Ophthalmology Flashcards

(34 cards)

1
Q

what are some risk factors for open angle glaucoma?

A
  • increasing age
  • family history
  • black ethnic origin
  • myopia (shortsightedness)
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2
Q

what treatment is recommended for open angle glaucoma?

A
  • 360 degrees selective laser trabeculoplasty
  • during this, a laser is directed at the trabecular meshwork, improving drainage
  • it may delay or prevent the need for eyedrops
  • a second procedure may be needed at a later date
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3
Q

apart from first line eye drops, what are some others than can be used in open angle glaucoma?

A
  • beta blockers (eg. timolol): reduces the production of aqueous humour
  • carbonic anhydrase inhibitors (eg. dorzolamide): reduces the production of aqueous humour
  • sympathomimetic (eg. brimonidine): reduces the production of aqeuous fluid and increases uveroscleral outflow
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4
Q

what is episcleritis usually associated with?

A

inflammatory disorders such as RA and IBD

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5
Q

although less commonly due to infection, what bacteria can cause scleritis?

A

pseudomonas or s.aureus

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6
Q

what are some systemic conditions associated with scleritis?

A

RA and vasculitis (particularly granulomatosis with polyangiitis)

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7
Q

what is the treatment for wet AMD?

A
  • anti-VEGF medications eg. ranibizumab, bevacizumab
  • these block VEGF, slowing the development of new blodo vessels
  • they’re injected directly into the vitreous chamber of the eye (intravitreal) once a month
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8
Q

what is the macula?

A
  • found in the centre of the retina
  • generates high definition colour vision in the central visual field
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9
Q

how does AMD present?

A
  • tends to be unilateral
  • gradual loss of central vision
  • reduced visual acuity
  • crooked or wavy appearance to straight lines (metamorphophsia)
  • gradually worsening ability to read small text
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10
Q

key examination findings of ARMD?

A
  • reduced visual acuity
  • scotoma
  • amsler grid test to see distortion of straight lines
  • drusen on fundoscopy
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11
Q

what might recurrent cases of uveitis need?

A

DMARDs and anti-TNF medications

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12
Q

how does CRAO present?

A
  • sudden painless vision loss
  • RAPD
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13
Q

how does CRAO present on examination?

A

pale retina with cherry red spot

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14
Q

how does retinal detachment present?

A
  • painless
  • peripheral vision loss (often sudden)
  • blurred vision
  • flashes or floaters
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15
Q

what can abrasions due to contact lenses be associated with & what’s an important differential?

A
  • pseudomonas infection
  • herpes keratitis (antivirals for treatment)
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16
Q

what are some different eye drops for corneal abrasions and how do they differ in viscocity?

A
  • hypromellos (least viscous, effect lasts 10 minutes)
  • polyvinyl alcohol drops (middle viscous)
  • carbomer eye drop (most viscous, alsts around 30-60 minutes)
17
Q

how does a primary infection of herpes simplex keratitis present?

A

mild symptoms of blepharoconjunctivitis (inflammation of eyelid margins and conjunctiva)

18
Q

how can a recurrent infection of herpes keratitis present?

A
  • painful
  • red
  • photophobia
  • vesicles
  • foreign body sensation
  • watery discharge
  • reduced visual acuity
19
Q

what are the features seen in hypertensive retinopathy?

A
  • silver/copper wiring
    • where the walls of the arterioles become thickened and sclerosed and reflect more light on examination
  • AV nipping
    • where the arterioles cause compression of the veins where they cross due to sclerosis and hardening of the arterioles
  • cotton wool spots
    • fluffy white spots that appear in the retina due to nerve fibre damage from ischaemia
    • caused by ischaemia and infarction of the retina, causing damage to the nerve fibres
  • hard exudates
    • caused by damaged vessels leaking lipids onto the retina
  • retinal haemorrhages
    • caused by damaged vessels rupturing and releasing blood into the retina
  • dot and blot haemorrhages
    • occur deeper, in the inner nuclear layer or outer plexiform layer
  • flame haemorrhages
    • occur in the nerve fibre layer
  • papilloedema
    • caused by ischaemia to the optic nerve, resulting in optic nerve oedema
20
Q

what are the 3 management options for retinal detachment?

A
  • vitrectomy
  • scleral buckling
  • pneumatic retinopexy
21
Q

what are the treatment options for proliferative diabetic retinopathy?

A
  • pan retinal photocoagulation: lasers on the retina to suppress the formation of new blood vessels
  • anti-VEGF
  • surgery (vitrectomy) if severe
22
Q

what are some complications of PRP?

A
  • reduction in visual field, due to damage to the peripheral retina
  • night vision difficulties
23
Q

what does fundoscopy examination show in retinal vein occlusion?

A
  • dilated tortuous retinal veins
  • flame and blot haemorrhages
  • retinal oedema
  • cotton wool spots
  • hard exudates
24
Q

management options for CRVO?

A
  • anti-VEGF therapies (eg. ranibizumab)
  • dexamethasone intravitreal implant for macular oedema
  • laster photocoagulation to treat new vessels/retinal neovascularisation
25
what does blockage of a retinal vein cause?
- venous congestion in the retina - increased pressure in the retinal veins results in fluid and blood leaking into the retina, causing macular oedema and retinal haemorrhages - this results in retinal damage and vision loss
26
=-[p0for patients with thyroid eye disease, which symptoms/signs should indicate the need for urgent review by an opthalmologist?
- unexplained deterioration in vision - change in intensity or quality of colour vision in one or both eyes - disc swelling - cornea visible when eyelids are shut - corneal opacity - globe subluxation (history of eyes suddenly popping out)
27
features of thyroid eye disease?
- exophthalmos - conjunctival oedema - optic disc swelling - opthalmoplegia - inability to close the eyelids leading to sore, dry eyes - if severe and untreated, risk of exposure keratotherapy
28
what are the causes of central/1st order neurone lesions in Horner's syndrome?
4S's - stroke - multiple sclerosis - swelling (tumours) - syringomyelia (cyst in spinal cord)
29
what are the causes of pre ganglionic/2nd order neurone lesions in Horner's syndrome?
4T's - tumours (pan coast) - trauma - thyroidectomy - top rib
30
what are the causes of post ganglionic/3rd order neurone lesions in Horner's syndrome?
4C's - carotid aneurysm - cavernous sinus thrombosis - carotid artery dissection - cluster headache
31
how can you test for Horner's syndrome?
- **cocaine eye drops** - it acts on the eye to **stop noradrenaline re-uptake at the NMJ, therefore increasing the noradrenaline levels** - this causes a **normal eye to dilate** as **noradrenalin stimulates the dilator muscles** of the iris - in horner’s syndrome, the **nerves aren’t releasing noradrenaline/sympathetic response is loss/weakened so the dilator muscles won't respond to the cocaine and increased noradrenaline levels** - this means the pupil will be smaller (may constrict or dilate a tiny amount) - therefore an affected pupil won't dilate properly, indicating Horner's syndrome
32
what is Holmes Adie pupil caused by and features?
- damage to the post ganglionic parasympathetic fibres - dilated - sluggish to react to light - responsive to accommodation (pupils constrict well when focusing on a near object) - slow to dilate following constriction ('tonic' pupil)
33
what is Argyll-Robertson pupil found in and features?
- neurosyphilis - constricted pupil - accommodates when focusing on near objects - doesn't react to light - irregularly shaped
34
how does anterior uveitis and acute angle closure glaucoma affect the pupil shape?
- **anterior uveitis** - can cause **adhesions** in the iris → irregular pupil shape - **AACG** - **ischaemic damage to the muscles** of the **iris** and an abnormal pupil shape, usually a **vertical oval**