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Opthalmology > Passmedicine > Flashcards

Passmedicine Flashcards

1
Q

What is orbital cellulitis?

A

Infection of fat and muscle posterior to the orbital septum within the orbit but not involving the globe

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2
Q

What tends to cause orbital cellulitis?

A

Spreading URTI from sinuses

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3
Q

How is orbital cellulitis managed?

A

Medical emergency req. hospital admission + urgent senior RV

Req. IV antibx

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4
Q

What is periorbital cellulitis?

A

Aka. preseptal cellulitis

Less serious infection anterior to orbital septum, due to superficial injury (e.g. chalazion, insect bite etc.)

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5
Q

What can periorbital cellulitis progress to?

A

Orbital cellulitis

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6
Q

What are risk factors for orbital cellulitis?

A 
Childhood
Prev. sinus infection 
Lack of Hib vaccination 
Recent eyelid infection/insect bite on eyelid (periorbital cellulitis)
Ear or facial infection
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7
Q

How does orbital cellulitis present?

A 
Redness/swelling around eye
Severe ocular pain 
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema + ptosis
Drowsiness, NV in meningeal involvement
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8
Q

How do you differentiate orbital from periorbital cellulitis?

A

Reduced visual acuity, proptosis, ophthalmoplegia/pain w eye movement are NOT consistent with preseptal cellulitis

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9
Q

What investigations should you do for orbital cellulitis and what results will they find?

A

FBC - WBC raised, raised inflammatory markers
CT with contrast scan of orbits, sinuses and brain - inflammation of orbital tissues deep to septum, sinusitis
Blood culture + microbiological swab to determine organism

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10
Q

What are the most common causes of orbital cellulitis?

A

Streptococcus
Staphylococcus aureus
Hib

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11
Q

What things will you see on Ex with orbital cellulitis?

A 
Decreased vision 
Afferent pupillary defect
Proptosis
Dysmotility
Oedema
Erythema
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12
Q

What are causes of optic neuritis?

A

MS
DM
Syphilis

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13
Q

What are the features of optic neuritis?

A

Unilateral decrease in visual acuity over days-hrs
Poor discrimination of colours, red desaturation
Pain worse on eye movement
Relative afferent pupillary defect
Central scotoma

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14
Q

How do you manage optic neuritis?

A

High dose steroids

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15
Q

How long does recovery from optic neuritis normally take?

A

4-6 weeks

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16
Q

If >3 white matter lesions are found on MRI what is the risk of developing MS in the next 5 years?

A

50%

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17
Q

What is optic neuritis very commonly the first presentation of?

A

MS

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18
Q

What are cataracts?

A

Condition of eye where lens gradually opacifies, i.e. becomes cloudy

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19
Q

What does the opacification of the lens in cataracts mean?

A

It’s more difficult for light to reach the retina –> reduced/blurred vision

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20
Q

What is the leading cause of curable blindness world wide?

A

Cataracts

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21
Q

What % of >65yos have a visually impairing cataract in 1 or both eyes?

A

30%

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22
Q

What is the commonest cause of cataracts?

A

Normal ageing

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23
Q

What are other causes of cataracts?

A 
Smoking
Increased alcohol consumption 
Trauma
DM
Long term corticosteroids
Radiation exposure
Myotonic dystrophy
Hypocalcaemia
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24
Q

What is a typical presentation of cataracts?

A

Gradual onset of reduced vision, faded colour vision (difficulty distinguishing colours), glare and halos around lights

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25
Q

What is glare?

A

Lights appearing brighter than they are

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26
Q

What are signs of cataracts?

A

Red reflex defect (cataracts prevent light getting to retina)

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27
Q

What investigations should be done for suspected cataracts?

A

Ophthalmoscopy after pupil dilatation (should have normal fundus + optic n)

Slit lamp examination will identify visible cataract

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28
Q

What are the different types of cataracts?

A

Nuclear
Polar
Subcapsular
Dot opacities

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29
Q

What is a nuclear cataract?

A

Forms in the nucleus (centre of lens)
Changes lens refractive index
Common in old age

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30
Q

What is a polar cataract?

A

Localised opacity
Commonly inherited
Lie in visual axis

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31
Q

What is a subcapsular cataract?

A

Lie just deep to lens capsule in visual axis

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32
Q

What most commonly causes subcapsular cataracts?

A

Steroid use

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33
Q

In which patients are dot opacity cataracts most commonly seen?

A

Common in normal lenses, diabetics, myotonic dystrophy

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34
Q

How are cataracts managed non-surgically?

A

Early stages - age related cataracts managed with stronger glasses/contact lenses, using brighter lighting (optimises vision but doesn’t slow down cataract progression, surgery will be needed eventually)

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35
Q

What is the surgical management of cataracts?

A

Removal of cloudy lens and replacement with artificial lens

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36
Q

When should individuals be referred for cataract surgery?

A

If visual impairment present, impact on quality of life and patient wishes to have surgery

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37
Q

What information should patients be provided with before cataract surgery?

A

Information on the refractive implications of various types of intraocular lenses

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38
Q

What information should patients be provided with after cataract surgery?

A

Advise on the use of eye drops and eyewear

What to do if vision changes + management of other ocular problems

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39
Q

How successful is cataract surgery?

A

85-90%

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40
Q

What are post-surgical complications of cataract

surgery?

A

Posterior capsule opacification (thickening of lens capsule)
Retinal detachment
Posterior capsule rupture
Endopthalmitis

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41
Q

What is endopthalmitis?

A

Inflammation of aqueous +/- vitreous humour

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42
Q

Why is it important to do a contrast CT scan of orbits, sinuses and brain in those presenting with orbital cellulitis?

A

Support the diagnosis

Search for possible complications, e.g. abscesses which may req. surgical drainage

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43
Q

What is the commonest cause of blindness in the UK?

A

Age related macular degeneration

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44
Q

What occurs in age related macular degeneration?

A

Degradation of the central retina (macula)

Features usually bilateral

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45
Q

What is ARMD characterised by?

A

Degeneration of the retinal photoreceptors –> formation of drusen

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46
Q

What can you use to see drusen?

A

Fundoscopy, retinal photography

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47
Q

What was the traditional classification of ARMD?

A

Dry + wet

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48
Q

What are the features of dry ARMD and how common is it?

A

90%

Geographic atrophy, drusen, yellow round spots in Bruch’s membrane

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49
Q

What are the features of wet ARMD and how common is it?

A

10%
Exudative
Choroidal neovascularisation, leakage of serous fluid + blood
Can lead to rapid loss in vision

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50
Q

Of wet and dry ARMD which has the worse prognosis?

A

Wet

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51
Q

What is the more updated classification of ARMD?

A

Early ARMD - non-exudative, age related: drusen + alterations to retinal pigment epithelium

Late ARMD - neovascularisation, exudative

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52
Q

What is the average age of presentation of ARMD?

A

70y

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53
Q

What are risk factors for ARDM?

A 
Advanced age - biggest RF (>75)
Smoking 
FH
Hypertension
Dyslipidaemia
DM
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54
Q

How does ARMD typically present?

A

Reduction in visual acuity, particularly for near field objects
Difficulties in dark adaption, poor vision at night
Fluctuations in visual disturbance (varies from day to day)
Photopsia (flickering/flashing lights, glare around objects)

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55
Q

What sign may be seen in ARMD?

A

Distortion of line perception on Amsler grid testing

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56
Q

What changes may be seen in dry ARMD on fundoscopy?

A

Drusen, yellow areas of pigment deposition in macular area which later may become confluent and scar

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57
Q

What changes may be seen in wet ARMD on fundoscopy?

A

Well demarcated red patches (may be intra-retinal/sub-retinal fluid leakage or haemorrhage)

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58
Q

What is the investigation of choice in ARMD?

A

Slit lamp microscopy (will identify pigmentary, exudative or haemorrhagic changes)
Usually accompanied w. colour fundus photography so have a baseline to identify future changes against

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59
Q

What investigations should be done in neovascular ARDM?

A

Fluorescein angiography (to guide intervention with anti-VEGF therapy)

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60
Q

What other investigation may be done in ARMD?

A

Ocular coherence tomography (look at retina in 3D and reveal areas of dx not seen by microscopy)

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61
Q

What is the management of dry ARMD?

A

Zinc, vitamin A, C, E (to reduce dx progression)

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62
Q

What is the management of wet ARMD?

A

Anti-VEGF - can stabilise/reverse visual loss

Start within first 2m of diagnosis if possible

Laser photocoagulation slows progression of ARMD where neovascularisation is present but risk of acute visual loss after Rx so anti-VEGF preferred

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63
Q

Give e.g.s of anti-VEGF agents

A

Ranibizumab, bevacizumab, pegaptanib

Given 4wkly by injection

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64
Q

What is papilloedema?

A

Swelling of optic disc caused by increased intracranial pressure

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65
Q

What are the features of papilloedema on fundoscopy?

A 
Usually bilateral 
Venous engorgement first sign
Loss of venous pulsation 
Blurring of optic disc margin
Elevation of optic disc
Loss of optic cuo
Paton's lines
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66
Q

What are Paton’s lines?

A

Concentric/radial retinal lines cascading from optic disc due to papilloedema

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67
Q

What causes papilloedema?

A 
Space occupying lesion - neoplastic/vascular
Malignant hypertension
Idiopathic intracranial hypertension
Hydrocephalus
Hypercapnia

rare: hypoparathroidism, hypocalcaemia, vit A toxicity

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68
Q

What is a classic history of raised intracranial pressure?

A

Headache worse in the morning associated with blurred vision and vomiting

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69
Q

What is the pathophysiology of primary open angle glaucoma?

A

Iris is clear of the meshwork, trabecular network functionally offers an increased resistance to aqueous flow –> raised intraocular pressure

(basically slow clogging of trabecular meshwork)

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70
Q

What are the causes of primary open angle glaucoma?

A

Increased age

Genetics

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71
Q

What are the symptoms of primary open angle glaucoma?

A

Slow rise in intraocular pressure (asymptomatic for long time)
Typically present following an ocular pressure measurement during routine ex by optometrist

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72
Q

What are the signs of a primary open angle glaucoma?

A

Increased intraocular pressure
Visual field defect
Pathological cupping of optic disc

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73
Q

What are glaucomas?

A

Group of eye diseases characterised by increased intraocular pressure which if left untreated can lead to pressure on the optic nerve and blindness

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74
Q

Describe the path which aqueous humour usually takes in the eye

A

AH secreted by ciliary epithelium, travels in space between lens and iris and into the trabecular network (like a spongey drain), this funnels the AH into the canal of schlemm and then into aqueous veins then into episcleral veins

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75
Q

What is the pathophysiology of glaucoma?

A

AH drainage pathway becomes blocked –> increased pressure in ant. chamber eye –> optic nerve damage –> vision loss

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76
Q

Define intraocular pressure

A

Pressure >21mmHg

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77
Q

What is the most common type of glaucoma?

A

Open angle

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78
Q

What kind of vision loss do you get with primary open angle glaucoma?

A

Initially peripheral vision loss, as pressure increases which can lead to loss in central vision as well

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79
Q

What is the pathophysiology of closed angle glaucoma?

A

Angle between iris and cornea too small, so passage for AH outflow is too narrow

Due to lens being pushed against iris –> rapid build up on intraocular pressure and symptoms

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80
Q

What investigations should be done for suspected primary open angle glaucoma?

A

Automated perimetry to assess visual field
Slit lamp ex with pupil dilatation to assess optic n. + fundus for baseline
Applanation tonometry to measure IOP
Central corneal thickness measurement
Gonioscopy to assess peripheral anterior chamber configuration + depth
Assess risk of future visual impairment

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81
Q

How do you assess risk of future visual impairment?

A

Assess risk factors e.g. IOP, central corneal thickness, FH, life expectancy

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82
Q

How are the majority of patients with primary open angle glaucoma managed?

A

Eye drops that lower IOP

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83
Q

What is the 1st line Rx for primary open angle glaucoma?

A

Prostaglandin analogue eye drop

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84
Q

What is the 2nd line Rx for primary open angle glaucoma?

A

Beta-blocker, carbonic anhydrase inhibitor or sympathomimetic eyedrop

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85
Q

What are treatment options for more advanced primary open angle glaucoma?

A

Surgery/laser Rx

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86
Q

Why is reassessment essential in primary open angle glaucoma?

A

Exclude progression + visual fiel loss

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87
Q

Which patients who have had primary open angle glaucoma need more frequent reassessment?

A

If IOP uncontrolled, patient high risk or there is progression

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88
Q

Give an example of a prostaglandin analogue

A

Latanoprost

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89
Q

How do prostaglandin analogues work in the treatment of primary open angle glaucoma?

A

Increase uveoscleral outflow

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90
Q

What are SEs of latanoprost?

A

Brown pigmentation of iris, increased eyelash length

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91
Q

How do beta blockers work in the treatment of primary open angle glaucoma?

A

Reduce aqueous production

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92
Q

What beta blockers are used to treat primary open angle glaucoma?

A

Timolol, betaxolol

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93
Q

What patients should you not use timolol in for treatment of primary open angle glaucoma?

A

Asthmatics, those with heart block

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94
Q

How do sympathomimetics work in treating primary open angle glaucoma?

A

Reduces aqueous production + increases outflow

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95
Q

Give an e.g. of a symphathomimetic used to treat primary open angle glaucoma

A

Brimonidine (alpha2-adrenoceptor agonist)

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96
Q

What are SEs of brimonidine?

A

Hyperaemia

Cannot be used with MAOI/TCAs

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97
Q

How do carbonic anhydrase inhibitors work in treating primary open angle glaucoma?

A

Reduce aqueous production

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98
Q

How do miotics work in treating primary open angle glaucoma?

A

Increases uveoscleral outflow

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99
Q

Give an e.g. of a carbonic anhydrase inhibitor

A

Dorzolamide

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100
Q

Give an e.g. of a miotic

A

Pilocarpine (muscarinic receptor agonist)

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101
Q

What are SEs of carbonic anhydrase inhibitors?

A

Systemic absorption may –> sulphonamide-like reactions

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102
Q

What are SEs of miotic agents?

A

Constricted pupil, headache, blurred vision

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103
Q

What kind of surgery may be offered for refractory primary open angle glaucoma?

A

Trabeculectomy

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104
Q

What features are associated with episcleritis?

A

Red eye
Classically not painful (maybe mildly painful)
watering
Mild photophobia

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105
Q

How can you differentiate between episcleritis and scleritis?

A

Phenylephrine drops - blanches episceral vessels but not scleral, so if redness improves after phenylephrine –> episcleritis

Clinically - scleritis usually painful, episcleritis usually not

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106
Q

How is episcleritis managed?

A

Conservative, e.g. NSAIDs/steroids (resistant cases)

Artificial tears

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107
Q

Define mydriasis

A

Dilated pupil

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108
Q

What can cause mydriasis?

A 
Third nerve palsy 
Holmes-Aldie pupil
Traumatic iridoplegia
Pheochromocytoma 
Congenital
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109
Q

What drugs can cause mydriasis?

A

Topical mydriatics: tropicamide, atropine
Sympathomimetic drugs: amphetamines, cocaine
Anticholingeric drugs: TCAs

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110
Q

What tend to be the causes of Argyll-Roberston pupil?

A

DM

Syphillis

111
Q

What are the features of Argyll-Robertson pupil?

A

Small irregular pupils, no response to light but response to accommodate

ARP - accommodation reflex present, PRA - pupillary reflex absent

112
Q

What is the first line treatment of primary open angle glaucoma in those with asthma?

A

Latanoprost

113
Q

Define blepharitis

A

Inflammation of eyelid margins typically leading to red eye

114
Q

Define stye

A

Infection of glands of eyelid

115
Q

Define chalazion

A

Retention cyst of the Meibomian gland

116
Q

Define entropion

A

In-turning of the eyelids

117
Q

Define ectropion

A

Out-turning of the eyelids

118
Q

What are the different types of styes?

A

External (hordeolum externum)

Internal (hordeolum intenum)

119
Q

What causes a hordeolum externum?

A

Infection (usually staph) of gland of Zeis (sebum producing) or glands of Moll (sweat glands)

120
Q

What causes a hordeolum internum?

A

Infection of Meibomian glands

May leave residual chalazion

121
Q

What is involved in the management of s tye?

A

Hot compresses
Analgesia
Topical antibx ONLY if assoc. conjunctivitis

122
Q

How does a chalazion present?

A

Firm, painless lump in eyelid

123
Q

How do you manage a chalazion?

A

Usually resolve spontaneously

Sometimes req. surgical drainage

124
Q

How can an ectropion/entropion present?

A

Watering and pain in affected eye

125
Q

What is the other name for anterior uveitis?

A

Iritis

126
Q

What is anterior uveitis?

A

Inflammation of the anterior portion of the uvea (iris + ciliary body)

127
Q

What HLA allele is anterior uveitis associated with?

A

HLA-B27

128
Q

What are the features of anterior uveitis?

A 
Acute onset
Ocular discomfort + pain (may increase with use) 
Pupil may be small + irregular 
Intense photophobia
Blurred eye
Red eye
Lacrimation
Ciliary flush
Hypopyon
Visual acuity initially normal -->. impaired
129
Q

What is hypopyon?

A

Pus and inflammatory cells in the anterior chamber often resulting in a visible fluid level

130
Q

What conditions are associated with anterior uveitis?

A 
Ankylosing spondylitis
Reactive arthritis
Ulcerative colitis, Crohn's disease
Behcet's disease
Sarcoidosis: bilateral disease may be seen
131
Q

How do you manage anterior uveitis?

A

Urgent ophthalmology RV
Cyloplegics
Steroid eye drops

132
Q

What are cytoplegics?

A

Substances that dilate the pupil and help to relieve pain + photophobia

133
Q

Give e.g.s of cytoplegics

A

Atropine, cyclopentolate

134
Q

What are slit lamp findings for anterior uveitis?

A

Keratic precipitates, flares, hypopyon, posterior synechiae

135
Q

What is the name of the classification system used for hypertensive retinopathy?

A

Keith-Wagener

136
Q

What is the classification of hypertensive retinopathy?

A

Stage 1 - arteriolar narrowing + tortuosity, increased light reflex, silver wiring

Stage 2 - AV nipping

Stage 3 - cotton wool exudates, flame + blot haemorrhages

Stage 4 - papilloedema

137
Q

What causes diabetic retinopathy?

A

Hyperglycaemia –> increased retinal blood flow + abnormal metabolism in retinal vessel walls –> damage to endothelial cells + pericytes –> endothelial dysfunction –> increased vascular permeability

Pericyte dysfunction –> microaneurysm formation

Neovasculisation is due to production of growth factors in response to retinal ischaemia

138
Q

What was the traditional classification of diabetic retinopathy?

A

Background retinopathy - microaneurysms, blot haemorrhages (=< 3), hard exudates

Pre-proliferative retinopathy - cotton wool spots, >3 blot haemorrhages, venous beading/looping, deep/dark cluster haemorrhages, commoner in T1DM

139
Q

What is the new classification of diabetic retinopathy?

A

Split into non-proliferative diabetic retinopathy and proliferative diabetic retinopathy

Mild NPDR
1 or more microaneurysm

Moderate NPDR
microaneurysms
blot haemorrhages 
hard exudates
cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant

Proliferative retinopathy
Retinal neovascularisation (may lead to vitreous haemorrhage), fibrous tissue forming anterior to retinal disc, more common in T1
140
Q

What is maculopathy based on?

A

Location as opposed to severity, anything is potentially serious

141
Q

What does maculopathy look like?

A

Hard exudates + other background changes on macula

142
Q

In which type of diabetes is maculopathy more common?

A

T2

143
Q

What is herpes zoster ophthalmicus?

A

Reactivation of varicella zoster virus in area supplied by ophthalmic division of trigeminal nerve

144
Q

What are the features of HZO?

A

Vesicular rash around eye, may or may not involve eye

145
Q

What is Hutchinson’s sign?

A

Rash on tip/side of nose

Indicates nasociliary involvement and strong risk factor for ocular involvement (anterior uveitis)

146
Q

How do you manage HZO?

A

Oral antivirals 7-10d
Started wi 72h
IV antivirals if severe infection/pt immunocompromised
Topical corticosteroids for inflammation of eye
Ocular involvement req. urgent ophthalmology RV

147
Q

What are the complications of HZO?

A

Oocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-herpetic neuralgia

148
Q

What are the features of allergic conjunctivitis?

A

Bilateral symptoms conjunctival erythema and swelling (chemosis)
Itch
Eyelids may be swollen
Hx of atopy/may be seasonal or perennial

149
Q

What allergens may cause seasonal allergic conjunctivitis?

A

Pollen

150
Q

What allergens may cause perennial conjunctivitis?

A

Dust mites, washing powder

151
Q

What is 1st line treatment for allergic conjunctivitis?

A

Topical antihistamines

Systemic antihistamines if other symptoms, e.g. rhinosinusitis

152
Q

What is 2nd line treatment for allergic conjunctivitis?

A

Topical mast cell stabilisers, e.g. sodium cromoglicate/nedocromil

153
Q

Define transient monocular visual loss

A

Sudden, transient loss of vision lasting less than 24h

154
Q

What are the most common causes of sudden painless loss of vision?

A

Ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis, this includes central retinal artery and vein occlusions)

Vitreous haemorrhage

Retinal detachment

Retinal migraine

155
Q

What is amaurosis fugax?

A

Temporary painless sudden loss in vision that is due to a vascular cause

156
Q

What can cause amaurosis fugax?

A

Large artery dx e.g. atherothrombosis, embolism, dissection
Small artery disease, e.g. anterior ischaemic optic neuropathy or vascularitis, e.g. TA

May be due to a TIA (should be treated with 300mg aspirin)

157
Q

How does amaurosis fugax commonly present?

A

Curtain coming down

158
Q

What causes ischaemic optic neuropathy?

A

Occlusion of the short posterior ciliary arteries causing damage to the optic nerve

159
Q

What can cause central retinal vein occlusion?

A

Glaucoma
Polycythaemia
HTN

160
Q

What is seen on fundoscopy in central retinal vein occlusion?

A

Severe retinal haemorrhages

161
Q

What can cause central retinal artery occlusion?

A

TE, arteritis (e.g. TA)

162
Q

What does central retinal artery occlusion appear like on fundoscopy?

A

Pale retina, cherry red spot

163
Q

What feature is common on examination in central retinal artery occlusion?

A

Afferent pupillary defect

164
Q

What can cause vitreous haemorrhage?

A

DM, bleeding disorders, anticoagulants

165
Q

What are typical features of vitreous haemorrhage?

A

Sudden visual loss, dark spots

166
Q

What are features of retinal detachment?

A

Features of vitreous detachment, which may precede retinal detachment including flashing light/floaters

167
Q

What are features of posterior vitreous detachment?

A

Flashes of light (photopsia) in peripheral field of vision

Floaters often on temporal side of vision

168
Q

What are features of retinal detachment?

A

Dense shadow that starts peripherally and progresses towards central vision
A veil/curtain over field of vision
Straight lines appear curved
Spider web like flashing flights around vision
Central visual loss

169
Q

What are the features of vitreous haemorrhage?

A

Large bleeds cause sudden vision loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters

170
Q

What is strabismus?

A

Squint - misalignment of visual axes

171
Q

How are squints categorised?

A

Concomitant

Paralytic

172
Q

What causes a concomitant squint?

A

Imbalance of extraocular muscles

173
Q

What causes a paralytic squint?

A

Due to paralysis of extraocular muscles (rare)

174
Q

Which of convergent and divergent squints are most common?

A

Convergent more common

175
Q

How can you diagnose a squint?

A

Corneal light reflection test - hold light source 30cm from face to see if light reflects symmetrically on pupils

176
Q

What is the cover test used to determine?

A

The nature of the squint

177
Q

Describe how to carry out the cover test

A

Ask child to focus on object
Cover one eye
Observe movement of uncovered eye
Cover other eye and repeat test

On covering the eye without the squint, the other eye should move to take up fixation

178
Q

How do you manage squint?

A

Eye patch to prevent amblyopia

Refer to secondary care

179
Q

What is esotropia?

A

Squint in which eye deviates towards the nose

180
Q

What is exotropia?

A

Squint in which eye deviates towards the temples

181
Q

What is hypertropia?

A

Squint in which eye deviates superiorly

182
Q

What is hypotropia?

A

Squint in which eye deviates inferiorly

183
Q

What causes blepharitis?

A

Meibomian gland dysfunction (posterior blepharitis, common) or seborrheic dermatitis/staph infection (less common, anterior blepharitis)

184
Q

What is the function of the Meibomian glands?

A

Secrete oil on to surface of eye to prevent rapid evaporation of tear film

Dysfunction –> drying of eyes and irritation

185
Q

What are the features of blepharitis?

A

Usually bilateral
Grittiness, discomfort around eyelid margin
Eyes may be sticky in morning
Eyelids margins may be red/swollen (swollen in staphylococcal blehapritis)
styes/chalazions more common
Secondary conjunctivitis may occur

186
Q

How is blepharitis managed?

A

Hot compresses x2/day (to soften lid margin)
Lid hygiene
Artificial tears for those with dry eyes/abnormal tear film

187
Q

What is involved in lid hygiene?

A

Mechanical removal of debris from lid margin

Cotton wool buds dipped in cooled boiled water and baby shampoo or sodium bicarb

188
Q

What are the features of dry eye syndrome?

A

Commonly effects elderly
Bilateral gritty feeling, symptoms worse at end of day
Assoc with pain

189
Q

What are the features of an acute angle closure glaucoma?

A

Severe pain - may be ocular/headache
Decreased visual acuity, haloes
Semi-dilated pupil
Hazy cornea

190
Q

What are the features of anterior uveitis?

A

Acute onset
Pain
Blurred vision, photophobia
Small, fixed, oval pupil, ciliary flush

191
Q

How can the discharge from conjunctivitis help distinguish between a bacterial/viral causses?

A

Purulent discharge = bacterial

Clear discharge = viral

192
Q

What clues in the hx may point toward subconjunctival haemorrhage being the cause of red eye?

A

Hx trauma or coughing bouts

193
Q

What is endophthalmitis?

A

Inflammation of the anterior + posterior chambers of the eye

194
Q

What is the typical presentation of endophthalmitis?

A

Red eye, pain, visual loss following intraocular surgery

195
Q

What is preseptal cellulitis?

A

Inflammation of the soft tissue anterior to the orbital septum - includes eyelids, skin, sc tissue of face

196
Q

What tends to cause preseptal cellulitis?

A

Tends to be spread of infection from breaks in skin/local infections (e.g. sinusitis/URTI)

197
Q

What are the most frequent causative organisms for preseptal cellulitis?

A

Staph aureus
Staph epidermis
Strep
Anaerobic bacteria

198
Q

How does preseptal cellulitis tend to present?

A

Red, swollen, painful eye of acute onset

May have fever

199
Q

What are the signs of preseptal cellulitis?

A

Erythema/oedema of eyelids, can spread to surrounding skin
Partial/complete ptosis due to eyelid swelling
Orbital signs must be ABSENT

200
Q

What investigations should be done in preseptal cellulitis?

A

Bloods - raised inflammatory markers
Swabs of discharge
Contrast CT of orbit may help distinguish preseptal and orbital cellulitis

201
Q

How should preseptal cellulitis be managed?

A

Always refer to secondary care
Oral antibx (co-amoxiclav)
Admission for observation if child

202
Q

What are complications of preseptal cellulitis?

A

Bacterial infection can spread into orbit –> orbital cellulitis

203
Q

What is posterior vitreous detachment?

A

Separation of vitreous membrane from retina

204
Q

Why does posterior vitreous detachment occur?

A

Due to natural changes to vitreous fluid of eye with ageing

205
Q

What are the features of posterior vitreous detachment?

A

Doe not causes pain/loss of vision but can lead to tears/detachment of retina

206
Q

Why is it important to rule out retinal tears/detachment in those presenting with posterior vitreous detachment?

A

Retinal tear/detachment can lead to permanent loss of vision

207
Q

Why can posterior vitreous detachment happen with age?

A

Vitreous fluid becomes less viscous and doesn’t hold its shape as well so pulls vitreous membrane away from retina towards the centre of the eye

208
Q

What eye condition predisposes to posterior vitreous detachment and why?

A

Myopia

myopic eye has longer axial length

209
Q

What are the symptoms of posterior vitreous detachment?

A 
Sudden appearance of floaters
Flashes of light
Blurred vision 
cobweb across vision 
Dark curtain coming down over vision = retinal detachment
210
Q

What is a sign of posterior vitreous detachment?

A

Weiss ring on ophthalmoscopy = detachment of vitreous membrane around optic nerve forms ring shaped floater

211
Q

How should suspected vitreous detachment be investigated?

A

Examination by ophthalmologist within 24h to rule out retinal tears/detachment

212
Q

How do you manage vitreous detachment?

A

As it does not cause permanent loss of vision, symptoms generally resolve over 6m - so no Rx necessary

213
Q

How do you manage a retinal tear/detachment?

A

Surgery

214
Q

What factors predispose to acute angle closure glaucoma?

A

Hypermetropia
Pupillary dilatation
Lens growth associated with age

215
Q

What are the features of acute angle closure glaucoma?

A 
Severe pain (ocular/headache)
Decreased visual acuity
Symptoms worse with mydriasis (e.g. watching TV in dark room)
Hard, red eye 
Haloes around lights
Semi-dilated non-reacting pupil 
Corneal oedema results in dull/hazy corneal 
Systemic upset (e.g. NV)
216
Q

How is closed angle glaucoma managed?

A

Urgent referral to ophthalmology

Reduce aqueous secretions - acetazolamide + inducing pupillary constriction with topical pilocarpine

217
Q

What thing may contraindicate giving supplements to prevent the progression of ARMD?

A

Being a smoker - beta-carotene has been found to increase lung cancer risk

218
Q

What drugs can precipitate angle closure glaucoma?

A

Mydriatic eye drops

219
Q

What are the features of Horner’s syndrome?

A

Miosis (small pupil)
Ptosis
Enophthalmos (sunken eye)
Anhidrosis (loss of sweating on 1 side)

220
Q

What central lesions may cause anhidrosis?

A 
Stroke
Syringomyelia
Tumour
MS
Encephalitis
221
Q

Where do central lesions cause anhidrosis?

A

The face, arms, trunk

222
Q

Where do pre-ganglionic lesions cause anhidrosis?

A

The face

223
Q

What pre-ganglionic lesions can cause anhidrosis?

A

Pancoast tumour
Thyroidectomy
Trauma
Cervical rib

224
Q

Do post-ganglionic lesions cause anhidrosis?

A

No

E.g.s of these lesions: carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis, cluster headache

225
Q

What are risk factors for vitreous haemorrhage?

A 
DM
Trauma
Anticoagulants
Coagulation disorders
Severe short sightedness
226
Q

What conditions are associated with blepharitis?

A

Acne rosacea
Dry eye syndrome
Seborrheic dermatitis

227
Q

What kind of visual defect do glaucomas primarily cause?

A

Impairs peripheral visual fields

228
Q

What is the epidemiology of primary open angle glaucoma?

A

2% of population over 40y are affected

229
Q

What are risk factors for primary open angle glaucoma?

A 
Genetics
Black 
Myopia
HTN
DM
Corticosteroid
230
Q

How does POAG tend to present?

A

Often insidious presentation and detected during routine optometry appointments

231
Q

What are potential features of POAG?

A

Peripheral visual loss
Decreased visual acuity
Optic disc cupping

232
Q

What are the fundoscopy signs of POAG?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
233
Q

Why is proliferative diabetic retinopathy a risk factor for vitreous haemorrhage?

A

New vessels that grow into the vitreous are fragile + bleed easily

234
Q

What is vitreous haemorrhage?

A

Bleeding into the vitreous humour

235
Q

What is the biggest cause of vitreous haemorrhage?

A

Proliferative diabetic retinopathy

Other two major causes are posterior vitreous detachment and ocular trauma

236
Q

What investigations should be done in suspected vitreous haemorrhage?

A

Dilated fundoscopy: may show haemorrhage in the vitreous cavity
Slit-lamp examination: RBCs in anterior vitreous
USS: rule out retinal tear/detachment + if haemorrhage obscures the retina
Fluorescein angiography: identify neovascularization
Orbital CT: used if open globe injury

237
Q

Which investigation is papilloedema a contraindication for?

A

LP - due to risk of coning

238
Q

Where does drusen tend to collect around in ARMD?

A

Macula

239
Q

What is retinitis pigmentosa?

A

Genetic disorder of the eye that affects primarily the peripheral retina resulting in tunnel vision

240
Q

What are the features of retinitis pigmentosa?

A

Night blindness is usually the initial sign

Tunnel vision due to loss of peripheral retina

241
Q

What things do you see on fundoscopy in retinitis pigmentosa?

A

Black bone spicule-shaped pigmentation in the peripheral retina, mottling of retinal pigment epithelium

242
Q

What diseases are associated with retinitis pigmentosa?

A 
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport's syndrome
243
Q

What is central retinal vein occlusion said to look like on fundoscopy?

A

Cheese and tomato pizza

244
Q

Who gets glaucoma screening and what does it involve?

A

Those with a positive FH should be screened annual from age 40

This usually takes place at the opticians

245
Q

Why is screening of high risk groups essential for glaucoma?

A

It has a strong hereditary component and because initial stages of the disease are asymptomatic

246
Q

What is a typical presentation of infective conjunctivitis?

A

Sore, red eyes associated with a sticky discharge

247
Q

What are the types of infective conjunctivitis and how do you distinguish between them clinically?

A

Bacterial: purulent discharge, eyes may be stuck together in morning

Viral: serous discharge, recent URTI, preauricular lymph nodes

248
Q

Does infective conjunctivitis settle without treatment?

A

Usually settles within 1-2w without treatment

249
Q

What treatment can you offer patients with infective conjunctivitis?

A

Topical antibiotics, e.g. chloramphenicol drops 2-3hrly

250
Q

What should you offer pregnant women with infective conjunctivitis?

A

Topical fusidic acid

251
Q

What advice should you give to those with infective conjunctivitis?

A

Do not share towels
Do not wear contact lenses for duration of illness
School exclusion is not necessary

252
Q

If a neonate presents with conjunctivitis with purulent discharge how should they be managed?

A

Urgent swabs of discharge for microbiological investigation and start systemic antibx

Want to check for gonococcus/chlamydia

253
Q

What is involved in the treatment of an entropion?

A

Definitive: surgery

Can use tape (to pull eyelid down) and lubricants in meantime

254
Q

What are the features of Holmes-Adie pupil?

A

Unilateral (80%)
Dilated pupil
Once pupil constricts stays small for abnormally long time + is slowly reactive to accommodation but very poorly to light (if at all)

255
Q

What is Holmes-Adie pupil associated with?

A

Absent ankle/knee reflex

256
Q

What is the typical presentation of a chalazion?

A

Firm, painless lump on eyelid - these resolve spontaneously

257
Q

In which group of people are corneal ulcers most common in ?

A

Contact lens users

258
Q

What are the features of corneal ulcers?

A

Eye pain
Photophobia
Watering of eye
Focal fluorescein staining of cornea

259
Q

What is a corneal ulcer?

A

Infection of cornea by a bacteria, fungus or protist

260
Q

How do you treat corneal ulcers?

A

Eyedrop tailored to the cause

261
Q

What drug can predispose to corneal ulcer formation?

A

Steroid eye drops as they supress the immune system to an infection

262
Q

What is the most common presentation of herpes simplex keratitis?

A

Dendritic corneal ulcer

263
Q

What are the features of herpes simplex keratitis?

A 
Red, painful eye
Photophobia
Epiphora
Visual acuity may be decreased
Fluorescein staining may show epithelial dendritic ulcer
264
Q

What is the management of herpes simplex keratitis?

A

Immediate referral to ophthalmology

Topical aciclovir

265
Q

What is the commonest cause of persistent watery eye in infants?

A

Nasolacrimal duct obstruction

266
Q

What causes nasolacrimal duct obstruction?

A

Imperforate membrane, usually at the lower end of the lacrimal duct

267
Q

How is nasolacrimal duct obstruction managed?

A

Teach patients lacrimal duct massage

Most resolve within 1y, if doesn’t refer to ophthalmology for consideration of probing (done under LA)

268
Q

What is Hutchinson’s pupil?

A

Unilaterally dilated pupil which is unresponsive to light

Due to compression of oculomotor nerve on same side by an intracranial mass

269
Q

What causes Horner’s syndrome?

A

Damage to the sympathetic trunk on the same side as the symptoms, e.g. due to trauma, compression, infection, ischaemia

270
Q

What is Marcus-Gunn pupil?

A

Relative afferent pupillary defect, seen during swinging light ex of pupil response (pupil appears to dilate when light is shone on it)

Mostly caused by damage to optic n (e.g. optic neuritis) or severe retinal dx

271
Q

What causes Adie pupil?

A

Damage to parasympathetic innervation of eye due to viral/bacterial infection

272
Q

Describe the pathway of pupillary light reflex

A

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

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

273
Q

What is the most effective intervention to slow the progression of dry ARMD?

A

Stopping smoking

Opthalmology (6 decks)

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