strabismus
  • intra-ocular inflammation
  • increased IOP
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129
Q

What symptoms are common during PVD?

A

flashes and floaters

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130
Q

PVD can cause what other three things

A

RD
retinal haemorrhage
macular traction syndrome (and possible macula hole)

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131
Q

Lattice degeneration represents areas of (1) and (2) which run circumferentially between what two structures (3/4)?

A

1) retinal thinning
2) capillary drop-out
3) ora serrata
4) equator

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132
Q

Snail track degeneration is likely a variant of what other condition?

A

lattice degeneration

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133
Q

Which two conditions can contain atrophic holes and which is less likely to cause RD?

A

lattice degeneration and snail track degeneration

snail track less likely to cause RD

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134
Q

What peripheral retinal condition is thought to be congenital (may be degenerative) is usually seen in the inferio/temporal quadrant is associated with areas of retinal thinning with loss of RPE with Bruch’s membrane intact and is of NO CONSEQUENCE

A

Pavingstone degeneration

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135
Q

Which peripheral retinal condition is very common, tends to increase with age and is characterised by cysts in the NFL or OPL and can be a precursor to what condition?

A

cystoid degeneration

retinoschesis

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136
Q

Which peripheral retinal condition can be mistaken for a RD, is usually bilateral, is flat, sharply demarcated and considered to be due to abnormal vitreo-retinal traction or a prominent vireous base (of no consequence)

A

white without pressure

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137
Q

RPE degeneration and disorganisation of pigment granules in the perpheral retina is characteristic of which condition? This condition can also have what characteristic which makes it look similar to RP?

A

1) reticular (pigmentary) degeneration
(a condition of no consequence)
2) can have bone spickle apperanace

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138
Q

What is retinoschesis (incl what layer is involved)

A

Splitting of neuro-retina (outer plexiform layer)

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139
Q

Retinoschesis is often associated with what other condition?

A

cystic degeneration

retinoschesis is a benign condition

140
Q

Which condition is caused by mutation of gene controlling ornithine keto-acid aminotransferase which leads to 2nd decade axial myopia, night blindness, cataract and CMO with poor prognosis for vision?

A

gyrate atrophy

141
Q

What are vitreo-retinal adhesions (tufts)?

A

abnormal areas of localised attachment of retina to vitreous with white tuft appearance

142
Q

Vitreo-retinal adhesions (tufts) require monitoring for what reason?

A

can cause retinal traction

143
Q

Define a retinal detachment

A

separation of the photoreceptors from the RPE

144
Q

RD can be classified as?

A
  • with retinal break (rhegmatogenous)
  • without retinal break (non-rhegmatogenous)
    • tractional
    • exudative/serous
145
Q

Retinal breaks can be classified as? (3)

A
  • U or V shaped with apex pointing to post pole
  • operculated (flap completely torn off)
  • dialyses (tears away from ora)
146
Q

Most retinal breaks are located where on the retina?

A

superio-temporal

147
Q

What are risks for retinal breaks? (7)

A
  • PVD
  • vitreous traction
  • lattice degeneration
  • snail track degeneration
  • white without pressure
  • retinoschisis
  • retinal traction
148
Q

PVD’s are generally assoc with no complications but they can cause what two things

A

retinal break

vitreous haemorrhage

149
Q

Following cataract surgery and YAG capsulotomy in myopia there is a higher risk of what?

150
Q

Risk factors for rhegmatogenous RD (6)

A
  • retinal holes/tears
  • myopia
  • FHx
  • RD other eye
  • Hx of trauma
  • Hx of intraocular surgery
151
Q

Symptoms of rhegmatogenous RD (3)

A
  • photopsia
  • floaters
  • VF defect
152
Q

Sign of rhegmatogenous RD (5)

A
  • Shafer’s sign
  • Tear/s or hole/s in retina
  • RAPD if extensive RD
  • decreased IOP if RD is large
  • mild anterior uveitis possible
153
Q

How can you tell the difference between a recent and longstanding rhegmatogenous RD? (3 each)

A

Recent
- affected retina appears opaque or gray
- tends to move with eye movements
- loss of visibility of underlying structures
Longstanding
- retina thins = some viewing of underlying structures possible
- high water mark of pigmentation forms at boundary
- intraretinal cysts may develop

154
Q

Compare and contrast a rhegmatogenous RD vs retinoschisis (write on paper - 9 points for each)

A

RD

  • looks whitish initially, semitransparent later
  • surface folds
  • tends to undulate on eye movements
  • retinal break present
  • pigmented demarcation line when longstanding
  • speed of enlargement variable
  • can invade posterior pole
  • symptoms common
  • usually treated

Retinoschisis

  • usually transparent
  • smooth, taut surface
  • no movement
  • inner and outer breaks possible
  • rarely has pigmented demarcation line
  • enlarge very slowly
  • rarely invades posterior pole
  • usually asymptomatic unless affects post pole
  • not usually treated unless inner and outer breaks
155
Q

Non-rhegmatogenous RDs can be due to what two things?

A 
proliferative retinopathy
proliferation of (epi) retinal membranes
156
Q

How does a tractional RD (without retinal break) compare to a rhegmatogenous RD? (3 main points)

A

tends to be slower onset and without flashes and floaters

affected retina not usually mobile

157
Q

Describe exudative RD

A

exudation from choriocapillaris into subretinal space (fluid passes through RPE) causing detachment

158
Q

What are the causes of exudative RD? (6)

A
  • central serous retinopathy
  • subretinal NV
  • choroidal tumours (75%)
  • posterior scleritis
  • severe hypertension
  • systemic corticosteroids
159
Q

Symptoms of exudative RD (3)

A
  • no flashes usually, might be present in acute presentation
  • absolute scotoma at site of lesion
  • metamorphopsia if central
160
Q

Signs of exudative RD (4)

A
  • no retinal breaks
  • smooth surface
  • RD can be deep and fluid may be seen to move with gravity
  • underlying cause may be seen (e.g. choroidal tumour)
161
Q

What is polypoidal choroidal vasculopathy?

A

network of branching inner choroidal vessels ending with polyp-like extensions which occupy the sub-retinal space and can cause fluid build up and haemorrhage

162
Q

Polypoidal choroidal vasculopathy is considered a unique form of _____ and has an appearance of ____, ____-like elevations and is diagnosed with what two tests?

A

CNV
sharp, dome-like elevations
OCT and FA

163
Q

How do you manage CSR if:

  • first episode
  • recurrent
A
  • if first episode monitor up to 3 months and refer if non-resolving
  • consider referral for recurrent cases
164
Q

What do you have to rule out for CSR?

A

other causes of serous detachments e.g. choroidal melanoma, ARMD

165
Q

What modality is required to confirm Dx of CSR?

166
Q

In all cases of flashes and floaters what must we do?

A

Rule out retinal breaks, RD, PVD

167
Q

Comment on time for surgery for macula-off RD (2)

A
  • Eyes treated up to 3 days have better outcomes than eyes treated after. No difference within the first 3 days.
  • should NOT postpone surgery for macula-off detachments
168
Q

Drug induced maculopathy can be caused by what 6 drugs?

A
  • Chloroquine and hydroxychloroquine
  • phenthiozines
  • tamoxifen
  • vigabatrin
  • methanol
169
Q

Cystoid macular oedema is characterised by ______ accumulations of fluid with _________ formations, typically in a _____ pattern.

A
  • intracellular accumulations of fluid

- microcystic formations, typically in a stellate pattern

170
Q

CMO symptoms and signs (5)

A
  • often asymptomatic in early stages
  • metamorphopsia
  • reduced vision
  • prolonged photostress recovery
  • subtle macular changes, increasingly obvious with progression
171
Q

Definitive Dx of CMO requires what modality

172
Q

CMO is associated with what conditions? (6)

A
  • post-ocular surgery
  • retinal vascular disorders
  • intraocular inflammation
  • retinal degeneration (RP, cellophane maculopathy, tumours)
  • idiopathic
  • drug related (epinephrine)
173
Q

What is the prognosis and Tx for CMO? (5 for Tx)

A
  • often self-limiting within 3 months
  • referral to consider:
    NSAIDS
    steroids
    anti-VEGFs
    CAIs
    laser
174
Q

Vitreomacular traction syndrome can cause what symptoms? (4)

A

metamorphopsia
decreased VA
micropsia
photopsia

175
Q

Pxs who get macular holes are usually? (2)

A

over 60

female

176
Q

Macular holes are considered to be caused by? (2)

A

vitreal traction forces and/or cystic formation

177
Q

Macular holes are usually unilateral and there is a __ yr risk of development in the other eye with no ___ with a chance of __-__%

A

5 year risk
PVD
20-30%

178
Q

Describe stage 1 macular hole (5)

A
  • loss of foveal depression
  • radial traction lines possible
  • metamorphopsia/distortion
  • VA might remain good
  • appearance of yellow spot possible (xanthophyll)
179
Q

Describe stage 2 macular hole (3)

A
  • VA drops to 6/12-6/30
  • foveal hole or tear develops
  • cuff of subretinal fluid
180
Q

Describe stage 3 macular hole (6)

A
  • further vitreo-foveal separation
  • enlargement of hole
  • positive Watzke-Allen test
  • operculum may be visible
  • white/yellow deposits may be visible in hole
  • VA 6/30-6/60
181
Q

Describe stage 4 macular hole (3)

A
  • Full thickness hole with PVD
  • operculum might be mobile
  • central absolute scotoma
182
Q

What is prognosis of stage 1 macular hole vs stage 2 or 3?

A

30-50% of stage 1 holes arrest and spontaneously resolve whereas less than 10% of stage 2 or 3 holes resolve

183
Q

Tx of macular holes? (4)

A

refer to retinal specialist to consider:

  • vitrectomy
  • vitreous peeling
  • gas tamponade
  • face down therapy
184
Q

Epiretinal membranes/cellophane retinopathy/macular pucker is due to?

A

proliferation of glial cells from retina

185
Q

Epiretinal membranes can be idiopathic or secondary. Secondary causes can be from? (6)

A
  • chronic RD
  • secondary glaucoma
  • chorio-retinitis
  • DR
  • ocular surgery
  • laser photocoagulation
186
Q

When should you consider referral for epiretinal membrane and what will the ophthal likely do?

A

when vision 6/12

membrane peel

187
Q

Signs of degenerative myopia? (6)

A
  • RPE atrophy
  • lacquer cracks
  • CNV
  • subretinal haemorrhagse
  • Foerster-Fuchs spot
  • macular hole
188
Q

What condition is characterised by orange peel effect seen at and temporal to the macula where cracks in thickened Bruch’s membrane radiate from the disc?

A

angioid streaks

189
Q

Characteristics of optic disc pits (4)

A
  • congenital
  • serous maculopathy in ~50% cases
  • metamorphopsia
  • VF defects
190
Q

direct sun gazing causes bilateral VA loss, chromatic changes in vision, metamorphopsia and causes foveo-macular retinitis. This condition is called?

A

Solar maculopathy

191
Q

Stargardt disease is _______ in inheritance is a __lateral condition and causes reduced _____ vision from about ____ years old to about 6/___ or less

A 
autosomal recessive
bilateral
central
10
6/60
192
Q

Fundus flavimaculatus can occur with or without Stargardt and has what characteristics? (4)

A
  • yellow white flecks (disruption of RPE)
  • accummulation of lipofuscin
  • variable effect on vision
  • 50% have Stargardt
193
Q

Best Disease is _____ in inheritance and reduces vision from about ___ years of age. It is characterised by what appearance?

A

autosomal dominant
10 yrs old
egg-yolk appearance due to lipofuscin accummulation

194
Q

Name the prostaglandins for glaucoma Tx (3)

A

latanoprost (Hysite)
travaprost (Travatan)
Bimatoprost (brand name same)

195
Q

Name the beta-blockers for glaucoma Tx (4)

A

Betaxolol (Betoptic)
levobunolol (Betagan)
Timolol (same)
Timolol XE (Timolol gel)

196
Q

Name the sympathomimetics (a2 agonists) for glaucoma Tx (2)

A

brimonidine (Alphagan)

apraclonidine (Iopidine)

197
Q

Name the carbonic anhydrase inhibitors for glaucoma Tx (3)

A

acetazolamide (Diamox)
Brinzolamide (Azopt)
Dorzolamide (Trusopt)

198
Q

Name the combination meds for glaucoma Tx (6)

A 
Latanoprost + timolol (Xalacom)
Travaprost + timolol (DuoTrav)
Brimonidine + timolol (Combigan)
Brinzolamide + timolol (Azarga)
Dorzolamide + timolol (Cosopt)
Bimatoprost + timolol PF (Ganfort)
199
Q

Glaucoma is an ____ _________ caused by chronic destruction of ______ cells with characteristic atrophy and functional loss with or without IOP elevation.

A

optic neuropathy

ganglion

200
Q

A visual field loss may only be detected after how many ganglion cells are lost?

201
Q

Mechanical theory of glaucomatous optic neuropathy

A
  • IOP damages neurons at lamina
  • compression/rearrangement of lamina cribrosa sheets
  • distortion/enlargement of lamina pores
  • altered lamina and ECM
  • results in axoplasmic stasis
  • necrosis
202
Q

Vascular theory of glaucomatous optic neuropathy

A
  1. ischaemia due to blood flow abnormalities or elevated IOP reduces perfusion
  2. autoregulation of blood flow in ON arteries abnormal
  3. slows axoplasmic flow
  4. damages optic nerve/peripapillary region
203
Q

What conditions are associated with POAG

A
  • systemic hypotension
  • decreased cardiac output or BP drop at night
  • migraine/vasospasm
  • diabetes
  • acute loss of blood
  • chronic vascular obstruction
  • hyperviscosity diseases
204
Q

What is the apoptosis theory of glaucomatous optic neuropathy?

A
  1. elevated IOP decreases axoplasmic flow
  2. Decreases effect of BDNF for ganglion cell survival
  3. initiates apoptosis response
205
Q

What two main factors are thought to be responsible for optic nerve injury/insult in glaucoma which leads to cell death –> excitotoxicity + decreased NTFs –> apoptosis

A

elevated IOP

decreased blood flow

206
Q

Define target pressure

A

the pressure at which the clinician expects the loss to be no greater than the age related rate

207
Q

What is the relation between IOP and corneal thickness?

A

0.3mmHg per 10um (Goldmann is calibrated for 515um)

208
Q

How can you mechanically increase outflow through the TM?

A

cholinergic agonists e.g. Pilocarpine

209
Q

What effect do steroids have on outflow?

A

steroid respones –> increase GAGs in TM –> increased outflow resistance

210
Q

What are the two main routes for aqueous outflow including outflow capacity %

A
  1. Canalicular/TM 85-95%

2. Extracanalicular/uveo-scleral outflow 5-15%

211
Q

What glaucoma drug increases outflow by acting on the CB and how?

A

Prostaglandins (e.g. Latanoprost) by decreasing CT density in CB and making it more porous

212
Q

Glaucoma patients with big diurnal spikes in IOP are best treated with what kind of drug?

A

Outflow drugs e.g. prostaglandins

213
Q

What are the avenues of treatment for glaucoma? (3)

A
  1. lowering IOP
  2. treating vascular diseases
  3. countering apoptosis/promoting neuroprotection
214
Q

What are the predictive factors for glaucoma (according to OHTS)? (6)

A
  • age (older)
  • race (african higher iop)
  • CD ratio (vertical more relevant)
  • IOP
  • corneal thickness
  • increased or asymmetric PSD
215
Q

Which glaucoma drug is a potential neuroprotective drug?

A 
Brimonidine
- impairs apoptotic pathways
- upregulates anti-apoptotic genes
- reduced excitatory aa release
- increased neuroprotective agents
BUT lack of clear evidence
216
Q

What are the risk factors for POAG? (7)

A
  • FHx
  • Ethnicity (african americans>caucasians>asians)
  • Age
  • IOP
  • Vascular conditions (hypo/hyperT, diabetes, reynauds, migraine)
  • Myopia
  • Obesity
217
Q

Comment on the characteristics of NTG (6)

A
  • more sensitive to ON damage
  • more splinter haemorrhages
  • ONH cupping larger and steeper at time of Dx
  • frequent inferotemporal displacement of cup
  • higher incidence of inferior focal rim compromise or notching
  • slower progressive VF loss
218
Q

Pseudoexfoliation glaucoma is characterised by what 2 things which can lead to what?

A
  • amyloid-like material in AC and TM
  • iris transillumination near pupil margin
  • material can lead to peripupillary ischaemia and PS leading to pigment release and further TM blocking
219
Q

What signs might you see with a patient with pigmentary glaucoma? (4)

A
  • spoke wheel iris transillumination
  • krukenbergs spindle
  • pigment deposit in TM
  • Sampaolesi line
220
Q

Which groups of people are at higher risk of steroid responsive glaucoma?

A
  • diabetic
  • high myopic
  • CT damage
  • children
221
Q

Name as many secondary open angle glaucomas as you can (7)

A 
pseudoexfoliation
pigmentary
steroid responsive
intraocular inflammatory
neovascular
lens-associated
traumatic
222
Q

Describe characteristics of sub-acute PACG (3)

A
  • intermittent pain/halos
  • precipitated at night or with dilation
  • frequent recurrence
223
Q

Describe characteristics of chronic PACG (2)

A
  • eye quiet with usually mildly shallow angles

- gonio shows narrow angle with broad areas of PAS

224
Q

What are the risk factors for PACG? (4)

A
  • shallow AC
  • plateau iris
  • large lens
  • iridocorneal syndromes
225
Q

Name 4 types of secondary ACG

A
  • intraocular inflammatory
  • subluxated lens
  • neoplasm of iris/CB
  • phacomorphic (secondary to hyper/mature cataract)
226
Q

What ocular signs do we need to consider when diagnosing glaucoma? (9)

A
  • abnormal NRR
  • laminar pore slits
  • cup size for ON size
  • peripapillary atrophy
  • retinal fibre layer loss
  • CD ratio >0.5
  • CD ratio asymmetry >0.2
  • non-central insertion of CRA
  • compromised AC
227
Q

What are the five rules (5+1) of ONH evaluation for glaucoma?

A
  • disc size
  • ISNT (looking more at notching or vert elongation)
  • disc haems
  • RNFL dropout
  • PPA
  • changes to BVs e.g. baring, bayoneting
228
Q

Give the 5 stages of Tubingen classification of glaucomatous defect (maybe write physically)

A 
Stage 0
- increased short term fluctuations in arcuate region (nasal step)
- review
Stage 1 (mild)
- relative defect - local loss in arcuate defect, nasal step
- act
Stage 2 (mild-moderate)
- absolute defect
- act
Stage 3 (moderate)
- ARCUATE DEFECT - joins blind spot
- act
Stage 4 (moderate-severe)
- multiple arcuate defects 
- peripheral break through threat to fixation 
Stage 5 (severe)
- end stage glaucoma
- act
229
Q

What is the target IOP for stage 1-2 (Tubingen)

230
Q

What is the target IOP for stage 3 (Tubingen)

231
Q

What is the target IOP for stage 4 (Tubingen)

232
Q

What is the target IOP for progressive glaucomatous defects

233
Q

What do we do to the IOP level for 60 and 70yo respectively

A

60yo - drop 1 IOP level

70yo - drop 2 IOP levels

234
Q

How is field loss in LTG/NTG different from POAG? (4)

A
  • more frequent damage within 5 degrees of fixation
  • higher probability in superior hemifield
  • field loss is steeper sided and more dense in NTG
  • more localised
235
Q

Is SWAP useful in glaucoma diagnosis?

A

probably picks up glaucoma earlier because it picks up on different GCs but the test is difficicult to do and takes a long time

236
Q

What are the three R’s to assess the results of threshold VF tests?

A

reliability
region affected
repeatibility

237
Q

What is the mean deviation (MD) in a VF test?

A

average deviation from age-matched normals

238
Q

What is the PSD in VF test?

A

average slope (drop off from hill of vision)

239
Q

What is the GHT in VFs?

A

uses 5 mirror image clusters of points

240
Q

what is the total deviation in VF test?

A

compares average sensitivity to normal

241
Q

What is the pattern deviation in VF test?

A

total deviation corrected for diffuse loss

242
Q

What % of FP is considered unreliable in VF?

243
Q

What % of fixation losses is considered unreliable in VF?

244
Q

What % of FN is considered unreliable in VF?

245
Q

Scotomas are characterised by which reliability indices?

A

high FN

high fixation loss

246
Q

Detection of local defects is the hallmark sign of POAG - what is important in regards to VF testing for reliability

A

repeat fields to confirm reliability

2-6 weeks later

247
Q

Definition of progression in glaucoma

A

if structural and/or functional changes, associated with the disease, are verifiably detected on clinical examination and/or testing

248
Q

VF progression is judged with what analysis?

A

event or trend analysis

249
Q

How many VF tests do you need to establish baseline?

250
Q

How many VF tests do you need to do per year to establish progression?

A

2 per year, within 2 years

251
Q

What is the problem with FDT compared to SAP in VF testing?

A

FDT provides poor progression data

252
Q

What is the gold standard glaucoma examination required under NHMRC guidelines? (5)

A 
Must do all of the following:
IOP
gonio
VF
optic disc images
RNFL images
253
Q

What is the suggested glaucoma work-up? (12)

A
  • Case Hx
  • BCVA
  • Pupils
  • Monocular CV
  • Gonio
  • Pachy
  • Anterior segment
  • Tono (GAT)
  • dilation
  • VF (threshold)
  • NFL assessment
  • ONH analysis
254
Q

Dry eye is a _________ disease of the ______ ______ characterised by a loss of _________ of the tear film, and accompanied by ocular ________, in which tear film _______ and ________, ocular surface ________ and damage, and ___________ abnormalities play _______ roles.

A

Dry eye is a multifactorial disease of the ocular surface characterised by a loss of homeostasis of the tear film and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles.

255
Q

The tear film has 4 main functions which are?

A
  • optical
  • mechanical
  • nutritional
  • defensive
256
Q

What four things can cause aqueous deficient dry eye (ADDE)?

A
  • Sjogren Syndrome
  • Non-Sjogren Syndrome (congenital, age)
  • Lacrimal gland obstruction
  • Hyposecretion due to lacrimal function unit (LFU) failure
257
Q

Evaporative dry eye (EDE) can be classified into two groups by?

A
  • lid related (obstructive MGD)

- ocular surface related (Vit A deficiency, mucin/glycocalyx deficiency, iatrogenic)

258
Q

What sort of triaging questions would you use when diagnosing dry eye? (3)

A

How severe is the eye discomfort?
Do you have any mouth dryness or enlarged glands?
How long have your symptoms lasted and was there any triggering event?
Is your vision affected and does it clear on blinking?
Are the symptoms or any redness much worse in one eye than the other?
Do the eyes itch, are they swollen, crusty or any discharge?
Do you wear CLs?
Have you been diagnosed with any general health conditions or taking any meds?

259
Q

What sort of risk factor questions could you ask when diagnosing dry eye?

A
  • smokin
  • diet
  • CL wear
  • General health
  • Medications
  • Environment
  • Screen/computer use
260
Q

What three diagnostic tests can you do for dry eye diagnosis?

A

TBUT (non-invasive via keratoscope or NaFl)
Osmolarity
Ocular surface staining

261
Q

What is the diagnostic criteria for osmolarity of tears to diagnose hyperosmolarity?

A

> 308mOsm/L
OR
inter-eye difference >8mOsm/L

262
Q

What is the diagnostic criteria for ocular surface staining?

number of corneal punctate spots, conjunctival spots, lid margin width

A

Corneal punctate spots >5
Conjunctival spots >9
Lid margin >2mm length and 25% width

263
Q

What are the diagnostic tear volume tests for aqueous deficient dry eye disease? (3)

A

tear meniscus height
Shirmer test
Phenol red test

264
Q

What are the diagnostic tests for evaporative dry eye disease? (5)

A
  • MG assessment (expressibility and oil flow)
  • Meibography
  • Interferometry
  • Blink and lid closure
  • Lid margin keratinisation
265
Q

What are the three main things to consider when managing dry eye?

A
  • protect eyes from environment
  • retain or supplement the tears
  • look after the eyelids
266
Q

What are the methods for tear conservation?

A
  • tear retention (reducing tear evap) with goggles

- punctal occlusion

267
Q

When is punctal occlusion contraindicated? (2)

A

not aqueous deficient dry eye

dry eye due to eyelid disease

268
Q

What therapeutic is good for reducing bacterial load for the lids?

A

Fusidic acid 1% (active against gram +ve)

269
Q

What other alternative therapy has been shown to be good for reducing bacterial load?

A

manuka honey

270
Q

What is the current recommendation for treating demodex?

A

lid hygiene with tea tree lid cleanswer daily for 4-6 weeks

271
Q

What are three methods for altering the composition of the oils for MGD?

A
  • systemic anti-inflammatory therapy
  • essential fatty acids
  • artificial supplementation (lipid based drops)
272
Q

Treatment with tetracyclines (e.g. low dose doxycycline for 2-3 months) does what?

A

laters meibum composition by improving lipid quality and irritation symptoms and dry eye signs

273
Q

Doxycycline is contraindicated in? (2)

A

growing children and pregnancy

274
Q

Is increasing omega-3 or omega-6 anti-inflammatory?

275
Q

The two main anti-inflammatory therapies for dry eye are?

A
  • topical glucorticoids

- non-glucocorticoid immunomodulators (cylcosporine, NSAIDs, tarcolimus)

276
Q

TD-OCT vs SD-OCT (5 points each - write)

A 
TD-OCT
- A-scan generated sequentially, 1 pixel at a time
- moving reference mirror
- 400 scans/sec
- low resolution
- slower than eye movement
SD-OCT
- entire A-scan generated at once
- stationary reference mirror
- 26000 scans/sec
- high resolution
- faster than eye movement
277
Q

In OCT which lesions are hyper-reflective? (3)

A

hard exudates
blood
scars

278
Q

In OCT which lesions are hypo-reflective? (2)

A

serous fluid

hypo-pigmented lesions of RPE

279
Q

What is the technique in OCT where A-scans are done anterior to posterior (instead of a cross-section)

280
Q

Define optic neuropathy

A

any pathological condition of the optic nerve

281
Q

Define optic neuritis

A

inflammation of the optic nerve

282
Q

Define optic atrophy

A

loss of neurons within the optic nerve due to cell death

283
Q

Define papilloedema

A

bilateral elevation of the optic nerve heads secondary to raised intracranial pressure

284
Q

What sort of cinical signs could you expect to find with optic nerve dysfunction? (6)

A
  • reduced VA
  • VF defects
  • impaired CV (red/green defects)
  • decreased brightness sensitivity
  • decrease CS
  • afferent pupillary defect
285
Q

How would the optic nerve appear with optic atrophy and why?

A

optic nerve pallor (pale or white coloration) due to astrocytes which fill the spaces where axons died

286
Q

There are many causes of optic atrophy, name 3? (6)

A
  • papillitis
  • compression (tumours, aneurysms)
  • Leber’s
  • Toxic/nutritional optic neuropathies (alcohol)
  • Ischaemia
  • chronic papilloedema
287
Q

What are signs of true disc swelling? (5)

A
  • blurred NFL
  • disc vessels partially/fully obscured
  • cup retained
  • dilated retinal veins
  • flame-shaped haemorrhages
288
Q

In which optic neuritis does the optic disc look normal? This optic neuritis is also the most common in adults and is frequently associated with what other condition?

A

retrobulbar optic neuritis

multiple sclerosis

289
Q

What is neuroretinitis?

A

papillitis with inflammation of retinal NFL and exudates at macula in a star pattern

290
Q

What are the 4 causes of optic neuritis?

A
  • demyelinating (most common)
  • parainfectious (following viral infection/immunisation)
  • infectious (cat scratch fever, syphillis, Lyme disease)
  • non-infectious (sarcoidosis, SLE)
291
Q

What are symptoms of optic neuritis? (6)

A
  • decreased VA (minimal to NLP)
  • decreased CV
  • decreased CS
  • VF abnormalities (vary)
  • pain around eye (esp with eye movements)
  • Uhthoff’s phenomenon (diff perception of motion between each eye)
292
Q

Describe the two signs of optic neuritis

A
  1. fundus appearance of optic disc
    - two thirds have normal appearance
    - one third show papillitis
    - exudates in pattern of macular star uncommon with demyelinating
  2. RAPD on affected side
293
Q

Describe the course of vison loss with optic neuritis (3)

A
  • variable levels of monocular vision loss progressing over 7-10 days
  • vision tends to recover after 2 weeks, mostly complete after 1 month
  • 90% achieve 6/12 or better
294
Q

Management of optic neuritis? (2)

A
  • most do not require Tx
  • corticosteroids may speed up recovery but does not influence final visual outcome (only prescribed under special circumstances)
  • MRI for prognosis
295
Q

Risk factors for NAION

A
  • age (55-70)
  • structural crowding of the ONH
  • predisposing systemic conditions
296
Q

Name predisposing systemic conditions for NAION (8)

A
  • HT
  • diabetes
  • hypercholesterolemia
  • sudden hypotensive events
  • cataract surgery
  • sleep apnoea
  • erectile dysfunction medications
297
Q

Signs of NAION? (6)

A
  • sudden, painless monocular vision loss
  • RAPD
  • VF defects (typically inf altitudinal)
  • dyschromatopsia (red/green)
  • diffuse or sectorial hyperaemic disc swelling
  • presence of known factors
298
Q

Management of NAION? (4)

A
  • urgent referral
  • no definitive treatment
  • address systemic predispositions
  • rule out GCA (ESR and CRP estimation)
299
Q

AAION is caused by ____ and has strong association with what condition?

A

giant cell arteritis

systemic polymyalgia rheumatica

300
Q

Signs of AAION (3)

A
  • sudden, profound unilateral vision loss and can be accompanied by periocular pain and/or preceded by TVO and flashing lights
  • systemic symptoms of GCA (headache, scalp tenderness, jaw claudication)
  • pale “chalky white” oedematous disc
301
Q

What is the gold standard method of diagnosing GCA?

A

temporal artery biopsy

302
Q

With a blood test, what would you expect to see with AAION?

A

elevated ESR and CRP

303
Q

Management for AAION? (2)

A
  • immediate referral

- systemic steroids for GCA - IV methylprednisolone 3 days followed by long taper of oral prednisolone

304
Q

What is PION?

A

ischaemia of the retrolaminar optic nerve

305
Q

PION occurs in specific scenarios which are? (3)

A
  • operative - especially spinal surgery w/ resultant bilateral poor vision
  • arteritic
  • non-arteritic (similar prognosis to NAION but not assoc with small discs)
306
Q

Parainfectious optic neuropathy is associated with?

A

various viral infections e.g. measles, mumps, chickenpox, rubella

307
Q

Parainfectious optic neuropathy usually occurs in ____ and is characterised by ______, ______ vision loss, - weeks after exposure and usually present with bilateral _____

A

children
acute, severe
papillitis

308
Q

Treatment for paraninfectious optic neuropathy?

A

none required in most cases (spont visual recovery)

- consider intravenous steroids if vision loss severe bilaterally or affecting only seeing eye

309
Q

Infectious optic neuropathy is a DIRECT result of?

A

infection by various organisms

310
Q

Give some examples of what can cause infectious optic neuropathy (3)

A
  • sinus-related
  • cat-scratch fever
  • syphillis
  • Lyme disease
  • crytococcal meningitis
  • varicella zoster
311
Q

How is infectious optic neuropathy treated?

A

appropriate anti-infective

312
Q

Sarcoid optic neuropathy causes what three things to the optic nerve?

A
  • compression
  • infiltration
  • ischaemia
313
Q

Signs of sarcoid optic neuropathy?

A
  • often presents like MS
  • “lumpy” disc possible
  • granulomatous uveitis (mutton fat KPs) common
314
Q

Tx of sarcoid optic neuropathy?

A

systemic steroids for ON involvment

topical/periocular steroids for uveitis

315
Q

Characteristics of Leber’s hereditary optic neuropathy (6)

A
  • caused by mutation of maternally inherited mitochondrial dna
  • males>females (9:1)
  • usually teens to early twenties
  • unilateral acute/subacute, painless, severe loss of central vision
  • second eye involved within weeks/months of first
316
Q

Signs of Leber’s hereditary optic neuropathy (5)

A
  • hyperaemia/elevation of optic disc
  • thickening of peripapillary retina
  • peripapillary telangiectasia
  • tortuosity of arterioles
  • optic disc atrophy
317
Q

Tx Leber’s hereditary optic neuropathy and prognosis?

A
  • no effective Tx

- very poor prognosis (most permanent bilateral 6/60 or worse)

318
Q

What is the most common inherited hereditary optic neuropathy characterised by bilateral progressive acuity loss and tritanopia

A

dominant optic atrophy (DOA)

319
Q

Nutritional optic neuropathy usually occurs with people who are _____, ______, ______ and experience ______, bi/unilateral vision loss with acquired _________.

A

alcoholics, smoke in excess, poor diets
progressive bilateral
dyschromatopsia

320
Q

Toxic optic neuropathy is commonly caused by (2)

A

methanol and ethylene glycol

321
Q

radiation optic neuropathy is probably a result of radiation induced what?

A

vascular occlusion

322
Q

What are the causes of increased intracranial pressure? (5)

A
  • intracrainal lesions (tumour, haem)
  • ventricular system obstruction
  • impairment of CSF absorption
  • severe systemic HT
  • idiopathic (pseudotumour cerebri)
323
Q

On refill write out the four different stages of papilloedema

A

Early

  • mildly elevated hyperaemic discs
  • loss of spontaneous venous pulsation
  • vision normal

Established

  • moderately elevated hyperaemic discs
  • venous engorgement, peripapillary haemorrhages and CW spots
  • TVOs + possible reduced VA

Chronic

  • marked elevated discs
  • lack of CW spots or haemorrhages
  • variable VA and VF constriction

Atrophic

  • slightly elevated, dirty grey discs
  • VA severely impaired
324
Q

Symptoms of papilloedema? (5)

A
  • possibly none initially
  • headache
  • nausea and vomiting
  • changes in vision (TVOs, horizontal diploplia, VA)
  • deterioration of consciousness
325
Q

What are the goals for management of papilloedema?

A

goal is to relieve headache and prevent vision loss

326
Q

idiopathic intracranial hypertension is normally seen in?

A
  • obese women of child bearing age

- associated with certain medications or sleep apnoea

327
Q

Which portion of the occipital lobe is responsible for central macula vision?

A

most posterior portion

328
Q

Which portion of the occipital lobe is responsible for peripheral vision?

A

mid-occipital portion

329
Q

Which portion of the occipital lobe is responsible for extreme temporal vision on the contra-lateral side

A

anterior most portion

330
Q

A lesion in the anterior occipital lobe causes?

A

monocular temporal crescent defect in contra-lateral eye

331
Q

A lesion in the mid-occipital lobe causes?

A

macula sparing congruous homonymous hemianopia

332
Q

A lesion at the posterior tip of the occipital lobe causes?

A

congruous homonymous central defect

333
Q

What is amaurosis fugax

A

sudden onset monocular vision loss

334
Q

What things should you check for a Px reporting amaurosis fugax? (5)

A
  • neck pain or Hx of neck injury
  • symptoms of GCA
  • emboli on funduscopy
  • pupils
  • CV
335
Q

Any patient with any form of homonymous hemianopia must have what done?

336
Q

What is the most common cause of homonymous VF loss?

337
Q

What is migraine aura?

A

neurological symptoms that precede, accompany or more rarely follow a migraine headache

338
Q

Symptoms of aura can be positive or negative. Name a few positive symptoms

A
  • scintillating scotomas
  • fortification spectra
  • flashes
  • heat waves
  • kleidoscope effects
  • fragmented vision
339
Q

Symptoms of aura can be positive or negative. Name a few negative symptoms

A
  • homonymous hemianopia
  • tunnel vision
  • cortical blindness
  • transient monocular vision loss
340
Q

What is retinal migraine

A

repeated episodes of monocular visual disturbances incl scintillations, scotomata or blindness assoc with migraine headache

341
Q

DDx for migraine aura (3)

A
  • photopsia from vitreous traction
  • TIAs from retinal emboli
  • transient visual obscurations
342
Q

DDx of migraine HA

A
  • arteriovenous malformation
  • HZO
  • trigeminal neuralgia
343
Q

Tx and management of migraine?

A

avoidance of triggers

medications

344
Q

Migraine without aura vs tension type headaches?

A

finish this card for before exams

345
Q

Characteristics of a cluster headache?

A

finish this card for exams

346
Q

Characteristics of Charles Bonnet Syndrome

A

finish this card for exams

OPTOM 450 (2 decks)

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