Optho

Question 1

causes of optic neuritis

Answer 1

MS
diabetes
syphilis

Question 2

optic neuritis investigations?

Answer 2

MRI of the brain and orbits with gadolinium contrast

Question 3

management of optic neuritis?

Answer 3

high-dose steroids
recovery usually takes 4-6 weeks

Question 4

How does optic neuritis present?

Answer 4

• Central scotoma. This is an enlarged blind spot.
• Pain on eye movement
• Impaired colour vision
• Relative afferent pupillary defect

Question 5

risk factors for scleritis?

Answer 5

RA
SLE
sarcoidosis
granulomatosis with polyangiitis

Question 6

How does scleritis present?

Answer 6

red eye
painful
watering / photophobia
gradual decrease in vision

Question 7

Management of scleritis?

Answer 7

1. same-day assessment by an ophthalmologist
2. oral NSAIDs - first-line
3. oral glucocorticoids - severe presentation
4. immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)

Question 8

complications of scleritis?

Answer 8

Perforation of the globe
glaucoma
cataracts
raised intraocular pressure
retinal detachment
uveitis.

Question 9

eye deviated ‘down and out’ + ptosis = ?

Answer 9

third nerve palsy

Question 10

What is orbital cellulitis?

Answer 10

the result of an infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe.

usually caused by spreading URTI

Question 11

What is preorbital cellulitis?

Answer 11

a less serious superficial infection anterior to the orbital septum, resulting from a superficial tissue injury (chalazion, insect bite etc…).

can progress to orbital cellulitis

Question 12

How does orbital cellulitis present?

Answer 12

-Redness / swelling around the eye
- Severe ocular pain
- Visual disturbance
- Proptosis
- Ophthalmoplegia/pain with eye movements
- Eyelid oedema and ptosis
- Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)

Question 13

How do you differentiate preorbital and orbital cellulitis?

Answer 13

reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements = orbital cellulitis

Question 14

Investigations of orbital cellulitis?

Answer 14

CT with contrast
FBC
blood culture

Question 15

Management of orbital cellulitis?

Answer 15

Admission to hospital for IV antibiotics

Question 16

What is glaucoma?

Answer 16

a group of disorders characterised by optic neuropathy due to raised intraocular pressure (IOP).

Question 17

What is acute close angle glaucoma?

Answer 17

Rise in IOP secondary to an impairment of aqueous outflow.

Question 18

Risk factors for Acute close angle glaucoma?

Answer 18

• hypermetropia (long-sightedness)
• pupillary dilatation
• lens growth associated with age

Question 19

Clinical presentation of acute close angle glaucoma?

Answer 19

• severe pain: may be ocular or headache
• decreased visual acuity
• symptoms worse with mydriasis (e.g. watching TV in a dark room)
• hard, red-eye
• haloes around lights
• semi-dilated non-reacting pupil
• corneal oedema results in dull or hazy cornea
• systemic upset may be seen, such as nausea and vomiting and even abdominal pain

Question 20

What is acute close angle glaucoma?

Answer 20

when the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away. This leads to a continual build-up of pressure in the eye.

Question 21

Management of acute close angle glaucoma?

Answer 21

Same day referral to ophthalmologist

Eye drops (beta-blocker, pilocarpine, alpha-2 antagonist) + IV acetazolamide (reduces secretions)

laser iridotomy - definitive management

Question 22

Normal intraocular pressure?

Answer 22

10-21mmHg

Question 23

What is open angle glaucoma?

Answer 23

Gradual increase in resistance through the trabecular meshwork. This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.

Question 24

Presentation of open angle glaucoma?

Answer 24

peripheral vision - tunnel vision
fluctuating pain
headaches
blurred vision
halos

Question 25

Investigations for glaucoma?

Answer 25

Goldmann applanation tonometry - check the intraocular pressure.

Fundoscopy - optic disc cupping and optic nerve health.

Visual field assessment - peripheral vision loss.

Gonioscopy

Question 26

Management of open angle glaucoma?

Answer 26

Prostaglandin analogue eye drops (e.g. latanoprost) - first line.

Second line:
Beta-blockers (e.g. timolol) reduce the production of aqueous humour
Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow

Trabeculectomy - if eye drops fail

Question 27

What is retinal detachment?

Answer 27

When the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium. It is a reversible cause of visual loss (as long as it doesn’t affect the macula)

Question 28

Risk factors for retinal detachment?

Answer 28

Diabetes
myopia (nearsightness)
age
previous cataract surgery
eye trauma e.g. boxing

Question 29

Clinical presentation of retinal detachment?

Answer 29

• new onset floaters and flashes
• sudden onset, painless + progressive loss of vision (described as curtain/shadow arising peripherally going centrally)
• relavant afferent pupillary defect may be seen
• Fundoscopy - red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms

Question 30

Management of retinal detachment?

Answer 30

Urgent referral to ophthalmology (<24hrs)

Question 31

adverse effects of prostaglandin analogues?

Answer 31

brown pigmentation of the iris
increased eyelash length

Question 32

How do beta blockers in acute angle glucoma work?

Answer 32

by reducing aqueous production

Question 33

Vision worse while going down stairs - what is most likely affected?

Answer 33

Trochlear nerve