Ophthalmology AS Flashcards

1
Q

What is an afferent defect?

A

No direct response but intact consensual response
Cannot initiate consensual response in contralateral eye
Dilatation on moving light from normal to abnormal eye.

Due to a total CN II lesion.

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2
Q

What is a relative afferent pupillary defect?

A

Marcus-Gunn Pupil

Features

  • Minor constriction to direct light
  • Dilatation on moving light from normal to abnormal eye
  • RAPD = Marcus Gunn Pupil

Damage to the affect pathway (retina or optic nerve). Due to consensual pupillary relaxation response form healthy eye.

Due to:
optic neuritis
Optic atrophy
retinal disease

Afferent: retina → optic nerve → lateral geniculate body → midbrain

efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve

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3
Q

What is the efferent defect?

A

Features

  • Dilated pupil does not react to light
  • Initiate consensual response in contralateral pupil
  • Ophthalmoplegia + ptosis
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4
Q

What is the cause of an efferent defect?

A

3rd nerve palsy

- The pupil is often spared in a vascular lesion as pupillary fibres run in the periphery.

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5
Q

Differential for a fixed dilated pupil?

A

Mydriatics - tropicamide
Iris Truma
Acute Glaucoma
CN3 Compression: tumour, coning.

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6
Q

Features of Holmes- Adie Pupil?

A

Young women with sudden blurring of near vision.

Initially unilateral and then bilateral pupil dilatation

Dilated pupil has no response to light and sluggish response to accommodation
- A tonic pupil

Investigations

  • Iris shows spontaneous wormy movements on slit-lamp examination
  • Iris streaming
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7
Q

Cause of a holmes-adie pupil?

A

Damage to postganglionic parasympathetic fibres

- Idiopathic: may have viral origin

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8
Q

Holmes-Adie Syndrome?

A

Tonic pupil + absent knee/ankle jerks + decreased BP.

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9
Q

Horner’s syndrome features?

A

Damage to sympathetic nerves

Ptosis: partial
Enophthalmos
Anhydrosis
Small pupil

Ptosis + constricted pupil = Horner’s

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10
Q

Causes of horner’s syndrome?

A

Distinguishing cause

  • Heterochromia (difference in iris colour) in congenital Horner’s.
  • Anhidrosis

Central = Anhidrosis in face, arm and trunk.

  • Syringomyelia
  • MS
  • Wallenberg’s Lateral Medullary Syndrome
  • Tumour
  • Encephalitis

Pre-ganglionic - Anhidrosis of face

  • Pancoast tumour: T1 nerve root lesion. Presents with shoulder and arm pain due to Brachial plexus invasion. Check smokign history.
  • Trauma: CVA insertion or CEA
  • Thyroidectomy
  • Cervical rib

Post-ganglionic

  • Cavernous sinus thrombosis
  • Usually 2ndry to spreading facial infeciton via the ophthalmic vein
  • CN 3, 4, 5, 6 palsies.
  • Cluster headache
  • Carotid artery dissection
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11
Q

What is an Argyll robertson pupil?

A

Features

  • Small, irregular pupils
  • Accommodate but doesn’t react to light. Prostitute.
  • Atrophied and depigmented iris

Caused by

  • DM
  • Quaternary Syphilis
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12
Q

What are the features of optic atrophy?

A
Decreased acuity
Decreased colour vision
Central scotoma
Pale optic disc
RAPD
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13
Q

Causes of Optic atrophy?

A

MS and glaucoma most common.

Congenital: Leber’s hereditary optic neuropathy
Hereditary motor + Sensory neuropathy
Friedrich’s ataxia
retinitis pigmentosa

  • EtOH
  • Ethambutol
  • Lead
  • B12 deficiency

Compression

  • Neoplasia: optic glioma, pituitary adenoma
  • Glaucoma
  • Paget’s
Vascular: DM, GCA
Inflammatory: MS, Devic's 
Sarcoid/other granulomatous
Infection: herpes zoster
Oedema: papilloedema 
Neoplastic infiltration: lymphoma, leukaemia
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14
Q

Visual history - Red eye history, exam and differential?

A

Vision

  • Blurred
  • Distorted
  • Diplopia
  • Field defect/Scotoma
  • Floaters

Sensation

  • Irritation
  • Pain
  • Itching
  • Photophobia
  • FB

Appearance

  • Red? Distribution
  • Lump
  • Puffy lids

Discharge

  • Watery
  • Sticky
  • Stringy
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15
Q

Key examination questions for red eye?

A
Inspect from anterior to posterior 
Is acuity affected
Is the globe painful 
Pupil size and reactivity 
Cornea: intact, cloudy? Use florescein
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16
Q

Signs of serious disease in red eye?

A

Photophobia
Poor vision
Corneal fluorescein staining
Abnormal pupil

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17
Q

What are the differentials for the eyelid?

A

Mechanical - ectropion (lower eyelid sags) , entropion (sages inwards) , trichiasis (eyelashes rubbing eyes)

Inflammation - Blepharitis, Chalazion (blockage of mebobian gland)

Infection

  • Preseptal cellulitis
  • Orbital cellulitis
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18
Q

What are the differentials for conjunctiva?

A

Mechanical - Sub conjunctival haemorrhage

Inflammation - allergic conjunctivitis

Infection - Conjunctivitis

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19
Q

What are the differentials for the sclera

A

Mechanical - Perforation

Inflammation - chemical burn, episcleritis, scleritis
Infection

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20
Q

What are the differnetials for the cornea?

A

Foreign body
Abrasion

Keratitis - infection

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21
Q

What are the differentials for anterior chamber?

A

Acute Glacuoma
Iritis/Uveitis
Endophthalmitis

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22
Q

How does acute glaucoma present?

A
  • Very painful
  • NO photophobia
  • Decreased acuity - loss of peripheral vision first.
  • Hazy/cloudy cornea
  • Pupil is large
  • very increased IOP

Systemic upset may be seen, such as nausea, vomiting and abdo pain.

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23
Q

How does anterior uveitis present?

A
Painful 
photophobia 
Decreased acuity 
normal cornea 
small pupil 
Normal IOP
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24
Q

How does conjunctivitis present?

A
  • a little pain
  • Photophobia
  • Normal acuity
  • normal cornea
  • normal pupil
  • normal IOP
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25
Q

What is acute closed angle glaucoma?

A

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

Pupil dilatation (e.g at night) worsens the blockage

Intraocular pressure rises from 15-20 –> >60mmHg.

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26
Q

Risk factors of ACAG?

A
  • Hypermetropia (long-sightedness)
  • Shallow anterior chamber
  • Female
  • FH
  • Increased Age

Drugs

  • Mydriatic drops
  • Anti-cholinergics
  • Sympathomimetics
  • TCAs
  • Anti-histamines
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27
Q

Symptoms of ACAG?

A

Prodrome: rainbow haloes around lights at night-time

  • Severe pain with n/v
  • Decreased acuity and blurred vision
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28
Q

Examination of ACAG?

A

Cloudy cornea with circumcorneal injection

Fixed, dilated, irregular pupil. DILATED!

Increased IOP makes eye feel hard.

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29
Q

Investigations of ACAG?

A

Tonometry: increased IOP (>40)

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30
Q

Acute management for ACAG?

A

Refer to ophthalmologist
- Pilocarpine: 2-4 drops stat: miosis opens blockage. Miosis is constricting the pupil.
- Topical B-B: timolol decreased aqueous formation
- Acetazolamide 500mg IV stat: decreased aqueous formation.
Analgesia and antiemetics.

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31
Q

Subsequent management of ACAG?

A

Bilateral YAG peripheral iridotomy once IOP decreased medically.

A Yag capsulotomy is a special laser treatment used to improve your vision after cataract surgery. It is a simple, commonly performed procedure which is very safe.

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32
Q

What is the pathophysiology of anterior uveitis?

A

Uvea is pigmented part of eye and includes: iris, ciliary body and choroid

Iris + ciliary body = anterior uvea

Iris inflammation involves ciliary body too

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33
Q

Symptoms of anterior uveitis?

A
Acute pain and photophobia
Blurred vision (Aqueous precipitates)
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34
Q

Examination of eye in anterior uveitis?

A
Small pupil initially, irregular later.
May be small, fixed oval shaped. 
Circumcorneal injection 
Hypopyon: pus in anterior chamber
White precipitates on back of cornea 
Talbots test: increased pain on convergence
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35
Q

Associations with uveitis?

A

Seronegative arthritis: AS, psoriatic, Reiter’s

HLA-B27

Still's/JIA
IBD
Sarcoidosis 
Behcet
Infection: TB, leprosy, syphilis, HSV, CMV.
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36
Q

Management of anterior uveitis?

A

Refer to ophthalmologist
prednisolone drops
Cyclopentolate drops: Dilates pupil and prevents adhesions between iris = atropine too! = mydriatic

Stay on TROP = Big/wide.
piLOWcapine = Small

Steroid eye drops.

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37
Q

What is episcleritis?

A

PAINLESS = Episcleritis

Inflammation below the conjunctiva in the episclera

Presentation

  • Localised reddening; can be moved over sclera
  • watering and mild photophobia.
  • Painless/mild discomfort
  • Acuity preserved
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38
Q

Causes of episcleritis?

A

Usually idiopathic
May complicate RA or SLE

Management: Topical or systemic NSAIDs.

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39
Q

What is scleritis?

A

Painful = SCLERA

Vasculitis of the sclera

Presentation
- Severe pain: worse on eye movement
- Generalised scleral inflammation
Vessels wont’ move over sclera

  • Conjunctival oedema.
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40
Q

What are the causes of scleritis?

A

WEgener’s
RA
SLE
Vasculitis

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41
Q

Management of scleritis?

A

Refer to specialist

Most need corticosteroids or immunosuppressants

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42
Q

Complications of scleritis?

A

Scleromalacia - globe perforation

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43
Q

What is conjunctivitis?

A

Presentation
- Often bilateral with purulent discharge
Bacterial: Sticky (staph, strep, haemophilus)
Viral: watery

  • Discomfort
  • Conjunctival injection: Vessels may be moved over the sclera.
  • Acuity, pupil responses and cornea are unaffected.
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44
Q

Causes of conjunctivitis?

A

Viral: adenovirus. Serous discharge, recent URTI, preauricular lymph nodes.

Bacterial: staph, chlamydia, gonococcus. Eyes may be stuck together in morning.

Allergic

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45
Q

Manangement of conjunctivitis?

A

Don’t share towels, school exclusion not necessary.

Bacterial: chloramphenical 0.5% ointment. Given 2-3hrly initially where as ointment is given qds initially.

Use fusidic acid in pregnant women.

Allergic: anti-histamine drops e.g emedastine

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46
Q

What is a corneal abrasion ?

A

Epithelial breech without keratitis
- Cause: trauma

Symptoms

  • Pain
  • Photophobia
  • Blurred vision

Investigations
- Slit lamp: fluorescein stains defect green.

Management
- Chloramphenicol ointment for infection prophylaxis.

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47
Q

Causes of a Corneal ulcer + keratitis (corneal inflammation)

A

Causes
- Bacterial, herpetic, fungal, protozoea, vasculitic (RA).

Due to steroid eye drop which leads to fungal infection leading to corneal ulcer. Not causative

May get a dendritic ulcer = Herpes Simplex. This leads to herpes simplex keratitis. Gold crusted lesions = Herpes.

Acanthamoeba: Protazoal infection affecting contact lens wearers swimming in pools.

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48
Q

Presentation of corneal ulcer?

A
  • Pain, photophobia
  • Conjunctival hyperaemia
  • Decreased acuity
  • White corneal opacity.
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49
Q

Risk factor of corneal ulcer?

A

Contact lens wearer

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50
Q

Investigations for corneal ulcer?

A

Green with fluorescein on slit lamp.

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51
Q

Management of corneal ulcer?

A

Refer immediately to specialist who will

  • Take smears + Cultures
  • Abx drops, oral/topical aciclovir
  • Cycloplegics/mydriatics ease photophobia
  • Steroids may worsen symptoms: professional only

Can lead to scarring and visual loss.

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52
Q

What is ophthlamic shingles ? - Herpes Zoster Ophthalmicus

A

20% of all shingles
Presents with pain in CNV1, dermatome precedes blistering rash

40% –> keratitis, iritis.

Hutchinson sign - nose-top zoster due to involvement of nasociliary nerve also supplies globe. Likely to have ocular involvement.

if this is present there is risk of ocular development therefore MUST be referred to ophthalmology.

Ophthalmic involvement
- Keratitis + corneal ulceration (fluorescein stains)
± iritis.
- Post-herpetic neuralgia

Management

  • Oral antiviral treatment for 7-10 days.
  • ideally started within 72hrs.
  • IV antivirals given for very severe infection.
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53
Q

Key questions in sudden vision loss?

A

Sudden painless loss of vision
- Ischaemic/vascular (thrombosis, embolism, temporal arteritis). Included recognised syndromes (Occlusion of central retinal vein + occlusion of central retinal artery). Amaurosis fugax (can be large or small artery occlusion). Can be from a TIA therefore give aspirin 300mg.
Curtain coming down.

Central retinal vein occlusion

Central retinal artery occlusion

Vitreous haemorrhage

Retinal detachment

  • Dense shadow that starts peripherally progresses towards the central vision
    A veil or curtain over the field of vision
    Straight lines appear curved
    Central visual loss

Vitreous haemorrhage
- Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters

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

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54
Q

What is anterior ischaemic optic neuropathy?

A
  • Optic nerve damaged if posterior ciliary arteries blocked by inflammation or atheroma.

Pale/swollen optic disc.

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55
Q

What can cause anterior ischaemic optic neuropathy?

A

Arteritic AION: Giant cell arteritis

Non-arteritic AION: HTN, DM, Increased lipids, smoking.

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56
Q

What is optic neuritis?

A
  • Unilateral loss of acuity over hrs-days usuallynot immediately.
  • decreased colour discrimination (Dyschromatopsia) - red desaturation
  • Eye movement may hurt
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57
Q

Signs of optic neuritis?

A
  • Decreased acuity
  • Decreased colour vision
    enlarged blind spot
  • Optic disc may be: normal, swollen, blurred.
  • Afferent defect
  • Central scotoma.
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58
Q

Causes of optic neuritis?

A

MS (45-80% over 15yrs) if >3 white matter lesions.
DM
Drugs: ethambutol, chloramphenicol
Vitamin Deficiency
Infection: zoster, lyme disease, syphilis.

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59
Q

Management of optic neuritis?

A

High-dose methyl-pred IV for 72hrs

Then oral pred for 11/7.

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60
Q

What is a vitreous haemorrhage?

A

Bleeding

  • From new vessels: DM
  • Retinal tears/detachment/trauma

RF: Diabetes, trauma, anticoagulants, severe short sightedness.

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61
Q

Presentation for vitreous haemorrhage?

A

Small bleeds –> Small black dots/ring floaters. Red tinged vision along with dark spots.!!!!

Large bleed can obscure vision –> No red reflex, retina can’t be visualised.

Patients present with cobwebs in the eye, which are floaters. Past medical history of DM, 50% due to proliferative diabetic retinopathy.

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62
Q

Investigations of vitreous haemorrhage?

A

May used B scan US to identify cause

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63
Q

Management of vitreous haemorrhage?

A

VH undergoes spontaneous absorption

Vitrectomy may be performed in dense VH/

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64
Q

Central retinal artery occlusion?

A
  • Dramatic unilateral visual loss in seconds
  • Afferent pupil defect (may precede retinal changes)
  • Pale retina with cherry-red macula. Very pale with bright red macula.
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65
Q

Causes of CRAO?

A

GCA

Thromboembolism: clot, infective, tumour

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66
Q

Management of central retinal artery occlusion?

A

If seen within 6hr aim is to return retinal blood flow by decreased IOP.

  • Ocular massage
  • Surgical removal of aqueous
  • Anti-hypertensive (local and systemic)
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67
Q

Central Retinal vein occlusion?

A

Central
- commoner than arterial occlusion

Causes : arteriosclerosis, Increased BP, DM, Polycythaemia

Presentation: Sudden unilateral visual loss with RAPD

Fundus: Stormy sunset appearance/Pizza.

  • Tortuous dilated vessels
  • haemorrhages
  • Cotton wool spots

Complications

  • Glaucoma - can be due to glaucoma.
  • Neovascularization

Prognosis: possible improvement for 6mo-1yr.

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68
Q

Branches of the retinal vein occlusion?

A

Present - Unilateral visual loss

Fundus: segmental fundal changes

Complication: Retinal ischaemia –> VEGF release and neovascularization (management: laser photocoagulation) .

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69
Q

Retinal detachment presentation and management?

A

Holes/tear in retina allow fluid to separate sensory retina from retinal pigmented epithelium.
- May be secondary to cataract surgery, trauma, DM.

  • Floaters: Numerous, acute onset, ‘spiders-web’
  • Flashes
  • Field loss
  • Fall in acuity
  • Painless
  • Curtain down the wall.

Fundus: grey, opalescent retina, ballooning forwards.

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70
Q

Management of retinal detachment?

A

Urgent surgery + referral ot ophthalmologist.

Vitrectomy + gas tamponade with laser coagulation to secure the retina?

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71
Q

Causes of transient visual loss?

A

Vascular: TIA, migraine
MS
Subacute glaucoma
Papilloedema

72
Q

What is the cause of gradual visual loss?

A

Common

  • Diabetic retinopathy
  • Age related macular degeneration
  • Cataracts
  • Open-angle glaucoma
73
Q

Rarer causes of gradual visual loss?

A

Genetic retinal disease: retinitis pigmentosa

HTN

Optic atrophy

74
Q

What is age-related macular degeneration (ARMD)

A

Commonest cause of blindness >60

30% of >75yr old will have dry AMD

75
Q

Risk factors for ARMD?

A

Smoking
increased age
Genetic factors

76
Q

What is the presentation of ARMD?

A

Elderly pts
central visual loss
Loss of vision of near field objects.
Blurring of small words and straight lines appearing curvy.
Difficulties in dark adaption.
Fluctuations in visual disturbance which may vary significantly from day to day.
Photopsia

77
Q

Dry ARMD: geographic atrophy?

A

Drusen: fluffy white spots around macula. D for Dry
Degeneration of macula
Slow visual decline over 1-2 yrs.

78
Q

Wet ARMD: subretinal neovascularitisation?

A

Aberrant vessels grow into retina from choroid and –> haemorrhage

Rapid visual decline (sudden/days/wks) with distortion.

Fundoscopy shows macular haemorrhage –> scarring.

Amsler grid detect distortion

79
Q

Investigations for gradual visual loss?

A

Fluorescein angiography = neovascular ARMD is suspected. Guide intervention with anti-VEGF therapy. May see choroid neovascularization.

OCT: optical coherence tomography

Gives high resolution images of the retina.

80
Q

Management of wet AMRD?

A

Wet

  • Intravitreal VEGF inhibitors
  • Bevacizumab (Avastin)
  • Ranibizumab

This is for dry! Vitamins, photodynamic then photocoagulation. Antioxidant vitamins (A,C,E, K) + zinc may help early ARMD.

81
Q

Chronic simple (open-angle glaucoma)

A

Pathogenesis
- Depends on susceptibility of pts retina and optic nerve to increased IOP damage.

  • Trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP.
    Here- iris is clear of meshwork.

IOP >21mmHg –> decreased blood flow and damage to optic nerve –> optic disc atrophy + cupping.

82
Q

Presentation of CS (open-angle) glaucoma?

A

Peripheral visual field defect: superior nasal first.

Central field is intact therefore acuity maintained until late

  • Presentation delayed until optic nerve damage is irreversible.
83
Q

Screening for CS glaucoma?

A
  • > 35
  • Afro-Caribbean
  • FH
  • Drugs: Steroids
  • Co-morbidities: DM, HTN, - migraines
  • Myopia (different to hypermetropia in acute closure glaucoma).

If there is a family history - screen form 40yrs. Normally at opticians.

84
Q

Investigtions for CS glaucoma?

A

Tonometry: IOP >24 mmHg
Fundoscopy: cupping of optic disc.
- Optic disc cupping >0.7. Occurs as loss of disc substance makes optic cup widen and deepen.
- OPtic disc pallor - indicating optic atrophy.
- Bayonetting of vessels - breaks as they disappear into deep cup.
Visual field assessment: peripheral loss
Corneal thickness measurement
- Gonioscopy to assess peripheral anterior chamber

85
Q

Management of CS glaucoma?

A

Life-long f/up.

86
Q

Eye-drops to decrease IOP?

A

1st line: Prostaglandin analogues

  • Latanoprost, travoprost
  • Increased uveoscleral outflow. once a day. Post so after so increase outflow.

SE: increased eyelash length iris pigmentation and periocular pigmentation.

2nst line: b-blockers

  • Timolol, betaxolol
  • Decreased aqueous production
  • Caution in asthma, heart failure

alpha2-agonist

  • Brimonidine, apraclonidine
  • decreased aqueous production and increased uveoscleral outflow
  • AVOID if taking MAOI or tricyclic antidepressant.

Carbonic anhydrase inhibitors
- Dorzolamide, acetazolamide

Miotics
- Pilocarpine

87
Q

Non-medical options for open-angle glaucoma?

A

Laser trabeculoplasty
-Surgery (trabeculectomy) is used if drugs fail
New channel allows aqueous to flow into conjunctival bleb.

88
Q

Commonest cause of blindness worldwide?

A
Trachoma 
Cataract
Glaucoma
Keratomalacia: vitamin A deficiency 
Onchocerciasis 
Diabetic Retinopathy
89
Q

The problem with diabetes in the eye?

A

DM is the leading cause of blindess up to 60yrs
30% have ocular problems @ presentation

BP<130/80 and normoglycaemia –> Decreased diabetic retinopathy

90
Q

How does DM increase risk of cataract?

A

DM accelerates cataract formation

Lens absorbs glucose which is converted to sorbitol by aldose reductase

91
Q

How does DM increase risk of retinopathy?

A
  • Microangiopahty –> occlusion
  • Occlusion –> ischaemia –> new vessel formation in retina

Bleed –> vitreous haemorrhage
Carry fibrous tissue with them –> retinal detachment

Occlusion also -> cotton wool spots (ischaemia)
Vascular leakage -
> Oedema and lipid exudates

Rupture of microaneurysms –> blot haemorrhages

92
Q

Screeening for diabetic retinopathy?

A

All diabetics should be screened annually
Fundus photography
Refer those with maculopathy, NPDR and PDR to ophthalmologist

93
Q

Investigation for DM in eye?

A

Fluorescein angiography

94
Q

Management of DM in eye?

A

Good BP and glycaemic control
Rx concurrent disease: HTN, dyslipidaemia, renal disease, smoking, anaemia

Laser photocoagulation
- Maculopathy: focal or grid

Nice concentric circles.

  • Proliferative disease: pan-retinal (Macula spread).
95
Q

CN palsies in diabetes?

A

CN 3 (pupil may be spared) and 6 Palsies may occur

96
Q

Fundoscopy findings in background retinopathy?

A

Background retinopathy: Leakage

  • dots: Microaneurysm
  • Blot haemorrhages
  • Hard exudates: yellow lipid patches
97
Q

Fundoscopy findings in pre-proliferative retinopathy?

A

Cotton-wool spots (infarcts - soft exudates)
Venous beading
Dark haemorrhages
Intra-retinal microvascular abnormalities

Severe preproliferative = widespread microaneurysms and dot-and-blot haemorrhages, venous beading in 2 or more and IRMA in at least one quadrant.

Mild = Only microaneurysm

Moderate PPDR = Not severe.

98
Q

Findings on proliferative retinopathy?

A

New vessels
Pre-retinal and vitreous haemorrhage
REtinal detachment

99
Q

Maculopathy?

A

Caused by macular oedema
Decreased acuity may be only sign
Hard exudates within one disc width of macula

100
Q

What is the presentation of cataracts?

A
  • Increasing myopia (near sightedness)
  • Blurred vision –> gradual visual loss
  • Dazzling in sunshine/bright lights
  • Monocular diplopia

A defect on red reflex - reddish orange reflection through ophthalmoscope when light is shone on retina.

Types of cataracts
- Nuclear: change lens refractive index, common in old age

  • Polar: localized, commonly inherited, lie in the visual axis
  • Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
  • Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
101
Q

Causes of cataracts?

A
Age: 75% of >65yrs old 
DM
Steroids - especially subcapsular. Located behind the capsule. Often present with glare from bright lights. 
Congenital 
- Idiopathic
- Hypocalcaemia 
- DM 
- Downs 
- Long-term steroids
- Infection: rubella
- Metabolic: Wilson's
- Myotonic dystrophy = dot cataracts. 
- myopia = nuclear cataracts 
- Allopurinol = less strong associated with subcapsular.
102
Q

Investigation of cataracts?

A

Visual acuity
Dilated fundoscopy
Tonometry
Blood glucose to exclude diabetes

103
Q

Conservative management of cataracts?

A

Glasses

Mydriatic drops and sunglasses may give some relief

104
Q

Surgery for cataracts?

A

Consider if symptoms affect lifestyle or driving

NICE - refer to surgery dependent on whether a visual impairment is present + impact on quality of life. Therefore even if there is minor affect on visual acuity refer.

Day case surgery under LA
- Phacoemulsion + lens implant

1% risk of serious complications

  • Anterior uveitis/iritis
  • VH
  • Retinal detachment
  • Secondary glaucoma
  • Endophthalmitis

Post-op capsule thickening is common - manage with laser capsulotomy.
Retinal detachment
Posterior capsule rupture
Endophthalmitis

Post-op eye irritation is common and requires drops.

105
Q

What is the retina?

A
  • Outer pigmented layer in contact with the choroid
  • Inner sensory layer in contact with vitreous
  • At centre is fovea
106
Q

Optic disc colour?

A

Should be pale pink

Paler in optic atrophy

107
Q

Contour of optic disc?

A
  • Margins blurred in papilloedema and optic neuritis
108
Q

Cup of the optic disc?

A

Physiological cup lies centrally and should occupy 1/3 of disc diameter
Cup widening and deepening in glaucoma.

109
Q

Retinitis pigmentosa?

A

Most prevalent inherited degeneration of the macula

Various modes of inheritence

  • Mostly AR
  • AD has good prognosis

Presentation

  • night blindness
  • Decreased visual fields - tunnel vision
  • Most are registrable blind by mid 30s (<3/60).

Fundoscopy
- Pale optic disc: optic atrophy
- Peripheral retina pigmentation: spares the macula.
- Bone spicule appearance with thinner, blacker lines.
= Mottling of the retinal pigment epithelium .

110
Q

Associations of retinitis pigmentosa?

A
Friedrich's ataxia
Refsum disease
Usher's syndrome
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome 
Alports
111
Q

Retinoblastoma?

A

Comonest intraocular tumour in children
- Hereditary type differers.

5% occurs with pineal or other tumours
- Increaed risk of osteosarcoma and rhabdomyosarcoma

Signs

  • Stabismus
  • Leukocoria (white pupil) –> no red reflex

Rx

  • depends on size
  • Options include: chemo, radio,enucleation
112
Q

What is a stye?

A

Abscess or infection in a lash follicle which points outwards
- Local abx - fusidic acid

  • External: (hordeolum externum) infection of gland of Zeis or glands of Moll (sweat)
  • Internal (hordeolim internum): infection of Meibomian glands leaving residual chalazion
  • Management = Hot compression and analgesia.
113
Q

What is a chalazion?

A

Abscess of the meibomian gland which points inwards onto conjunctiva
- Sebaceous gland of eyelid

Most resolve spontaneously but some require surgical drainage.

114
Q

What is blepharitis?

A

Chronic inflammation of eyelid
Causes: Seborrhoeic dermatitis, staphs - dry skin of the eyes. Also common with patients with rosacea.

Meibomian gland secrete oil to prevent rapid evaporation of tear film.

Features

  • Red eyes
  • Gritty/itchy sensation
  • Scales on lashes
  • Often associated with rosaea

Management - Clean crusts of lashes with warm soaks
May need fusidic acid drops.
Lid hygiene - mechanical removal of debris from lid margins. Artificial tears.

Styes and chalazions more common.

115
Q

Entropion?

A

Lid inversion –> corneal irritation
Degeneration of lower lid fascia
If left untreated this patient may develop a corneal ulcer.

Definitive management of entropion is surgical although eye lubircants + tap may be used whilst waiting for surgery.

116
Q

Ectropion?

A

Low lid eversion –> watering and exposure keratitis

Associated with ageing and facial nerve palsy.

117
Q

Ptosis?

A

Ture ptosis is intrinsic LPS weakness - Levator palpebrae superioris

118
Q

Causes of bilateral ptosis?

A

Congenital
Senile
MG
Myotonic dystrophy

119
Q

Causes of unilateral ptosis?

A

3rd nerve palsy
Horner’s syndrome
Mechanical: xanthelasma, trauma.

120
Q

Lagophthalmos

A

Difficulty in lid closure over the globe which may –> Exposure keratitis

Causes: exophthalmos, facial palsy, injury.
Management - Lubricate eye with liquid parafinn ointment
Temporary tarsorrhaphy may be needed if corneal ulcers develop

121
Q

Pinguecula?

A

yellow vascular nodules either side of cornea

122
Q

Pteryguim?

A

Similar to pinguecula but grows over the cornea - decreased vision

Benign growth of conjunctiva
Associated with dusty, wind-blown lifetyles, sun exposure.

123
Q

What is orbital cellulitis?

A

Infection from paranasal sinuses, eyelid or external eye

Staph, pneumococcus, GAS.

124
Q

Presentation of orbital cellulitis?

A

Usually a child with inflammation of the orbit + lid swelling
Pain and decreased range of eye movement
Exophthalmos
Systemic signs - fever
± tenderness over the sinuses

NB: reduced visual acuity, proptosis, ophthalmoplegia, pain with eye movements are NOT consistent with periorbital cellulitis.

125
Q

Management of orbital swellings?

A

when suspected - contrast enhanced CT scan of the orbits, sinuses and brain should be considered to support the diagnosis and to search for possible complications.

Medical emergencies.

IV Abx: Cefuroxime

Complications

  • Local extension –> Meningitis and cavernous sinus thrombosis
  • Blindness due to optic nerve presure
126
Q

What is a carotico-carvernosus fistula?

A

May follow carotid aneurysm rupture with reflux of blood into cavernous sinus

Causes: spontaneous, trauma

Presentation - engorgement of eye vessels

  • Lid and conjunctival oedema
  • Pulsatile exophthalmos
  • Eye bruit

Manage with oral antiviral: aciclovir

127
Q

Exophthalmos/Proptosis?

A

Protrusion of one or both eyes

Graves disease - Anti-TSH abds –> retro-orbital inflammation and lymphocyte infiltration –> swelling.

Orbital cellulitis

Trauma

128
Q

Other causes of exophthalmos?

A
Idiopathic orbital inflammatory disease 
Vasculitis: Wegeners 
- Neoplasm -
 Optic glioma 
lyphoma 

Carotico-carvernous fistula

129
Q

Myopia?

A

Short sightedness
Distant objects are focussed too far forward

Causes

  • Genetic
  • Excessive close work in the early decades

Solution
- Concave lenses

130
Q

Astigmatism?

A

Cornea or lens doesn’t have same degree of curvature in horizontal and vertical planes

  • Image of object is distorted longitudinally or vertically

Need correcting lenses

131
Q

Hypermetropia- long-sightedness

A

Eye is too short
When eye relaxed and not accomodating, objects behind the retina.

Need convex lenses.

132
Q

What is esotropia?

A

Convergent squint
- Commonest type in children

Towards the nose.

When covering left eye will move laterally from nasal to take up fixation.

Features ambylopia

133
Q

What is exotropia

A

Divergent squint
- Older children

Towards to temporals.

Superiorly = Hypertropia 
Inferiorly = Hypotropia. 

Ambylopia. Don’t normally have double vision as they adapt.

134
Q

Non-paralytic squint

A

Concomitant = imbalance in extraocular muscles.

Corneal reflection: should fall centrally and symmetrically over each cornea

Cover test: movement of uncovered eye to take up fixation demonstrates manifest squint.

135
Q

Management of non-paralytic squint?

A

Refer to ophthalmologist and orthoptist.

Optical: correct refractive errors

Orthoptic: patching good eye encourages use of squinting eye

Operations: e.g resection + recession of rectus muscle - help alignment

136
Q

What is a paralytic squint?

A

Diplopia is most on looking in direction of pull of paralysed muscles
Eyes won’t fixate on covering
Cover each eye in turn: which ever eye sees the outer image is malfunctioning

137
Q

CNIII

A

Ptosis (LPS)
Fixed dilated pupil (no parasympathetic)
Eye looking down and out

Causes

  • Medical: DM, MS, infarction
  • Surgical: Increased ICP, cavernous sinus thrombosis, posterior communicating artery aneurysm
138
Q

CNIV

A

Diplopia especially on going down stairs
Head tilt
Test: Can’t depress in adduction

  • Cause
    Peripheral: DM, trauma, compresion
    Central: MS, vascular, SOL
139
Q

CNVI

A
Eye is medially deviated and cannot abduct
Diplopia in the horizontal plane
Causes 
- Peripheral: DM, compression trauma 
- Central: MS, vascular, SOL 

Managment: botulinum toxin can eliminate need for surgery

140
Q

What is orbital blowout frature?

A

Blunt injury –> Sudden increased in orbital pressure with herniation of orbital contents into maxillary sinus

Presents
- Ophthalmoplegia + diplopia
Tethering of inferior rectus + inferior oblique

  • Loss of sensation to lower lid skin = Infraorbital nerve injury
  • Ipsilateral epistaxis: Damage to anterior ethmoidal artery

Decreased acuity
Irregular pupil that reacts slowly to light.

141
Q

Management of orbital blowout fracture?

A

Fracture reduction + muscle release necessary

142
Q

Chemical injury to eye?

A

Alkalmine solutions are really bad.

Manage = copious irrigation
Specialist referral.

143
Q

What are floaters?

A

Small dark spots in the visual field

Sudden shower of floaters in one eye may be due to blood or retinal detacment

144
Q

Causes of floaters?

A
Retinal detachment 
VH 
Diabetic retinopathy 
Old retinal branch vein occlusion 
Syneresis
145
Q

Flashes cause?

A

Either from intraocular or intracerebral pathology
Headache, n/v, migraine
Flashes and floaters: retinal detachment

146
Q

Haloes?

A

Usualyl just diffractive phenomena
May be caused by hazy ocular media –> Cataract, corneal oedema, acute glaucoma

Haloes + Eye pain - Acute glaucoma.

jagged haloes which change shape are usually migrainous .

147
Q

Allergic eye disease - seasonal allergic conjunctivits?

A

50% of allergic eye disease
Small papillae on tarsal conjunctiviae (Bulging)

  • Management: Antazoline - antihistamine drops topically.
    Cromoglycate: inhibitis mast cell degranulation need to be applied for several weeks to attain optimal prophylactic benefit.
148
Q

Perennial allergic conjunctivitis?

A

Symptoms all year with seasonal exacerbation

- Manage with olopatadine (antihistamine + mast cell stabiliser)

149
Q

Giant papillary conjunctivitis?

A

Iatrogenic FBs: Contact lension, sutures

Giant papillae on tarsal conjunctivae therefore remove FB/

150
Q

Management of allergic eye disease?

A
Remove allergen
General measurs 
- Cold compression
- Artificial tears 
- Oral antihistamines: Loratadine 

Eye drops

  • ANtihistamines: antazoline
  • Mast cell stabilisers: cromoglycate
  • Steroids - dexamethasone
  • NSAIDS: diclofenac
151
Q

What is a trachoma?

A

Caused by chlamydia trachomatis
spread by flies
- inflammatory reaction under lids –> scarring –> lid distortion –> entropion –> Eyelashes scatch cornea
–> ulceration –> blindness

Management = tetracycline 1% ointment.

152
Q

What is onchocerciasis (river blindness)

A

Caused by nematode Onchocerca
- spread by flies

Invades eye, leads to fibrosis, corneal opacitiies and synechiae

Ivermectin as management

153
Q

What is xerophthalmia and keratomalcia?

A

Manifestations of Vitamin A deficiency

  • Night blindness + dry conjunctivae (xerosis)
  • Corneal ulceration + perforation

Manage with Vitamin A palmitate reverses early corneal changes.

154
Q

What are the stages of hypertensive retinopathy?

A
  1. Tortuosity and silver wiring
  2. AV nipping
  3. Flame haemorrhages + soft/cotton wool spots. If they just have cotton-wool spots makes it 3.
  4. Papilloedema

SAFE

  • Silver wiring + Tortuosity. Arteriolar narrowing.
  • AV nipping
  • Flame and cotton wool
  • Papilloedema.
155
Q

Which granulomatous disorders causes uveitis and choriodoretinitis?

A

TB, Sarcoid, Toxo, leprosy, brucella

156
Q

Which inflammatory diseases cause conjunctivitis

A

SLE, reactive arthritis, IBD

157
Q

Which inflamamtory diseases cause scleritis/epislepritis?

A

RA, vasculitis, SLE, IBD

158
Q

Which inflammatory disease cause iritis?

A

Ank Spond
IBD
Sarcoid

159
Q

Which inflammatory disease can cause retinopathy?

A

Dermatomyositis

160
Q

What is keratoconjunctivitis Sicca?

A

Sjogrens

  • Decreased tear production (Schirmer’s <5mm in 5m ins
  • Dry eyes and dry mouth
  • Primary or secondary: SLE, RA, Sarcoid

Management with artificial tears or saliva

161
Q

Amaurosis fugax?

A

GCA

Carotid atheroemboli

162
Q

Microemboli of the eye?

A

Roth spots

Infective endocarditis

163
Q

Kayser-fleisher rings

A

Wilsons

164
Q

Exophthalmos

A

Graves

165
Q

Corneal calcification

A

HPT

166
Q

HIV eye related disease?

A

CMV retinitis: Pizza-pie fundus + flames

HIV retinopathy: cotton wool spots

167
Q

What are mydriatics?

A

Eye dilators

Anti-muscarinics
- Tropicamide
Duration: 3hr

Cyclopentolate
- duration:24hr (paediatrics)

Used in pupil dilatation
Cyclopelgia –> blurred vision

Sympathomimetics

  • Para-hydroxyamphetamine
  • may be used with tropicamide
  • Don’t affect the light reflex.

Indications
- Eye examination

168
Q

Miotics?

A

Effects
- Constrict pupil

Pilocarpine
- Muscarinic agonist

Used in –> Acute closed-angle glaucoma

169
Q

Papilloedema?

A

Optic disc swelling that is caused by increased intracranial pressure. Almost always bilateral.

  • On fundoscopy =
    venous engorgement,
    the loss of venous pulsation.
    Blurring of optic disc margin. elevation of optic disc.
    Loss of optic cup.
    Paton’s lines: concentric/radial retinal lines cascading from optic disc.

Causes of papilloedema

  • SOL
  • Malignant HTN
  • Idiopathic intracranial HTN
  • Hydrocephalus
  • Hypercapnia

Therefore hypocapnia via hyperventilation can be used to reduced ICP. Increased PaCO2 leads to arterial vasoconstriction lowing cerebral blood flow.

170
Q

Hutchinson’s pupil?

A

Unilateral dilated pupil is unresponsive to light. A result of compression of the oculomotor nerve of the same side. By an intracranial mass.

171
Q

Nasolacrimal duct obstruction?

A

Persistent watery eye in an infant. Caused by imperforate membrane.

Usually at the lower end of the lacrimal duct.

teach parents to massage the lacrimal duct
symptoms resolve in 95% by the age of one year. Unresolved cases should be referred to an ophthalmologist for consideration of probing, which is done under a light general anaesthetic

172
Q

Tunnel Vision?

A
Papilloedema
Glaucoma
retinitis pigmentosa
Choroidoretinitis
Optic atrophy secondary to tabes dorsalis
hysteria
173
Q

Causes of mydriasis?

A
Third nerve palsy 
Holmes-Adie Pupil
Traumatic iridoplegia
Phaechromocytoma
Congenital 

Drugs
- Topical: tropicamide, atropine
Sympathomimetic drugs: amphetamines, cocaine
- Anticholinergic drug: tricyclic antidepressants.

174
Q

Macular hole?

A

Similar to age-related macular degeneration.

Well-defined round or oval lesions in the macular with yellow deposits at the base.

No choroidal neovascularisation

175
Q

Differentials for red eye?

A

Acute angle closure glaucoma

  • severe pain (may be ocular or headache)
  • decreased visual acuity, patient sees haloes
  • semi-dilated pupil
  • hazy cornea

Anterior uveitis

  • acute onset
  • pain
  • blurred vision and
  • photophobia
  • small, fixed oval pupil, ciliary flush

Scleritis
- Severe pain and tenderness
(episcleritis = painless)

Conjunctivits
- Purulent discharge or clear if viral

Subconjunctival haemorrahge
- history of trauma or coughing bouts

Endophthalmitis
- Typically red eye, pain and visual loss following intraocular surgery.

176
Q

Babies with minor purulent discharge?

A

Take swab samples to detect chlamydia and gonococcus.

Must take swabs first.

177
Q

Posterior vitreous detachment

A

Natural changes to the vitreous fluid of the eye with ageing. Not associated with pain or loss of vision. Can ead to tear of the membrane. Therefore need to rule this out.

Highly myopic (near sighted) patients have an increased risk.

vitreous shrinks and pulls away from retina. 10% of patients with PVD develop retinal tear.

  • Flashes of light (photopsia) - in the peripheral field of vision
    Floaters, often on the temporal side of the central vision

Weiss ring on ophthalmoscopy.

Investigations
- patients must be seen by ophthalmologist within 24hrs.

Management
- Normally does not need treatment as improves and not associated with permanent loss of vision.