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MSRA > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What is glaucoma?

A

A group of disorders characterised by optic neuropathy secondary to raised intraocular pressure

Types:
1. Open-angle
2. Closed-angle

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2
Q

What are the features of closed-angle glaucoma?

A

Rise in IOP secondary to an impairment of aqueous flow causing:
- severe ocular pain/headache
- decreased visual acuity
- symptoms worse in darkened room
- hard red eye
- haloes around lights
- semi-dilated non-reacting pupil
- corneal oedema results in dull or hazy cornea
- systemic upset

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3
Q

What are the predisposing factors for closed angle glaucoma?

A

Hypermetropia (long-sightedness)
Pupillary dilatation
Lens growth associated with age
Can be precipitated by mydriatic drops

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4
Q

What do investigations show in glaucoma?

A

Tonometry - elevated IOP
Gonioscopy - special lens that allows visualization of angle
Fundoscopy - optic disc cupping/pallor, bayonetting of vessels

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5
Q

How is glaucoma managed?

A

Open-angle:
1st line - 360deg selective laser trabeculoplasty (if IOP>24)
2nd line - eyedrops, see below
Prostaglandin analogues eg. latanoprost - increase uveoscleral outflow
Beta blockers eg. timolol, betazolol - reduces aqueous production
Sympathomimetics eg. brimonidine - reduces aqueous production and increases outflow
Carbonic anhydrase inhibitors eg. dorzolamide - reduces aqueous production
Miotics eg. pilocarpine - increases outflow

Closed-angle:
Urgent opthalmology referral
Eye drops as above +/- IV acetazolamide and steroids
Laser irodotomy - creates hole in iris to relieve pressure

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6
Q

What is the pathophysiology of ARMD?

A
  • Bilateral degeneration of central retina (macula) photoreceptors causing formation of drusen
  • RFx include age, smoking, family history, CHD
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7
Q

What are the 2 types of ARMD?

A

Dry/early - 90% of cases, atrophic, drusen (yellow round spots) seen

Wet/late- 10% of cases, exudative, choroidal neovascularisation and rapid visual loss > poor prognosis

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8
Q

What are the signs, symptoms and investigations seen in ARMD?

A

Symptoms:
- Subacute visual loss particularly for near objects
- Difficulties adapting vision at night
- Flickering/flashing lights (photopsia) and glare
- Visual hallucinations (Charles-Bonnet syndrome)

Signs:
- Distortion of line perception on Amsler grid testing
- Drusen (yellow pigment) seen on macula
- In wet ARMD you can see well demarcated red patches which represent intra-retinal or sub-retinal fluid leakage or haemorrhage

Investigations:
- Slit lamp microscopy
- Fluorescein angiography if neovascular ARMD
- Optical coherence tomography for 3D picture

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9
Q

How is ARMD managed?

A

REFER TO OPHTHALMOLOGY IN 1 WEEK IN CASE IT IS WET

DRY: Vitamins + zinc to reduce progression, no cure otherwise

WET: Vascular endothelial growth factor (-mab,-nib)

Laser photocoagulation can slow progression but may cause acute visual loss

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10
Q

What are the features of allergic conjunctivitis?

A
  • Bilateral erythema, swelling and itch
  • History of atopy
  • Seasonal or perennial (dust mite, washing powder)
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11
Q

How is allergic conjunctivitis managed?

A

1st line - topical/systemic antihistamines
2nd line - topical mast cell stabilisers eg. sodium cromoglicate and nedocromil

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12
Q

What are the features of anterior uveitis?

A
  • Acute red eye, pain, photophobia and blurred vision
  • Small and irregular pupil due to sphincter muscle contraction
  • Ciliary flush (ring of red spreading out)
  • Hypopyon (pulse and inflammation in aterior chamber causing a visible fluid level)
  • Associated with HLA-B27 (ank spon, reactive arthritis, IBD, Behcet’s, sarcoid)
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13
Q

How is anterior uveitis managed?

A
  • Urgent opthalmology review
  • Cycloplegics to dilate pupil and relieve symptoms eg. atropine, cyclopentolate
  • Steroid eye drops
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14
Q

What is an argyll-robertson pupil?

A

Small, irregular pupils which DON’T respond to light but DO accommodate

Caused by diabetes or neurosyphilis

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15
Q

What are the features of blepharitis?

A
  • Inflammation of eyelid margin
  • Can be posterior (due to meibomian gland dysfunction) or anterior (due to seborrhoeic dermatitis/staph infection)
  • More common with rosacea
  • Bilateral grittiness, discomfort, stickness, redness
  • Can cause secondary conjunctiviit
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16
Q

What are the meibomian glands?

A

Glands that secret oil on to the eye surface to prevent rapid evaporation of the tear film

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17
Q

How is blepharitis managed?

A
  • Hot compresses
  • Lid hygeine (remove debris with baby shampoo/sodium bicarb)
  • Artificial tears
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18
Q

What are the features of cataracts?

A
  • Clouding of the lens causing reduced/blurred vision and halos/glare
  • Associated with female sex, smoking, alcohol, trauma, DM, steroids, radiation, myotonic dystrophy, hypocalcemia
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19
Q

What do investigations show in cataracts?

A

Fundoscopy - defect in red reflex
Opthalmoscopy - normal fundus/optic nerve
Slit lamp examination - visible cataract

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20
Q

How are cataracts managed?

A

Non-surgical - prescribe stronger glasses, encourage brighter lighting

Surgery - replace cloudy lens with artificial one

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21
Q

What are the complications of cataract surgery?

A

Posterior capsule opacification
Retinal detachment
Posterior capsule rupture
Endopthalmitis (inflammation of aqueous or vitreous humour)

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22
Q

What is central retinal artery occlusion?

A

Sudden painless unilateral visual loss due to thromboembolism or arteritis

Examination:
- RAPD
- Cherry red spot on pale retina

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23
Q

How is central retinal artery occlusion managed?

A
  • Treat underlying condition
  • Intraarterial thrombolysis if acute presentation
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24
Q

What is central retinal vein occlusion?

A

Sudden painless unilateral loss of vision due to occlusion of a vein

Examination:
- Widespread hyperaemia
- Severe retinal haemorrhages (stormy sunset)

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25
Q

How is central retinal vein occlusion managed?

A

Usually conservative
If macular oedema > intravitreal anti-vascular endothelial growth factor agents
If retinal neovascularization > laser photocoagulation

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26
Q

What is chororetinitis?

A

A form of posterior uveitis causing inflammation of the choroid and retina

Associated with syphilis, CMV, toxoplasmosis, sarcoidosis, TB

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27
Q

How does a corneal abrasion present and how is it investigated?

A

Presents as eye pain, lacrimation, photophobia, foreign body sensation

Investigate with fluorescein staining - shows yellow-stained abrasion to naked eye which is enhanced by use of a cobalt blue filter or Woods lamp

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28
Q

How is a corneal abrasion managed?

A

Topical antibiotic to prevent secondary bacterial infection

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29
Q

What are the features of a corneal ulcer aka keratitis? how is it managed?

A
  • Presents as eye pain, lacrimation, photophobia
  • Can be bacterial, fungal, viral or acanthamoeba (contact lens)
  • Typically staph but pseudomonas seen in contact lens wearers
  • Vitamin A deficiency is a risk factor

Management:
- Same day opthalmology
- Topical abx (quinolones)
- Cyclopentolate for pain relief

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30
Q

When should corneal injuries be referred to secondary care?

A
  • Penetrating injury
  • Significant trauma
  • Chemical injury
  • Unable to remove safely
  • Severe pain/irregular pupils/blood or pus in anterior chamber/corneal opacity
  • Large or deep abrasion
  • Infection/corneal ulcer

If suitable for primary care - irrigate with normal saline +/- apply topical anaesthetic and sweep a sterile cotton applicator

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31
Q

What is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in vessel walls > damage to endothelial cells> increased vascular permeability > EXUDATE > pericyte dsyfunction predisposiong to formation of microaneurysms

Neovasculization due to growth factor production in response to retinal ischaemia

32
Q

What are the subtypes of diabetic retinopathy?

A
  1. Non-proliferative
    - characterised by microaneurysms, blot haemorrhages and cotton wool spots
  2. Proliferative
    - characterised by NEOvascularisation and fibrous tissue formation > common in T1DM and high risk of blindness
  3. Maculopathy
    - any kind of macular damaged, common in T2DM
33
Q

How is diabetic retinopathy managed (by subtype)?

A

All:
Optimise glycemic control, BP and lipids

Non-proliferative:
Regular observation +/- panretineal laser photocoagulation

Proliferative:
Panretinal laser photocoagulation
Intravitreal VEGF inhibitors eg. ranibizumab

Maculopathy:
If change in visual acuity > VEGF inhibitors

34
Q

What is the episclera?

A

Thin layer of tissue that lies between the conjunctivia and the sclera

35
Q

How does episcleritis present and how is it managed?

A
  • Acute painless red eye
  • Blood vessels inflamed and dilated, can be palpated/mobile
  • Often idiopathic but may be associated with RA, IBD
  • 50% bilateral

Manage conservatively with artificial tears

36
Q

How do you differentiate between episcleritis and scleritis?

A

Phenylephrine drops

Episcleritis
- Blanched vessels > eye redness improves

37
Q

How does scleritis present and how is it managed?

A
  • Painful red eye (may be mild)
  • Gradual decrease in vision
  • Associated with RA, SLE, sarcoid, GwP

Refer urgently to Opthalmology > oral NSAIDs or glucocorticoids if severe

38
Q

What is a stye? How is it managed?

A

AKA hordoleum - bacterial infection of an oil gland in the eyelid

Types:
1. External (staph infection of Moll/Zeis glands)
2. Internal (infection of Meibomian glands)

Management:
Hot compresses and analgesia
Topical abx if conjunctiviits

39
Q

What is a chelazion? How is it managed?

A

Retention cyst of the Meibomian gland - presents as a firm painless lump in eyelid

Management:
Spontaneous resolution, if not may need surgical drainage

40
Q

What are the features of herpes zoster opthalmicus?

A
  • Reactivation of VZV in ophthalmic division of trigeminal nerve
  • Vesicular rash +/- eye involvement
  • Hutchinson’s sign: rash on tip or side of nose indicating nasociliary involvement > strong RF for ocular involvement
41
Q

How is herpes zoster ophthalmicus managed?

A

Oral antivirals for 7-10 days, start within 72h

Give IV if very unwell/immunosuppressed

42
Q

What is a holmes-adie pupil?

A
  • Benign dilated pupil
  • Once constricted remains small for LONG TIME
  • Slowly reactive to accommodation
  • Associated with absent ankle/knee reflexes
43
Q

What are the 4 features of Horner’s syndrome?

A
  1. Miosis
  2. Ptosis
  3. Enopthalmos (sunken eye)
  4. Anhydrosis
44
Q

What causes Horner’s syndrome?

A

Heterochromia is seen in congenital Horners. Otherwise, use location of anhidrosis to localise lesion.

Central lesions ie. stroke, syringomyelia, MS, tumour, encephalitis > anhidrosis of face, arm and trunk

Pre-ganglionic lesions ie. pancoasts tumour, thyroidectomy, trauma, cervical rib
> anhidrosis of face

Post-ganglionic lesions ie. carotid pathology, cluster headache, cavernous sinus thrombosis > no anhidrosis

45
Q

How is hypertensive retinopathy classified and managed?

A

1 - arteriolar narrowing, silver wiring
2 - AV nipping
3 - cotton wool exudate, flame and blot haemorrhages
4 - papilloedema

46
Q

What are the features of infective conjunctivitis? How is it managed?

A

Bacterial - purulent discharge
Viral - serous discharge, LNs, recent URTI

Management:
- Usually self-limiting
- Can give topical chloramphenicol
- Topical fusidic acid if pregnant
- If contact lens wearer, use topical fluorescein to identify corneal staining

47
Q

What causes lens dislocation?

A
  • Marfans: upwards
  • Homocystinuria: downwards
  • Ehlers-Danlos syndrome
  • Trauma
  • Uveal tumours
  • AR ectopia lentis
48
Q

What causes mydriasis (large pupil)?

A
  • Third nerve palsy
  • Holmes-Adie pupil
  • Traumatic iridoplegia
  • Phaeochromocytoma
  • Congenital

Drugs:
Topical > tropicamide, atropine
Sympathomimetics > amphetamines, cocaine
Anticholinergics > TCAs

49
Q

What is nasolacrimal duct obstruction and how is it managed?

A

Imperforate membrane at lacrimal duct causing persistent watery eye in infant

Will resolve by 1 year old, parents should be taught to massage lacrimal duct

If persistent can refer to Ophthalmologist for probing

50
Q

What is hyphema? How is it managed?

A

Blood in the anterior chamber of the eye - warrants urgent referral to Opthalmology due to risk of blindness secondary to raised intraocular pressure

Managed with strict bed rest and pressure checks

51
Q

What is orbital compartment syndrome? How is it managed?

A

TRUE OPHTHALMIC EMERGENCY

Features include eye pain, swelling, proptosis, roch hard eyelids RAPD

Management:
- Urgent lateral canthotomy to decompress the orbit

52
Q

What are the risk factors for orbital cellulitis?

A
  • Often has had recent URTI/sinus infection/ear infection/periorbital cellulitis
53
Q

How does orbital cellulitis present?

A

Basically every eye symptom incl visual distrubance/redness/pain/proptosis

54
Q

How is orbital cellulitis managed?

A

Urgent opthalmology assessment with bloods, CT with contract, blood cultures to determine organisms

Admit for IV antibiotics

55
Q

What is optic neuritis?

A

Inflammation of the optic nerve causing unilateral decreased visual acuity over hours or days

Features:
- Poor colour discrimination
- Pain on eye movements
- RAPD
- Central scotoma (blind spot)

56
Q

What scan is diagnostic for optic neuritis?

A

MRI of brain and orbits with gadolinium contrast - if >3 lesions, high risk of developing MS

57
Q

How is optic neuritis managed?

A

High-dose steroids
Recovery takes 4-6 weeks

58
Q

What is papilloedema? What do you see on fundoscopy?

A

Optic disc swelling secondary to increased ICP

Fundoscopy shows venous engorgement and changes to the optic disc

Can be caused by malignant hypertension, SOL, hydrocephalus, hypercapnia, hypoparathyroidism, hypocalcemia, vitamin A toxicity

59
Q

What is the most common cause of blindness in a) the UK, b) the world? c)aged 35-65?

A

a) Age related macular degeneration
b) Cataracts
C) Diabetic retinopathy

60
Q

What is a relative afferent pupillary defect?

A

AKA marcus-gunn pupil

Swinging light test - pupils dilate when a bright light is swung from the unaffected eye to the affected eye. It is caused be a lesion anterior to the optic chiasm ie. optic nerve or retina (Afferent = away from the eye)

61
Q

What is retinitis pigmentosa?

A

A genetic disorder of the eyes causing tunnel vision and night blindness due to breakdown and loss of retinal cells

Fundoscopy shows BLACK BONE SPICULE-SHAPED PIGMENTATION in the peripheral retina

62
Q

What are the features of retinal detachment?

A

Seperation of the inner retina from the underlying retinal pigment epithelium, allowing vitreous fluid to accumulate in the subretinal space

Leads to progressive loss of vision (starts peripherally and progresses centrally)

more common in myopia

63
Q

How is retinal detachment managed?

A
  • Urgent ophthalmology assessment if visual acuity loss, or slit lamp in 24h if not
  • They will perform surgery to close retinal tears or reattach retina
64
Q

What are the two types of squint?

A

Concomitant (common):
- Due to imbalance in extraocular muscles
- Usually converent

Paralytic (rare):
- Due to paralysis of extraocular muscles

Detetion is important as if uncorrected it may lead to amblyopia (brain fails to process input from one eye and over time favours the others)

65
Q

How is a squint detected and managed?

A

Corneal light reflection - check for asymmetrical reflection
Cover test - ask child to focus on object, cover one eye and observe movement of unconvered eye

Refer to secondary care - give eye patch whilst waiting

66
Q

What is a subconjunctival haemorrhage? How is it managed?

A

Unilateral asymptomatic flat red patch on conjunctiva
Normal vision and fundoscopy
Check if hypertensive/on anticoagulation
May need CT head if unable to see whole borders
If recurrent > investigate for bleeding disorder

MANAGE IS CONSERVATIVE, SHOULD RESOLVE IN 2-3 WEEKS

67
Q

What causes sudden painless loss of vision?

A
  1. Amaurosis fugax (ischaemic/vascular) > curtain coming down
  2. Vitreous haemorrhage > dark spots,
  3. Retinal detachment > floaters, flashes ‘curtain/veil’
  4. Retinal migraine
  5. Central retinal vein occlusion > retinal haemorrhage
  6. Central retinal artery occlusion > cherry red, RAPD
  7. Vitreous detachment > flashers/floaters peripherallly, assoc with HTN/T2DM
68
Q

What causes tunnel vision?

A

Papilloedema
Glaucoma
Retinitis pigmentosa
Choroidoretinitis
Optic atrophy

69
Q

What are the features and management of orbital lymphoma?

A

Features:
- Slowly progressing, painless orbital process
- Salmon pink conjunctiva (may be mistaken for conjunctivitis pinkish tinge)
- Mass (if present) may be S shaped in the lacrimal gland (lateral)
- Mass (if present) may cause ptosis if involving superior orbital and levator muscle
- Eyelid swelling and double vision are common complaints

Management:
- Radiation
- Chemo (not indicated unless systemic lymphoma)
- Surgery for biopsy and histology
- Cryotherapy may be beneficial

70
Q

What is a common complication of Bell’s palsy?

A

Dry eye syndrome - should use lubricants and tape eye shut.

On slit lamp would see punctate fluorescein staining of cornea

71
Q

How does herpes simplex keratitis usually present? How is it managed?

A

Dendritic corneal ulcer
Red, painful eye with photophobia, epiphora, feathery uptake on fluorescein staining, decreased visual acuity

Management:
- Refer immediately to ophthalmologist
- Topical aciclovir

72
Q

What are the features of chorioretinitis?

A
  • A form of posterior uveitis
  • Pizza pie appearance on fundoscopy
  • Caused by HIV, syphilis, CMV, toxoplasmosis, sarcoidosis, tuberculosis
73
Q

What is the most common occular manifestation of RA?

A

Keratoconjunctivitis sicca

74
Q

What is endophthalmitis?

A

Red eye, pain and visual loss following intraocular surgery > urgent ophthalmology referral

75
Q

How can someone be qualified as legally blind?

A
  • Vision <3/60 in the better eye
  • Needs to be certified by consultant ophthalmologist
76
Q

What is keratoconus?

A
  • Progressive eye condition in which the normally dome-shaped cornea thins and begins to bulge causing burred vision
  • Cause is unknown
  • In severe disease you see Munson’s sign (lower lid indented by cornea when patient gazes down)
  • Manage with rigid contact lenses +/- transplant/graft
  • Can slow progresison with corneal collagen cross-linking

MSRA (24 decks)

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