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Sem1revcards > Mx Exam Revision > Flashcards

Mx Exam Revision Flashcards

1
Q

What is the 1st-choice pharmaceutical treatment for reducing IOP in glaucoma and why?

A

Prostaglandin Analogues [specifically Xalatan]: highest efficacy [30% reduction] and once-daily usage [24hr IOP control] is convenient.

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2
Q

List 4 potential side effects of prostaglandin analogues

A

Darker iris
Lash growth
Loss of orbital fat
Red eye [either short term or long term]

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3
Q

List 4 different options for prostaglandin analogues, including their dosage percentages

A

Latanaprost [Xalatan 0.005% NOCTE]
Travaprost [Travatan 0.004% NOCTE]
Bimatoprost [Lumigan 0.03% NOCTE]
Tafluprost [Zioptan 0.0015% NOCTE]

** that’s right lumigan is actually 0.03%

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4
Q

What alternative prostaglandin can you consider if Xalatan is only achieving a small reduction (IOP redcution <5mmHg)? Why?

A

Travatan: it binds better to PGF2alpha

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5
Q

What downside may occur in switching from xalatan to travatan?

A

May have more adverse/side effects

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6
Q

Of the 4 mentioned prostaglandin options, which results in the least side effects and least conjunctival hyperaemia?

A

Xalatan.

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7
Q

List 3 contraindications for prostaglandin analogues

A

Uveitis
Pregnancy
HSV

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8
Q

List 2 prostaglandin analogues to consider for a patient with ocular surface disease or sensitivity to BAK preservative

A

Travaprost [uses an ionic buffered preservative]

Tafluprost [preservative free]

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9
Q

Aside from PGAs, list 3 other drug classes that can be used to reduce IOP in open angle glaucoma

A

Carbonic Anhydrase Inhibitors
Beta Blockers
Alpha Agonists

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10
Q

Which drug class makes the best adjunct to PGAs?

A

CAIs. Because PGAs secondary action promotes the action of CAIs.

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11
Q

What is the ideal patient for PGAs?

A

Those with a chronic, non-acute IOP elevation (i.e. POAG and NOT aacg or post-op iop spike)

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12
Q

List 2 topical CAI options for reducing IOP

A

Dorzolamide [Trusopt 2% TiD]

Brinzolamide [Azopt 1% BiD]

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13
Q

List 4 benefits for topical CAIs

A

Reduces diurnal fluctuation
Good vascular nocturnal profile
Fast effect [1 hr]
Good adjunct to PGAs

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14
Q

Which topical CAI has less stinging? Dorzolamide or Brinzolamide? Why?

A

Brinzolamide. It coms in a 10mg/ml suspension which means it has a slower release and therefore less stinging.

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15
Q

List 1 contraindication for CAIs

A

Corneal graft/corneal compromise. Topical CAIs can result in corneal deturgescence.

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16
Q

Which glaucoma drops are safest to use in the first trimester?

A

Brimonidine [an alpha agonist] may be the safest option for the first trimester. [** it’s also generally the safest drug as it’s a category B1 drop]

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17
Q

Which glaucoma drops are safest to use in the second trimester? (3)

A

Brimonidine
Beta blockers [with regular fetal heart rate/growth monitoring]
CAIs [with fetal growth monitoring]

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18
Q

Which glaucoma drops are safest to use in the third trimester? (3)

A

Brimonidine [must discontinue late in 3rd trimester to avoid CNS depression in newborns]
Beta blockers
Topical CAIs
**All to be used with caution

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19
Q

What are the main risks associated with glaucoma surgery in pregnant patients? (4)

A

the usage of local anaesthetics
post-operative meds
gastro-oeseophageal reflux
increased risk of aortic + vena cava compression in 2nd/3rd trimester

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20
Q

Name an alternative to traditional glaucoma surgery that can be safer for pregnant patients. Why? (4)

A

Selective Laser Trabeculectomy (SLT):

  • only uses topical anaesthesia
  • upright positioning during procedure
  • faster rehab
  • reduced need for post-op meds [both dosage + duration]
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21
Q

When is the ideal time to consider surgery for a pregnant patient?

A

Before their (planned) pregnancy, as a way to manage IOP without having them on drops

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22
Q

Does IOP naturally rise or lower during pregnancy? By how much? Why? When is this most pronounced?

A

IOP diminishes by up to 10% during pregnancy, most pronounced in the 3rd trimester. Is attributed to fluctuating hormones [β-human chorionic gonadotropi and progesterone]

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23
Q

Is MIGS-iStent safe for pregnant patients?

A

Yeah-ish. About as safe as SLT anyway.

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24
Q

List the IOP reduction efficacies, in percentage, for the 4 different drug classes used in primary open angle glaucoma

A

PGAs: 30%
Beta Blockers: 25-30%
Topical CAIs: 20%
Alpha agonists: ~25% ish. Unsure. Expect maybe a 5-6mmhg reduction.
[update on the role of alpha agonists in glaucoma management]

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25
Q

Name 3 scenarios where you might consider MIGS-iStent

A

Pregnancy/Planned pregnancy
Drops not working
Patient about to undergo cataract surgery [can get iStent at same time]

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26
Q

When might you consider oral CAI [i.e. Diamox]? (2)

A

Topical therapy not working

AACG management

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27
Q

What effect does Diamox have on IOP?

A

~50% IOP reduction

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28
Q

What dosage of diamox would you use for glaucoma where topical is not working?

A

250mg Diamox po per day

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29
Q

What dosage of diamox would you use as an initial dose for AACG patients?

A

2x250mg Diamox + 500mg KCl

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30
Q

List 3 contraindications to Diamox

A

Kidney disease
Alergy to sulfa drugs
COPD [get GP advice]

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31
Q

Are there any fixed combination drugs containing both a PGA and CAI?

A

No. Not on the PBS at least. I couldn’t find any.

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32
Q

Are there any fixed combination drugs containing both a PGA and a beta blocker?

A

Yes.
Combigan: Bimataprost + Timolol
Xalacom: Latanaprost + Timolol

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33
Q

How would a typical glaucoma treatment pathway look? (4)

A

Start with PGA1
If PGA1 not working properly (<5mmHg reduction), switch to PGA2
If PGA working but not enough, Add topical CAI
If still not enough, turn CAI into a combo with a beta blocker or alpha agonist

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34
Q

Are beta blockers effective at night?

A

No

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35
Q

List 2 options for beta-blockers to reduce IOP

A

Timolol 0.5% QD [once per day] or BiD
Betaxolol 0.5% sol BiD [safest b-blocker for asthmatics]

https://www.aaopt.org/detail/knowledge-base-article/timoptic-05-bid-or-qd-which-controls-glaucoma-more-effectively - suggests timolol 0.5% BiD is better than qd

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36
Q

List 6 contraindications of beta blockers

A 
Low tension glaucoma
Bradycardia (<50bpm)
Asthma/COPD [can use betaxolol with caution]
MG
Diabetes
Depression
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37
Q

List the benefit of alpha agonists for glaucoma treatment

A

Good pulsatile ocular blood flow (POBF) effect. Particularly good for low tension glaucoma, especially when IOP = 14. (NB: though if IOP 15-21 in NTG, PGAs are still good, just don’t use xalatan, it has less effect.).

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38
Q

List 2 glaucoma drops that are good for treating the vascular nature of normal tension glaucoma

A

Brimonidine
Topical CAIs also good.
**Neuroprotective effect.

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39
Q

How was brimonidine postulated to have a neuroprotective effect in normal tension gluacoma?

A

it was compared to timolol in the LOGTS [Low-Pressure Gluacoma Treatment Study] and was found to result in lower likelihood of having VF progression.

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40
Q

List 2 alpha agonist options for treating glaucoma

A

Alphagan [Brimonidine 0.2% Tid (max) or BiD (adjunct)]

Apraclonidine [Iopidine 0.5% Tid (max) or BiD (adjunct)]

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41
Q

Which is the most commonly used alpha agonist?

A

Alphagan

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42
Q

What is the benefit of Apraclonidine?

A

Large fast IOP lowering which is good for IOP spikes, such as post-surgical IOP spikes (however not on PBS).

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43
Q

List 4 contraindications of alpha agonists

A

Tricyclic antidepressants
MAO inhibitors
Severe cardiovascular disease
Heavy machinery usage.

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44
Q

What is the main use for pilocarpine?

A

Low dose (0.16%) treatment for PDS/PGS, where miosis and reduced iris movement is desired

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45
Q

Why is pilocarpine not used much for open angle glaucoma?

A

too many adverse effects (e.g. CME, angle closure, variable myopia, RD, chol. toxicity, tachycardia, fever)

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46
Q

What is the primary IOP management for secondary glaucoma?

A

Same as POAG really. It depends. Can try Apraclonidine to treat IOP spikes for instance.
Avoid PGAs if secondary to uveitis.

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47
Q

What is the first aid treatment for AACG?

A

1 drop of: BB [timolol] + AA [alphagan] + CAI [trusopt] + pilo 2%. Also steroid drop if inflammation.
Then Oral diamox [2x250mg + 500mgK+] if kidneys ok

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48
Q

What is required for the diagnosis of POAG? (4)

A

NRR loss or RNFL defect
Typical VF defect (repeatable. Need baseline x3 for monitoring)
Open un-occluded angle
IOP >21mmHg (at some stage)

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49
Q

How many signs do we need to make a general glaucoma diagnosis? [Graham L.]

A

3 structural signs of glaucomatous disease that all match with each other

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50
Q

List 7 signs on fundus that should make you more suspicious of glaucoma (add +1 to OHTS for each)

A 
Vertical notching
Loss of ISNT (sup/inf thinning)
High CDR (0.7+) + increasing over time [standard disc size]
CDR asymmetry >0.2
Deepening of cup
Drance Haem
Barring of circumlinear vessels
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51
Q

What should you do if you see an isolated drance haemorrhage in an otherwise normal patient?

A

While it is less likely to be glaucoma, you should still monitor every 3 months for the first 2 years. Including baseline visual fields.

Repeated drance haemorrhages that occur in this time are much more suggestive of glaucoma

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52
Q

How long does an isolated drance haemorrhage typically last?

A

about 3 months, sometimes longer. If it lasts longer, it should still be faded and less noticeable on 3 month review.

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53
Q

List 6 high ocular risk factors for OAG

A 
Myopia
RVO
Oc injury/sx
Iris degen
Past/present papilloedema
High IOP
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54
Q

List 4 low risk factors for OAG

A

Female
DM
MIgraine
Sleep apnoea

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55
Q

List 6 other risk factors for OAG (6)

A 
Fam Hx
African-american
High BP or very low BP
Aggressive BP control
Low CCT
Steroid use [prednisolone - e.g. for COPD]
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56
Q

List 9 risk factors for NTG

A 
Age >65yo
Fam Hx
Japanese
High myopia
Aggressive BP control
CV disease
DM
Migraine
Sleep apnoea
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57
Q

What are the 5 main factors to consider for the OHTS risk calculator for 5 year prognosis of OAG?

A 
Age
Mean IOP (avg of 2 eyes)
Mean CCT
Mean vertical CDR (avg of 2 eyes)
Pattern Standard Deviation on VF
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58
Q

Describe a suggested sequence for performing a glaucoma workup

A

Slit lamp –> IOP –> Gonio –> Pachymetry –> VF (dilate as doing) –> OCT –>Fundus Lens –>Repeat IOP

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59
Q

Why would you perform a gonio on a glaucoma patient?

A

Check for signs of neovascularisation or secondary glaucoma

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60
Q

Describe an early VF defect in glaucoma

A

MD >/= -6.00dB + one of:

  • > /= 3 pts cluster p<5%, with at least 1pt in cluster p<1% on pattern dev plot
  • Pattern SD p<0.05
  • GHT “outside normal limits”
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61
Q

Describe a moderate VF defect in glaucoma

A

MD -6.01dB to -12.00dB + one of:

  • 25-50% p<5%, with at least 15-25%p<1% on pattern dev plot
  • > /= 1pt in central 5 deg <15dB, but none <0dB
  • Only 1 hemifield containing a pt <15dB in central 5deg
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62
Q

Describe an advanced VF defect in glaucoma

A

MD -12.01dB to -20.00dB + one of:

  • 50-75% p<5%, with at least 25-50% p<1%
  • > /= 1pt in central 5 deg <0dB
  • Both hemifields containing a pt <15dB in central 5deg
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63
Q

Describe a severe VF defect in glaucoma

A

MD >/= -20.00dB + one of:
>/=75% p<5%, with at least 50% p<1%
- >/= 50% pts in central 5 deg <0dB
- Both hemifields conta`ining >50% of pts <15dB in central 5deg

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64
Q

Describe an end-stage VF defect in glaucoma

A

Unable to perform VF in “worst eye” (due to central scotoma or VA = 6/60)

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65
Q

You should advance 1 grade in VF defect for glaucoma if there is a “threat to fixation”, what does this refer to?

A

4 points within central 3 degrees @ 16-25dB

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66
Q

When would a threat to fixation make you advance to advanced VF defect?

A

if 1 point within central 3 degrees @ 0-15dB

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67
Q

List 4 signs of PXS

A

White deposits (GAGs) on ant lens/iris/tm
Iris transillumination at pupil margin
Pigment loss/dispersion from iris collar
Gonio pigment

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68
Q

List 3 risk factors for PXS

A

Often 60-80yo men
Myopia
Scandinavian/Meditteranean

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69
Q

How does the prognosis of PXS differ from POAG?

A

Prognosis is worse than POAG, with faster rates of progression and poorer response

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70
Q

List 4 signs of PDS

A

Backward iris bowing
Pepper pigment deposits on anterior iris, lens capsule, corneal endothelium
Gonio pigment
Possible red eye post exercise

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71
Q

Why might a PDS patient acquire a red eye post exercise?

A

IOP spike (from the pigment)

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72
Q

Where are the pigment deposits on the anterior iris located in PDS?

A

Mostly inferior, due to gravity

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73
Q

How does pigment from PDS appear on the corneal endothelium

A

Appears as “Krukenberg’s Spindle” - a vertical line of pigment on the corneal endothelium

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74
Q

List 6 risk factors for PDS

A 
M>F
30yo M or Older F
Myopic
African
Concave iris
Flat cornea
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75
Q

Is PDS usually unilateral or bilateral?

A

bilateral

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76
Q

Is PXF usually unilateral or bilateral?

A

unilateral

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77
Q

List the 3 main steps for managing a secondary glaucoma like PDS/PXF

A

Treat underlying disorder
Manage IOP (aq suppress) if long term elevated IOP
Rev 24 hours: if IOP still >/=30 with tx, refer for sx

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78
Q

How frequently should you monitor PXS/PDS (no glaucoma)?

A

4-12 monthly

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79
Q

How frequently should you monitor PXG/PDG?

A

4 monthly

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80
Q

List 7 risk factors for PAC

A 
50-70yo
Female
Fam Hx
Fellow eye
Asian
Narrow angle
Forward lens + shallow AC
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81
Q

What 3 measurements and values would constitute a forward lens and shallow AC?

A

Lens vault >/= 0.6 [forward lens]
ACD <2.1 [shallow AC]
AC width <11.7

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82
Q

What two tests combined should be used to screen for high risk PAC suspects?

A

Iris shadow test and VH

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83
Q

What is considered a fail on the shadow test?

A

> 33% shadow

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84
Q

When a OAG diagnosis is established, and treatment chosen, how should you proceed with follow up?

A

Follow up in 1 month, then 3 months, then 4 months, then 6 months or 1yr.

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85
Q

How many baseline VF tests should you do on the 1 month review for OAG?

A

2 Visual Fields [making 3 total baseline VFs when adding original VF from month prior].

**NB: patient may feel uncomfortable sitting through 2 VFs, so perhaps schedule the 2nd VF for a week later. This is also good for timing purposes. NB: you should also be doing OCT/photo on this and subsequent visits too. And check IOP.

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86
Q

What is required for a PACS diagnosis?

A

PTM not visible in 2 mirrors

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87
Q

What is required for a PAC diagnosis?

A

PACs [PTM not visible in 2 mirrors] + IIS [Ischemic iris changes]

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88
Q

What constitutes Ischemic Iris Changes? List 3 examples.

A

increased pigment (2+) in sup PTM
iris atrophy
glaucomflecken

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89
Q

What is required for a PACG diagnosis?

A

PAC + NRR loss or RNFL defect

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90
Q

How do you manage PACG?

A

Peripheral laser Iridotomy

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91
Q

What is required for an AACG diagnosis

A

Angle closure with IOP >/= 24mmHg and
2 or more symptoms (pain/nausea/blur) and
2 or more signs (red/corneal oedema/mid-dilated pupil/shallow AC)

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92
Q

List 8 indications for a PLI

A 
APAC/PACs/PAC/PACG
Contralateral eye in APAC
2ndary angle closure with pupil block
Plataeu iris configuration/syndrome
Aqueous misdirection
Malignant Glaucoma
Ciliary Block
PDS
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93
Q

List 4 contraindications for a PLI?

A

corneal oedema
ac inflammation
uveitis
very flat ac

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94
Q

List the 3 primary combination glaucoma IOP reduction drugs not involving a PGA

A

Combigan [Brimonidine + timolol]
Cosopt [Dorzolamide + timolol]
Simbrinza [Brimonidine + Brinzolamide]

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95
Q

What is the prevalence of glaucoma in siblings of patients?

A

10.4% [population family study]

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96
Q

What is the prevalence of glaucoma in children of patients?

A

1.1%

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97
Q

Which optic nerve disease in a 60yo women could be mimic the appearance of primary open angle glaucoma?

A

AION: Anterior Ischemic Optic Neuropathy

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98
Q

List 4 symptoms of AION

A

Sudden painless vision loss
TIAs/Amaurosis Fugax
Diplopia
Flashes/flicker/colour scintillations

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99
Q

List 4 GCA specific symptoms

A

HAs [50%]
Tender/swollen temporal artery
Jaw claudication
Scalp tender/pain

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100
Q

List 5 ocular signs of AION

A 
Central scotoma
Achromatopsia/Dyschromatopsia
RAPD
Peri-papillary non-perfusion
Optic neuropathy
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101
Q

Describe the optic neuropathy that occurs in AION

A

Disc oedema + pp haem + CWPs OR …

White pallid disc with mild pp oedema

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102
Q

List 6 differentials for AION

A

NAION
ON inflammation via syphilis, sarcoidosis
Infiltrative optic neuropathies
Anterior orbital lesions with ON compression
Diabetic papillopathy
Open angle glaucoma.

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103
Q

What are the 5 steps for GCA Management

.

A
  1. Hospital Emergency ward: referral with mention of your suspicion
  2. Urgent blood test: ESR + CRP
  3. Systemic Steroid [Prednisolone 60mg qd po]
  4. Urgent temporal artery biopsy
  5. Low dose maintenance steroid typically for 1-2 days, after which stopping tx can be considered depending on ESR levels. Tx may be lifelong however.
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104
Q

How can you differentiate NAION from AION?

A

Lack of arteritis. Diagnosis of exclusion from AION.

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105
Q

List 5 features of NAION

A 
Sudden painless vision loss [6/30]
RAPD
RG defect + red desaturation
VF: altitudinal (inf) or arcuate defect
Unilateral disc oedema
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106
Q

Where is unilateral disc oedema most marked in NAION?

A

superiorly

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107
Q

How long after unilateral disc oedema in NAION does optic atrophy ensue?

A

after 1-2 months

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108
Q

List 6 systemic associations with NAION

A 
Arteriorsclerosis
DM
Hypertension
Hyperlipidemia
Anemia 
Sleep apnoea
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109
Q

How would you manage NAION [4]

A

Monitor [no effective tx for NAION]
GP referral: check for systemic associations like CV/DM
Review 1 month
Council on risk to contralateral eye

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110
Q

What percentage of NAION patients show mild improvement in vision over 3-6 months?

A

Up to 40%

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111
Q

Which 3 classes of glaucoma drugs reduce IOP by reducing aqueous production?

A

CAIs
Beta Blockers
Alpha agonists

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112
Q

Which 2 classes of glaucoma drugs reduce IOP by increasing aqueous outflow? Which pathway does each use?

A

PGAs - via uveoscleral pathway

Pilocarpine - via uveoscleral pathway indirectly which outweighs reduction in outflow from tm pathway

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113
Q

How does angle recession occur?

A

ocular blunt force trauma can cause shearing forces that tear between the longitudinal and circular fibres of the ciliary muscle, causing the circular fibres to displace posteriorly along the iris root, causing angle recession

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114
Q

How does angle recession glaucoma occur?

A

the ocular blunt force trauma causes damage to trabecular meshwork, making it dysfunctional

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115
Q

Which class of glaucoma drop is contrainidcated in angle recession glaucoma? Why?

A

pilocrapine: causes a pardoxical IOP rise in some

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116
Q

Which classes of glaucoma drops are preferred in treating angle-recession glaucoma? [3]

A

Aqueous suppressants: CAIs, Beta Blockers, Alpha agonists

[*So something like timolol 0.5% QiD is a good choice here]

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117
Q

When can angle recession glaucoma occur post trauma?

A

Can be anytime from days to years later

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118
Q

Are argon laser trabeculectomy (ALT) and selective laser trabeculectomy (SLT) effective in treating patients with angle recession glaucoma? When will better responses occur?

A

Rarely. Better responses will occur when more of the TM is intact on gonio.

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119
Q

When max tolerated medical therapy fails to control IOP adequately in angle recession glaucoma, which filtering surgical option is ideal?

A

Trabeculectomy with antimetabolites
[Mermoud et al, 1994]
[https://glaucomatoday.com/articles/2012-may-june/clinical-approach-to-angle-recession-glaucoma]

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120
Q

How often are patients with angle recession typically monitored for development of glaucoma?

A

yearly, in the absence of other findings.

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121
Q

What can early onset angle recession gluacoma present alongside?

A

Iritis with or without hyphaema

[treat with topical steroids like aau]

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122
Q

How many mirrors should be open to PTM on gonio to be safe to dilate?

A

3 mirrors.

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123
Q

List 3 epidemiological risk factors for Optic Neuritis

A

Typically 20-45yo. F>M [2x]. Caucasian

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124
Q

List 5 systemic associations with Optic Neuritis

A 
Infections 
Multiple Sclerosis
Tumours/compressive lesions
Vascular diseases
Idiopathic
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125
Q

What is the main cause of retrobulbar neuritis?

A

Multiple Sclerosis

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126
Q

How often does multiple sclerosis cause retrobulbar neuritis?

A

75%

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127
Q

List 4 ocular signs of retrobulbar neuritis

A

RAPD
Orbital pain/pain with eye movement
Acute vision loss
Brightness/CV defects

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128
Q

After how many weeks of untreated retrobulbar neuritis, might a patient experience mild disc oedema? Why?

A

1-2 weeks. Due to axoplasmic stasis (doesn’t always happen)

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129
Q

After how many weeks of untreated retrobulbar neuritis, might a patient experience RNFL loss on OCT?

A

6-8 weeks

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130
Q

After how long of retrobulbar neuritis, might a patient experience optic atrophy?

A

3-6 months

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131
Q

What are the 2 main causes of papillitis?

A

GCA [beware bilateral spread]

MS

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132
Q

How does the presentation of papilitis differ from retrobulbar neuritis?

A

There’s also disc oedema [mostly swelling, few retinal haems]

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133
Q

Is neuroretinitis usually associated with multiple sclerosis?

A

No

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134
Q

What are the 2 main causes of neuroretinitis?

A

infectious

inflammatory

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135
Q

Is orbital pain always present in neuroretinitis?

A

No. It’s actually not as common compared to retro/papilitis

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136
Q

Can neuroretinitis present with a macula wing/star exudate?

A

Yes.

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137
Q

List 5 differential diagnosis for optic neuritis

A 
Ischemic optic neuropathy
Acute papilloedema
Severe systemic hypertension
ON compression (tumour)
Intracranial mass
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138
Q

How do you perform the photostress test?

A

Hold light 2-3cm from patient’s eye [other eye occluded] for 10 seconds, then remove light.
– Ask patient to read line of best VA after central scotoma has disappeared. Time how long it takes to read at least 2/3rd of the line of their best VA.

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139
Q

What is an abnormal photostress test?

A

> 50 seconds = abnormal.

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140
Q

List what possible tests you can do for a patient with suspected optic neuritis (9)

A 
VA 
Screening [confrontation/HH/pupils/red cap
Lid ax/FAT: if lid protosis or ptosis present
Refraction/Ret
IOP
Ocular health
VIsual fields: 30-2?
Photostress test
OCT: check RNFL thinning
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141
Q

What eye movement condition is MS associated with? What percentage of patients may acquire this? Explain the condition.

A

~30% of MS patients may have INO [Internuclear Ophthalmoplegia]. INO: sluggish or absent contralateral adduction.

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142
Q

What type of evidence do you need to diagnose MS?

A

evidence of CNS damage that is “disseminated in time and space”

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143
Q

What tests are required for diagnosing multiple sclerosis (2)

A

MRI scans: for lesions

CSF-specific marker: needs lumbar puncture

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144
Q

Other than MS testing, what other referred tests might be considered in a patient with optic neuritis? (list 5)

A 
CBC
ESR
ACE level
FTA-ABS
Chest x-ray or CT.
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145
Q

Should blood pressure be checked in a patient with optic neuritis?

A

yes

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146
Q

How often should you review a patient with optic neuritis?

A

Review 4-6 weeks after presentation, and then every 3-6 months thereafter

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147
Q

What is CDMS and who should patients at high risk of this be referred to?

A

Clinically Definitive Multiple Sclerosis. High risk patients should be referred to a neurologist for evaluation and mx of possible MS.

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148
Q

How can we treat MS? Does this improve final outcome?

A

IV Methyl pred. Hastens recovery but doesn’t improve final outcome

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149
Q

Why don’t we use oral pred for MS?

A

Oral pred increases the rate of recurrence of MS

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150
Q

What is the NHMRC target IOP for Ocular Hypertension (OHT)?

A

-20% or =24mmHg [whichever is less]

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151
Q

When would be an appropriate time to start treatment for OHT prior to seeing evidence of any glaucomatous damage?

A

There is no real consensus on the minimum IOP threshold for this. But generally IOPs >24* with a normal CCT is a good guide.

**In these cases, diurnal IOP should ideally be measured as well

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152
Q

At what time of day is IOP normally highest?

A

For most normal eyes the pressure is highest in the early morning between 6am and 8am.

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153
Q

At what time of day is IOP normally lowest?

A

Afternoon

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154
Q

Why does IOP vary throughout the day?

A

hormonal fluctuation

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155
Q

With what type of CCT value is IOP overestimated?

A

Thicker CCTs

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156
Q

Normal CCT value

A

555

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157
Q

What is the NHMRC target IOP for Early OAG?

A

-20% or = 18mmHg, whichever is less

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158
Q

What is the NHMRC target IOP for OAG [starting point] and Moderate OAG?

A

-25% or = 18mmHg, whichever is less

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159
Q

Should you write the target pressure in the management section of sunix/optomate for someone you have begun treating for glaucoma?

A

Yes, you should

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160
Q

What is the NHMRC target IOP for Advanced OAG [or high risk early/mod OAG]?

A

-30% or =12mmHg, whichever is less

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161
Q

What is the NHMRC target IOP for LTG [MD

A

-30% or =12mmHg, whichever is less

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162
Q

Describe the surgical treatment pathway for OAG (4)

A

SLT/MIGs –> Filtering sx + antimiotic –> aqueous shunt or cyclodestructive sx –> low vision care

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163
Q

Define papilloedema

A

bilateral optic disc swelling secondary to elevated intracranial pressure

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164
Q

List 3 potential causes of papilloedema

A

Intracranial tumour
Malignant hypertension [must always check for this]
Idiopathic intracranial hypertension

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165
Q

Define Malignant Hypertension

A

Diastolic blood pressure >120mmHg

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166
Q

What should you suspect if a young person presents with malignant hypertension?

A

Kidney failure.

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167
Q

How do you manage malignant hypertension? [and even if not malignant but DBP >110]

A

Immediate referral to ICU/emergency department for cardiac monitoring, urine analysis, and neurological status assessment.

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168
Q

What are 6 potential symptoms of elevated ICP associated with papilloedema?

A 
Severe headaches
Nausea
Vomiting
Slight blur
Diplopia
Pulse-like ringing sound in ears
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169
Q

What are 4 additional tests you can do for a patient with papilloedema?

A

Blood pressure
VF [check for stroke/signs of cortical VF loss]
Refer to neuro for MRI + Lumbar puncture

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170
Q

What are 5 indications for urgent hospital referal in patients with papilloedema

A

Recent onset [within 1-2 months] with unusual headaches
Transient vision loss [<1min complete blackout]
EOM abnormality - diplopia
new related VF loss
Other new neuro problems like muscular paralysis, palsy, cognition issues

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171
Q

How can you treat pseudotumour cerebri? [3]

A

Weight loss +/- spinal tap
Oral diamox 250-500mg BiD for progressive vision loss on monitoring
Shunt surgery if still progressing on diamox

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172
Q

What is considered normotensive blood pressure?

A

<140/90

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173
Q

What is considered borerline high blood pressure?

A

140/90 - 160/95

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174
Q

What is considered primary hypertension?

A

> 160/95

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175
Q

What percentage of hypertensive cases are secondary to a renal or endocrine condition?

A

5%

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176
Q

List 8 systemic risk factors for hypertension/hypertensive retinopathy

A 
duration of high bp
heart disease
atherosclerosis
diabetes
smoking
high cholesterol
overweight
fatty/sugary diet
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177
Q

How does grade 1 [minimal] hypertensive retinopathy present on fundus examination? [Keith-Wagener-Barker Classification]

A

Mild general retinal arteriolar narrowing [reduced AVR]

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178
Q

How does grade 2 [mild] hypertensive retinopathy present on fundus examination? (2)

A

Focal arteriolar narrowing + AV nipping

Potential “copper wiring” of arteriolar walls

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179
Q

How does grade 3 [moderate] hypertensive retinopathy present on fundus examination? (3)

A

G2 + any of the following:
Retinal Haems (mostly flame)
Exudates
CWPs

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180
Q

How does grade 4 [severe] hypertensive retinopathy present on fundus examination?

A

Severe G3 + OD swelling [a marker of “malignant” hypertension]

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181
Q

T/F: The increasing severity of hypertensive retinopathy makes it more likely that it is secondary to other issues

A

True

182
Q

Rank the 4 most important fundus signs for detecting early hypertension

A
  1. Focal arteriolar constriction
  2. Vein occlusions
  3. Banking {particularly with shunt vessels]
  4. Atherosclerotic signs
183
Q

When would you refer a hypertension suspect to the GP for blood pressure and systemic workup?

A

GP referral when signs of recent origin seen: haems, CWPs, papilloedema, RVO

(NB: also do ophthalm referral if needed)

184
Q

What percentage of strokes are ischaemic vs haemorrhagic?

A

Ischemic: 80%
Haemorrhagic: 20%

185
Q

Over what age do most strokes occur?

A

50 years old.

186
Q

List 4 systemic risk factors for stroke

A

Uncontrolled hypertension
Diabetes
prior attacks/TIAs
Atheerosclerosis

187
Q

List 2 lifestyle risk factors for stroke

A

sedentary lifestyle

smoking

188
Q

In what time period do major stroke events often occur following TIA?. How long after do the patients continue to be a high risk for stroke?

A

Within the first week. High risk within next 2 years.

189
Q

Describe a transient ischemic attack (TIA)

A

Temporary blockage of blood flow causing a visual blackout typically lasting a few minutes

190
Q

On what side would a visual blackout occur in a patient with carotid stenosis?

A

ipsilateral side

191
Q

What are 4 potential ocular signs of carotid insufficiency?

A

Venous Stasis Retinopathy (i.e. type 1 non-ischemic CRVO)
Ocular Ischemic Syndrome
Asymmetric Cataract
Dilated conj/scleral vessels

192
Q

What are 3 atherosclerotic signs of carotid insufficiency?

A

BRAO [old or recent]
Hollenhorst plaque [cholesterol]
Fisher plug [fibrin]

193
Q

How can visual signs of stroke manifest?

A

Depends on where the stroke occurs

194
Q

List 6 possible visual manifestations of stroke

A 
Hemianopia
Diplopia/EOM palsy
CN5 palsy [loss of sensation to one side of face]
CN7/Bell's palsy
Nystagmus/gaze palsy
Visual processing/visual memory issues
195
Q

How can you manage carotid insufficiency? (3)

A 
Refer to GP for stroke workup. 
Anticoagulant therapy (e.g. aspirin daily)
carotid endarterectomy (surgical removal of a plaque)
196
Q

If you see ocular signs of carotid insufficiency, what should you ask the patient?

A

Any temporary visual blackouts in the past? When did they occur?

197
Q

How long after a stroke do you need to wait before the patient can safely undergo elective surgery (e.g. cataract surgery). Why?

A

3 months post stroke. To avoid increased risk of adverse cardiovascular events.
[Jorgensen et al. 2014]

198
Q

List 8 differentials for “localised areas of no vision”

A 
BRVO
RD
DR
Pre-retinal haem
AMD
Vitritis
Ret infection
Vit haem
199
Q

What should you do if a patient presents with localised area of no vision and you suspect posterior pathology but the angle is not open on gonio?

A

Same day referral to the ophthalmologist so you can deal with the narrow anterior chamber and the presenting problem today.

200
Q

What does sectoral retinal hemorrhaging and painless positive scotoma most likely indicate?

A

BRVO

201
Q

Where are flame haemorrhages localised in the retina?

A

GCL and RNFL

202
Q

Where are dot/blot haemorrhages localised in the retina?

A

INL and OPL

203
Q

List 6 potential retinal signs of BRVO

A 
Dilated veins/Banking
Tortous veins
Haems [typically flame]
CWPs
Ret oedema/thickening
Vit haem
204
Q

What type of ocular issues lead to positive scotomas? [i.e. area of black]

A

retinal problems like RVOs, haemorrhages

205
Q

What type of ocular issues lead to negative scotomas?

[i.e. area of blank]

A

optic nerve or posterior visual pahway disease [glauc/on glioma/optic neuritis, etc]

206
Q

Should you refer a patient with BRVO and no macular involvement? Explain

A

Non-urgent referral to GP and Retinal specialist. The retinal specialist can perform fluorescein angiography after the haemorrhage has cleared enough, to assess the level of capillary damage and non-perfusion. GP is for systemic workup.

207
Q

How long do the haemorrhages in BRVO typically take to clear up enough so that adequate fluorescein angiography can be performed by the ophthalmologist?

A

Somewhere around 6-12 weeks usually. During your 2nd [8wks]/3rd [12wks] review you can assess this and decide if it’s appropriate to refer to ophthalm now.

208
Q

How should you monitor a BRVO?

A

Monthly review for 3 months to check for development of neovasc or any macula oedema, and then review every 3 months until resolution.

209
Q

Within what time period do BRVOs typically resolve?

A

Within 6-12 months.

210
Q

What are 2 treatment options for macula oedema in BRVO patients?

A

aVegF [1st choice]

Laser photocoagulation [grid]

211
Q

What are the 3 factors contributing to thrombosis and subsequent vein occlusions [known as Virchow’s Triad]

A

Vessel damage
Venous Stasis
Hypercoagulability

212
Q

List 5 systemic or lifestyle risk factors for RVO

A 
Hypertension
DM
Hyperlipidemia
Smoking
Renal Disease
213
Q

How can glaucoma be a risk factor for CRVO?

A

can cause compression + backward bowing of the lamina cribrosa, which can lead to pinching of axons and blockage of axonal flow

214
Q

What percentage of CRVO are ischemic vs non-ischemic?

A

Ischemic: 20%

Non-ischemic: 80%

215
Q

What type of vision loss is ischemic CRVO best characterised by?

A

Painless marked vision loss within hours to days resulting in very poor VA (e.g. 6/60)

216
Q

What type of vision loss is non-ischemic CRVO best characterised by

A

painless less obvious vision loss ocurring within days to weeks resulting in slightly reduced VA (e.g. 6/7.5-6/9.5)

217
Q

What features of CRVO can indicate that it’s ischemic? (4)

A

CWPs
Marked vision loss
RAPD (is worse with increasing ischemia)
Macula oedema >600 um

218
Q

List 5 differentials for CRVO

A 
Severe DR
Ocular Ischemic Syndrome
Retinitis
Coats Disease
Benign Intracranial Hypertension
219
Q

What is the prognosis of untreated non-ischemic CRVO

A

10-20% improve but around 35-50% get worse

220
Q

How should you manage CRVO?

A

More urgent referral of all new cases to GP and retinal specialist. Should be within a week.

221
Q

What is rubeosis?

A

Neovascular glaucoma (a secondary angle closure like glaucoma) that develops around 90 days following CRVO in 50% of cases due to increased vegF as a result of retinal ischemia.

Ret ischemia –> increased vegF –> Iris neovasc –> Neovascular glaucoma/ACG.

222
Q

How often should you monitor patients with ischemic CRVO? What test should you perform each time on review?

A

Monitor monthly for 6 months (checking for development of iris neovasc, so perform gonio each time)

223
Q

When should you review non-ischemic CRVO (without mac oedema)?

A

Review in 4-6 weeks to monitor for oedema and/or ischemia or prn if vision deteriorates

224
Q

Provide 2 options for treating macula oedema associated with CRVO

A

AvegF

IV Triamcinolone

225
Q

How often should you review clinically significant macula oedema?

A

Monthly review for OCT and tx response for 1st 4 months, then quarterly until resolution.

226
Q

What is the criteria to diagnose CSMO (Clinically Significant Macula Oedema)? [3]

A

Ret thickening within 500um of centre of fovea
Lipid exudate within 500um of centre of fovea
Ret thickening >1500um, which is within <1500um of centre of fovea

227
Q

What is the average normal macula thickness?

A

=250um

[Chan et al. 2007]

228
Q

What is considered abnormal thickening of the macula?

A

> 300um

229
Q

What are the main 3 important causes of CRAO?

A

Cholesterol plaque/embolus
Thrombosis
Giant Cell Arteritis

230
Q

List 5 signs of CRAO

A 
superficial retinal whitening
cherry red spot
attenuated arterioles
retinal embolus visible
cattle tracking
231
Q

why might CRAO present with a possible sector of normal retinal colour?

A

Dual blood supply from ciliomacular artery

232
Q

Does everyone have a ciliomacular artery/dual blood supply?

A

No. About 25% of patients have it

233
Q

What must we rule out when we see a patient with CRAO? What implications does this have for ophthalmic testing?

A

GCA. Therefore, as a rule, when patients over 50yo present with CRAO, fluorescein angiography must be performed to find out if there is any underlying PCA occlusion as well.

[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7933845/]

234
Q

What does an underlying PCA occlusion in a patient with a CRAO suggest?

A

It is virtually diagnostic of a CRAO due to GCA.

Such patients require immediate and aggressive corticosteroid therapy to prevent catastrophic visual loss.

235
Q

What is the key differentiator between CRAO and an ophthalmic artery occlusion? How does the treatment differ?

A

Ophthalmic artery occlusion usually has no cherry red spot. Treatment is the same

236
Q

What should you do if a patient with CRAO does not have an embolus on fundus examination? (2)

A
  1. Immediate hospital referral with blood test for ESR + CRP

2. Start high dose systemic steroids [hospital handles this]

237
Q

How can you attempt to treat a CRAO with embolus while in clinic? How does this technique work and what is the logic behind it?

A

Ocular massage: use the gonioscope to push on the eye [10 seconds on/5 seconds off].

Doing this will increase the IOP to hopefully increase artery pressure behind the embolus enough to dislodge it. Doesn’t always work, but worth trying.

238
Q

How should you refer for a patient with CRAO with an embolus and without suspicion of GCA? [2]

A

Refer to ophthalm: super urgent [particularly if onset <48 hours]
Refer to neurologist for stroke assessment and management

[*super urgent = same day referral]

239
Q

After referring and treatment, how should you monitor a patient with CRAO?

A

Monthly monitoring to check for development of neovascularisation/NVG.

(Wills Eye Manual says 1-4 week follow up)

240
Q

What is the prognosis like for CRAO?

A

Poor

241
Q

How does the management of BRAO differ from CRAO?

A

It doesn’t. Mx as per CRAO.

242
Q

What is the incidence of choroidal naevus in caucasian?

A

6.5% [Blue Mountain Eye Study]

243
Q

What does TFSOM-HHD stand for? [identifying choroidal melanoma]

A 
Thickness >2mm
Subretinal Fluid
Symptoms [reduced vision, floaters]
Orange pigment
Margin touching optic disc
Hollowness in ultrasound
Halo absent around lesion in fundus
244
Q

What percentage of choroidal naevi meeting one criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?

A

3%

245
Q

What percentage of choroidal naevi meeting 2 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?

A

38%

246
Q

What percentage of choroidal naevi meeting 3 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?

A

58%

247
Q

What percentage of choroidal naevi meeting more than 3 criteria from TFSOM-HHD is likely to progress to choroidal melanoma in 5 years?

A

Likely already melanoma

248
Q

When should you refer a choroidal naevus to the ophthalmologist? (2)

A

Any new symptoms

Change in size

249
Q

How long does it take choroidal naevi to acquire pigmentation?

A

After it’s been there for about 6-10 years

250
Q

What dietary choice promotes progression of AMD? [1]

A

Saturated fats

251
Q

What dietary choice has a protective effect towards AMD? [2]

A

Omega-3

AREDS 2 supplements [Macuvision]

252
Q

Is smoking a risk factor for AMD?

A

Yes

253
Q

When should you refer AMD to the retinal specialist? [3]

A

Foveal thickness >300 microns
Central retinal thickness >350 microns
Wet AMD [for aVegF]

254
Q

What size drusen is considered normal ageing?

A

small [druplets] <63 microns [<1/4 BV]

255
Q

What size drusen is considered early amd?

A

Intermdiate drusen 63-125 microns [<1/2 BV]

256
Q

What size drusen is considered intermediate amd?

A

large drusen >125 microns [size of vein @ disc]

257
Q

What is required for a grading of late amd? [2]

A

Geographic atrophy or neovascularization

258
Q

Within what range from the fovea is pathology counted for AREDS calculation?

A

Pathology 2DD away from the fovea is assessed, however modifiers can be anywhere

259
Q

List the 5 components towards AREDS calculation for the risk of AMD progression to Late AMD in 5 years

A 
Hyper/hypo/disrupted pigment (>1/4DD) = +1
Large drusen = +1
*Reticular drusen = +1
*Bilateral intermediate drusen = +1
*End-stage AMD in fellow eye = +1
  • = modifier.
260
Q

A good mnemonic for things to consider in AMD patients is DRUSEN. What does it stand for?

A 
Diet
Relatives
Use of amsler
Smoking
Eye tests
Nutritional supplements
261
Q

At what stages of AMD are nutritional AREDS 2 supplements mainly used for? (2)

A

Intermediate AMD

The fellow eye of one eye with late amd

262
Q

What is the benefit of taking AREDS 2 supplements?

A

reduce the risk of progression of intermediate AMD to late AMD

263
Q

Can AREDS2 supplements stop progression from early amd to intermediate?

A

No. They can only stop progression from intermediate to late.

[https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/age-related-macular-degeneration/nutritional-supplements-age-related-macular-degeneration]

264
Q

What is the benefit of AREDS2 supplements compared to AREDS1?

A

AREDS2 does not contain beta carotene, which can increase the risk of lung cancer in people who smoke or used to smoke.

265
Q

At what stage of AMD for either eye is home monitor with amsler grid most appropriate?

A

Intermediate AMD. This stage can be unpredictable, and monitoring at home can be useful for early diagnosis of CNV. [The earlier the diagnosis, the better the outcome]

266
Q

What are 7 indications to perform amsler grid in clinic? [i.e. suspected or confirmed conditions]

A 
Wet AMD/CNV
CSCR
ERM + other vitreoretinal interface diseases
Acute Macula Neuroretinopathy
CME
NAION
Pituitary tumour
267
Q

How might CSCR appear on amsler?

A

it can cause a round or oval central scotoma, depending on the shape of the neurosensory retinal detachment

268
Q

How might CME appear on amsler?

A

things may appear smaller (micropsia)

269
Q

How might NAION appear on amsler?

A

it may reveal an altitudinal visual field defect.

270
Q

How may a pituitary tumour appear on amsler

A

it may be used to demonstrate a bitemporal hemianopia

271
Q

What is another name for dry amd and wet amd?

A

Atrophic amd

Exudative amd

272
Q

Can late stage AMD with geographic atrophy progress to wet AMD?

A

They are 2 distinctly different entities, however it is possible for exudative AMD/CNV to develop in an eye that already has late stage geographic atrophy.

273
Q

Would amsler grid home monitoring be appropriate in an eye with late stage atrophic AMD [geographic atrophy]? Or should it just be reserved for the fellow eye only?

A

It depends on their level of vision and the size + location of the geographic atrophy. If they still have acceptable area of central vision, you could monitor for wet amd in those regions

274
Q

Can wet amd occur in an area with existing geographic atrophy?

A

No, I’d imagine not. The RPE, which generates vegF, has died at the site of geographic atrophy. So any wet amd/cnv that subsequently occurs would be outside of this area, where vegF is still being produced.

275
Q

Briefly explain the pathogenesis of geographic atrophy

A

Insufficient vegF delivery from the RPE to the choriocapillaris due to thicker BLinD and accumulation of lipofuscin in RPE results in the atrophy of both.

276
Q

What risk does an AREDS score of 0-1 represent?

A

Low risk [3%]

277
Q

What risk does an AREDS score of 2 represent?

A

Medium risk [12%]

278
Q

What risk does an AREDS score of 3 represent?

A

High risk [25%]

279
Q

What risk does an AREDS score of 4 represent?

A

Very High risk [50%]

280
Q

What might drusen regression on OCT precede?

A

Progression to geographic atrophy

281
Q 
How often should you review the following AREDS scores:
0-1:
2:
3:
4:
A

0-1: 2 years

2: 1 year
3: 6 months
4: 3 months

282
Q

Which AREDS scores should home monitor with amsler?

A

2+ points.

283
Q

Is early AMD worth monitoring at home with amsler?

A

Not really, unless it’s the fellow eye of a late stage AMD.

284
Q

When should you refer wet AMD?

A

immediately. It’s urgent. Because of the rapid growth of CNVMs.

285
Q

What is the prognosis breakdown for wet AMD patients following aVEGF

A

1/3rd benefit forever

2/3rds will decline in 2 years

286
Q

How soon should fluorescein angiography be performed on a patient with CNV?

A

Because of the rapid growth of CNVMs, Fluorescein angiography should be performed no sooner than 72 hours prior to treatment. [i.e. the treatment should stabilize it, to allow a better idea from FA results I guess?]

[AMD Clinical Practice Guidelines 6]

287
Q

When after aVEGF treatment should the patient be evaluated?

A

2 weeks post treatment. I believe the ophthalmologist may handle this.

288
Q

When no further leakage is detected from a wet AMD/CNV patient, what should the review schedule look like?

A

Rev 6 weeks, then every 3 months for 1 year, then every 4-6 months thereafter

{AMD Clinical Practice Guidelines 6]

289
Q

List 5 signs of CNV recurrence

A 
Decrease in VA
New scotomas or dysmorphopsia
New areas of focal hypopigmentation at the edge of an area of laser treatment
Persistent subretinal or sub-RPE fluid
New specks of subretinal blood
290
Q

What grade is the AMD in the eye of a patient with intermediate drusen and PED?

A

Intermediate AMD. The existence of PED makes it intermediate, instead of early.

291
Q

What general percentage of wet AMD patients will develop PED [Pigment Epithelial Detachment]?

A

About 80% [Fibrovascular in particular is present in 62-80% of eyes with wet AMD]

292
Q

Can PED occur in patients with intermediate amd?

A

Yes

293
Q

What are the 3 types of PEDs associated with AMD?

A

Serous PED
Drusenoid PED
Fibrovascular/Haemorrhagic PED

[https://link.springer.com/article/10.1007/s40123-020-00291-5]

294
Q

Briefly explain the pathophysiology of serous PED in AMD patients

A

Increased thickness and lipid deposition in the bruch’s membrane reduces it’s conductivity and makes it more hydrophobic. This creates a barrier to fluid passage from the RPE to the choriocapillaris.

295
Q

Briefly explain the pathophysiology of drusenoid PED in AMD patients

A

Thought to be a product of enlargement and coalescence of soft drusen

296
Q

How does the AREDS study differentiate large drusen from drusenoid PED?

A

Large drusen: >125 microns

Drusenoid PED: >350 microns

297
Q

Briefly explain the pathophysiology of fibrovascular PED in AMD patients

A

CNV - new vessels access the sub-RPE space through breaks in bruch’s membrane. The new vessels usually proliferate laterally between the RPE and bruch’s membrane.

298
Q

How do serous PEDs appear on OCT?

A

Dome-shaped elevations of the RPE with sharp borders over a uniform hyporeflective space.

299
Q

What finding on an OCT of a serous PED can imply the presence of CNV? (2)

A

The presence of intraretinal (IRF) or subretinal fluid (SRF)
Hyper-reflective structures within the PED

[http://assets.markallengroup.com/article-images/image-library/147/uploads/sites/9/2014/07/772507Figure-7.jpg]

300
Q

What is a more definitive way we can rule out CNV in a patient with serous PED with suspected CNV?

A

Fluorescein Angiography

301
Q

How do drusenoid PEDs appear on OCT?

A

They appear as RPE elevations over homogenous mildly hyper-reflective spaces

[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig4_HTML.png?as=webp]

302
Q

How do druesnoid PEDs appear on fundus?

A

Well-circumscribed yellow-white elevations of the RPE that are usually within the posterior pole. Their borders are usually scalloped and they may have an irregular surface with areas of hyperpigmentations.

[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig3_HTML.png?as=webp]

303
Q

How do serous PEDs appear on fundus?

A

Dome-shaped elevations of the RPE with sharp borders

304
Q

How do fibrovascular PEDs appear on OCT?

A

Irregular elevations of the RPE with an interior that is optically not empty [there are areas of both hyper and hypo-reflectivity]

[https://media.springernature.com/lw685/springer-static/image/art%3A10.1007%2Fs40123-020-00291-5/MediaObjects/40123_2020_291_Fig7_HTML.jpg?as=webp]

305
Q

What additional test can you perform in clinic when you suspect vascularisation in your PED?

A

OCT-angiography. Check for presence of abnormal vascular complex.

306
Q

What percentage of AMD patients present with a serous avascular PED?

A

10%

307
Q

What percentage of serous PEDs will progress to CNV?

A

32-39%

308
Q

What percentage of serous PEDs will eventually flatten and become atrophic?

A

21-38%

309
Q

What percentage of serous PEDs will remain unchanged within an average follow up period {between 6 months to 2 years]?

A

22%

310
Q

Are any treatments available for serous avascular PEDs?

A

No

311
Q

Do serous avascular PEDs usually constitute and immediate threat to vision?

A

No

312
Q

How are serous avascular PEDs managed?

A

Regular follow up and monitoring

313
Q

What percentage of AMD patients will have drusenoid PEDs at some point?

A

8%

314
Q

Are there any recommended treatments for drusenoid PEDs?

A

Currently no.

315
Q

How should drusenoid PEDs be managed?

A

Regular follow up and monitoring

316
Q

What percentage of patients with fibrovascular PEDs will experience significant vision loss (> 3 lines) during their first year if no treatment?

A

50%

317
Q

What should you do if you see a fibrovascular/haemorrhagic PED?

A

Refer to ophthalm. They will need aVegF.

318
Q

What is one important complication of PEDs in wet AMD patients that we should look out for?

A

RPE tears

319
Q

How do RPE tears appear on fundus?

A

Large areas of bare choroid adjacent to an area of hyperpigmentation

320
Q

How do RPE tears appear on OCT?

A

Focal, sharp disruption of the RPE, with hyper-reflectivity of the underlying choroid at the area of absent RPE

321
Q

Where in association with the PED does an RPE tear typically form?

A

At the base of the PED, near the intersection of attached and detached RPE

322
Q

Should aVegF treatment be continued in patients with PED and an RPE tear?

A

Yes. There is a degree of controversy, but currently multiple studies suggest continuing aVegF improves visual outcomes, and that aVegF treatment following an RPE tear can be of benefit.

323
Q

What is CSCR?

A

Central Serous Chorioretinopathy. Is when you have subretinal fluid with RPE thinning +/- choroidal thickening.

(NB: subretinal fluid is directly above the RPE, so RPE intact unlike PED)

324
Q

Briefly describe the pathophysiology of CSCR

A

Damaged RPE leaks fluid towards the retina

325
Q

which age and gender most commonly present with CSCR?

A

20-40 year old males

326
Q

What are the main risk factors for CSCR? (2)

A

High stress or psychiatric disorder [e.g. depression]

Type A personality

327
Q

Are corticosteroids a risk factor for CSCR?

A

yes

328
Q

How does CSCR typically affect vision? (2)

A

Sudden unilateral painless central vision loss/disturbance [typical VA 6/9 - 6/36]
Hypermetropic shift [~+0.75]

329
Q

How might CSCR affect visual field?

A

Relative central or paracentral scotoma

330
Q

Is metamorphopsia a symptom of CSCR?

A

yes

331
Q

How does CSCR appear on fundus?

A

Oval/round lesion about 1-4DD wide, clear SRF. Is hard to see [translucent + gentle slopes]

332
Q

How does classic CSCR [aka local serous detachment] appear on OCT?

A

Usually a central + foveal elevation which occurs directly above the RPE, leaving a hyporeflective/dark space undernath

333
Q

What proportion of CSCR cases are local serous detachment?

A

25%

334
Q

How does CSCR appear on FAF?

A

Localised lesion with prominent bright halo

335
Q

How does CSCR appear in late-stage of fluorescein angiography?

A

smoke stack

336
Q

How do we normally manage cscr?

A

No treatment usually, monitor every 6 to 8 week until resolution [wills eye manual]. [CSCR lecture says 4 weekly review]

337
Q

Should you do a dilated eye exam if you spot a cscr? Why?

A

yes. To rule out a choroidal tumour or rRD.

338
Q

When is fluorescein angiography indicated in a patient with CSCR? [3]

A

If diagnosis is uncertain/atypical presentation
If CNV is suspected
If considering laser treatment

339
Q

How long do local serous detachment CSCRs typically take to resolve?

A

75% of patients spontaneously resolve in 6-9 weeks

340
Q

What is the typical prognosis for a local serous detachment CSCR?

A

Excellent

341
Q

When is laser surgery indicated in a patient with CSCR?

A

Persistence of a serous detachment for several months
Recurrence in an eye that sustained a permanent visual defect from a previous episode
Occurrence in contralateral eye after a permanent visual defect from a previous episode
Patient requiring prompt restoration of vision (e.g. occupational necessity)

342
Q

Does laser therapy for CSCR come with an increased risk of CNV development?

A

Yes it can, hence they use low laser intensity to help mitigate that

343
Q

What type of non-laser treatment might chronic CSCR respond to? What can this treatment do?

A

Photodynamic therapy: can reduce SRF. Particularly good for if very diffuse pattern

344
Q

How is Diffuse Retinal PIgment Epitheliopathy (DRPE) distinguished from classic serous detachment cscr? [3]

A

Areas of RPE atrophy [best seen on FAF with RPE dropout and long “tail”]
Choroid thicker than normal [>300 microns]
Often occurs alongside a focal PED.

345
Q

What percentage of CSCR is DRPE?

A

75%

346
Q

What type of laser surgery is used in chronic cases of cscr/drpe?

A

focal laser

347
Q

How long would you typically observe CSCR for late recovery until deciding to do laser?

A

Up to 26 weeks at most. Would probably refer before that.

348
Q

When may be a good time to refer patients with chronic cscr?

A

After 12+ weeks have passed without resolution, can refer for a fluorescein angiography to assess the state of the choroid.

349
Q

What is the prevalence of epiretinal membrane in patients over 50 years old?

A

6%

350
Q

Can epiretinal membrane occur in children?

A

yes but rare

351
Q

What percentage of epiretinal membranes will be secondary to a PVD of some kind?

A

90%

352
Q

Other than PVD, list 3 other posterior conditions an epiretinal membrane may be secondary to

A

Vascular retinopathy
Diabetic retinopathy
Blunt/penetrating trauma

353
Q

What surgeries/treatments can potentially lead to epiretinal membrane? [4]

A

Cataract surgery
rgRD surgery
Laser
Retinal cryotherapy

354
Q

What is the incidence of symptomatic epiretinal membrane following rgRD surgery?

A

4-8%

355
Q

What actually is an epiretinal membrane? Briefly describe it.

A

abnormal fibrocellular tissue/fibrosis on the retinal surface. Usually relates to an inflammatory process (b/c fibrosis)

356
Q

What proportion of idiopathic epiretinal membranes are bilateral?

A

20-30%

357
Q

What is the main symptom of epiretinal membrane and what does this tell us?

A

mild blur +/- metamorphopsia (if macula region is involved]

358
Q

According to Gass’ classification of epiretinal membrane, what is Grade 0?

A

Translucent membrane with no retinal distortion

359
Q

According to Gass’ classification of epiretinal membrane, what is Grade 1?

A

Irregular wrinking of the inner retinal surface + retinal distortion

360
Q

According to Gass’ classification of epiretinal membrane, what is Grade 2?

A

Opaque thick membrane, macula pucker/distortion of foveal pit

361
Q

What may present as an early sign of epiretinal membrane on OCT?

A

Hyper-reflective little bump on the retinal surface

362
Q

What should you look out for on the OCT of a patient with epiretinal membrane? (2)

A

Traction

Macula thickening + oedema

363
Q

What might a patient commonly report in history if suffering with an epiretinal membrane, VMT, or any condition that has elicited metamorphopsia?

A

closing one eye to read [the eye with distortions/metamorphopsia]

364
Q

What percentage of ERM patients also have vitreous adherence to the macula [VMA]?

A

About 57%

[https://www.aaojournal.org/article/S0161-6420(15)01270-1/pdf - ERM and VMT preferred practice patterns]

365
Q

What is the difference between Vitreo-macular adhesion (VMA) and Vitreo-macula traction (VMT)?

A

Vitreomacular adhesion is when the vitreous gel is adhered to the macula/fovea. VMT is when this adherence causes the fovea to be raised due to a tractional force.

So VMT is VMA, but with traction.

366
Q

Are epiretinal membranes stable or progressive?

A

The majority of epiretinal membranes will remain relatively stable and do not require therapy

367
Q

Should patients with epiretinal membranes self-monitor with amsler grid at home?

A

Yes

368
Q

Explain the pathophysiology behind why most patients experience little to no symptom progression after initial diagnosis.

A

Membrane contraction of the epiretinal membrane usually occurs soon after its formation and then stabilises

369
Q

What percentage of epiretinal membrane patients show decline in VA over time? How long does this take?

A

10-25%. Progression can vary from months to years

370
Q

What percentage of epiretinal membranes actually regress by themselves over 5 years?

A

25%

371
Q

are epiretinal membranes usually treated?

A

Usually not treated unless progression is found to be faster. Watch + monitor

372
Q

Can uveitis cause an epiretinal membrane?

A

yes

373
Q

How is a decision for surgical management of epiretinal membrane made?

A

The recommendation to simply monitor or to perform surgery is mainly based on the patients’ discomfort with their vision, along with their understanding of the associated risks [e.g. cataract]

374
Q

Is surgery urgent in patients with epiretinal membrane?

A

No. It’s elective.

375
Q

What is the go to surgery for epiretinal membrane and VMT?

A

Vitrectomy with membrane peel

376
Q

What is the level of risk of cataract formation post vitrectomy?

A

pretty high. Such progression occurs at different rates, and may be age dependent. Typically it’s progressive nuclear cataract

377
Q

How does vitrectomy surgery for epiretinal membrane affect VA

A

Usually improves VA but complete recovery is rare.

378
Q

List 3 intraoperative complications to vitrectomy

A

vitreous haemorrhage
retinal surface damage
peripheral retinal breaks

379
Q

List 3 post operative complications to vitrectomy

A

recurrence
cataract
retinal detachment

380
Q

When should epiretinal membrane patients be counselled to seek optometric/ophthalmic advice? (4)

A

increase in floaters
loss of visual field
metamorphopsia
decrease in VA

381
Q

What would be your biggest concern when you see a VMT?

A

Worried about potential of future retinal detachment

382
Q

Suppose you saw a VMT lifting up the fovea creating a small area of serous fluid underneath, how would you manage this patient? [1st time diagnosis]

A

Review in 3-4 months. Then 6 months after that.

383
Q

When would you consider surgery/vitrectomy (pars-plana vitrectomy) in a patient with VMT?

A

When the VMT causes vision loss that start to interfere with a person’s normal daily activities

384
Q

When is an appropriate review period for an epiretinal membrane?

A

once or twice a year is fine.
Could do a 6 month review for a first time diagnosis on a more noticeable epiretinal membrane. But if it’s mild on first time diagnosis just see them in a year.

385
Q

What is our target Hba1c to have good control of a patients diabetes

A

Less than 7%

386
Q

Is a Hba1c of 7.5% ok?

A

it’s ok. Room for improvement but its fine really. Actually is a good target for those taking insulin and self monitoring glucose.

387
Q

What is our target systolic BP in diabetics?

A

<130mmHg

388
Q

What is our target LDL cholesterol in diabetics?

A

<2.5 mmol/L

389
Q

What is our target triglyceride level in diabetics?

A

<2.0mmol/L

390
Q

What is the recommended blood glucose level range for a diabetic?

A

4.4-7.2 mmol/L

[Mayo clinic - american diabetes association]

391
Q

What our targets for good diabetic control? (5)

A 
Hba1c < 7%
Systolic BP <130mmHg
LDL cholesterol <2.5mmol/L
Triglycerides <2.0mmol/L
BGL 4.4-7.2
392
Q

What should you suspect when a diabetic patient presents with a hyperopic shift?

A

Macula Oedema.

therefore must do OCT

393
Q

How many diabetics are undiagnosed?

A

1 in 5 diabetics

394
Q

What is the incidence of diabetes in australia?

A

4.9% (i.e. 5%)

395
Q

According to the beaver dam study, what was the incidence of any retinopathy (e.g. MAs, haems) in non-diabetics?

A

6.8%

[5.1% were MAs only, 1.2% were haems only, remainder was both]

396
Q

If you find a dot/blot haemorrhage in a patient that has not been diagnosed with diabetes, what should you do?

A

Send a referral letter to the GP for a BGL/systemic workup. In the letter, classify the haemorrhage as a mild Non-proliferative diabetic retinopathy.

397
Q

What is a good screening test for a diabetic who has either had a hyperopic shift or severe reduction in vision in one eye?

A

Amsler grid: check for metamorphopsia from a macula oedema

398
Q

Is smoking a risk factor for diabetic retinopathy?

A

yes

399
Q

According to wisconsin grading, define minimal NPDR

A

MAs only

400
Q

According to wisconsin grading, define mild NPDR

A

MAs and >/=1 of: haem, HEx, CWS, but not meeting moderate NPDR definition

401
Q

define moderate NPDR

A

MAs + haems in at least 1 quadrant + 1 or more of: CWS, VB, IRMA, but not meeting severe

402
Q

define severe NPDR

A

4:2:1 rule
MAs + Haems in all 4 quadrants
Venous beading in 2 quadrants
IRMA in 1 quadrant

403
Q

define PDR [3]

A

Any of:
NVD and/or NVE
Vit/pre-ret haem
NVE <1/2 disc area without NVD

404
Q

define high risk PDR (2)

A

Any of:
NVD >1/4 to 1/3 disc area or existing with vit/pre-ret haem
NVE >1/2 disc area with vit/pre-ret haem

405
Q

define advanced PDR

A

High risk PDR with tractional detachment involving macular or vitreous haemorrhage obscuring ability to see/grade NVD + NVE

406
Q

define macula oedema

A

retinal thickening within 2DD of macula centre

407
Q

Define CSME

A

Ret thickening within 500um of foveal centre
Hard lipid exudate within 500um of foveal centre
Ret thickening of >1500u which is <1500u from centre of fovea

[NB: 1500u = 1 disc diameter]

408
Q

What is the rate of progression % of moderate NPDR to PDR in 3 years?

A

30-48%

409
Q

What is the rate of progression % of severe NPDR to PDR in 1 year?

A

52%

410
Q

How often should you review a diabetic with no retinopathy?

A

yearly

411
Q

How often should you review a diabetic with mild NPDR?

A

6 months

412
Q

How often should you review a diabetic with severe NPDR?

A

3 months

413
Q

when would you provide a prompt referral to the ophthamologist in a diabetic? (4)

A

Severe NPDR
PDR
Unexplained vision loss
Macula oedema

414
Q

Within what time frame should a referral to the ophthalmologist be made for a moderate NPDR?

A

within 12 weeks [ranzco].

From here on, monitoring of retinopathy should be coordinated alongside and ophthalmologist.

415
Q

Within what time frame should a referral to the ophthalmologist be made for a severe NPDR?

A

within 4 weeks [ranzco]

416
Q

Within what time frame should a referral to the ophthalmologist be made for a PDR?

A

within 1 week [ranzco]

417
Q

Within what time frame should a referral to the ophthalmologist be made for a sudden severe visual loss [vit haem, RD, or rubeotic gluacoma]?

A

same day [ranzco]

418
Q

When should a referral to the ophthalmologist be made for diabetic retinopathy?

A

Moderate or worse.

419
Q

What treatment is typically administered for PDR and CSMO?

A

aVegF

Also can try PRP/focal PRP

420
Q

When may vitrectomy be considered in a diabetic retinopathy patient?

A

last resort if poor outcome with other interventions

421
Q

is a retinal hole safe when it is pigmented or unpigmented?

A

pigmented

422
Q

What is the prevalence of WWOP in the general population?

A

up to 30%

423
Q

List 2 risk factors for WWOP

A

High myopia

Age

424
Q

What is WWOP indicative of in a highly myopic retina?

A

indicative of an area where the retina has been stretched, and is correlated with an increased risk for future retinal detachment in these eyes.

[https://www.optometrystudents.com/clinical-guide-to-degenerative-myopia/]

425
Q

How should you manage WWOP?

A

Watch annually and warn of RD

426
Q

Aside from WWOP, what other peripheral retinal degenerations are associated with retinal detachment? (4)

A

lattice degeneration
snail track
cystoid degeneration
retinoschisis

[mx similar to wwop]

427
Q

What percentage of eyes with rRD also have lattice degen?

A

60%

428
Q

What does typical lattice degeneration look like?

A

Sharply bordered white lines +/- pigment

429
Q

What does atypical lattice degeneration (2)

A

No white lines

Local accumulation of “snowflakes” [frost like appearance]

430
Q

What is the prevalence of lattice degeneration in the general population?

A

8-10%

[https://www.asrs.org/content/documents/fact-sheet-33-lattice-degeneration.pdf]

431
Q

Where does regular retinoschisis occur?

A

splitting along the OPL plane

432
Q

Where does reticular retinoschisis occur?

A

INL or NFL

433
Q

Which form of retinoschisis is more serious: regular or reticular?

A

reticular is more serious [but rarely reaches posterior pole]

434
Q

Define PVD

A

separation of vitreous from the ILM

435
Q

List the 4 stages of PVD on OCT

A
  1. Shallow +/- foveal spot (traction)
  2. PVD reaches fovea but doesn’t include foveola
  3. Shallow ONH attachment + foveal traction
  4. Complete PVD
436
Q

What are 2 symptoms a patient with PVD may experience?

A

Large central ring-shaped floater (weiss ring)

Flashes [occurring opposite in the visual field to where retinal traction is]

437
Q

What are flashes indicative of in general?

A

traction

438
Q

List 3 signs of PVD on fundus examination (3)

A

Weiss ring
Hyaloid face pulled forwards from retina
Small pre-ret or vit haemorrhage +/- pale ret due to traction

439
Q

What signs of trouble should you look for in patients with PVD? (6)

A 
Tobacco dust (pigment in ant vitreous)
ret/vit haem
cells
traction (white retina)
tears
persistent unexplained photopsia/flashes
440
Q

How should you manage PVD if no concerning signs of trouble?

A

Follow up review in 2 months with DFE, then reassure + advise to return if symptoms worsen

441
Q

How should you manage PVD if there ARE concerning signs of trouble?

A

refer urgently.

442
Q

What does asteroid hyalosis look like?

A

yellow/white specs with clear zone [lipid/calcium deposits]

443
Q

Is asteroid hyalosis unilateral or bilateral?

A

often unilateral

444
Q

is asteroid hyalosis symptomatic or asymptomatic?

A

often asymptomatic

445
Q

In what age group is asteroid hyalosis common?

A

older patients (7th/8th decade)

446
Q

What does synchisis scintillans look like?

A

White/golden cholesterol crystals found in liquified vitreous

447
Q

Is synchisis scintillans unilateral or bilateral?

A

Bilateral

448
Q

How do you manage asteroid hyalosis and synchisis scintillans?

A

No management/treatment.

449
Q

What is asteroid hyalosis associated with? (4)

A

DM
Hypertension
Atherosclerosis
Hyperopia

450
Q

Is asteroid hyalosis associated with PVD?

A

Asteroid hyalosis is never found in eyes with PVD

451
Q

How does synchisis scintillans relate to PVD?

A

Only found in eyes with/after PVD [younger patients after PVD]

452
Q

Things that still need to be covered:

A

For posterior:
Retinal Detachment + Hole
Macular hole
corneal FB/trauma

For anterior, need to cover:
AAU, episcleritis/scleritis, cataract, bacterial keratitis, herpetic keratitis, conjunctivitis (bacterial, viral, allergic), ocular injury/fb

Sem1revcards (19 decks)

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