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Medicine > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is glaucoma?

A
  • Optic nerve damage caused by intraocular pressure rise
  • Due to blockage in aqueous humour trying to escape eye
  • 2 types-> open + closed angle
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2
Q

What is the anterior chamber?

A
  • Between cornea + iris

- Aqueous humour-> gives nutrients to cornea

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3
Q

What is the posterior chamber?

A
  • Between lens and iris

- Aqueous humour

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4
Q

What is aqueous humour?

A
  • Produced by ciliary body
  • Flows around lens and under iris, through trabecular meshwork + into canal of Schlemm
  • Found in anterior and posterior chamber
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5
Q

What is the normal intraocular pressure?

A
  • 10-21mmHg

- Resistance to flow through trabecular meshwork into canal of Schlemm

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6
Q

What is the pathophysiology of open angle glaucoma?

A
  • Gradual increase in resistance through trabecular meshwork
  • Hard for aqueous humour to flow + exit the eye
  • Pressure builds slowly
  • Can cause optic cupping-> optic cup in disc centre becomes larger + wider
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7
Q

What are the risk factors for developing open angle glaucoma?

A
  • Age
  • FH
  • Black
  • Myopia (near sighted)
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8
Q

What is the vitreous chamber?

A
  • Filled with vitreous humour

- Behind lens-> most of eye

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9
Q

How does open angle glaucoma present?

A
  • Asymptomatic + found on screening
  • Tunnel vision (peripheral)
  • Gradual onset
  • Pain, headaches, blurred vision, halos around lights at night
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10
Q

How is intraocular pressure measured?

A
  • Non-contact tonometry machine-> puff of air + measure corneal response
  • Goldmann applanation tonometry-> contact with cornea + more accurate measurement
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11
Q

How is open angle glaucoma diagnosed?

A
  • Goldmann applantation tonometry
  • Fundoscopy-> cupping + nerve health
  • Visual field assessment
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12
Q

How is open angle glaucoma managed?

A
  • Treatment started at >24mmHg
  • Latanaprost-> prostaglandin analogue eye drops (increase uveoscleral outflow)
  • Timolol-> beta-blocker to reduce humour production
  • Dorzolamide or brimonidine
  • Surgery-> trabeculotomy ie new channel + bleb for drainage
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13
Q

What is latanaprost?

A
  • prostaglandin analogue eye drops (increase uveoscleral outflow)
  • used in open angle glaucoma
  • can cause eyelid + iris pigmentation
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14
Q

What is the pathophysiology of acute angle-closure glaucoma?

A
  • Iris bulge forward + seal off trabecular meshwork from anterior chamber
  • Prevents aqueous humour drainage
  • Pressure builds in posterior chamber
  • Iris bulges
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15
Q

What are the risk factors for acute angle-closure glaucoma?

A
  • Age
  • Female
  • Family history
  • Chinese + East Asian (rare in black people)
  • Shallow anterior chamber
  • Medications-> noradrenaline, oxybutynin, amitriptyline
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16
Q

How does acute angle-closure glaucoma present?

A
  • Unwell
  • Severe red eye pain
  • Blurred vision
  • Halos around lights
  • Headache
  • Nausea + vomiting
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17
Q

What examination findings might be present in acute angle-closure glaucoma?

A
  • Red + teary eye
  • Hazy cornea
  • Decreased acuity
  • Dilated/fixed pupil
  • Firm eyeball
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18
Q

How is acute angle-closure glaucoma managed?

A
  • Same day assessment from ophthalmology
  • Lie on back without pillow
  • Pilocarpine eye drops
  • Acetazolamide
  • Timolol (beta-blocker)
  • Hyperosmotic agents-> glycerol or mannitol
  • Laser iridotomy-> laser hole in eye
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19
Q

What are pilocarpine eye drops?

A
  • Act on muscarinic receptors in sphincter muscles of iris-> pupil constriction
  • Miotic agent
  • Ciliary muscle contraction
  • Cause flow of aqueous humour pathway to open
  • Used in acute angle-closure glaucoma
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20
Q

What is acetazolamide?

A
  • Carbonic anhydrase inhibitor
  • Reduces aqueous humour production
  • Used in acute angle-closure glaucoma
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21
Q

What is age-related macular degeneration?

A
  • Degeneration of macula-> part of retina responsible for central + colour vision
  • Dry (90%) or wet (10%)
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22
Q

What does the macula consist of?

A

Central + colour vision…

  • Choroid layer-> BV supply
  • Bruch’s membrane
  • Retinal pigment epithelium
  • Photoreceptors
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23
Q

What is drusen?

A
  • Fundoscopy finding in age-related macular degeneration
  • Deposits of protein + lipids between Bruch’s membrane + retinal pigment epiethlium
  • Larger + greater than normal-> early sign
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24
Q

What is the pathophysiology of wet age-related macular degeneration?

A
  • New vessels grow from choroid layer into retina
  • Due to vascular endothelial growth factor (VEGF)
  • Leak fluid/blood-> oedema + rapid vision loss
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25
Q

What are the risk factors for age-related macular degeneration?

A
  • Older
  • Smoking
  • White
  • Chinese
  • Family history
  • CVD
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26
Q

How does wet age-related macular degeneration present?

A
  • Central visual field loss-> over few days then full over a few years
  • Reduced acuity
  • Crooked/wavy appearance to straight lines
  • Often progress to bilateral
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27
Q

How does dry age-related macular degeneration present?

A
  • Gradual central visual field loss
  • Reduced acuity
  • Crooked/wavy appearance to straight lines
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28
Q

How is age-related macular degeneration investigated?

A
  • Full eye exam
  • Slit lamp biomicroscopic fundus exam
  • Optical coherence tomography (wet)
  • Fluorescein angiography
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29
Q

How is dry age-related macular degeneration managed?

A
  • Ophthalmology referral

- Lifestyle-> smoking, HTN control, vitamin supplements

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30
Q

How is wet age-related macular degeneration managed?

A
  • Ophthalmology referral

- Anti-VEGF meds-> ranibizumab injections

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31
Q

What causes diabetic retinopathy?

A
  • Blood vessels in retina damaged by prolonged exposure to hyperglycaemia
  • Progressive degeneration of retina health
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32
Q

What is the pathophysiology of diabetic retinopathy and its features?

A
  • Hyperglycaemia-> retinal small vessel + endothelial damage
  • Increased vascular permeability-> leakage from BVs, blot haemorrhages
  • Hard exudates-> yellow/white
  • Microanurysms-> weakness in walls causes bulges
  • Venous bleeding-> veins like beads
  • Nerve fibre damage-> cotton wool spots (fluffy white on retina)
  • Intraretinal microvascular abnormalities-> dilated capillaries + can act as shunt
  • Neovascularisation-> GFs released + cause new BV formation
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33
Q

What are some features of diabetic retinopathy?

A
  • Blot haemorrhages
  • Lipid deposits/exudates
  • Microaneurysms
  • Venous bleeding
  • Cotton wool spots
  • Neovascularisation
  • Intraretinal microvascular abnormalities
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34
Q

What are the two categories of diabetic retinopathy?

A
  • Proliferative

- Non-proliferative

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35
Q

What are the categories + features of non-proliferative diabetic retinopathy?

A
  • Mild-> microaneurysms
  • Moderate-> + blot haemorrhages, hard exudates, cotton wool spots, venous bleeding
  • Severe-> blot haemorrhages + microaneurysms in 4 quadrants, venous beating in 2 quadrants, IMRA in any quadrant
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36
Q

What are the features of proliferative diabetic retinopathy?

A
  • Neovascularisation

- Vitreous haemorrhage

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37
Q

What is diabetic maculopathy?

A

Macular oedema + ischaemic maculopathy

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38
Q

What are the complications of diabetic retinopathy?

A
  • Retinal detachment
  • Vitreous haemorrhage
  • Optic neuropathy
  • Cataracts
  • Rebeosis iridis-> new BVs on iris
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39
Q

What is the management of diabetic retinopathy?

A
  • Laser photocoagulation
  • Anti-VEGF-> ranibizumab
  • Vitreoretinal surgery-> severe
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40
Q

What is the pathophysiology of hypertensive retinopathy?

A
  • Damage to small BVs in retina related to systemic HTN

- Develops from chronic or malignant HTN

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41
Q

What are the retinal signs of hypertensive retinopathy?

A
  • Silver/copper wiring-> thick + sclerosed arteriole walls
  • AV nipping
  • Cotton wool spots-> ischaemia + infarction causes nerve fibre damage
  • Hard exudates
  • Retinal haemorrhages
  • Papilloedema-> ischaemia to optic nerve so swells
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42
Q

What is the Keith-Wagener classification?

A

For hypertensive retinopathy…

  • Stage 1-> mild narrowing of arterioles
  • Stage 2-> focal constriction of BVs + AV nicking
  • Stage 3-> cotton-wool patches, exudates, haemorrhages
  • Stage 4-> papilloedema
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43
Q

How is hypertensive retinopathy managed?

A

Control HTN + risk factors-> smoking, lipids etc

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44
Q

What is anterior uveitis?

A
  • Inflammation in anterior part of uvea (iris + ciliary body + choroid)
  • Inflammation + immune cell infiltration of anterior chamber-> floaters
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45
Q

What is the choroid?

A

Layer between retina + sclera all the way around the eye

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46
Q

What can cause anterior uveitis?

A
  • Autoimmune
  • Infection
  • Trauma
  • Ischaemia
  • Malignancy
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47
Q

What is associated with anterior uveitis?

A
  • HLAB27 conditions-> IBD, reactive arthritis, ankylosing spondylitis
  • Chronic-> sarcoidosis, syphilis, Lyme’s, TB, herpes
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48
Q

What is chronic anterior uveitis and how does it present?

A
  • More granulomatous-> increased macrophage infiltration of anterior chamber
  • Less severe than acute
  • Over 3+ months
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49
Q

How does anterior uveitis present?

A
  • Unilateral, spontaneous + without trauma
  • May get flare up if have chronic condition
  • Pain-> dull, on movement
  • Red eye + ciliary flush (red ring)
  • Vision-> reduced acuity, floaters, flashes, photophobia
  • Pupil-> miosis + abnormal shape as adhesions pull
  • Excess lacrimation
  • Hypopyon-> yellow fluid (WBC) in lower iris
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50
Q

How is anterior uveitis managed?

A
  • Same say ophthalmology
  • Steroids
  • Immunosuppressants-> DMARDs, TNF-inhibitors
  • Laser therapy
  • Cyclopentolate or atropine eye drops
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51
Q

How do atropine eye drops work?

A
  • Cycloplegic-mydriatic
  • Paralyse ciliary muscle + dilate pupils
  • Antimuscarinics
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52
Q

What is episcleritis?

A
  • Benign + self-limiting

- Inflammation of episclera-> outer layer of sclera under conjunct

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53
Q

Who is episcleritis most common in?

A
  • Young
  • Middle aged
  • Associated with RA + IBD
  • Not usually infection
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54
Q

How does episcleritis present?

A
  • Acute onset
  • Unilateral
  • None to mild pain
  • Patch of redness in lateral sclera
  • Foreign body sensation
  • Dilated episcleral vessels
  • Watery eye
  • No discharge
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55
Q

How is episcleritis managed?

A
  • Recovers in 1-4 weeks
  • No treatment needed usually
  • Lubricating eye drops
  • Analgesia + cold compression
  • Safety netting
  • Severe-> systemic NSAIDs, topical steroid eye drops
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56
Q

What are cataracts?

A

Lens becomes cloudy + opaque over time due to age + risk factors-> reduced acuity

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57
Q

How does the lens of the eye work?

A
  • Focuses light into eye + retina
  • Held by suspensory ligaments attached to ciliary body
  • Ciliary body relaxes-> increased tension of suspensory ligaments-> lens narrows
  • Nourished by surrounding fluid (no blood supply)
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58
Q

What are the risk factors for cataracts?

A
  • Older age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypoglycaemia
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59
Q

How does cataracts present?

A
  • Asymmetrical reduction + blurring of vision
  • Colour vision change-> brown/yellow
  • Starbursts around lights at night
  • Loss of red reflex
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60
Q

How does vision loss in cataracts compare to loss in other eye conditions?

A
  • Cataracts-> general reduction in acuity + starbursts
  • Glaucoma-> peripheral vision loss + halos round lights
  • Macular degeneration-> central vision loss + wavy/crooked appearance to straight lines
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61
Q

How are cataracts managed?

A
  • None if symptoms manageable

- Surgery-> drill + break lens then remove + implant artificial one

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62
Q

What are the complications of cataract surgery?

A
  • Prevent detection of other pathology eg macular degeneration
  • Poor visual acuity
  • Endophthalmitis-> infection/inflammation of inner eye contents + can cause loss of vision
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63
Q

What causes pupillary constriction?

A
  • Circular muscles in iris
  • Stimulated by parasympathetic nervous system-> travels to eye via CNIII
  • Involved acetylcholine NT
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64
Q

What causes pupil dilation?

A
  • Dilator muscles from inside to outside of iris
  • Stimulated by sympathetic nervous system
  • Adrenaline NT
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65
Q

What can cause an abnormal pupil shape?

A
  • Cataract surgery
  • Trauma
  • Adhesions/scars from infection
  • Anterior uveitis
  • Acute angle closure glaucoma
  • Rubeosis iridis
  • Coloboma
  • Tadpole pupil-> from migraines
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66
Q

What is mydriasis?

A

Dilated pupil

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67
Q

What can cause mydriasis (dilated pupil)?

A
  • CNIII palsy
  • Raised ICP
  • Holmes-Adie syndrome
  • Congenital
  • Trauma
  • Stimulants (cocaine)
  • Anticholinergics
68
Q

What is miosis?

A

Constricted pupil

69
Q

What can cause miosis (constricted pupil)?

A
  • Horner’s
  • Cluster headache
  • Argyll-Robertson pupil (syphillis)
  • Opiates
  • Nicotine
  • Pilocarpine
70
Q

Which way will an eye affected by CNIII palsy look and why?

A
  • Down and out

- Supplies all muscles apart from superior oblique (CNIV) + lateral rectus (CNVI)

71
Q

How does third nerve palsy present?

A
  • Down + out eye (divergent strabismus)
  • Dilated fixed pupil
  • Palsy
  • Ptosis
72
Q

Why do patients with third nerve palsy get ptosis?

A

Supplies levator palpebrae superioris muscle which lifts upper eyelid-> lost in palsy

73
Q

Why do patients with third nerve palsy get dilated fixed pupil?

A

Parasympathetic fibres to sphincter muscles of iris act to constrict pupil-> lost in CNIII palsy

74
Q

What can cause third nerve palsy (with pupil sparing)?

A

Microvascular-> DM, HTN, ischaemia

75
Q

What can cause third nerve palsy (with full compression)?

A
  • Cavernous sinus thrombosis
  • Posterior communicating artery aneurysm
  • Idiopathic
  • Tumour
  • Trauma
  • Raised ICP
76
Q

What causes Holmes-Adie pupil?

A

Damage to post-ganglionic PSNS fibres

77
Q

How does Holmes-Adie pupil present?

A
  • Unilateral dilated pupil
  • Sluggish to react to light
  • Slow dilation after constriction
  • Smaller over time
78
Q

What causes Argyll-Robertson pupil?

A

Neurosyphillis

79
Q

How does Argyll-Robertson pupil present?

A
  • Constricted pupil that accommodates to near object but doesn’t react to light
  • History of neurosyphillis
80
Q

What is the pathophysiology of Horner’s syndrome?

A

Sympathetic nerve damage to nerves supplying the face

81
Q

Where do the sympathetic nerves that are affected by Horner’s syndrome run?

A
  • Start in spinal cord in chest as pre-ganglionic nerves
  • Into sympathetic ganglion (at base of neck)
  • Post ganglionic nerves run alongside internal carotid artery
82
Q

How does Horner’s syndrome present?

A
  • Ptosis
  • Miosis
  • Anhidrosis
83
Q

How can the location of the cause of Horner’s syndrome be determined?

A

Anhidrosis…

  • Central lesion-> arm + trunk
  • Pre-ganglionic-> face
  • Post-ganglionic-> none
84
Q

What are the causes of Horner’s syndrome?

A
  • Central lesions (4Ss)-> stroke, MS, swelling (tumour), syringomyelia
  • Pre-ganglionic (4Ts)-> tumour (pancoast’s), trauma, thyroidectomy, top rib (cervical)
  • Post-ganglionic (4Cs)-> carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache
  • Congenital
85
Q

What is associated with congenital Horner’s syndrome?

A

Heterochromia (different coloured eyes)

86
Q

How is Horner’s syndrome investigated?

A

Cocaine eye drops…

  • Stop noradrenaline re-uptake at NMJ + normal eye dilates (more NA to stimulate iris dilator muscles)
  • Horner’s-> nerves don’t release NA-> blocking makes to difference-> no reaction
87
Q

What is blepharitis?

A

Inflammation of eyelid margins

88
Q

What causes blepharitis?

A
  • Meibomian gland dysfunction (secrete oil onto eye surface)

- Inflammation of eyelid margins

89
Q

What are the symptoms of blepharitis?

A

Gritty, itchy, dry, can cause styes + chalazions

90
Q

How is blepharitis managed?

A
  • Hot compresses
  • Gentle cleaning
  • Hypromellose eye drops
91
Q

What is a stye?

A
  • Hodeolum externum-> gland of Zeis (sebaceous at eyelash base) or glands of Moll (sweat at eyelash base) infection
  • Hordeolum internum-> Meibomian gland infection
92
Q

How do styes present?

A
  • Hodeolum externum-> red + tender lump along eyelash base +/- pus
  • Hordeolum internum-> deep + more painful, may point in towards eyeball
93
Q

What is a chalazion?

A

Meibomian gland blocks + swells-> cyst

94
Q

What are the symptoms of a chalazion?

A
  • Swelling
  • Non tender
  • Red
95
Q

How is chalazion treated?

A
  • Hot compress
  • Analgesia
  • Chloramphenicol
  • Surgical drainage
96
Q

What is entropion?

A

Eyelid turns in with lashes against eyeball

97
Q

How does entropion present?

A
  • Eyelid turns in with lashes against eyeball
  • Pain
  • Corneal damage + ulcers
98
Q

How is entropion managed?

A
  • Tape eyelid down
  • Eye drops
  • Surgery
  • Same day referral if sight risk
99
Q

What is ectropion?

A

Eyelid turns outwards with inner lid exposed

100
Q

What is the complication of ectropion?

A

Exposure keratopathy

101
Q

How is ectropion managed?

A
  • None
  • Regular drops
  • Surgery
  • Same day referral if sight risk
102
Q

What is trichiasis?

A

Inward growth of eyelashes

103
Q

How does trichiasis present?

A
  • Inward growth of eyelashes
  • Pain
  • Corneal damage
  • Ulcers
104
Q

How is trichiasis managed?

A
  • Epilation-> removal of eyelashes
  • Electrolysis
  • Cryotherapy
  • Laser-> prevent regrowth
  • Same day referral is sight risk
105
Q

What is periorbital cellulitis?

A

Eyelid and skin infection in front of orbital septum

106
Q

How does periorbital cellulitis present?

A
  • Swelling
  • Hot & red skin
  • Around the eye
107
Q

What investigation should be done in periorbital cellulitis?

A

CT-> rule out orbital cellulitis

108
Q

How is periorbital cellulitis managed?

A
  • Systemic antibiotics

- Admission-> if suspect/risk of orbital cellulitis (eg kids)

109
Q

What is orbital cellulitis?

A

Infection around eyeball + tissues behind orbital septum

110
Q

How does orbital cellulitis present?

A
  • Pain on eye movement
  • Reduced movement
  • Change in vision
  • Abnormal pupil reaction
  • Proptosis (eyeball moves forward)
111
Q

How is orbital cellulitis managed?

A
  • Admission
  • IV antibiotics
  • Surgical drainage if abscess
112
Q

What is conjunctivitis?

A

Inflammation of conjunctiva (thin tissue covering inside of eyelids + sclera)

113
Q

What are the three types of conjunctivitis?

A
  • Bacterial
  • Viral
  • Allergic
114
Q

How does conjunctivitis present (in general)?

A
  • Uni or bilateral
  • Red
  • Bloodshot
  • Itchy
  • Gritty
  • Discharge
  • NOT pain, photophobia or reduced acuity
115
Q

How does bacterial conjunctivitis present?

A
  • Uni or bilateral (spread to other eye)
  • Red
  • Bloodshot
  • Itchy
  • Gritty
  • Discharge-> purulent
  • Worse on a morning-> eyes stuck together
  • Highly contagious
116
Q

How does viral conjunctivitis present?

A
  • Uni or bilateral
  • Red
  • Bloodshot
  • Itchy
  • Gritty
  • Discharge-> clear
  • Associated-> cough, sore throat, tender preauricular lymph nodes
  • Contagious
117
Q

What are the differentials for painful red eye?

A
  • Glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions
  • Ulcers
  • Keratitis
  • Foreign body
  • trauma
  • Chemical injury
118
Q

What are the differentials for painless red eye?

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
119
Q

How is conjunctivitis managed (in general)?

A
  • Usually resolves in 1-2 weeks
  • Good hygiene + avoiding contact lenses
  • Sterile water cleaning
120
Q

How is bacterial conjunctivitis managed?

A
  • Good hygiene
  • Chloramphenicol
  • Fuscidic acid
121
Q

What should happen if a neonate (<1 month) presents with conjunctivitis?

A

Urgent review-> may be gonococcal + lead to sight loss/pneumonia

122
Q

How does allergic conjunctivitis present?

A
  • Swelling of conjunctival sac + eyelid
  • Discharge
  • Itch
123
Q

How is allergic conjunctivitis treated?

A
  • Antihistamines

- Mast-cell stabilisers for few weeks (chronic/seasonal)

124
Q

What is scleritis?

A

Inflammation of full thickness of sclera-> not infection usually + more serious

125
Q

What are the complications of scleritis?

A
  • Necrosis
  • Perforation
  • Visual impairment
126
Q

What conditions are associated with scleritis?

A

RA, SLE, IBD, sarcoidosis, granulomatosis + polyangiitis

127
Q

How does scleritis present?

A
  • Acute
  • 50% bilateral
  • Severe pain worsened by movement
  • Photophobia
  • Watery eye
  • Reduced acuity
  • Abnormal pupil reactions
  • Tender on palpation
128
Q

How is scleritis managed?

A
  • Sam day ophthalmology
  • Topical or systemic steroids
  • NSAIDs
  • Immunosuppressant relevant to underlying condition
129
Q

What can cause corneal abrasions?

A
  • Contact lens
  • Foreign body
  • Nails
  • Eyelashes
  • Entropion (eyelid inward)
130
Q

What can corneal abrasions caused by contact lenses be associated with?

A

Pseudomonas infection

131
Q

How does corneal abrasion present?

A
  • History
  • Painful red eye
  • foreign body sensation
  • Watery
  • Blurred vision
  • Photophobia
132
Q

How is corneal abrasion diagnosed?

A

Fluorescein stain + slit lamp exam

133
Q

How is corneal abrasion managed?

A
  • Same day ophthalmology
  • Analgesia
  • Lubricating eye drops
  • Chloramphenicol
  • Review in 1 week
  • Often heal in 2-3 days
134
Q

What is herpes keratitis?

A

Inflammation of the cornea (especially epithelial layer) due to herpes simplex

135
Q

What can cause keratitis (inflammation of the cornea)?

A
  • Herpes simplex (most common)
  • Bacteria-> pseudomonas, staph
  • Fungus
  • Contact lens
  • Exposure keratitis
136
Q

What complications can occur in keratitis and when?

A

If inflammation to stroma (between epithelium + endothelium)…

  • Stromal necrosis
  • Vascularisation
  • Scarring
  • Blindness
137
Q

How does herpes keratitis present?

A
  • Painful red eye
  • Photophobia
  • Vesicles around eye
  • Foreign body sensation
  • Watery
  • Reduced acuity
138
Q

How is herpes keratitis diagnosed?

A
  • Fluorescein stain-> dentritic (branched/spreading) corneal ulcer
  • Slit lamp exam
  • Corneal swabs/scraping-> culture/PCR
139
Q

How is herpes keratitis managed?

A
  • Same day assessment
  • Acyclovir
  • Ganciclovir gel
  • Topical steroids
  • Corneal transplant-> eg when scarred + resolved
140
Q

What is subconjunctival haemorrhage?

A

Small vessels in conjunctiva ruptures causing blood to accumulate between sclera + conjunctiva

141
Q

What causes subconjunctival haemorrhage?

A
  • Triggers-> heavy coughing, weight lifting, trauma
  • Idiopathic
  • HTN
  • Bleeding disorder
  • Whooping cough
  • Warfarin + DOACs
  • Non-accidental injury
142
Q

How does subconjunctival haemorrhage present?

A
  • Bright red blood patch covering eye
  • Painless
  • Not affect vision
  • Often triggered by something
143
Q

How is subconjunctival haemorrhage managed?

A
  • Resolves in 2 weeks approx
  • Address causes
  • Lubricating eye drops
144
Q

What is the pathophysiology of posterior vitreous detachment?

A
  • Vitreous body-> gel in eye to keep retina pressed on choroid
  • Less firm as get older
  • In posterior vitreous detachment-> gel comes away from retina
145
Q

How does posterior vitreous detachment present?

A
  • Painless
  • Spots of vision loss
  • Floaters
  • Flashing lights
146
Q

How is posterior vitreous detachment managed?

A
  • None-> vision improves as brain adjusts

- Retinal tear/detachment risk-> need urgent assessment if suspect

147
Q

What causes retinal detachment?

A
  • Retina separates from choroid

- Usually retinal tear-> lets vitreous fluid out under retina + fills space

148
Q

Why is retinal detachment a sight-threatening emergency?

A

Outer retina relies on choroid vessels for supply-> may die if too long

149
Q

What are the risk factors for retinal detachment?

A
  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Trauma
  • Retinal malignancy
  • Older
  • Family history
150
Q

How does retinal detachment present?

A
  • Flashes/floaters
  • Peripheral vision loss
  • Blurred/distorted vision
151
Q

How is retinal detachment managed?

A
  • Immediate referral
  • Tears-> adhesion via laser/cryotherapy
  • Reattachment
  • Vitrectomy + replacement
  • Scleral buckling
  • Pneumatic retinoplexy
152
Q

What is the pathophysiology of retinal vein occlusion?

A
  • Thrombus in retinal veins-> block blood draining from retina
  • Fluid + blood leaks-> macular oedema + retinal haemorrhage
  • Causes tissue damage in retina + loss of vision
  • Central vein through optic nerve made from 4 branches-> not as bad if branch thrombus
153
Q

How does retinal vein occlusion present?

A

Sudden painless loss of vision

154
Q

What are risk factors for retinal vein occlusion?

A
  • HTN
  • High cholesterol
  • DM
  • Smoking
  • Glaucoma
  • SLE
155
Q

What fundoscopy findings might be present in retinal vein occlusion?

A
  • Flame + blot haemorrhages
  • Optic disc oedema
  • Macular oedema
156
Q

How is retinal vein occlusion managed?

A
  • Immediate referral
  • Laser photocoagulation
  • Intravitreal steroids
  • Anti-VEGF (eg ranibizumab)
157
Q

What is the blood supply to the retina?

A

Internal carotid artery-> opthalmic artery-> central retinal artery

158
Q

What causes central retinal artery occlusion?

A

Blockage from artherosclerosis or vasculitis (giant cell arteritis)

159
Q

What are the risk factors for central retinal artery occlusion?

A
  • General-> older, FH, smoking, alcohol, HTN, DM, obesity

- Secondary to GCA-> over 50, female, polymyalgia rheumatica

160
Q

How does central retinal artery occlusion present?

A
  • Sudden painless loss of vision

- Relative afferent pupillary defect

161
Q

What is relative afferent pupillary defect?

A
  • Pupil in affected eye constricts more when light shone in other eye
  • Normal retina senses consensual light reflex
  • Indicates CNII problem (light signal not going in properly)
162
Q

What fundoscopy signs might be present in central retinal artery occlusion?

A
  • Pale retina-> lack of perfusion

- Cherry red spot-> macula thinner + shows red choroid below

163
Q

How is central retinal artery occlusion managed?

A
  • Immediate referal
  • Test for GCA-> ESR + temporal artery biopsy
  • Ocular massage-> try dislodge thrombus
  • Inhaled carbogen
  • Isosorbide mononitrate
  • 2ndary prevention of CVD
164
Q

What is retinitis pigmentosum?

A

Congenital and inherited degeneration of rods + cones-> isolated or with systemic disease

165
Q

How does retinitis pigmentosum present?

A
  • Often in childhood
  • Night blindness
  • Decreased vision-> peripheral then central
166
Q

What fundoscopy findings might be present in retinitis pigmentosum?

A
  • Bone spicule pigmentation-> bone matrix appearance mostly in mid-peripheral retina
  • Narrow arterioles
  • Waxy/pale optic disc
167
Q

How is retinitis pigmentosum managed?

A
  • Referral
  • Genetic counselling
  • Vision aids
  • Driving limits
  • Regular follow up

Medicine (13 decks)

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