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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
Treatment of retinoblastoma
Moving away from eye removal surgery and towards other options such as chemo, targeted radio, enucleation etc
26
What is esotropia
One eye turned in aka convergent squint - commonest type in children
27
What is exotropia
Divergent squint, one eye turns out - more common in older children and often intermittent
28
Management of squint
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
29
What happens in 3rd CN palsy
Oculomotor nerve affected - ptosis and proptosis due to decreased recti tone Fixed pupil dilation and eye looking down and out
30
What happens in 6th CN palsy
Abducens nerve - diplopia in horizontal plane, eye medially deviated and cannot move laterally from midline (lateral rectus paralysed)
31
Causes of 6th CN palsy x4
Tumour causing raised ICP and pushing nerve against temporal bone Trauma to base of skull MS Vascular
32
What happens in 4th CN palsy
Trochlear Nerve - Diplopia - eye looks upward and adducted - cannot look down and in (superior oblique is paralysed)
33
Causes of 4th CN palsy x4
Trauma 30% Diabetes 30% Tumour Idiopathic
34
What does inferior oblique do
Rotates eye upwards and inwards
35
Signs and symptoms of acute closed angle glaucoma
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
36
What causes ACAG?
Blocked flow of aqueous humour from the anterior chamber via the canal of Schlemm
37
Why is ACAG worse at night
Because pupil dilates with low light and this causes increased blockage
38
Danger with ACAG
Blockage causes raised IOP which causes pupil to become fixed and dilated and axonal death can occur
39
Pressure changes with ACAG
Normally IOP is 15-20mmHg and in ACAG will rise to above 30
40
Management of ACAG
``` 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 ```
41
What is keratitis
Corneal inflammation
42
Management of a corneal abrasion
Not infected (infected is corneal ulcer and needs expert help) - treat with chloramphenicol drops
43
Difference between episcleritis and scleritis
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
Treatment of episcleritis
Topical or systemic NSAIDs
45
Cause of episcleritis
No cause found in 70% | Can complicate rheumatic fever, PAN and SLE
46
Cause of scleritis
Can be associated with systemic disease such as connective tissue diseases
47
Treatment of scleritis
Oral steroids/immunosuppression - ciprofloxacin, topical fortified amikacin and vancomycin (if staphylococcal)
48
Symptoms of conjunctivitis
Itching, burning, lacrimation and photophobia | Bilateral with eyelids sticking together
49
Signs of conjunctivitis
Red eye with mobile vessels | Acuity and pupillary reflexes are unaffected
50
Causes of conjunctivitis
Adenoviruses (small lymphoid follicular aggregates on conjunctiva) Bacterial (more purulent discharge) Allergic
51
Treatment of conjunctivitis
Chloramphenicol or fusidic acid | Antihistamine for allergic
52
When does arteritic anterior ischaemic optic neuropathy occur?
Giant cell arteritis
53
Symptoms of arteritic anterior ischaemic optic neuropathy (and GCA)
Malaise, jaw claudication, tender scalp and temporal arteries + sudden painless vision loss
54
Treatment of arteritic anterior ischaemic optic neuropathy
Also treatment for gca | Start prednisolone
55
What is non-arteritic anterior ischaemic optic neuropathy
More common type which occurs in people with cardiovascular risk factors It is a white matter stroke of the optic nerve
56
Symptoms of non-arteritic anterior ischaemic optic neuropathy
Sudden painless vision loss Often in the morning Often half field covered with a shadow and often nasal field
57
Treatment of non-arteritic anterior ischaemic optic neuropathy
Recent evidence shows corticosteroid treatment may improve regain of vision Otherwise treat risk factors to protect other eye
58
What is vitreous haemorrhage?
Retinal bleed from new retinal vessels (diabetes, CRVO) retinal tears, retinal detachment or trauma
59
Presentation of vitreous haemorrhage
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
Prognosis of vitreous haemorrhage
Undergoes spontaneous resorption | If large VH then may need vitrectomy to removed blood
61
What is main cause of subacute loss of visual acuity over hours/days
Optic neuritis
62
How does optic disc appear on fundoscopy in anterior ischaemic optic neuropathy?
Pale/swollen optic disc
63
Symptoms of optic neuritis
Subacute onset - colour vision affected (dyschromatopsia) - reds appear less red 'red desaturation' Eye movements hurt Pupil shows afférent defect
64
Prognosis of optic neuritis
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
What occurs with central retinal artery occlusion
Dramatic visual loss within seconds of occlusion (embolic) often to finger counting or less RAPD
66
Signs of central retinal artery occlusion
Retina is white with a cherry red spot in the macula
67
Management of central retinal artery occlusion
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
Features of central retinal vein occlusion
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
What are two types of central retinal vein occlusion
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
Management of central retinal vein occlusion
Pan-retinal photocoagularion to prevent or treat neovascularisation - but prognosis is still poor
71
What is seen on fundoscopy with central retinal vein occlusion
Hyperaemia and haemorrhages - known as stormy sunset appearance
72
What is the chief cause of registrable blindness?
Age-related macular degeneration
73
How does ARMD present?
Deteriorating central vision
74
Two types of ARMD
Wet and dry
75
Features of dry ARMD
Mainly drusen (signify axonal degeneration) and degenerative changes at the macular - slow progression
76
What are drusen?
signify axonal degeneration leading to intracellular mitochondrial calcification - axons rupture, mitochondria extruded into extra-cellular space and calcium is deposited
77
Features of wet ARMD
Occurs when aberrant vessels grow from choroid into the retina and leak Vision deteriorates rapidly, distortion is a key feature
78
What is seen on ophthalmoscopy with wet ARMD
Fluid exudation, localised detachment of the pigment
79
Lifestyle advice for ARMD
Stop smoking and eat lots of green vegetables
80
Treatment of wet ARMD
Intravitreal vascular endothelial growth factor (veg-f) inhibitors - bevacizumab and ranibizumab Intravitreal steroids e.g. Triamcinolone Screening Antioxidants and vitamins
81
What do you think of if gradual visual loss in teenagers
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
Optic disc in optic atrophy
Pale
83
Which type of glaucoma is the chronic glaucoma
Open angle glaucoma
84
What % if registered blindness does open angle glaucoma account for?
7%
85
What is glaucoma?
Optic neuropathy with death of retinal ganglion cells and their optic nerve axons
86
Definition of glaucoma pathologically
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
What happens to vision in glaucoma
Peripheral vision loss Nasal and superior fields are lost first Temporal fields lost last
88
What happens to optic disc cups in glaucoma
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
Management of glaucoma
Reducing IOP stops visual field loss but does not reverse it
90
Who needs screening for glaucoma
High risk patients - screen when over 35 if: | positive family history, Afro-Caribbean, myopia, diabetic/thyroid disease
91
Treatment of glaucoma
Prostaglandin analogues (latanoprost, travoprost) B-blockers (tinolol, betaxolol) Alpha adrénergic agonists (brimonidine, apraclonidine) Etc
92
Role of prostaglandin analogues in the treatment of glaucoma
Increase uveoscleral outflow | E.g. Latanoprost and travoprost
93
Role of beta blockers in glaucoma treatment
Decrease aqueous production | E.g. Timolol and betaxolol
94
Role of alpha adrenergic agonists in treatment of glaucoma
E.g. Brimonidine and apraclonidine | Decrease aqueous production and increase uveoscleral outflow
95
Role of carbonic anhydride inhibitors in glaucoma treatment
E.g. Dorzolamide and brinzolamide drops and acetazolamide PO | Decrease production of aqueous
96
Role of miotics in treatment of glaucoma
E.g. Pilocarpine Decrease resistance to aqueous outflow Causes miosis, decreased acuity and brow ache from ciliary muscle spasm
97
Type of surgery in glaucoma treatment
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
What is normal optic cup to disc ratio
0.4-0.7
99
When is cupping said to be severe
When ratio is >0.9
100
Sudden painless vision loss with RAPD
RVO or RAO

Opthalmology (6 decks)

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