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Ophthalmology > Oph Lectures > Flashcards

Oph Lectures Flashcards

1
Q

What are rods for?

A

Low light and peripheral vision

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2
Q

What are cones for?

A

Detailed and colour vision

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3
Q

What is emmetropia?

A

No refractive error

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4
Q

What is hypermetropia?

A

Long sighted

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5
Q

What is myopia?

A

Short sighted

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6
Q

What is astigmatism?

A

When the lens is more oval and circular

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7
Q

What commonly causes bacterial conjunctivitis in infants?

A

Staph aureus, neiserria gonorrhoea, chlamydia trachomatis

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8
Q

Common causes of bacterial conjunctivitis

A

H. influenza, staph aureus and strep pnuemoniae

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9
Q

What treatment is given for bacterial conjunctivitis?

A

Chloramphenicol

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10
Q

In what scenario should chloramphenicol be avoided?

A

Confirmed allergy or aplastic anaemia

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11
Q

In what forms can chloramphenicol be given?

A

Drops - QDS and kept in the fridge

Ointment - can cause blurred vision

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12
Q

What bacteria will chloramphenicol not treat?

A

Pseudomonas aerguinosa

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13
Q

What bacteria does fusidic acid treat?

A

Staph aureus

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14
Q

What bacteria will gentamicin treat?

A

Coliforms

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15
Q

Common viruses causing viral conjunctivitis

A

Herpes simplex, herpes zoster, adenovirus

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16
Q

Chronic, bilateral conjunctivitis with urethritis is probably caused by what?

A

Chlamydia

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17
Q

What causes scarring on the eyelids ad “rice grains” in the eye?

A

Chlamydial conjunctivitis

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18
Q

What must you do if taking a swab for chlamydia?

A

Inform the patient and do contact tracing

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19
Q

Short history of red eye, pain, decreased vision and hypopyon is classic of what?

A

Bacterial keratitis

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20
Q

How is bacterial keratitis treated?

A

Ofloxacin drops hourly

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21
Q

What organism does ofloxacin not treat?

A

Strep pneumoniae

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22
Q

What happens if bacterial keratitis is not treated?

A

The eye can perforate

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23
Q

What is the most common cause of viral keratitis?

A

Herpes

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24
Q

What commonly presents with a dendritic ulcer?

A

Viral kertitis

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25
Q

Is viral keratitis painful?

A

So painful patient can’t open their eyes.

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26
Q

What should you never give in viral keratitis?

A

Steroids. Can make the ulcer spread and thin - potentially burst

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27
Q

Bilateral infection, following URTI, sub-epithelial infiltrates are all signs of what?

A

Adenoviral keratitis

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28
Q

How is adenoviral keratitis treated?

A

Mild steroids to speed up recovery + topical antibiotics

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29
Q

Common causes of fungal keratitis

A

Pseudomonas aeruginosa or acanathamoeba

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30
Q

How does fungal keratitis commonly present?

A

History of trauma, vegetation and hypopyon

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31
Q

How does orbital cellulitis commonly present?

A

Pain on eye movement, redness, swelling, proptosis, pus, fever

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32
Q

What can cause orbital cellulitis?

A

Insect bites, surgery

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33
Q

What is a complication of orbital cellulitis?

A

Infection can spread to the brain

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34
Q

What investigation should be done in orbital cellulitis?

A

CT to identify any abscesses

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35
Q

What are symptoms of endopthalmitis?

A

Pain, decreasing vision, loss of vision

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36
Q

Common bacterial cause of endopthalmitis?

A

Staph epidermidis

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37
Q

What is the treatment for endopthalmitis?

A

Intravitreal amikacin, ceftazidime or vancomycin. With topical antibiotics

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38
Q

What condition is CMV retinitis associated with?

A

HIV/AIDS

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39
Q

What is a common cause of chorioretinitis?

A

Toxoplasma gondii

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40
Q

How can toxoplasma gondii be contracted?

A

Froms cats and raw meat

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41
Q

What is toxocara canis?

A

A worm affecting cats and dogs, but cannot replicate in humans - larvae remain the body

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42
Q

How is bacterial keratitis investigated?

A

Corneal scrape

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43
Q

How is endopthalmitis investigated?

A

Aqueous or vitreous humour culture

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44
Q

How is toxoplasma and toxocara investigated?

A

Serology

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45
Q

How does chloramphenicol work?

A

Inhibits peptidyl transferase enzyme to stop bacterial protein being produced

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46
Q

Complications of chloramphenicol

A

Aplastic anaemia or grey baby syndrome

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47
Q

What antibiotic should be used if there is a chloramphenicol allergy?

A

Gentamicin

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48
Q

How do penicillins and cephalosporins work?

A

Inhibit cell wall formation

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49
Q

How do quinolones (ofloxacin) work?

A

Inhibit DNA gyrase

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50
Q

What is a common contaminant of bottles of eye drops?

A

Pseudomonas

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51
Q

How are antivirals given in ophthalmology?

A

Tablets which excrete 3% acyclovir in the tears

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52
Q

What are the three factors which make a DNR legal?

A

Signed, witnessed and in writing

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53
Q

Where is CSF produced?

A

Choroid plexus

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54
Q

At what rate is CSF produced?

A

500-600ml / day

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55
Q

Where does CSF circulate?

A

In the subarachnoid space before being absorbed by granules into the venous system

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56
Q

What is the role of CSF?

A

Supplying water, AAs, ions

Removes metabolites

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57
Q

How is CSF obtained for testing?

A

Lumbar puncture at L3/4/5

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58
Q

What should CSF look like?

A

Clear and colourless

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59
Q

What is the physiological composition of CSF?

A

15-45 mg/dl protein

1-5cells/ml IGs

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60
Q

What are the main functions of CSF?

A

Mechanical protection - absorbing shock to brain tissue
Homeostatic function - pH affects pul ventilation and cerebral blow flow as well as hormone transport
Circulation - exchange of nutrients and waste products between the blood and brain

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61
Q

What embryonic structure gives rise to the brain’s ventricles?

A

Neural canal

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62
Q

What connects the lateral ventricles to the third ventricle?

A

Foramen of Monroe / intraventricular foramen

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63
Q

What connects the third ventricle to the fourth?

A

Aqueduct

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64
Q

What connects the fourth ventricle to the subarachnoid space?

A

Foramen of magendie

Laterally, the foramina of Luschka

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65
Q

What makes up the blood brain barrier?

A

Brain capillaries, basal membranes and perivascular astrocytes.

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66
Q

In which gland is melanin produced?

A

Pineal gland

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67
Q

What is the purpose of the BBB?

A

To protect the brain from infection

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68
Q

What is hydrocephalus?

A

An accumulation of CSF in the ventricular system or around the brain due to obstruction or overproduction. This results in the enlargement of the ventricles and increase in CSF pressure

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69
Q

What is idiopathic cranial hypertension?

A

Idiopathic intracranial hypertension is a condition which causes headache, visual disturbance, increase in CSF but no hydrocephalus

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70
Q

What is papilloedema?

A

Optic disc swelling due to increased ICP

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71
Q

What symptoms can papilloedema cause?

A

Blind spots, blurred vision, loss of vision

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72
Q

What is aqueous humour and what is for?

A

A fluid which bathes the eye and provides O2, metabolites and bicarbonate and act as a buffer

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73
Q

Where are H+ ions produced in the eye?

A

Cornea and lens

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74
Q

Where is aqueous humour?

A

Anterior chamber of the anterior segment

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75
Q

Where does aqueous humour drain to?

A

through the trabecular meshwork to the scleral venous sinus

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76
Q

What is glaucoma?

A

Raised IOP causing damage to the optic nerve

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77
Q

What causes glaucoma?

A

Imbalance between the rates of secretion and removal of aqueous humour

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78
Q

How is glaucoma treated?

A

Carbonic anhydrase inhibitors reduce aqueous humour production
Dorzolamide is topical drops to avoid systemic effects. Acetazolamide is oral but affects the kidney

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79
Q

What are the 4 things that must occur in order to see an object?

A

Pattern of the object must fall on rods and cones
Lighting must be regulated
Energy converted to electrical signals
Brain interprets signals

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80
Q

What are the four main regions of a photoreceptor?

A

Outer segment, inner segment, cell body and synaptic terminals

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81
Q

What is the resting membrane potential of a photoreceptor?

A

~ -20mV

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82
Q

What happens to photoreceptor Vm on light exposure?

A

Hyperpolarises (becomes more negative) due to closing of the cGMP gated Na channel

83
Q

What modulates the “dark current” in the eye?

A

Retinal opsin (rhodopsin)

84
Q

How is retinal opsin activated?

A

Light converts 11-cis-retinal (in retinal opsin) to trans-retinal to activate transducing, decreasing cGMP and closing the channel

85
Q

What is visual acuity?

A

How well you can see

86
Q

What determines visual acuity?

A

Photoreceptor spacing and

87
Q

What is the function of rod shaped photoreceptors?

A

Seeing in dim light

88
Q

What is the function of cone shaped photoreceptors?

A

Seeing in normal light, seeing in colour

89
Q

What is amblyopia?

A

A variety of visual disorders where there is no problem but one eye is better than the other

90
Q

What can cause amblyopia?

A

Strabismus/lazy eye in infancy

91
Q

What are the two types of immunity?

A

Innate and adaptive

92
Q

When is the innate immune system active?

A

4-96 hours past exposure

93
Q

When is the adaptive immune system active?

A

After 96 hours post exposure

94
Q

What chemicals do tears contain for a immune barrier? (10 things)

A

Lysozyme; lactoferrin; transferrin; tear lipids; angiogenin; IgA; complement; IL-6, IL-8 and MIP

95
Q

What is the role of lysozyme in the tears?

A

To protect against gram -ve bacteria and fungi

96
Q

What is the role of lactoferrin and transferrin in the eye?

A

To protect against gram +ve bacteria

97
Q

What is the role of tear lipids in the tears?

A

Attack cell membranes

98
Q

Which part of the eye is the only part with lymphatic drainage?

A

Conjunctiva

99
Q

What is immune privilege?

A

Ability to tolerate the antigens without an inflammatory response

100
Q

Which sites of the body exhibit immune privilege

A

Brain, testes, placenta, eyes

101
Q

What is sympathetic opthalmia?

A

Granulomatous uveitis due to trauma or surgery to one eye which then affects both eyes

102
Q

What is autoimmune uveoretinitis?

A

Inflammation of the uvea and retina

103
Q

What is a Dalen-Fuchs nodule?

A

Cluster of epithelial cells in the retinal layers

104
Q

What is keratoconjunctivitis sicca?

A

Dry eyes

105
Q

Explain type II hypersensitivity.

A

Direct cell killing by machrophages, NK cells or complement

106
Q

In which ophthalmology condition is type II HS observed?

A

Ocular cictricial pemphigoid

107
Q

Explain type III hypersensitivity

A

Immune complex mediated response

108
Q

In which ophthalmology condition is type III observed?

A

Autoimmune corneal melting

109
Q

Explain type IV hypersensitivty

A

Delayed type, when T helper cells are activated causing clonal expansion. Then an exaggerated response on re-exposure.

110
Q

In which ophthalmology condition is type IV HS observed?

A

corneal graft rejection

111
Q

What are symptoms of raised ICP?

A

Transient blurred vision, double vision, loss of vision, pupillary changes

112
Q

Where is the subarachnoid space located?

A

Between the arachnoid and pia

113
Q

What are the three meninges in the brain?

A

Dura mater, arachnoid mater, pia

114
Q

Which nerve supplies sensory innervation to dura mater

A

CN V, trigeminal

115
Q

At which spinal levels can a lumbar puncture be done to obtain CSF?

A

L3/4/5

116
Q

At which spinal level does subarachnoid space end?

A

S2

117
Q

What is the falx cerebri?

A

Sickle shaped fold of dura mater in the midline of the cerebral hemispheres

118
Q

What is the tentorium cerebelli?

A

Crescent shaped fold of dura mater which forms a roof over the posterior cranial fossa and covers the upper surface of the cerebellum.

119
Q

What is the tentorial notch?

A

Gap in the tentorium cerebelli which the midbrain passes through

120
Q

What is the falx cerebelli?

A

A small fold of dura mater between the cerebral hemispheres

121
Q

What is the diapharagma sellae?

A

Dura mater which forms a roof for the sell turcica

122
Q

What features should make you suspicious of a penetrating foreign body? (3)

A

Irregular pupil, shallow anterior chamber, gross inflammation

123
Q

Side effects of topical steroids?

A

Cataract and glaucoma

124
Q

Side effects of steroids?

A

Proliferation of herpes keratitis

125
Q

Side effects of vigabatrin?

A

Field defects

126
Q

Side effects of alcohol and ethambutol?

A

Optic atrophy

127
Q

Side effects of rifampicin?

A

Red/orange body fluids (incl tears)

128
Q

Side effects of digoxin?

A

Changes in colour vision

129
Q

Side effects of chloroquine?

A

Maculopathy

130
Q

Side effects of amiodarone?

A

Corneal verticullata

131
Q

How does diabetic retinopathy occur?

A

Chronic hyperglycaemia causes glycosylation of the basement membranes

132
Q

What are signs of diabeteic retinopathy? (4)

A

“Dot and blot” haemorrhages, hard exudates, cotton wool patches, abnormalities of venous system

133
Q

What effect does phosphate have on steroids?

A

Makes it more hydrophillic

134
Q

What drug is used in glaucoma to lower IOP?

A

Bimatoprost 0.03%

135
Q

How do you limit systemic absorption of topical drugs?

A

Occluding the punctum

136
Q

Describe R0 retinopathy

A

No retinopathy. Rescreen in 12 months

137
Q

Describe R1 retinopathy

A

Background diabetic retinopathy - presence of haemorrhages; micro aneurysms; hard exudates; cotton wool spots. Rescreen in 12 months.

138
Q

Describe R2 retinopathy

A

Four or more haemorrhages in one hemi field (sup/inf). Rescreen in 6 months.

139
Q

Describe R3 retinopathy

A

Four or more haemorrhages in both fields, venous beading; IRMA. Refer to oph

140
Q

Describe R4 retinopathy

A

Neovasculature or vitreous haemorrhage. Refer to oph

141
Q

Describe R6 retinopathy

A

Retina not sufficiently visible. Rearrange screening.

142
Q

How does central retinal artery occlusion present?

A

Sudden, painless, profound loss of vision.

143
Q

How to manage central retinal artery occlusion?

A

Massage vessels to attempt to move the clot to a minor arterial branch. Rarely recovers.

144
Q

How does central retinal vein occlusion present?

A

Sudden, painless visual loss. May be profound or insignificant.

145
Q

How can giant cell arteritis present?

A

Headache, jaw claudication, malaise, raised PV, visual loss

146
Q

What condition is giant cell arteritis strongly a/w?

A

Polymyalgia rhuematica

147
Q

What is thyroid eye disease associated with?

A

Thyroid disease, commonly Grave’s or hyperthyroidism

148
Q

How can thyroid eye disease present?

A

Proptosis, lid retraction, oedema, lid lag, lid pigmentation, optic nerve swelling, choroidal folds

149
Q

How to manage thyroid eye disease?

A

Treat underlying thyroid problems

150
Q

What ophthalmological symptom can SLE cause?

A

Occular inflammation

151
Q

Which ophthalmological problems can rheumatoid arthritis be associated with?

A

Keratoconjunctivits sicca (dry eyes); scleritis or corneal melt

152
Q

Which ophthalmological problems can Sjogren’s syndrome present with?

A

Keratconjunctivitis sicca (dry eyes) and inflammation of lacrimal glands.

153
Q

Which ophthalmological problems can Steven-Johnson’s syndrome present with?

A

Conjunctivitis, occlusion of lacrimal glands and corneal ulcers

154
Q

What are signs of central retinal artery occlusion?

A

Relative afferent pupillary defect; pale retina; oedema; thread like vessels

155
Q

What is amaurosis fugax?

A

Transient painless visual loss lasting approx. 5 mins which is a/w central retinal artery occlusion. “Like a curtain coming down”

156
Q

What can be seen on examination of amaurosis fugax?

A

Nothing

157
Q

How to manage amaurosis fugax?

A

Give aspirin and refer to stroke clinic

158
Q

What can be seen in central retinal vein occlusion?

A

Haemorrhages; dilated/torturous veins; macular swelling; papilloedema.

159
Q

How is a central retinal vein occlusion managed?

A

Anti-VEGF given and risk factors assessed

160
Q

How does ischaemic optic neuropathy present?

A

Sudden, profound visual loss with a swollen disc. Temporal headache; jaw claudication; scalp tenderness; amaurosis fugax; malaise; high ESR, PV and CRP.

161
Q

What are the two types of ischaemic optic neuropathy?

A

Arteritic with inflammation or non-arteritic with athersclerosis

162
Q

Describe the pathogenesis of ischaemic optic neuropathy.

A

Lumen of the artery becomes occluded due to inflammation or atherosclerosis.

163
Q

How does a vitreous haemhorrge present?

A

Loss of vision and/or floaters. Loss of red reflex

164
Q

How does retinal detachment present?

A

Painless loss of vision, flashes, floaters, RAPD

165
Q

What are risk factors for age related macular dengeration?

A

Age, smoking, FHx, malnutrition

166
Q

What are the two types of age related macular dengeration?

A

Wet - suddent visual loss

Dry - gradual visual loss

167
Q

Describe the pathogenesis of wet age related macular degeneration.

A

New blood vessels grow under the retina, leakage causes a build up of fluid and scarring

168
Q

How does wet age related macular degeneration present?

A

Central visual loss, distortion/metamorphopsia, haemorrhage, exudates.

169
Q

What is the treatment for age related macular degeneration?

A

Intra-ocular anti-VEGF

170
Q

What is glaucoma?

A

Progressive optic neuropathy most likely due to high IOP resulting in nerve damage and visual loss.

171
Q

What are the two types of glaucoma?

A

Open and closed angle

172
Q

What is the pathogenesis of closed angle glaucoma?

A

Aqueous humour comes up against resistance through the iris and lens channels. This causes the peripheral iris to come forward and obstruct the trabecular meshwork.

173
Q

How does closed angle glaucoma present?

A

Visual loss, headache, n&v.

174
Q

How is open angle glaucoma managed?

A

Lower IOP with drops or oral medication ASAP nad perform laser iridotomy to open the angle

175
Q

How do cataracts present?

A

Hazy, blurred vision, intense glare, cloudy lens

176
Q

How are cataracts managed?

A

Surgical removal with intra-ocular lens implant - only if patient is symptomatic

177
Q

What is seen on examination of open angle glaucoma?

A

Cupped disc, visual field defect, high IOP

178
Q

What is papilloedema?

A

Disc swelling from raised ICP

179
Q

What should always be considered in bilateral papilloedema?

A

Space occupying lesion(s) in the brain until proven otherwise - also consider hypertension.

180
Q

Describe the pathogenesis of papilloedema

A

Increase ICP is transferred to the sub-arachnoid space which surrounds the brain and optic nerve. This causes interruption of axoplasmic flow and venous congestion so discs become swollen.

181
Q

What is the Monro-Kellie hypothesis?

A

The ICP is made of the brain, blood and CSF. An increase in one will result in an decrease of another.

182
Q

What can happen to the brain with increased ICP?

A

Can be squeezed through the foramen magnum, compressing the brainstem resulting in death

183
Q

What is blepharitis?

A

Inflamed eyelids

184
Q

How does blepharitis present?

A

Gritty eyes, foreign body sensation, mild discharge,

185
Q

What are meibomian glands?

A

Tarsal glands which secrete Meibomian fluid (oily part of tears) to stop tears evaporating

186
Q

What can be seen on examination of blepharitis?

A

Seborrhoeic scales on the lashes, distorted lashes, red lid margin, meibomian gland dysfunction, styes

187
Q

How is blepharitis treated?

A

Daily warm bathing and compress of the eyes, tear drops, oral doxycycline for 2-3 months

188
Q

How does bacterial conjunctivitis present?

A

Red eye, gritty eye, stick discharge

189
Q

How is bacterial conjunctivitis manages?

A

Self-limiting over 14 days

190
Q

What are common causes of bacterial conjunctivitis?

A

Staph aureus, strep pneumo, H influenzae

191
Q

What are common causes of follicular conjunctivitis?

A

Adenovirus, herpes simplex/zoster, chlamydial, iatrogenic

192
Q

What dermatological condition is follicular conjunctivitis a/w?

A

Molluscum contagiosum

193
Q

What is a hypopyon?

A

Leukocytic exudate in the anterior chamber

194
Q

How do corneal ulcers present?

A

Severe “needle-like” pain; photophobia; profuse lacrimation; redness and reduced vision

195
Q

How is a corneal ulcer investigated?

A

Corneal scrape for gram stain and culture

196
Q

How are corneal ulcers managed?

A

Ofloxacin hourly for bactieral
Acyclovir ointment 5x per day if viral
Steroids for autoimmune

197
Q

How does anterior uveitis present?

A

Pain; reduced vision; photophobia; circumcorneal redness; flare; hypopyn; small irregular pupil

198
Q

How is anterior uveitis managed?

A

Topical steroids over 4-8 weeks and mydratics (eg cyclopentolate 1% BD).

199
Q

What rheumatic condition can episcleritis be a/w?

A

Gout

200
Q

How is episcleritis managed?

A

Lubricant, topical NSAIDs , mild steroids but is normally self limtiing

201
Q

How does scleritis present?

A

Lotsa pain, violaceous hue.

202
Q

What test should be doen in scleritis?

A

Phenylephrine test

203
Q

What is a phenylephrine test?

A

When drops are administered to one ptotic eye, the eyelids raise and proves that the eye was previously ptotic.

204
Q

How is scleritis managed?

A

NSAIDs, oral steroids and steroid sparing agents

Ophthalmology (2 decks)

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