Visual Loss Flashcards

1
Q

Describe the normal anatomy of the optic disc

A
  • The areas of the optic disc and optic cup are correlated to each other (i.e. the larger the disc, the larger the cup)1
  • The size of the optic cup may vary tremendously1
  • In most normal eyes the rim tissue area is constant1
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2
Q

Patient history for glaucoma

A
  • History of presenting complaint
  • Including incidence, duration, severity and triggers of visual symptoms of glaucoma
  • Ophthalmic history
  • Trauma, previous eye surgery or laser, previous ophthalmic medications
  • Medication history
  • Social history
  • Family history
  • Risk factors in family
  • Blindness or eye disease in the family
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3
Q

All patients with suspected glaucoma should undergo a physical eye examination that includes the following investigations:

A
  • Slit-lamp examination
  • Applanation tonometry
  • Gonioscopy
  • Optic nerve head and retinal nerve fibre layer evaluation
  • Visual field examination (perimetry)
  • Visual acuity
  • Pachymetry
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4
Q

features of POAG normal pressure glaucoma

A
  • > 35 years
  • Normal IOP without treatment
  • Asymptomatic until field loss advanced
  • ONH: typical damage
  • VF: typical, paracentral defects
  • Gonio: open anterior chamber angle*
  • No history or signs of other eye diseases or steroid use

OAG suspect
• VF, ONH and RNFL normal or suspicious

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5
Q

features of Ocular hypertension

A
  • IOP > 21 mm Hg
  • VF: normal
  • ONH/RNFL: normal
  • Gonio: open anterior angle*
  • No other risk factors
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6
Q

Acute angle-closure signs

A
  • IOP > 21 mm Hg, often to 50 to 80 mm Hg
  • Decreased visual acuity
  • Corneal oedema
  • Shallow or flat peripheral anterior chamber
  • Peripheral iris pushed forward
  • Gonio:iridotrabecularcontact360degrees
  • Pupil mid dilated and reduced with no reactivity
  • Gonioscopycluesfromothereye
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7
Q

Signs of Intermittent angle- closure

A
  • Features vary according to amount of iridotrabecular contact • Optic disc rim may show atrophy with an afferent pupil defect • Mild,intermittentsymptomsofacuteangle-closuretype
  • Resolves spontaneously
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8
Q

signs of Chronic angle-closure

A
  • Gonio: peripheral anterior synechiae of any degree
  • IOP > 21 mm Hg
  • Visual acuity may be normal
  • ONH damage compatible with glaucoma
  • Superimposed iridotrabecular contact possible
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9
Q

OVERVIEW OF PHARMACOLOGICAL treatment of glaucoma

A

• IOP reduction is the only treatment option we have
• Neuroprotection
Glaucoma & IOP reduction • 20% reduction in IOP reduces progression by 50%

  • Beta blockers (1978)
  • Timolol, betaxolol (betagan)
  • Prostaglandin analogues (1996)
  • Latanoprost (xalatan), bimatoprost (Lumigan), travoprost (Travatan) • Alpha agonists(1988)
  • Brimonidine (alphagan), iopidine
  • Carbonic anhydrase inhibitors (1995)
  • Dorzolamide (Trusopt), brinzolamide (Azopt)
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10
Q

side effects of Beta blockers for glaucoma

A
  • Beta blockers (1978)
  • Timolol 0.25% & 0.5%, betaxolol (betagan)
  • 20-27% reduction in IOP • Twice daily regime
  • Bronchospasm
  • Bradycardia
  • Hypotension
  • One drop of 0.5% may lead to 10mg oral dose equivalent
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11
Q

What drug os first line for glaucoma? list some side effects

A
Prostaglandin analogues
• 20-35% reduction in IOP
• Associated with decreased rate of glaucoma surgery in 1990s • First line
• Once daily at night
• Well tolerated
• lash growth
• Iris darkening
• Dark circles under eyes
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12
Q

Cataracts Definition

A
  • An opacity that forms within the lens of the eye which can reduce the transparency of the lens
  • Most common cause of blindness in the world
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13
Q

Cataracts clarification

A

• Often classified according to part of lens primarily affected
• Nuclear – central part of lens, most common, change the refractive index
• Cortical – in the outer layer
• Sub-capsular – directly under lens capsule,
anterior or posterior
• Sub-classifications sometimes used by specialists, including severity, maturity and aetiology

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14
Q

Risk factors for acquired cataract

A
  • Ageing (most occur in >60s)
  • Trauma (blunt or penetrating injury, electric shock, radiation, surgery)
  • Systemic disease (diabetes mellitus, myotonic dystrophy, NF type 2, severe atopic dermatitis)
  • Drugs- corticosteroids
  • Family history
  • Social history- Smoking/ Cumulative exposure to UV light
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15
Q

Ocular conditions associated with cataract

A
  • Trauma
  • Uveitis
  • High myopia
  • Topical medication (particularly steroid drops) • Intraocular tumour
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16
Q

Clinical features cataract

A
  • Unilateral cataracts may often be unnoticed but loss of stereopsis may affect distance judgement
  • Gradual and painless reduction in V/A (difficulty in reading, recognising faces, watching TV)
  • Difficulties due to glare (problems with bright sunshine, oncoming headlights when driving at night)
  • Frequent changes of spectacle prescription
  • Monocular diplopia
  • Opacities and reduced red reflex on ophthalmoscopy
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17
Q

Differential diagnosis Other causes of painless gradual visual disturbance include

A
• Refractive error
• Age-related macular degeneration
• Primary open-angle glaucoma
• Presbyopia
• Some types of corneal disease
• Chronic uveitis
• Chemicals or drugs — eg methanol, chloroquine, hydroxychloroquine, isoniazid, thioridazine, isotretinoin, tetracycline, ethambutol
• Pituitary tumour
• Diabetic lens — undiagnosed or uncontrolled diabetes can cause vision
changes
• Diabetic retinopathy/maculopathy
• Retinoblastoma — nearly always affects children <5 (pupil may look white (loss of red reflex),
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18
Q

Management cataract

A
  • If not already seen optometrist, encourage patient to see one (to assess V/A and exclude other causes of visual impairment)
  • Provide advice on fitness to drive
  • Consider referral for surgery
  • Visual impairment which is affecting lifestyle (eg driving, reading)
  • Comorbidity that may benefit from surgery (eg risk of falls)
  • Surgery would facilitate treatment/monitoring of other eye conditions eg retinal screening for diabetics
  • If person has capacity to cooperate with exams, surgery and post-op drops
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19
Q

Post-op complications cataracts

A
  • Intraoperative:
  • Posterior capsule rupture and/or vitreous loss (communication between anterior and posterior chambers)
  • Early complications:
  • Bruising of eye or eyelids
  • Infective endophthalmitis (very rare, may lead to loss of sight or eye)
  • Refractive surprise (unexpectedly large need for glasses)
  • Later complications
  • Posterior capsule opacification (takes months to years) – treatable by laser, most common complication
  • Detached retina (may occur weeks or months after surgery
  • Dislocation of implant lens
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20
Q

Cataracts in children

A
  • Much less common than in adults
  • Babies screened for congenital cataracts at birth and at 6-8 weeks of age
  • Present with poor vision, a white/grey pupil, nystagmus, strabismus, light sensitivity
  • Unilateral cataracts usually idiopathic and non-hereditary
  • Bilateral cataracts either idiopathic in 60% cases or
  • Hereditary (most often autosomal dominant)
  • Intrauterine infections (rubella, varicella, CMV, HSV, toxoplasmosis) • Genetic syndromes (Down syndrome, Edward’s syndrome)
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21
Q

Cataracts Prognosis

A

Adults
• Without treatment
Prognosis
• Steady decline in V/A without chance of recovery (rate of progression variable and unpredictable), leading to severe visual impairment
• With surgery
• Around 95% will have 6/12 best corrected vision on a Snellen chart
(meeting UK driving requirements)
• Generally very safe procedure but small minority develop complications which can be sight-threatening
• Children
• If congenital ones not removed within about 6 weeks of life, deprivation
amblyopia and lifelong visual impairment likely to occur
• Some visual improvement may be possible if treatment delayed or

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22
Q

lid lacerations management

A

if it closes lid margin medial canthus, lacrimal apparatus, or associated iwrh globe perforations must be referred to ophthalmologist. all others repaired with 6/0 mono filament
remember tetanus

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23
Q

periorbital heamatomas

A

check for other ocular damage e.g. orbital floor fracture, globe perforation hyphaema
if bone injury suspected x rY
analgesia

24
Q

Management of blow out fracture

A

x ray - tear drop sign

refer to ophthalmology or max fax

25
Q

symptoms and signs of blow out fracture

A

orbital pian on occular movements, diplopia, parasthesia over maxilla

enopthalmos
bony tenderness
surgical emphysema
sensation over v2 districultuin

26
Q

Hyphaema symptoms and signs

A

blurred vision, watering, photophobia

blood in the anterior chamber

27
Q

Hyphaema management

A

look for globe perforation, refer to ophthalmologist, usually admit, bed rest, topical steroids, reduce intraoccqular pressure

28
Q

Ruptured globe management

A
tetanus prophylaxis
x-ray
plastic shield
primary repair
secondary repair
29
Q

toxic foreign bodies in eye

A

Copper Thorn Twig Wood Soil Hair follicle

30
Q

Intraocular foreign bodies management

A

refer and systemic antibiotics e.g. ciprofloxacin

31
Q

chemical burns to eye management

A

copies irrigation urgent feral

32
Q

Acute Closed Angle Glaucoma signs and symptoms

A

Blocked drainage of aqueous from anterior chamber via the canal of Schlemm.
Pupil dilatation (e.g. @ night) worsens the blockage.
Intraocular pressure rises from 15-20 >60mmHg

Symptoms
Prodrome: rainbow haloes around lights at night-time.
Severe pain ̄c n/v
acuity and blurred vision

33
Q

Acute Closed Angle Glaucoma acute management

A

Pilocarpine 2-4% drops stat: miosis opens blockage
Topical -B (e.g. timolol): aqueous formation
Acetazolamide 500mg IV stat: aqueous formation
Analgesia and antiemetics

34
Q

Sudden Loss of Vision: Key Questions

A

Headache associated: GCA
Eye movements hurt: optic neuritis
Lights / flashes preceding visual loss: detached retina
Like curtain descending: TIA, GCA
Poorly controlled DM: vitreous bleed from new vessels

35
Q

Optic Neuritis signs and symptoms

A

Symptoms
Unilateral loss of acuity over hrs – days
colour discrimination (dyschromatopsia)
Eye movements may hurt
Signs
acuity
colour vision
Enlarged blind-spot
Optic disc may be: normal, swollen, blurred
Afferent defect

36
Q

Optic Neuritis causes

A
Multiple sclerosis (45-80% over 15yrs)
  DM
  Drugs: ethambutol, chloamphenicol
  Vitamin deficiency
  Infection: zoster, Lyme disease
37
Q

Retinal Detachment: presentation

A

Holes/tears in retina allow fluid to separate sensory retina from retinal pigmented epithelium
May be 2O to cataract surgery, trauma, DM
Presentation: 4 F’s
Floaters: numerous, acute onset, “spiders-web”
Flashes
Field loss
Fall in acuity
Painless

38
Q

Orbital Cellulitis pathophysiology

A

Pathophysiology
Infection spreads locally: e.g. from paranasal sinuses, eyelid or external eye.
Staphs, pneumococcus, GAS

39
Q

Orbital Cellulitis presentation

A
Presentation
  Usually a child  ̄c inflammation of the orbit + lid swelling   Pain and   range of eye movement
  Exophthalmos
  Systemic signs: e.g. fever
  ± tenderness over the sinuses
40
Q

Orbital Cellulitis management

A

IV Abx: Cefuroxime (20mg/kg/8h IV)

41
Q

4 areas of visual function

A

visual acuity
eye movements
visual fields
light reflex and pupil function

42
Q

primary function of superior oblique muscle

A

incyclorotation

43
Q

primary function of inferior oblique muscle

A

excyclorotation

44
Q

Patient has complete loss of vision in one eye - where is the site of the lesion?

A

ipsilateral optic nerve

e.g. optic neuritis, foreign body occluding, dense cataract.

45
Q

Patient has bitemporal hemianopia - where is the site of the lesion?

A

optic chiasm

bitemporal hemianopia
optic chiasm lesion e.g. pituatuary defect

46
Q

Patient has binasal hemianopia - where is the site of the lesion?

A

optic chiasm

47
Q

Patient has left homonymous hemianopia - where is the site of the lesion?

A

Right optic tract/radiation

48
Q

Patient has right homonymous hemianopia - where is the site of the lesion?

A

Left optic tract/radiation

49
Q

Patient has Homonymous quadrantanopia - where is the site of the lesion?

A

Contralateral optic tract/radiation
Top – temporal region
Bottom – parietal region

50
Q

Patient has scotoma visual field defect - where is the site of the lesion?

A

Occipital region

51
Q

What muscles contract to constrict pupil?

A

Circular muscles contract

radial muscles relax

52
Q

What muscles contract to dilate pupil?

A

circular muscles relax

radial muscles contract

53
Q

What do you look for on direct ophthalmoscopy of ocular media?

A

Red reflexes; are there any dark or light areas.
Distinguish between out-of-focus disc and light areas.
‘White eye in photos’.

54
Q

What do you look for on direct ophthalmoscopy of optic disc/nerve head?

A
Is the disc margins sharp or swollen?
Is the disc (neuro-retinal rim) pink or is there pallor?
Are the vessels normal looking?
Are there any haemorrhages.
What is the cup-to-disc ratio?
55
Q

What do you look for on direct ophthalmoscopy of macula?

A

The macula is a small darker patch compared with the of the
rest of the retina.
The bright spot is the fovea/foveola.
Are there any haemorrhages or drusen?

56
Q

What do you look for on direct ophthalmoscopy of (Central)

Retinal blood vessels?

A

Any tortuosity of the vessels?
Are there any changes in calibre. Are the reflections bright?
Are there any blockages, haemorrhages or occlusions?

57
Q

What do you look for on direct ophthalmoscopy of peripheral retina?

A

Are there any haemorrhages or changes in colour?
Are there any lesions?
What is the size of the lesions c/w disc diameters?
Where is it on the retina as a polar co-ordinate?
What colour is it? Are its margins sharp? Is it raised?