Ophthalmology - Gradual Vision Loss (Open Angle Glaucoma, ARMD and Cataracts) Flashcards

1
Q

What is the pathophysiology of Open Angle Glaucoma (AOG)?

A

-Gradual increase in resistant through trabecular meshwork - more difficult for aqueous humour to exit the eye.

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2
Q

What are risk factors for OAG?

A
  • Increase age
  • Family Hx (screen from age 40 if have 1st degree affected relative)
  • Black ethnic origin
  • Nearsightedness (myopia)
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3
Q

What is the PC (sx) of OAG?

A
  • Usually diagnosed at routine optometry screening
  • Peripheral vision affected first, gradually turns into tunnel vision
  • Visual acuity is maintained until late stages
  • Gradual onset of fluctuating pain, headaches, blurred vision and halos around light (night time)
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4
Q

What investigations should you perform on a patient with suspected OAG?

A

Measure intraocular pressure

  • Non-contact tonometry: ‘puff of air’ blown at cornea (less accurate)
  • Goldman applanation tonometry: gold standard, applies different pressures to cornea to measure IOP (must have been calibrated for corneal thickness)

Other

  • Corneal thickness measurement
  • Fundoscopy: check for optic disc cupping (>0.5 of optic disc is bad)
  • Visual field assessment: peripheral vision loss
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5
Q

How do you manage OAG?

A

-Treat a IOP of 24mmHg and above

Medication

  • 1st line: Prostaglandin analogue (latonoprost) increases uveoscleral flow (increases drainage from ant chamber to iridocorneal angle) but SEs are eyelash growth, eyelid pigmentation and iris pigmentation
  • Beta Blockers: timolol reduces production of aqueous humour
  • Carbonic anhydrase inhibitors: dorzolamide reduces production of aqueous humour
  • Sympathomimetics: bromonidine reduces production of aqueous humour and increases uveoscleral flow
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6
Q

How do you manage OAG if medications are not effective?

A

-Trabeculectomy: creation of new canal from anterior chamber, through sclera to location under conjunctiva, where aqueous humour drained and is then reabsorbed into general circulation

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7
Q

What is age-related macular degeneration (ARMD)?

A
  • Degeneration of the macula that causes progressive deterioration in vision
  • Dry: 90% of cases, Drusen (yellow deposits of proteins and lipids) appear between the retinal pigment epithelium and Bruch’s membrane (common to both wet and dry) + degeneration of macula
  • Wet: 10% of cases and worst prognosis, neovascularisation growing from choroid layer into the retina. These vessels leak fluid/blood and cause oedema (more rapid loss of vision)

Common features

  • Atrophy of retinal pigment epithelium
  • Degeneration of photoreceptors
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8
Q

What are some risk factors for ARMD?

A

-Age -Smoking -White/Chinese origin -FHX -CVS disease

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9
Q

How will a patient with ARMD present?

A

-Gradually worsening central visual field loss (bilateral usually)
-Reduced visual acuity (esp near field objects)
-Crooked or wave appearance of straight lines
-Fluctutations in visual disturbance which vary significantly from day to day
*Wet ARMD will present more acutely and often progresses to full loss of vision over 2-3 years.

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10
Q

What type of ARMD is this?

A
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11
Q

What type of ARMD is this?

A
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12
Q

What investigations will you perform on someone with suspected ARMD?

A
  • Snellen chart: reduced visual acuity
  • Fields of vision: scotoma
  • Amsler grid test: distortion of straight lines
  • Fundoscopy: Drusen visible
  • Optical coherence tomography (1st line for wet ARMD) - shows cross sectional view of layers of retinal
  • Fluorescein angiography (2nd line if OCT doesn’t confirm wet ARMD) - looks at blood supply to retina and will show any oedema and neovascularisation
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13
Q

How to you manage dry ARMD?

A
  • No specific treatment for dry ARMD
  • Management is focused on lifestyle: no smoking, controlled BP, vitamins supplementation
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14
Q

How to you manage wet ARMD?

A
  • Anti VEGF medications injected into vitreous chamber every month
  • Eg: ranibizumab, bevacizumab - slow and even reverse progression of disease
  • Must be started within 3 months to be beneficial
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15
Q

What are cataracts? Name some causes of congenital catarcts

A
  • Lens of the eye becomes cloudy and opaque - reduces visual acuity by reducing the light that reaches the retina.
  • Must cataracts develop with advanced age but you can also have congenital cataracts (idiopathic, rubella, Wilson’s disease/Galactoseamia
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16
Q

Name some risk factors for cataracts

A
  • Increasing age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypocalcaemia
17
Q

How would someone with cataracts present?

A
  • Sx usually asymmetrical as both eyes are affected separately
  • Very slow reduction in vision/myopia
  • Progressive blurring of vision
  • Change in colour vision (colours become more brown/yellow)
  • “starburst’’ or glare around lights (esp at night)
18
Q

What investigations would you perform on someone with suspectec cataracts?

A
  • Visual acuity (decreased)
  • Fundoscopy with dilatation of pupil: lens will onstruct view
  • Tonometry
  • BM/diabetic assessment to exclude diabetes
19
Q

How would you manage a patient with cataracts?

A

Conservative Mx

  • If sx are manageable, can wait on surgery
  • Stronger glasses/contact lenses
  • Use of brighter lights

Surgical treatment

  • Not worth delaying in patients who are symptomatic (very cost effective and rreally educe morbidity)
  • Drilling and breaking lens into pieces and implanting an artificial lens into remaining capsule.
20
Q

Name some important complications and post-op care for cataract surgery

A

Complications:

  • Anterior uveitis/iritis
  • Retinal detachment
  • Secondary glaucoma
  • Posterior capsule opacification
  • Endophthalmitis: rare but serious inflammation (infection) of inner eye - requires intravitreal antibiotics and can lead to loss of vision (0.1%)

Post-op care:
-Post-op eye irritation is common
-Antibiotic and steroid drops given
-Shield place on eye
*Local anaesthesia day case procedure