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Special Senses > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

Painless Vision loss is usually secondary to what events ?

A

Vascular events: - vitreous haemorrhage - central retinal artery occlusion - optic neuropathy - ARMD

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2
Q

Painful vision loss is usually secondary to what events ?

A

Inflammatory events: - Uveitis - Acute angle closure glaucoma - keratitis - optic neuritis

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3
Q

Sudden visual loss is usually due to:

A
  • vascular events (most are sudden) - Retinal detachment - Acute angle closure glaucoma
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4
Q

Chronic visual loss is usually due to:

A
  • Cataracts - ARMD - Uveitis - Keratitis
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5
Q

What are the ophthalmic manifestations of a stroke?

A
  • CN palsies - VF loss
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6
Q

Ophthalmic manifestations of MS?

A
  • Optic neuritis - Nystagmus
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7
Q

Ophthalmic manifestation of IBD?

A

Uveitis

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8
Q

Ophthalmic manifestation rheumatoid arthritis?

A

Scleritis

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9
Q

How might contact lenses cause involution ptosis?

A

May cause levator aponeurosis to detach from tarsal plate

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10
Q

what is entropion?

A

Lid inturning: typically due to degeneration of lower (rarely upper) lid fascuak attachments and their muscles - Usually >40 yrs - inturned lashes irritate cornea

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11
Q

Management of entropion?

A
  • Tape lower lid to cheek - Botulinum toxin injection - Surgery for long lasting relief
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12
Q

What is Ectropion?

A

Lower lid eversion: causes eye irritation, watering +/- ketaitis

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13
Q

what is blepharitis?

A
  • Lid inflammation - due to staphs, seborrhoeic dermatitis - causes burning, itching , red margins with crusting on lashes
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14
Q

what are dendritic ulcers of the eye ? treatment?

A
  • Corneal ulcer due to HSV infection - treat with steroid eye drops and aciclovir
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15
Q

signs of nasolacrimal duct non-canalization?

A
  • child with persistent watery eyes - prone to attacks of conjunctivitis
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16
Q

what Ig is prevalent in tears ?

A

IgA

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17
Q

Causes of dry eye syndrome (Keratoconjunctivitis sicca)

A
  • decreased tear production with age - Sjogren’s - mumps - sarcoidosis - amyloid - lymphoma, leukaemia - mucin deficiency in tears (e.g. Stevens-Johnson syndrome, pemphigoid etc)
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18
Q

causes of excess lacrimation

A
  • emotion - corneal abrasions - foreign body - entropion - conjunctivitis - acute glaucoma
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19
Q

What is considered to be the cause of a painful Horner’s syndrome until proven otherwise ?

A

Internal Carotid artery dissection - pain in the neck and side of head + Miosis

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20
Q

Causes of Horner’s syndrome?

A
  • PICA or basilar artery occlusion - Pancoasts tumour - MS - Cavernous sinus thrombosis - Klumpke’s palsy
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21
Q

What is Horner’s syndrome?

A

Disruption of the sympathetic fibres, so the pupil is miotic (smaller) and there is partial ptosis - the pupil does not dilate in the dark

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22
Q

Signs of third nerve palsy ?

A
  • Ptosis - Exopthalmos (as recti tone decreased) - Fixed pupil dilation - eye = down + out
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23
Q

Who is acute angle glaucoma most likely to affect ?

A
  • most common 60-70 (>40) - South Asians, Chinese - Females (4:1)
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24
Q

Presentation of acute angle glaucoma

A
  • Severe, rapid, progressive pain spreading around orbit + frontal headache - Blurred vision (Rapidly progressing to vision loss) + coloured haloes around light - Usually Unilateral - Nausea + vomiting, systemic malaise (may be presenting complaint in elderly)
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25
Q

Who is at greater risk of close angle glaucoma; long or short sighted people?

A

Long sighted (hypermetropes)

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26
Q

Precipitants of acute angle closure glaucoma attack:

A

times of mid-dilated pupil: - moments of stress/excitement - watching TV in dim lighting - topical mydriatics - systemic anticholinergics

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27
Q

Findings o/e in AAGC?

A
  • generally unwell - Red eye (Ciliary flush-redness around periphery of cornea) - Hazy cornea + non-reactive, mid-dilated pupils - Globe hard on palpation - IOP raised (norm = 10-21mmHg)
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28
Q

Diagnostic criteria for Acute Angle Closure?

A

Ocular pain, Nausea/Vomiting + History of intermittent blurring of vision with Haloes AND 3 of: - ICO >21 - Conjunctival infection - Corneal Epithelial oedema - Mid-dilated, fixed pupils - Shallow chamber

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29
Q

Differential Diagnoses of severe ocular pain with visual loss?

A
  • AACG - Anterior Uveitis - Scleritis - Optic Neuritis
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30
Q

Treatment of AACG?

A
  • Topical: B-blockers, steroids - Pilocarpine (miosis to open blockage) - IV carbonic anhydrase inhibitors e.g. Acetazolamide (decreases formation of aqueous) - Systemic analgesics +/- antiemetics - Peripheral Iridectomy - once IOP decreased: small pice of iris removed I nboth eyes to allow free circulation of aqeous
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31
Q

Pathogenesis of AACG?

A

Blocked drainage of aqeous from the anterior chamber via the canal of schlemm. - pupil dilatation worsens the blockage - IOP rises > 60 (norm = 10-21)

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32
Q

Complications of AACG

A
  • Permanent vision loss - Recurrent attacks - Attack in other eye - Central retinal artery/vein occlusion
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33
Q

What is primary open-angle glaucoma characterised by ?

A
  • Adult onset - IOP >21 - Open Iriocorneal angle - Glaucomatous optic neuropathy - Visual field loss (compatible with nerve fibre damage) - Absence of an underlying cause
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34
Q

Pathogenesis of open angle glaucoma?

A
  • Increased resistant to aqueous outflow within the trabecular meshwork -> causing IOP to rise -> damage to the optic nerve - raised IOP influences retinal ganglion apoptosis (mechanical compression of optic nerve head + compromise of local vasculature)
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35
Q

Which is the most common form of glaucoma ?

A

Primary open angle glaucoma (1-2% > 40)

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36
Q

Risk factors for primary open angle glaucoma?

A
  • Increasing age - Family history - Afrocarribean (presents earlier + more severe) - Ocular hypertension - Myopia (short sighted) - retinal disease - Diabetes and systemic hypertension
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37
Q

Presentation of primary open angle glaucoma?

A
  • usually don’t notice anything - by the time symptomatic 90% optic fibres irreversibly damaged - Abnormalities with IOPs + visual fields noticed incidentally at routine optician apt.
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38
Q

What is Gonioscopy ?

A

Measurement of the angle between the cornea and the iris to assess whether the glaucoma is open or closed angle. (Initial assessment only)

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39
Q

What is Tonometry

A

Objective measurement of IOP

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40
Q

Investigations in glaucoma?

A
  • Gonioscopy - Corneal thickness (affects IOP reading) - Tonometry - Optic disc:cup ratio (progression of disease) - Visual fields
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41
Q

Which drugs are used to control IOP ?

A
  • topical B-blockers - Prostaglandin analogues - Carbonic anhydrase inhibitors - Miotics - Sympathomimetics
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42
Q

What is the action of Carbonic Anhydrase Inhibitors?

A

reduce aqueous secretion by ciliary body. Weak diuresis in systemic use.

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43
Q

Contraindications of Carbonic Anhydrase Inhibitors?

A
  • renal impairment - metabolite imbalance - severe hepatic impairment - sulfonamide sensitivity (acetazolamide) - breast-feeding.
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44
Q

what structures are included in the uvea?

A

Pigmented part of the eye, including: iris, ciliary body (ant.) and choroid

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45
Q

Systemic diseases causing Uveitis?

A
  • ankylosing spondylitis - sarcoidosis - IBD - psoriasis - Behcets - Juvenile idiopathic arthritis
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46
Q

Presentation of Uveitis?

A
  • Acute, unilateral pain - photophobia - blurred vision (aqueous precipitates) - Lacrimation - circumcorneal redness (ciliary congestion) - Initial small pupil -> irregular or dilate irregularly due to adhesions
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47
Q

what is Talbot’s test ?

A

test for Uveitis: - pain worsens on convergence (accommodation)

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48
Q

Age group most commonly affected by Uveitis ?

A

20-50 (working age)

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49
Q

Characteristic sign if anterior uveitis on slit lamp exam?

A

presence of cells in aqueous humour - appears like bits of dust floating in the dark - cloudy - anterior chamber flare

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50
Q

Which infections are associated with anterior uveitis?

A

Herpes simplex Herpes Zoster - due to immune reaction to organism

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51
Q

What infections is granulomatous uveitis associated with?

A
  • Toxoplasmosis - CMV - TB - Syphilis - AIDS (CMV, HSV, Cryptococcus, candiasis)
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52
Q

Management of uveitis

A
  • Corticosteroids (reduce inflam. and prevents adhesions) - Cycloplegic-mydriatic drug (e.g. cyclopentolate) - paralyse ciliary body (relieves pain + prevents adhesions) - Abx if infectious
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53
Q

complications of uveitis

A

Vision loss due to: - crystalloid macular oedema - secondary cataracts raised IOP (with or without glaucoma) - retinal detachment - neovascularsation

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54
Q

Red flag considerations in a red eye

A
  • Acuity affected ? - painful globe ? (foreign body?) - Pupil respond to light ? - Cornea damaged? (use fluorescin eyedrops)
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55
Q

What is Keratitis?

A

Inflammation of cornea - white are on cornea representing collection of white cells

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56
Q

what organisms may be causative for infective corneal ulcers?

A
  • pseudomonas (progress srapidly) - HSV - Fungal: candida/aspergillus -Protozoal: acanthamoeba
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57
Q

Presentation of corneal ulcers

A
  • Pain - Photophobia - reduced visual acuity - red eye - systemic e.g. Headache, nauseated, generally unwell/run down
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58
Q

what is chloramphenicol?

A

topical treatment for bacterial eye infections

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59
Q

presentation of episcleritis

A
  • acute mild pain/gritty discomfort - localised or diffuse red eye - unilat or bilat - no associated ocular symptoms other than watering
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60
Q

Presentation of scleritis

A
  • subacute, severe boring pain radiating to forehead, brow and jaw - pain worse on eye movement + at night - watering, photophobia, gradual decrease in vision - 50% bilat - occasional systemic upset: fever, vom, headache
61
Q

management of episcleritis

A

topical and systemic NSAIDs - most self limiting 7-10 days

62
Q

management of scleritis

A

oral corticosteroids/immunosuppressives to control disease - refer to specialist

63
Q

what is a corneal abrasion?

A

breach of corneal epithelium without keratitis e.g. in trauma

64
Q

presentation of conjunctivitis ?

A
  • Red, inflamed conjunctiva - often bilat with discharge - eyes itch, burn and lacrimate hyperaemic vessels may be moved over sclera (gentle pressure on globe) - acuity, pupillary responses and corneal lustre unaffected
65
Q

how can you distinguish between viral and bacterial conjunctivitis on examination?

A
  • Bacterial = purulent discharge more prominent - viral = small lymphoid aggregates appear as follicles on conjunctiva
66
Q

when would you suspect the cause of conjunctivitis to be chlamydial?

A

In young, adults with prolonged conjunctivitis or those with sexual disease

67
Q

treatment of allergic conjunctivitis?

A
  • Antihistamine drops e.g. emedastine - sodium cromoglycate or steroid drops if not settling after few days/under specialist advice
68
Q

Signs/Symptoms of myopia ?

A
  • difficulty with distant vision- squinting, eye strain, headaches - Feeling fatigued when driving or playing sport - Typically starts in childhood (~6)
69
Q

What causes myopia?

A

Eye ball is too long relative to focusing power of cornea and lens - causes light rays to focus in front on the retina

70
Q

Treatment of myopia ?

A
  • Concave lenses - Refractive surgery
71
Q

What is Degenerative Myopia?

A
  • elongation of eyeball occurs rapidly - quick and severe progression of myopia leading to vision loss - increased risk of retinal detachment and cataracts
72
Q

What is presbyopia?

A

Age-related long sightedness

73
Q

What is astigmatism?

A

Refractive error due to unevenly curved cornea

74
Q

Symptoms of hypermetropia?

A
  • difficulty with near vision - tiring of eyes - headaches and uncomfortable vision - difficulty with depth perception - lazy eye if present from young age
75
Q

What causes hypermetropia?

A

Eye ball too short, object focus behind the retina and eye unable to accommodate properly so results in blurred vision

76
Q

What type of lenses correct hypermetropia?

A

Convex lenses

77
Q

sources for vitreous haemorrhage?

A
  • Neovascularisation (diabetes) - retinal tears - retinal detachment - trauma
78
Q

what is the most common cause of flashes and floaters?

A

Vitreous detachment

79
Q

Risk factors for vitreous detachment?

A
  • Increasing age - Myopia - Uveitis - Laser treatment - Eye surgery - Eye trauma
80
Q

Symptoms of Vitreous detachment?

A
  • 1+ floaters or wispy lace objects floating across vision - floaters = usually circle, ovoid, bent line (depending on completeness of detachment) - photopsia (if exerts traction on retina) - Painless + no effect on vision
81
Q

Symptoms of vitreous haemorrhage?

A

shower of black specks across vision (associated with retinal detachment)

82
Q

Signs of vitreous detachment?

A

Usually only seen on slit lamp unless associated retinal detachment: - Weiss ring: condensed, thickened posterior surface of vitreous that has become visible as it has pulled away from optic disc - thin irregular ring of translucent material floating in vitreous - haemorrhage occasionally

83
Q

Investigations to be done in suspected vitreous detachment?

A
  • Full slit lamp exam - ultrasound (if no haemorrhage) - if detachment - visual fields
84
Q

Complications of vitreous haemorrhage?

A
  • retinal tear - retinal detachment - vitreous haemorrhage (if part that has become detached happened to overlie a vessel)
85
Q

Triad of clinical features in optic neuritis?

A
  • reduced vision - eye pain (esp. on movement) - impaired colour vision (red desaturation)
86
Q

Types of optic neuritis?

A
  • acute demyelinating - ischaemic optic neuropathies - Inflammatory (+corticosteroid responsive) - Infectious - Nutritional - drugs and toxins - inherited
87
Q

Causes of ischaemic optic neuropathies?

A
  • Giant cell arteritis - Ant + Post optic neuropathy - Diabetic papillopathy
88
Q

Which vitamin deficiency can cause optic neuritis?

A

B12

89
Q

Drugs that can cause optic neuritis?

A
  • Amiodarone - Isoniazid - methanol intoxication -
90
Q

Feature of acute demyelinating optic neuritis?

A
  • Light flashes - Uhthoff’s phenomenon - worsening of symptoms with increased temperature - fatigue - fading of vision
91
Q

what is amblyopia?

A

Lazy eye - impaired or dim vision without obvious defect or change in the eye

92
Q

What is Strabismus?

A

aka squint: - the eyes do not look together in the same direction. Whilst one eye looks straight ahead, the other eye turns to point inwards, outwards, upwards or downwards

93
Q

What are the different types of squint?

A

•esotropia = eye turns inwards •exotropia = eye turns outwards •hypertropia = eye turns upwards •hypotropia = eye turns downwards

94
Q

What is a manifest squint?

A

The affected eye turns when the eyes are open and being used

95
Q

What is a latent squint?

A

The affected eye turns only when it is covered or shut but looks fine when eyes are open

96
Q

A squint where the angle is always the same in every direction is called what ?

A

Concomitant squint i.e. eyes move well, all muscles working, but the two eyes are always misaligned by same amount, despite which way they’re looking

97
Q

What is an incomitant squint?

A

the angle of squint can vary e.g. when you look to the left, there may be no squint and the eyes are aligned. But when you look to the right, one eye may not move as far and the eyes are then not aligned.

98
Q

What is Hirschberg test ?

A

Route estimate of degree of strabismus: - hold pen torch arms lenbth from patient and shine it in front of their eyes. - patient looking at the light - observe where reflection of pen torch lies with respect to cornea - should be central bilat. - if in the inner margin = outward deviation + vice vera

99
Q

Management of squint:

A
  • Treat refractive errors first - If
100
Q

What is a paralytic squint?

A

Refers to disease of CN II, IV, VI: - may be isolated or multiple nerve palsies - myopathies may give rise to diplopia or restricted movement

101
Q

What is orbital cellulitis

A

Infection of the soft tissue behind the orbital septum

102
Q

Pathophysiology of orbital cellulitis

A
  • Extension of infection from periorbital structures (usually paranasal sinuses esp ethmoid). + face, globe, lacrimal sac and dental infection (via intermediary maxillary sinusitis) - may be an extension of preseptal cellulitis esp. in children (septum not properly formed) - post traumatic - haematogenous spread from sdistant bacteraemia
103
Q

Pathogens most commonly involved in orbital cellulitis?

A

Aerobic: - Strep pneumoniae - staph aureus - strep pyogenes - H. ingluenzae

104
Q

What pathogen is associated with orbital cellulitis in patient who have DKA or are immunosuppressed?

A

Mucormycosis (fungi) - rare and rapidly spreading

105
Q

Presentation of orbital cellulitis:

A
  • Sudden onset of unilat swelling of conjunctiva and lids - proptosis - pain + restriction of eye movements - blurred vision, reduced acuity, diplopia - Fever, severe malaise - ~Relative afferent pupillary defect
106
Q

Complications of orbital cellulitis

A
  • Ocular: Leratopathy, Raised IOP, Central retinal artery/vein occlusion, optic neuropathy - Orbital abscess - Subperiosteal abscess - Intracranial: meningitis, brain abscess, cavernous sinus thrombosis
107
Q

what is giant cell arteritis?

A

Systemic immune mediated vasculitis of medium and large arteries

108
Q

Presentation of giant cell arteritis

A
  • Temporal headache, myalgia, malaise or fever - scalp tenderness - transient visual symptoms (blurred, diplopia, amaurosis fugax) - Jaw claudication/face pain - systemic: anorexia, fever, fatigue, malaise
109
Q

Signs of giant cell arteritis on examination?

A
  • Tempora; artery = prominent, beaded, tender + pulseless - fever - tender muscles/joints - fundoscopic evidence of ischaemic events
110
Q

Investigations and findings in giant cell arteritis

A
  • raised ESR - Abnormal artery biopsy (vasculitis characterised by mononuclear cell infiltration or granulomatous inflammation usually with multinnucleated giant cells
111
Q

Differential diagnoses of giant cell arteritis

A
  • Migraine - Tension headache - Trigeminal neuralgia
112
Q

Management of giant cell arteritis?

A
  • Corticosteroids (prednisolone) - Low-dose aspirin (+PPI
113
Q

Complications of Giant cell arteritis

A
  • Loss of vision - Aneurysm, dissections, stenotic lesions of the aorta/major branches Steroid-related complications
114
Q

What are Drusen:

A

Associated with dry AMD:

Collections of lipid and protein material beneath the outer layer of the retina (which may be seen on ophthalmoscopy as pale yellow spots on the retina).

115
Q

Changes associated with AMD

A
  • Drusen
  • Neovascularisation
  • Geographical atrophy
  • abnormalities of retinal pigement epithelium
116
Q

How does vision loss occur in dry AMD?

A

choroidal neovascularisation breaks through to the neural retina, leaking fluid, lipids, and blood, and leading to fibrous scarring.

117
Q

How does vision loss occur in wet AMD?

A

progressive atrophy of the retinal pigment epithelium, choriocapillaris and photoreceptors.

118
Q

Risk factors for AMD?

A
  • increasing age
  • Smoking
  • UV exposure (cumulative over lifetime)
  • CV risk factors
  • +ve fam. hist
119
Q

Symptoms of dry AMD?

A
  • insidious presentation, usually found on routine exam
  • When GA is bilateral and involves the fovea of both eyes, patients may complain of deterioration of central vision.
  • A common presentation is difficulty with reading initially with the smallest sizes of print and then later with larger print and or words.
120
Q

Presentation of wet AMD?

A
  • Central visual blurring and distortion
  • straight lines appear crooked or wavy.
  • sudden deteriorate to profound central visual loss due to bleed - preceded/accompanied by a shower of floaters
  • When in both eyes-patients suddenly become unable to read, drive, and see fine detail e.g. facial expressions
  • central dark patch in the visual field noticed at night, which clears within a few minutes as they adapt
121
Q

Findings on exam of dry AMD

A

+ normal/decreased acuity, pigment abn etc

122
Q
A

Wet AMD:

-

123
Q

Therapies for acute neovascular AMD?

A
  • Laser photocoagulation (for lesions away from fovea)
  • Photodynamic therapy (PDT) with verteporfin - destroy the neovascular membrane without damaging the overlying neurosensory retina
  • Anti-VEGF inhibitors* e.g. Aflibercept, Ranibizumab - interfere with angiogenesis by binding to VEGFs to prevent endothelial cell proliferation
  • Combination therapy: PDT and anti-VEGF - may have increased efficacy but not enough evidence
124
Q

What is amaurosis fugax?

A
  • painless, transient loss of all or part of the vision of an eye, lasting just seconds/minutes.
  • It is due to transient ischaemia and may be a feature of embolic, thrombotic, vasospastic, or haematological problems.
125
Q

Conditions associated with amaurosis fugax?

A
  • transient ischaemic attacks
  • giant cell arteritis
  • Takayasu’s disease
  • sickle cell disease
126
Q

most common ophthalmic emergency in the UK

A

Retinal detachment

127
Q

What is Rhegmatogenous retinal detachment?

A
  • sensory retina detaches due to a retinal break:
  • torn as a result of vitreous traction or chronic retinal atrophy may result in a hole.
  • Liquefied vitreous seeps through the break into the potential space between the sensory retina and the pigment epithelium, lifting the retina off
128
Q

What are the two types of non-Rhegmatogenous retinal detachment?

A
  • *Tractional**: the vitreous contracts, pulling sensory retina away with it. (uncommon)
  • *Exudative:** damage of the underlying Retinal Pigment Epithelium allows subretinal fluid to leak into the subretinal space under the sensory retina, so pushing this out and causing a detachment.

*Non-rhegmatogenous = NOT due to a Tear in the retinal

129
Q

Risk factors for retinal detachment?

A
  • Extreme myopia (short-sightedness)
  • Family history
  • History of RD in either eye
  • Eye trauma- especially blunt trauma
  • Previous cataract surgery
  • Proliferative diabetic retinopathy
  • Inflammatory conditions (eg, uveitis and scleritis)
  • Malignancy - eg, choroidal melanoma, haemangioma, metastasis
  • Congenital eye diseases - eg, glaucoma, cataract, or retinopathy of prematurity
130
Q

Presentation of retinal detachment:

A
  • photopsia
  • floaters: cobweb-like opacity or a shower of little spots
  • visual field defect= curtain descending over their vision
  • If macula involved = decreased visual acuity
131
Q

If Visual acuity is unchanged in a retinal attachment what does this mean?

A
  • Macula has not detached yet
  • urgent refferal - surgery can prevent macula from detaching therefore saving some acuity
132
Q

Signs of retinal detachment on fundoscopy ?

A
  • sheet of sensory retina billowing towards the centre of the globe, over which the vessels pass like paths over a hill.
  • There may be an associated tear visible
133
Q

Treatment for retinal detachment:

A
  • Laser - retinal break but a full-blown RD hasn’t yet developed
  • Surgery - Scleral buckle, Vitrectomy
  • Cryotherapy
134
Q

Risk factors for cataracts

A
  • Female
  • DM
  • Steroids.
  • Eye trauma.
  • Uveitis.
  • UV exposure.
  • Nutrition and socio-economic status.
  • Smoking and alcohol.
  • Dehydration/diarrhoeal crises.
  • Metabolic disorders - eg, galactosaemia in children.
135
Q

What are the 3 types of age related cataracts?

A
  • Nuclear sclerosis: formed by new layers of fibre compressing the nucleus of the lens.
  • Cortical: new fibres are added to the outside of the lens, which age and produce cortical spokes. These may not produce symptoms unless on the visual axis or the entire cortex is affected when it is ‘mature’.
  • Posterior subcapsular: opacities in the central posterior cortex. This may occur in younger patients and may cause glare ± deterioration in near vision.
136
Q

Causes of paediatric cataracts?

A
  • Congenital: hereditary/genetic, metabolic (eg, galactosaemia), in-utero infection (toxoplasmosis, other, rubella, cytomegalovirus, herpes simplex (TORCH)).
  • Developmental: genetic, metabolic (eg, galactokinase deficiency).
  • Acquired: metabolic (eg, diabetes mellitus), traumatic, post-radiotherapy.
137
Q

Symptoms of catarcts?

A
  • Gradual painless loss of vision.
  • Difficulties with reading.
  • Failure to recognise faces.
  • Problems watching TV.
  • Diplopia in one eye and haloes (less commonly).
138
Q

Signs of cataracts?

A
  • Opacities can be seen as defects in the red reflex (ophthalmoscope is held 60 cm away)
  • The lens may appear brown or white when a bright light is shone on the eye.
139
Q

Treatment of cataracts?

A

surgical removal

140
Q

Presentation of occlusion of central retinal artery

A
  • Sudden unilateral painless visual loss.
  • vision is usually reduced to counting fingers
  • There may be a history of amaurosis fugax

*In 1-2% of patients, the loss is bilateral

141
Q

Signs of central retinal artery occlusion on examination:

A
  • afferent pupillary defect
  • pale retina with attenuation of the vessels
  • segmentation of the blood column in the arteries (‘cattle-trucking’)
  • centre of the macula (supplied by the intact underlying choroid) stands out as a cherry-red spot.
142
Q

Management of central retinal artery occlusion:

A
  • Firm ocular massage
  • Lowering of intraocular pressure with an an anterior chamber paracentesis +/- acetazolamide
  • Intra-arterial fibrinolysis (still experimental)
143
Q

Presentation of retinal vein occlusion

A
  • unilateral, painless blurred vision,
  • metamorphopsia (image distortion)
  • ± a field defect (usually altitudinal).
  • Visual acuity depends on macula involvement
144
Q

Signs of retinal vein occlusion n fundoscopy?

A
  • vascular dilatation and tortuosity of the affected vessels
  • haemorrhages (Dot, blot, flame) in that area only

*look for an arc of haemorrhages, like a trail left behind a cartoon image of a shooting star*

145
Q

Pathogenesis of diabetic retinopathy (5 processes)

A
  • Microaneurysms - physical weakening of the capillary walls ->leakages.
  • Hard exudates - precipitates of lipoproteins/other proteins leaking from retinal blood vessels.
  • Haemorrhages - rupture of weakened capillaries: dot-blot/’flame’ haemorrhages
  • Cotton wool spots - build-up of axonal debris due to poor axonal metabolism at the margins of ischaemic infarcts.
  • Neovascularisation - an attempt (by residual healthy retina) to revascularise hypoxic retinal tissue.
146
Q

Treatment for diabetic retinopathy:

A
  • Laser treatment:
  • Intravitreal steroids
  • Anti-vascular endothelial growth factor treatments
  • Surgery (vitrectomy if haemorrhage + repair of any retinal detachment)
147
Q

Complications of diabetic retinopathy

A

Vision loss due to:

  • Macular oedema.
  • Macular ischaemia.
  • Vitreous haemorrhage.
  • Tractional retinal detachment.
148
Q

What changes are seen in hypertensive retinopathy?

A
  • Silver wiring (arterioles)
  • AV nipping
  • Tortuous vessels
  • Advanced = microaneurysms, blot hemorrhages and/or flame hemorrhages, cotton wool spots (ischaemic)

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