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Special Senses > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

what is the pathogenesis of diabetic eye disease

A

hyperglycaemia and htn ->

biochemical/haemodynamic pathways result in microvascular occlusion and leakage

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2
Q

how are patients with diabetes managed by ophthalmology

A

arrange annual fundoscopy and retinal photography

refer to ophthalmology if preproliferative changes or near the macula

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3
Q

if presymptomatic screening of diabetic retinopahty is undertaken, what can be done to manage it

A

laser photocoagulation to prevent angiogenesis

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4
Q

what are the three stages of diabetic retinopathy

A

1) background retinopathy
2) preproliferative retinopathy
3) proliferative retinopathy

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5
Q

what are the features of background diabetic retinopathy on examination of the retina

A
  • microaneurysms (dots)
  • haemorrhages (blotes)
  • hard exudates (lipid deposits)
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6
Q

what are the features of preproliferative diabetic retinopathy on examination of the retina

A
  • cotton wool spots (infarcts)
  • haemorrhages
  • venous beading
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7
Q

what are the features of proliferative diabetic retinopathy on examination of the retina

A

new vessel formation, rubeosis iridis

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8
Q

when should you suspect maculopathy in diabetic patients

A

reduced visual acuity

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9
Q

how is maculopathy managed in diabetic patients

A

prompt laser, intravitreal steroids and anti-angiogenic agents may be needed in macular oedema

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10
Q

what are the cataract types you would get in diabetic patients

A

juvenile “snowflake” or “senile”, occur earlier in diabetics

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11
Q

what is rubeosis iridis

A

new vessel formation on iris , which occurs late and may lead to glaucoma

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12
Q

what is the medical management for diabetic retinopathy

A

1) primary medical: good glycaemic control, bp, lipid control
2) antiplatelet
protein kinase c inhibitors
aldose reductase
gh/insulin like gf inhibitor

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13
Q

what is the surgical management for diabetic retinopathy

A
  • retinal laser
  • laser photocoagulation
  • intravitreal injection of vegf for maculopahthy
  • vitrectomy for vitreal haemorrhage
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14
Q

describe the afferent/efferent pathway for pupil reflexes

A
  • afferent pupillary fibres travel with the rest of the retinal fibres but leave the pathway just before the LGN
  • synapse with pretectal nucleus
  • from here the fibres travel to BOTH edinger-westphal nuclei
  • they synapse with the efferent pupillary fibres which travel from the CNIII nucleus to the ciliary ganglion via the CNIII to the sphincter pupillae
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15
Q

what happens in completely damaged optic nerve when shining a flashlight into it

A

no direct or consensual response if light on affected eye

direct and consensual response when light shone on the normal eye

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16
Q

what happens when light is shone into an eye with an incompletely damaged optic nerve

A

sluggish response from afferent system or affected eye but normal response of unaffected eye

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17
Q

describe RAPD testing with the swinging flashlight test

A

when light is swung onto normal eye, there is direct and consensual response (as efferent system is still intact in the affected eye)
but when light swung onto affected eye the pupil carries on dilating rather than constrict because the efferent system of the affected eye is overpowered by the intact system of the normal eye which demands dilation due to it being in the dark

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18
Q

list the causes of RAPD

A
  • optic neuritis (e.g. ms, infection)
  • optic nerve tumours, trauma, pressure, glaucoma
  • severe retinal pathology e.g. detachment, central retinal artery/vein occlusion
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19
Q

how are the recti muscles of the eye arranged

A

they form a fibrous cuff around the optic canal and attahc anteriorly at the sclera

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20
Q

which artery does the central artery of the retina come from

A

ophthalmic artery

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21
Q

where do ophthalmic veins drain into

A

cavernous sinus

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22
Q

what is the presentation of a sixth nerve palsy

A

Esotropia of the affected eye, with inability to abduct the eye.
Binocular diplopia worse in the direction of the impaired muscle
Patient may turn their head towards the direction of the impaired field

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23
Q

what are the causes of 6th nerve palsy

A
  • microvascular: htn, diabetes
  • macrovascular: stroke
  • acoustic neuroma
  • acute petrositis
  • raised ICP
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24
Q

what is the presentation of 4th nerve palsy

A

Vertical diplopia - difficulty walking downstairs
Hypertropia of affected eye
Hypertropia worse on opposite gaze therefore tilt head away from affected side

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25
Q

which muscles does the 3rd nerve supply

A

sr, ir, mr, io
lps
sphincter pupillae (parasymp)

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26
Q

what is the presentation of a 3rd nerve palsy

A

Ophthalmoplegia of affected supplied nerves

Affected eye is down and out, pupil may be dilated, ptosis

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27
Q

explain the importance of pupil involvement in the 3rd nerve palsy

A

it is more worrying if pupil is involved with 3rd nerve palsy (dilation) as the parasympathetic fibres that control constriction run on the outside of the nerve. Therefore, if the nerve is being compressed externally e.g. aneurysm or tumour, it will involve the pupil via more worrying causes
if pupil not involved, less dagnerous paralysis of nerve from ischaemia (e.g. diabetes, or htn)

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28
Q

when are swollen optic discs termed papilloedema

A

when known/proven raised icp is also present

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29
Q

what are the visual symptoms of papilloedema

A

enlarged blind spot, transient loss of vision esp when bending forward (and back again)

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30
Q

what are the factors associated with idiopathic intracranial htn

A

obesity, pregnancy, ocp, tetracycline

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31
Q

how s idiopathic intracranial htn diagnosed

A

mri/ct normal

increased opening pressure on LP

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32
Q

what is the treatment of idiopathic intracranial htn

A

diamox (acetazolamide), optic nerve decompression, neurosurgical shunts

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33
Q

what are the symptoms of optic neuritis

A
  • unilateral gradual visual loss
  • loss of colour vision
  • pain on movement of the eye
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34
Q

what are the causes of optic neuritis

A

MS most commonly, viral infection, granulomatous inflammation (TB, sarcoid, syphillis)

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35
Q

what is the treatment for optic neuritis

A

Observe vision, as it recovers with MS over 2-3 months
?do MRI
if other treatable cause, manage underlying infection/inflamm etc.

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36
Q

describe intranuclear ophthalmoplgia, and why is occurs

A

Weakness of adduction of the eye and horizontal jerk nystagmus of abducting other eye.
This is because there is a lesion to the MLF (medial longitudinal fasciculus) which connects cniii and cnvi on opposite sides. hence there is a disconnection between conjugate movement of lateral gaze of the eyes.
Impaired adduction of on eye and the other abducting eye experiences nystagmus

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37
Q

what is the most common cause of intranuclear opthalmoplegia

A

MS

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38
Q

which part of the orbit is most commonly affected by orbital blowout #

A

medial wall, or floor of the orbit

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39
Q

what are the types of deformity that result from orbital blowout #

A
  • open door type which is large, displaced and comminuted. it may cause the eye to “sink” downwards in the socket (hypotropia)
  • trapdoor tupe which is hinged and minimally displaced. Can entrap extraocular nerves and muscles
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40
Q

what are the characteristics of blowout fracture on examination, apart from sigs of trauma

A

double vision, sunken ocular globes, loss of sensation to upper cheek/lip
entrapment can cause painful eye movements, diplopia etc

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41
Q

which nerve can be damaged in orbital blowout fracture causing characteristic sensory loss

A

infraorbital nerve

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42
Q

what is the management of an orbital blowout fracture

A

may be left alone for up to two weeks to either resolve spontaneously or swelling to go down.
surgery can provide relief from sunken eye, diplopia, entrapped muscle etc.

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43
Q

what are the jobs of the cornea

A
  • maintain transparecny to look through
  • protect eye - corneal reflex
  • refraction of light
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44
Q

list the 5 layers of the cornea

A
  • epithelium
  • bowmans layer
  • stroma
  • descemets layer
  • endothelium
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45
Q

what type of epithelium is the corneal

A

non keratinised squamous

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46
Q

how does the cornea repair after damage

A

migration of cells from the periphery and basal layer when damaged. corneal stem cells at limbus

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47
Q

what does corneal oedema appear like

A

visible lines in the stroma (striae). These are visible stromal lamellae. hazy

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48
Q

once which corneal layer is breached, does corneal scarring occur

A

bowmans layer

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49
Q

what will happen if there is damage/cellular loss in the endothelium layer of the the cornea

A

corneal oedema and poor vision

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50
Q

describe the pupil reflex pathways

A

1) afferent pupillary fibres travel with the rest of the retinal fibres but come off just before the LGN
2) synapse at the pretectal nucleus
3) from here the fibres travel to both the edinger-westphal nuclei (CNIII)
4) then efferent fibres leave the edinger westphal nuclei and travel to the ciliary ganglion and sphincter pupillae

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51
Q

which structures make up the uveal tract

A

iris, ciliary body and choroid (pigmented and vascular structures)

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52
Q

what layers does the choroid lie between

A

retina and sclera

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53
Q

what is the function of the choroid

A
  • allows nerves and vessels to reach the anterior eye
  • remove waste products from outer retina
  • supplies essential nutrients
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54
Q

through which structure does the choroid attach to the retina

A

bruch’s membrane (between choroid and RPE)

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55
Q

what is the action of tropicamide on the eye

A

antimuscarinic - mydriasis

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56
Q

what is the action of phenylephrine on the eye

A

sympathomimetic - mydriasis

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57
Q

what is the action of pilocarpine on the eye

A

muscarinic agonist - miosis

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58
Q

what is the pathophysiology of posterior vitreous detachment

A

with age fluid fills in the potential space between the retina and vitreous - it may then detach from the retina. the detachment can tug on areas where it is attached to the retina, and predispose to retinal detachment

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59
Q

what are the symptoms of pvd

A

floaters and flashing lights (due to tugging on retina causing stimulation)

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60
Q

what are the two layers of the retina

A
  • inner neural retina

- outer rpe

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61
Q

what is the retina derived from

A

optic cup

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62
Q

what is the potential space between the two layers of the retina called, and why is it important

A 
subretinal space (fuses early in foetal life)
these two layers can separate e.g. by trauma  - leading to retinal detachment
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63
Q

what are the symptoms of retinal detachement

A

flashing lights, floaters, possible visual field defects

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64
Q

what are the firm attachments of the neural retina

A

optic nerve head posteriorly and ora serrata anteriorly

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65
Q

what are the functions of rods and cones in vision

A 
rods = contrast vision and motion - not good for detial "black and white vision"
cones = fine detail and colour
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66
Q

what is the blood supply to the retina

A

inner 2/3 = central retinal artery

outer 1/3 = choroidal blood supply

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67
Q

how does the blood supply of the macula and fovea differ

A

macula - dense capillary network

fovea - capillary free zone - dependent on underlying choriocapillaries

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68
Q

what is the appearance of the retina like when there is a central retinal artery occlusion

A

retina becomes pale and oedematous, with changes being irreversible within 1-2 hours.
Fovea can retain red colour however, and appear as a “cherry red spot” due to being supplied by the choriocapillaris

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69
Q

which optic fibres travel through the temporal and parietal lobes

A

parietal - superior fibres from the retina (which cary information from inferior visual field)
temporal - inferior fibres from the retina (which carry information from superior visual field)

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70
Q

at which level are the macula sparing visual field loss

A

striae cortex

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71
Q

what is the pattern of visual loss in ARMD

A

not complete blindness - just loss of central vision so unable to read/recognise faces/perform some adl’s

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72
Q

what is charles bonnet syndrome

A

visual hallucinations in armd patients - NOT a sign of mental illness

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73
Q

list the risk factors for armd

A
  • incresing age
  • smoking
  • caucasian
  • concomitant disease e.g. htn, cvd
  • genetics
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74
Q

what is drusen

A

hallmark of armd - undigested debris of rpe - yellow-white matter that builds up between the rpe and burch’s membrane

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75
Q

list the classification of armd

A
  • early
  • intermediate
  • advanced dry or wet
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76
Q

what are the characteristics of early armd

A

few medium-sized drusen and pigmentary abnormalities

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77
Q

what are the characteristics of intermediate armd

A

1 or more large drusen/numerous mendium sized drusen

geographic atrophy does not extend to macular centre

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78
Q

what are the characteristics of severe armd

A

can be dry or wet

  • dry = non exudative/atrophic drusen _ geographic atrophy extending to macular centre
  • wet = exudative, choroidal neovascs equelae, rpaid vision loss
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79
Q

describe conversion of dry to wet armd

A

dr amd -> inflammation -> monocytes + macrophages -> vegf + vegf signalling cascade -> aberrant vessel production and neovascularisation -> wet amd

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80
Q

how do you recognise the difference between armd and diabetic maculopathy

A
  • history features
  • on fundoscopy - diabetic maculopathy will have other typical changes in the retina of diabetic eye disease, which are not seen on armd.
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81
Q

what is the pathophysiology of dry armd

A

drusen accumulation between the rpe and burchs membrane leads to hypoxia and inflammation. visual loss is caused by atrophy or conversion to wet armd

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82
Q

what are the retinal photograph features of dry armd

A

confluent drusen (soft or hard), central nd paracentral degeneration, geographic atrophy extending to the foveal centre

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83
Q

what are the early symptoms of dry armd

A

mild visual loss
reduced visual acuity
loss of contrast sensitivity
abnormal dark adaptation

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84
Q

what are the late symptoms of dry armd

A

mild occassional metamorphosia (due to presence of drusen)
fluctuating vision
loss of central vision
limited night vision/under poor light

85
Q

what are the diagnostic tests you would perform on a patient with armd

A

1) contrast sensitivity test, and hue test for colour
2) amsler grid
3) snellen chart (at least 2 lines decline)
4) fundus photography
5) fluoroscein angiography (wet amd)
6) optical coherence tomography (slice image of retina)

86
Q

what is the management of dry armd

A
  • manage cvs risk factors
  • stop smoking!
  • green vegetables (lutein)
87
Q

what is the pathophysiology of wet armd

A

abnormal blood vessels are leaky and cause fibrosis and central vision loss
bleeding into and below the retina

88
Q

what is a disciform scar in armd

A

wet armd causes a disc like scar which represents a portion of the macula that has been permanently damaged
causes scotoma

89
Q

what is scotoma

A

blind spot in field of vision

90
Q

what are the symptoms of wet armd

A

loss of visual acuity
decreased contrast sensitivity
metamorphosia
central scotoma

91
Q

what is the treatment of wet armd

A

anti vegf injections - try and stop aberrant vessel growth

92
Q

give an example of anti vegf that is used in armd

A

ranibizumab

93
Q

what blood test is important to do in a patient with cataracts

A

bm’s to exclude diabetes mellitus

94
Q

list the different types of cataracts on ophthalmoscopy

A
  • nuclear
  • cortical
  • anterior and posterior polar
  • subcapsular
95
Q

what is the presentation of cataracts

A
  • bluured vision
  • loss of stereopsis if unilateral (causing difficulty judging vision)
  • gradual loss of vision
  • dazzle/glare
  • monocular diplopia may be present
96
Q

how may cataracts present in children

A

squint, loss of binocular function, white pupil, nystagmus/amblyopia in infants

97
Q

when is surgery offered with cataracts

A

impairing daily living activities, impairing driving, vision <6/12

98
Q

what are the risks of cataract surgery in terms of failure to work 100%

A

eyes may still suffer from dazzle/glare
distant specs often needed
posterior capsule thickening post opmay seem like “cataract is returning)
astigmatism
irritation and dryness
anterior uveitis
vitreous haemorrhages/detachment/glaucoma

99
Q

what drugs are prescribed for a couple of day post-op use in patients who have had cataract surgery

A

topical antibiotic and antiinflamms

100
Q

list the risk factors for cataracts

A
  • increasing age
  • genetic
  • diabetes mellitus
  • steroid use (topical/po/inhaled)
  • high myopia
  • dystrophia myotonica
101
Q

what is performed prior to surgery to choose appropriate lens type for patient

A

ocular biometry - measures curvature of the cornea and length of eye

102
Q

what is the post op advice for patients following cataract surgery

A
  • come in to eye casualty if red eye/loss of vision
  • lubricants
  • antiobiotics/antiinflamm
  • new specs
  • imbalance should sette within a few weeks
  • can resume activities next day after surgery
103
Q

what is the window for which congenital cataracts must be treated

A

4 weeks (to prevent significant deprivation/amblyopia)

104
Q

what screenng would you do in a baby presenting with congenital cataracts

A

TORCH screen

105
Q

what causes presbyopia

A

with age, the lens becomes flattened and harder so focusing capacity is reduced

106
Q

what is the name of the suspensory ligaments of the lens, arising from the ciliary body

A

zonular fibres

107
Q

what is the typical cataract shape in dm

A

snowflake

108
Q

what is the typical cataract shape in myotonic dystrophy

A

stellate post capsular

109
Q

what is the typical cataract shape in atopic dermatitis

A

shield-like ant capsular

110
Q

list some ophthalmological conditions that can cause secondary cataracts

A
  • chronic anterior uveitis (can be steroid induced too)
  • acute angle closure glaucoma
  • hereditary fundus dystrophies
  • high myopia
111
Q

list some factors that may contribute to cataract formation

A

diabetes, inflamm, trauma, steroid use

112
Q

list the steps for the surgical procedure of cataract removal

A

1) capsulorrhexis (open front surface of lens)
2) hydrodissection (seperate lens from capsule inro 4 chunks)
3) lens fragmentation - phaecoemulsfication (uss)
4) irrigation and aspiration
5) intraocular lens implantation

113
Q

what is the treatment of post-op posterior capsule opacification in cataract surgery

A

YAG laser

114
Q

what is a complication during surgery for cataracts

A

posterior capsular rupture and viterous loss

115
Q

when is red reflex checked for newborns

A

at 6 weeks

116
Q

define glaucoma

A

a group of eye conditions that result in progessive optic neuropathy and visual loss

117
Q

define glaucoma

A

a group of eye conditions that result in progessive optic neuropathy and visual loss
(IOP is a key factor but not always riased)

118
Q

what are the symptoms of closed angle glaucoma

A

severe eye pain, blurred vision, mid dilated pupil, red eye, nausea

119
Q

is visual loss due to glaucoma reversible

A

no - what is lost is permanent

120
Q

what are the “3 c’s” when looking at the optic nerve head on fundoscopy

A
  • colour
  • contour
  • cup (cup: disc ratio)
121
Q

where is aqueous humor produced

A

ciliary processes of the ciliary body

122
Q

where is the outlet of aqueous humor in the eye

A

drainage angle of the eye - trabecular meshwork + canal of schlemm

123
Q

what is the normal range for iop

A

10-21 mmhg

124
Q

does high iop always mean glaucoma

A

no - though it increases risk

125
Q

what is the effect of stimulating the alpha 2 receptor in the eye on ocular pressure

A

decrease iop by reducing aqeuous production and may increase outflow

126
Q

what is the effect of stimulating the beta 2 receptor in the eye on ocular pressure

A

stimulation increases iop by increasing aqueous production - therefore give beta blockers

127
Q

what is the name of the visual field test performed in glaucoma

A

humphrey visual field test

128
Q

what does humphrey visual field test show in glaucoma patients

A

arcuate scotoma, that obeys the horizontal line

129
Q

what are the surgical options for management of gluacoma

A
  • laser
  • trabeculectomy
    aim to increase drainage
130
Q

list the main classes of drugs used to treat glaucoma

A

a-agonists, b-blockers, carbonic anhydrase inhibitors, prostaglandin analogues

131
Q

what is the mechanism of a agonists and b blockers in reducing iop

A
  • a agonists: reduce aqueous production and increased drainage
  • b blockers: increase aqueous drainage
132
Q

what is the mechanism of carbonic anhydrase inhibitors in reducing iop

A

reduce aqueous production

133
Q

what is the mechanism of prostaglandin analogues in reducing iop

A

increase aqueous drainage

134
Q

what is the typical epidemiology of patients with acute angle closure glaucoma

A

over 50 y/o, female usually

135
Q

what time of the day is acute angle closure glaucoma most likely to present

A

evening typically

136
Q

what are the signs on examination of a patient with acute angle closure glaucoma

A

reduced vision, red eye corneal oedema, fixed mid-dilated pupil, visual halos
(tonometry = increased iop)

137
Q

what does increased cup to disc ratio represent in terms of pathology

A

loss of nerve fibres

138
Q

what is bayonette sign on fundoscopy

A

vessels appear misaligned when entering the optic disc, due to increased cup to disc ratio

139
Q

what are there symptoms in early open angle glaucoma

A

asymptomatic until visual fields are impaired, therefore screening

140
Q

what are the groups that are high risk and therefore screened for glaucoma

A
  • over 40(?) yo
  • afrocaribbean
  • myopia
  • diabetic/thyroid eye disease
141
Q

what is tested for when “screening” for glaucoma

A
  • visual field testing
  • document cup:disc ratio
  • increased iop
142
Q

what is the benefit of pilocarpine in treatment of glaucoma

A

miotic - reduces resistance to aqueous flow by “opening angle” with pupil constriction

143
Q

why should you take care with sympathomimetics (e.g. brimonidine) in glaucoma

A

arrhythmias/htn - be careful due to systemic side effects

144
Q

what is the cause of closure angle glaucoma

A

blocked flow of aqueous humor via the anal of schlemm

145
Q

what examination would be undertaken in eye casualty to examine the anterior chamber in angle closure glaucoma

A

gonioscopy

146
Q

which nerve supplies the obicularis oculi

A

cnvii

147
Q

list the layers of the eyelid

A

skin, obicularis oculi, tarsal plate (meiobian glands, lps), tarsal plate/tarsal muscle, bulbar/palpebral conjunctiva

148
Q

which test can prove shallow anterior chamber

A

oblique flashlight test

149
Q

whcih questions should you ask in the history of someone with acute red eye

A
  • pain, discomfort
  • grittiness, fb sensation, deep ache
  • photosensitivity
  • watering +/- dc
  • change in vision - blurring, halos etc
  • trauma
  • contact lens wear
  • previous ocular hx
  • nausea/vomiting
150
Q

what is trichiasis

A

abnormally-positioned eyelashes e.g. turned inwards

151
Q

give some differentials for deep intense eye pain

A

corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis

152
Q

list some differentials for photophobia

A

corneal abrasions, iritis, acute glaucoma

153
Q

where is the episclera located

A

between conjunctiva and sclera

154
Q

what is ciliary flush

A

injection of vessels of the eye - superificial or deep (not seen in conjunctivitis)

155
Q

what is blepharitis

A

inflammation of the lid margin, causing crusting, redness, telangiectasia, trichiasis

156
Q

what are the main causative organisms for blepharitis

A

staphylococcus and skin flora

157
Q

what does the tarsal plate contain

A

meiobian glands

158
Q

where do the tarsal glands open

A

at the lid margin

159
Q

what glands are found at the lid margin

A
  • glands of Moll - modified sweat glands

- glands of Zeiss - sebaceous glands

160
Q

how do external and internal hordeolums develop

A
  • meiobian cyst = obstruction to tarsal glands (internal)

- stye = obstruction to gland of moll/zeiss (external)

161
Q

which anatomical area is the lacrimal gland found

A

lacrimal fossa

162
Q

where does the nasolacrimal duct open

A

inferior meatus

163
Q

list some of the symptoms of blepharitis

A

grittiness, fb sensation, itching, redness, mild pain

164
Q

what is the treatment of blepharitis

A

lid hygeine, warm compress, topical antibiotics, lubricants

165
Q

when would you give doxycycline in eye problems

A

meiobian gland disease and rosacea

166
Q

what is marginal keratitis

A

inflammation of the cornea, leading to subepithelial marginal concentrate

167
Q

what is the treatment for marginal keratitis

A

topical low dose steroids

168
Q

what is the treatment for trichaisis

A

lubricants, epilation, electrolysis, cryotherapy

169
Q

what is an internal hordeolum

A

acute chalazion - meiobian gland staph infection

170
Q

what are the examination signs of internal hordeolum

A

tender nodule within tarsal plate, with or without associated cellulitis

171
Q

what is the treatment for internal hordeolum

A

hot compress, topical antibiotic ointment, incision and drainage once infection has subsided

172
Q

what is an external hordeolum

A

stye - staphylococcal abscess of lash follicle and its assocaites gland of zeiss/moll

173
Q

what is the treatment for external hordeolum

A

hot compress, epilation of lash with infected follicle, topical abx

174
Q

how do you manage subtarsal foreign body

A

evert eyelid with cotton bud while the patient looks down and remove fb with cotton bud
stain with fluoroscein to look for abrasion
+/- antiobiotics

175
Q

list some causes of dry eyes

A
  • systemic: ra, sjogrens
  • use of antihistamines
  • cnvii palsy
176
Q

what are the common organisms causing bacterial conjunctivitis

A

s aureus, s epidermidis, s pneumoniae, h influenzae

177
Q

what are the symptoms of conjunctivitis

A

redness, grittiness, burning, dc, often bilat

178
Q

what are the signs on examination of the conjunctivitis

A

crusty lids, conjunctival hyperaemia, mild papillary reaction, lids and conjunctiva may be oedematous

179
Q

when should swabs be taken for conjunctivitis

A

newborn, uncertain diagnosis

180
Q

what is the treatment for conjunctivitis

A

chloramphenicol or fusidic acid

topical abx 2-7days

181
Q

what are the signs and symptoms of chlamydial conjunctivitis

A

usually unilat, fb sensation, lid crusting with sticky dc, follicles

182
Q

what are the investigations for chlamydial conjucntivitis

A

swab/smear
direct monoclonal fluorescent ab icroscopy
pcr, naat

183
Q

what is the treatment for chlamydial conjunctivitis

A

topical tetracycline/po doxycycline or azithromycin

184
Q

what is the main viral cause of conjunctivitis

A

adenovirus

185
Q

what are the symptoms of viral conjunctivitis

A

usually bilateral watery eyes, dc, soreness, fb sensation,

186
Q

what is the management of viral conjunctivitis

A

usually self resolves by 2 weeks
give advice that it is contagious
give topical steroids if risk of keratitis

187
Q

what are the signs and symptoms of allergic conjunctivitis

A

itch, bilateral watery dc, oedema, papillae (cobblestone)

188
Q

what are the investigations for allergic conjunctivitis

A

ige levels, patch testing

189
Q

what is the treatment for allergic conjunctivitis

A

cold compress
remove allergen, nsaids, antihistamines
sodium cromoglycate (mast cell stabiliser)
topical corticosteroids
if steroid resistant - immunosuppression with ciclosporin
(lid steroid injection)

190
Q

what should you check in a patient with spontaneous suconjunctival haemorrhage

A

bp

191
Q

what is the treatment for spontaneous subconjunctival haemorrhage

A

lubricants for up to 14 days until it resolves itself

192
Q

what are the symptoms of episcleritis

A

mild tearing/irritation, tender to touch, blanching with phenylephrine

193
Q

what is the treatment for episcleritis

A

lubricants, nsaids,

rarely low dose steroids

194
Q

what is scleritis

A

scleral inflammation wtih maximal congestion in the deep vascular plexus

195
Q

what are the signs and symptoms of scleritis

A

pain (severe, boring)
ocular tenderness to movement and palpation
watering and photophobia
bluish red appearance

196
Q

what is the treatment of scleritis

A

manage underlying condition, nsaids, corticosteroids, immunosuppression

197
Q

what is pterygium

A

fibrous growth from the conjunctiva onto the cornea

198
Q

what is the management of pterygium

A

excision and covering with conjunctival autograft

mitomycin

199
Q

what is infective keratitis

A

disruption to the epithelial surface of the cornea, and can lead to infection here

200
Q

what are some of the trggers for bacterial keratitis

A

contact lens wear, small ulcer that has developed, dry eyes, fb, persisting corneal disease

201
Q

what are the symptoms of bacterial keratitis

A

pain, drop in visual acuity (corneal surface and tear film disruption), fb sensation, watering, photophobia, corneal oedema may be present

202
Q

what would you see on examination of eye with bacterial keratitis

A

white deposit on cornea (infiltrate) +/- collection of pus in the anterior chamber (hypopyon), “cell and flare” with slight lamp exam of anterior chamber, corneal oedema

203
Q

what is cell and flare representative of

A

proteins and leucocytes are visible floating in anterior chamber when light shone on pupil (come from leaky iris blood vessels in response to infection)

204
Q

what are the symptoms of corneal abrasion/fb

A

severe pain, especially with itching, watering

205
Q

what is the management of corneal abrasion

A 
remove fb with cotton bud if able to under topical
anaesthetic, exclude intraocular fb
refer if it crosses the visual pathway
chloramphenicol ointment
cyclopentolate
206
Q

list the common organisms causing bacterial keratitis

A

s aureus, strep pyogenes, s pneumoniae, p aeuruginosa

207
Q

what are the investigations for bacterial keratitis

A

culture

208
Q

what is the treatment for bacterial keratitis

A

topical ofloxacin, cyclopentolate tds,

steroids once cultures stable

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