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Opthalmology > Blurred Vision > Flashcards

Blurred Vision Flashcards

1
Q

How to test which eye is causing diplopia

A

Looking in direction of diplopia and cover one eye followed by the other - ask which eye is seeing the outer image - this is the eye which is malfunctioning

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2
Q

What is hypopyon

A

Pus in anterior chamber

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3
Q

What is hyphaema

A

Blood in anterior chamber

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4
Q

How are pupils in anterior uveitis

A

Small and irregular

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5
Q

How are pupils in acute glaucoma

A

Fixed, dilated and oval

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6
Q

What is the medical term for stye and what is it

A

Hordeolum externum - inflammatory eyelid swelling - open staphlococcal infection in the lash follicle. Point outwards and cause inflammation - treated with local antibiotic eg. fusidic acid

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7
Q

Name for stye that is not infected

A

Marginal cyst

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8
Q

What is chalazion

A

Also called hordeolum internum - internal abscess where opens into conjunctiva

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9
Q

What is blepharitis

A

Lid inflammation from staph, seborrhoeic dermatitis or rosacea. Burning itching red margins and scales on lashes
Treat by cleaning off crusts and then Tears Naturale, fusidic acid, steroid drops or oral doxy

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10
Q

What is entropion (eye)

A

Lid inturning associated with degeneration of lower lid fascial attachments and muscle
Causes irritation
Can taper lower lashes to cheek or botox or surgery for longer lasting effects

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11
Q

What is ectropion (eye)

A

Lower lid eversion causing irritation, watering and exposure keratitis
associated with old age and facial palsy
Surgical correction

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12
Q

What is a dendritic ulcer

A

Herpes simplex corneal ulcer which causes severe pain, photophobia and watering

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13
Q

Investigation of dendritic ulcer

A

1% fluorescein drops stain the lesion green

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14
Q

Treatment of dendritic ulcer

A

Treat with aciclovir 3% 5x daily

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15
Q

Features of orbital cellulitis

A

Inflammation of orbit, fever, lid swelling, decreased eye mobility

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16
Q

Cause of orbital cellulitis

A

Infection spread via paranasal sinuses, eyelid, dental injury/infection or external ocular infection
by Staphs, strep pneu, strep pyogenes or milleri

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17
Q

Treatment of orbital cellulitis

A

CT, ENT and opthalmic opinion
Antibiotics
Need to prevent spread to meninges or cavernous sinus

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18
Q

Risk with orbital cellulitis

A

Spread and also blindness from pressure on optic nerve or vessel thrombosis

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19
Q

Typical presentation of opthalmic shingles (herpes zoster opthalmicus)

A

Pain and neuralgia in opthalmic division followed by a blistering inflamed rash
50% have affected globe therefore having corneal signs with or without iritis

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20
Q

What is an indicator in HZO that the globe might be affected

A

If the nose tip is involved (Hutchisons sign) then the nasociliary branch is affected and this nerve also supplies the globe

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21
Q

Treatment of HZO

A

Famiciclovir - 750mg OD for 1 week - better regimen but more expensive than Aciclovir 800mg 5x day for 1 week (aciclovir also has more serious side effects eg. hepatitis and renal failure)

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22
Q

Signs of retinoblastoma

A

Strabismus and leukocoria (white pupil)

Red reflex is absent!!

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23
Q

Inheritance and genetics of retinoblastoma

A

Inherited autosomal dominant with 80% penetrance
RB gene is a tumour suppressor gene
Usually inherit one altered allele - if developing mutation occurs in other allele then tumour arises

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24
Q

What can occur as a secondary in retinoblastoma

A

Secondary malignancies such as osteosarcoma or rhabdomyosarcoma

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25
Q

Treatment of retinoblastoma

A

Moving away from eye removal surgery and towards other options such as chemo, targeted radio, enucleation etc

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26
Q

What is esotropia

A

One eye turned in aka convergent squint - commonest type in children

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27
Q

What is exotropia

A

Divergent squint, one eye turns out - more common in older children and often intermittent

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28
Q

Management of squint

A

3 O’s - Optical (cyclopentolate drops to see refractive error and if any other diagnoses - then give glasses)
Orthoptic - cover the good eye, forces bad eye to be used
Operation - rectus muscle resection and recession

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29
Q

What happens in 3rd CN palsy

A

Oculomotor nerve affected - ptosis and proptosis due to decreased recti tone
Fixed pupil dilation and eye looking down and out

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30
Q

What happens in 6th CN palsy

A

Abducens nerve - diplopia in horizontal plane, eye medially deviated and cannot move laterally from midline (lateral rectus paralysed)

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31
Q

Causes of 6th CN palsy x4

A

Tumour causing raised ICP and pushing nerve against temporal bone
Trauma to base of skull
MS
Vascular

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32
Q

What happens in 4th CN palsy

A

Trochlear Nerve - Diplopia - eye looks upward and adducted - cannot look down and in (superior oblique is paralysed)

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33
Q

Causes of 4th CN palsy x4

A

Trauma 30%
Diabetes 30%
Tumour
Idiopathic

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34
Q

What does inferior oblique do

A

Rotates eye upwards and inwards

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35
Q

Signs and symptoms of acute closed angle glaucoma

A

Headache, nausea and a painful red eye
Preceeded by blurred vision or haloes around lights at night
Raised IOP can cause eye to feel hard

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36
Q

What causes ACAG?

A

Blocked flow of aqueous humour from the anterior chamber via the canal of Schlemm

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37
Q

Why is ACAG worse at night

A

Because pupil dilates with low light and this causes increased blockage

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38
Q

Danger with ACAG

A

Blockage causes raised IOP which causes pupil to become fixed and dilated and axonal death can occur

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39
Q

Pressure changes with ACAG

A

Normally IOP is 15-20mmHg and in ACAG will rise to above 30

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40
Q

Management of ACAG

A 
Immediate gonioscopy (imaging of anterior chamber)
Pilocarpine drops (miosis) with acetazolamide (stops aqueous production) and may need mannitol
These reduce IOP and then surgery can be performed - peripheral iridectomy 
Also give analgesia, antiemetics and topical steroids and anti=hypertensives
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41
Q

What is keratitis

A

Corneal inflammation

42
Q

Management of a corneal abrasion

A

Not infected (infected is corneal ulcer and needs expert help) - treat with chloramphenicol drops

43
Q

Difference between episcleritis and scleritis

A

Episcleritis is slightly more superficial. It is less painful, more a numb aching compared to very painful scleritis. With a cotton bud the engorged vessels can be moved whereas in scleritis they are immobile
Episcleritis vessels blanch with phenylephrine - scleritis don’t
Visual acuity not affected in episcleritis but can be in scleritis

44
Q

Treatment of episcleritis

A

Topical or systemic NSAIDs

45
Q

Cause of episcleritis

A

No cause found in 70%

Can complicate rheumatic fever, PAN and SLE

46
Q

Cause of scleritis

A

Can be associated with systemic disease such as connective tissue diseases

47
Q

Treatment of scleritis

A

Oral steroids/immunosuppression - ciprofloxacin, topical fortified amikacin and vancomycin (if staphylococcal)

48
Q

Symptoms of conjunctivitis

A

Itching, burning, lacrimation and photophobia

Bilateral with eyelids sticking together

49
Q

Signs of conjunctivitis

A

Red eye with mobile vessels

Acuity and pupillary reflexes are unaffected

50
Q

Causes of conjunctivitis

A

Adenoviruses (small lymphoid follicular aggregates on conjunctiva)
Bacterial (more purulent discharge)
Allergic

51
Q

Treatment of conjunctivitis

A

Chloramphenicol or fusidic acid

Antihistamine for allergic

52
Q

When does arteritic anterior ischaemic optic neuropathy occur?

A

Giant cell arteritis

53
Q

Symptoms of arteritic anterior ischaemic optic neuropathy (and GCA)

A

Malaise, jaw claudication, tender scalp and temporal arteries + sudden painless vision loss

54
Q

Treatment of arteritic anterior ischaemic optic neuropathy

A

Also treatment for gca

Start prednisolone

55
Q

What is non-arteritic anterior ischaemic optic neuropathy

A

More common type which occurs in people with cardiovascular risk factors
It is a white matter stroke of the optic nerve

56
Q

Symptoms of non-arteritic anterior ischaemic optic neuropathy

A

Sudden painless vision loss
Often in the morning
Often half field covered with a shadow and often nasal field

57
Q

Treatment of non-arteritic anterior ischaemic optic neuropathy

A

Recent evidence shows corticosteroid treatment may improve regain of vision
Otherwise treat risk factors to protect other eye

58
Q

What is vitreous haemorrhage?

A

Retinal bleed from new retinal vessels (diabetes, CRVO) retinal tears, retinal detachment or trauma

59
Q

Presentation of vitreous haemorrhage

A

Vitreous floaters which appear to patient as small black dots or ring-like forms with clear centres - vision not massively obscured
Large enough bleed can cause no red reflex and retina not being able to be visualised

60
Q

Prognosis of vitreous haemorrhage

A

Undergoes spontaneous resorption

If large VH then may need vitrectomy to removed blood

61
Q

What is main cause of subacute loss of visual acuity over hours/days

A

Optic neuritis

62
Q

How does optic disc appear on fundoscopy in anterior ischaemic optic neuropathy?

A

Pale/swollen optic disc

63
Q

Symptoms of optic neuritis

A

Subacute onset - colour vision affected (dyschromatopsia) - reds appear less red ‘red desaturation’
Eye movements hurt
Pupil shows afférent defect

64
Q

Prognosis of optic neuritis

A

Recovery usually over 2-6 weeks but 45-80% develop MS in the next 15 years - high dose methylprednisolone for 72hr then prednisolone for 11 days may briefly delay onset of MS

65
Q

What occurs with central retinal artery occlusion

A

Dramatic visual loss within seconds of occlusion (embolic) often to finger counting or less
RAPD

66
Q

Signs of central retinal artery occlusion

A

Retina is white with a cherry red spot in the macula

67
Q

Management of central retinal artery occlusion

A

Increase retinal artery flow by reducing intraocular pressure (ocular massage or surgical removal of aqueous or antihypertensives)
Hyperbaric treatment has been tried with 70% getting improved acuity

68
Q

Features of central retinal vein occlusion

A

Incidence increased with age and cardiovascular risk factors are a feature
Pathology is sudden development than artery occlusion but may seem suddenly to patient
RAPD

69
Q

What are two types of central retinal vein occlusion

A

Non-ischaemic and ischaemic (cotton wool spots, swollen optic nerve, macular oedema and risk of neovascularisation)
Non-ischaemic have better visual prognosis but can become ischaemic therefore need follow up

70
Q

Management of central retinal vein occlusion

A

Pan-retinal photocoagularion to prevent or treat neovascularisation - but prognosis is still poor

71
Q

What is seen on fundoscopy with central retinal vein occlusion

A

Hyperaemia and haemorrhages - known as stormy sunset appearance

72
Q

What is the chief cause of registrable blindness?

A

Age-related macular degeneration

73
Q

How does ARMD present?

A

Deteriorating central vision

74
Q

Two types of ARMD

A

Wet and dry

75
Q

Features of dry ARMD

A

Mainly drusen (signify axonal degeneration) and degenerative changes at the macular - slow progression

76
Q

What are drusen?

A

signify axonal degeneration leading to intracellular mitochondrial calcification - axons rupture, mitochondria extruded into extra-cellular space and calcium is deposited

77
Q

Features of wet ARMD

A

Occurs when aberrant vessels grow from choroid into the retina and leak
Vision deteriorates rapidly, distortion is a key feature

78
Q

What is seen on ophthalmoscopy with wet ARMD

A

Fluid exudation, localised detachment of the pigment

79
Q

Lifestyle advice for ARMD

A

Stop smoking and eat lots of green vegetables

80
Q

Treatment of wet ARMD

A

Intravitreal vascular endothelial growth factor (veg-f) inhibitors - bevacizumab and ranibizumab
Intravitreal steroids e.g. Triamcinolone
Screening
Antioxidants and vitamins

81
Q

What do you think of if gradual visual loss in teenagers

A

Stargardt macular degeneration - central vision loss, wavy vision, blind spots, blurry vision and colour blindness
Look for prominent yellow flecks in retina
Average age onset 17
No treatment often progresses to registered blindness

82
Q

Optic disc in optic atrophy

A

Pale

83
Q

Which type of glaucoma is the chronic glaucoma

A

Open angle glaucoma

84
Q

What % if registered blindness does open angle glaucoma account for?

A

7%

85
Q

What is glaucoma?

A

Optic neuropathy with death of retinal ganglion cells and their optic nerve axons

86
Q

Definition of glaucoma pathologically

A

On visual field testing 3 or more locations are outside normal limits
Cup to disc ratio greater than that seen in 97.5% of population
IOP may be raised (but not part of definition)

87
Q

What happens to vision in glaucoma

A

Peripheral vision loss
Nasal and superior fields are lost first
Temporal fields lost last

88
Q

What happens to optic disc cups in glaucoma

A

Cups enlarge especially along vertical axis
With progressive atrophy the disc pales, cup widens and deepens (vessels appear to have breaks as they pass over the cup)

89
Q

Management of glaucoma

A

Reducing IOP stops visual field loss but does not reverse it

90
Q

Who needs screening for glaucoma

A

High risk patients - screen when over 35 if:

positive family history, Afro-Caribbean, myopia, diabetic/thyroid disease

91
Q

Treatment of glaucoma

A

Prostaglandin analogues (latanoprost, travoprost)
B-blockers (tinolol, betaxolol)
Alpha adrénergic agonists (brimonidine, apraclonidine)
Etc

92
Q

Role of prostaglandin analogues in the treatment of glaucoma

A

Increase uveoscleral outflow

E.g. Latanoprost and travoprost

93
Q

Role of beta blockers in glaucoma treatment

A

Decrease aqueous production

E.g. Timolol and betaxolol

94
Q

Role of alpha adrenergic agonists in treatment of glaucoma

A

E.g. Brimonidine and apraclonidine

Decrease aqueous production and increase uveoscleral outflow

95
Q

Role of carbonic anhydride inhibitors in glaucoma treatment

A

E.g. Dorzolamide and brinzolamide drops and acetazolamide PO

Decrease production of aqueous

96
Q

Role of miotics in treatment of glaucoma

A

E.g. Pilocarpine
Decrease resistance to aqueous outflow
Causes miosis, decreased acuity and brow ache from ciliary muscle spasm

97
Q

Type of surgery in glaucoma treatment

A

Trabeculectomy
Filtration surgery that makes a pressure valve at limbus so that aqueous can flow into a conjunctival bleb
Failure rates are high but can be delayed by cytotoxics e.g. Fluorouracil

98
Q

What is normal optic cup to disc ratio

A

0.4-0.7

99
Q

When is cupping said to be severe

A

When ratio is >0.9

100
Q

Sudden painless vision loss with RAPD

A

RVO or RAO

Opthalmology (6 decks)

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