gradual visual loss Flashcards

1
Q

generalised reduction in visual acuity with starburst around lights

A

cataracts

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2
Q

peripheral loss of vision with halos around lights

A

glaucoma

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3
Q

central loss of vision with crooked or wavy appearance to straight lines

A

macular degeneration

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4
Q

what produces aqueous humour

A

ciliary body

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5
Q

normal intraocular pressure

A

10-21

pressure is created by resistance to flow through trabecular meshwork into canal of schlemm

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6
Q

what can cause cupping of the optic disc?

A

increased pressure
optic cup is made wider + deeper
optic cup > 0.5 the size of optic disc = abnormal

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7
Q

investigations for glaucoma

A

goldmann applanation tanometry = gold standard
–> makes contact with cornea, applies diff pressures

non-contact tanometry
–> puff of air, used in screening

fundoscopy = disc cupping
peripheral field assessment

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8
Q

open angled glaucoma

A

poor drainage of aqueous humour through trabecular meshwork, slow onset

RF = black, near-sightedness (myopia)

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9
Q

presentation of open angled glaucoma

A

peripheral vision first - eventually tunnel vision
gradual onset fluctuating pain
headaches

halos appearing around lights
optic disc cupping

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10
Q

criteria for beginning management of open angled glaucoma

A

pressure of 24 mmHG

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11
Q

pharma management of open angled glaucoma

A

1st line = prostaglandin analogue (latanoprost)
–> increase outflow

others reduce aqueous production

  • timolol (BB)
  • carbonic anhydrase inhibitor
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12
Q

closed angle glaucoma

A

when irisi bulges forward + seals off trabecular meshwork from anterior chamber preventing drainage

increased pressure pushes irish forward more + more

medical emergency

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13
Q

medications that can predispose close angle glucoma

A

adrenergic - noradrenalin
anticholinergic - oxybutynin, solifenacin

tricyclic antidepressants - amitriptyline

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14
Q

closed angle glucoma presentation

A
haxy cornea
fixed pupil size
blurred vision
headache, N+V
firm eyeball on palpation
decreased visual acuity
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15
Q

initial management of closed angle glaucoma

A

pilocarpine - constrict pupils + contracts ciliary
–> opens pathway

acetazolamide - reduces production (carbonic anhydrase inhibitor)

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16
Q

definitive management of close angle glaucoma

A

laser iridotomy

–> zap hole in iris

17
Q

papilloedema

A

bilateral dic swelling SECONDARY to raised intracranial pressure

(suspect space occupying lesion until proved otherwise)

18
Q

causes of papilloedema

A

space occupying lesion
malignant hypertension - always check BP

idiopathic intracranial hypertension - young females

19
Q

causes of increased cranial pressure

A

obstruction to CSF circulation - congenital malformation
overproduction of CSF - choroid plexus tumour

inadequate absorption - subarachnoid haemorrhage

20
Q

endophthalmitis

A

inflammation of inner ocntents of eye

Mx = intravitreal antibiotics injected

21
Q

classification of hypertensive retinopathy

A

Keith-Wagener
1 = mild narrowing
2 = focal constriction

3 = cotton wool, exudates, haemorrhages
4 = papillodema
22
Q

hypertensive retinopathy presentation

A

cotton wool spots
atriovenous nipping - art compress veins where they cross
exudates
haemorrhages

papilloedmea - ischaemia to optic nerve resulting in optic nerve swelling + blurring of optic disc margins

23
Q

types of macular degeneration

A

dry (90%) - gradual

wet (10%) - sudden, vascular proliferation

24
Q

macular degeneration of funducopy

A

drusen = yellw deposits of protein + lipids

25
Q

diagnosis of wet macular degeneration

A

optical coherence tomography
–> atrophy of retinal pigment epithelium, degeneration of photoreceptors

(shows cross section ofretina layers)

26
Q

age related macular degeneration presentation

A

central vision loss - scotoma (blind spots/distortions)
wavy appearance to straight lines

(wet more acute - loss of vision over days)

27
Q

fluorescein angiography

A

given fluorescin contrast + photgraph retina to look in detail at the blood supply to retina

–> shows any oedema + neovascularisation

(2nd line diagnosis for wet ARMD after OCT)

28
Q

management of wet ARMD

A

anti-VGEF meds
ranibizumab, bavacizumab

injected directly into vitreous chamber once a month
slow + reverse progression

29
Q

management of dry ARMD

A

lifestyle measures - smoking, bp, vitamin supplementation

social support
magnifiers

30
Q

stages of diabetic retinopathy

A
  1. non proliferative
  2. proliferative
  3. diabetic maculopathy
31
Q

diabetic retinopathy on fundoscopy

A
hard exudates
microaneurysms
blot haemorrhages
neovascularisation
cotton wool spots
32
Q

what causes cotton wool spots

A

damage to nerve fibres

33
Q

pathophysio of diabetic retinopathy

A

hyperglycaemia leads to damage to retinal small vessels + endthelial cells
damage to wall leads to microaneurysms, venous beading

increased vascular permeability leads to leakage - blot haemmorhages + hard exudates

34
Q

management of diabetic retinopathy

A

yearly review

NP = observe, photocoag in severe

P = panretinal laser photpcoagulation, intravitreal VEGF inhibitors, vitereoretinal surgery in severe

maculopathy = intravitreal VEGF inhib if change in visual acuity

35
Q

difference between proliferative and non-proliferative diabetic retinopathy

A

prolif = retinal neovascularisation - may lead to virous haemorrhage

–> patient may complain of floaters or sever visual loss