High Yield Opthal and Derm

Question 1

What is normal intraocular pressure?

Answer 1

10-21 mmHg

It is created by the resistance to flow of aqueous humour through the trabecular meshwork

Question 2

Raised intraocular pressure causes cupping of the optic disc.

What is this?

Answer 2

In the centre of the optic disc is an indent called the optic cup, which is usually less than 50% of the size of the optic disc.

Raised intraocular pressure causes this indent to become wider and deeper, described as “cupping”. A cup-disk ratio greater than 0.5 is abnormal.

Question 3

Risk factors for open-angle glaucoma include:

Answer 3

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Hypertension
Diabetes mellitus
Corticosteroids

Question 4

In open-angle glaucoma, the rise in IOP may be asymptomatic for a long time and diagnosed by routine eye testing.

How may it present if symptomatic?

Answer 4

Peripheral visual field loss
Decreased visual acuity (blurred vision)
Fluctuating pain
Headaches
Halos around lights, particularly at night

Question 5

How does open-angle glaucoma present on fundoscopy?

Answer 5

1. Optic disc cupping - cup-to-disc ratio >0.7, 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

Question 6

When is treatment initiated for open-angle glaucoma?

Answer 6

at an intraocular pressure of 24 mmHg or above

Question 7

How can open-angle glaucoma be managed?

Answer 7

Prostaglandin analogue eye drops (e.g., latanoprost) are the first-line medical treatment - increase uveoscleral outflow

360° selective laser trabeculoplasty - laser is directed at the trabecular meshwork, improving drainage

Question 8

Other than prostaglandin analogues, what eye drops may be used in the mx of open angle glaucoma?

Answer 8

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 the uveoscleral outflow

Question 9

Risk factors for acute angle-closure glaucoma include:

Answer 9

Increasing age
Family history
Female (four times more likely than males)
Chinese and East Asian ethnic origin
Shallow anterior chamber

Question 10

How do patients with acute angle-closure glaucoma present?

Answer 10

Severely painful red eye
Decreased visual acuity (blurred vision)
Halos around lights
Associated headache, nausea and vomiting
Symptoms worse with mydriasis (e.g. watching TV in a dark room)

Question 11

What may be seen on examination of patients with acute angle-closure glaucoma?

Answer 11

Red eye
Hazy cornea
Semi-dilated non-reactive pupil
Hard eyeball on gentle palpation
Decreased visual acuity

Question 12

How can acute angle closure glaucoma be managed in the community?

Answer 12

Acute angle-closure glaucoma requires immediate admission!

Measures while waiting for an ambulance are:

Lying the patient on their back without a pillow
Pilocarpine eye drops (2% for blue and 4% for brown eyes)
Acetazolamide 500 mg orally
Analgesia and an antiemetic, if required

Question 13

How can acute angle closure glaucoma be managed in secondary care?

Answer 13

Pilocarpine eye drops

IV Acetazolamide

Hyperosmotic agents (e.g. IV mannitol)

Timolol, Dorzolamide - both reduce the production of aqueous humour via different mechanisms

Brimonidine - reduces aqueous humour production and increases uveoscleral outflow

Question 14

What is the most common cause of blindness in the UK?

Answer 14

Age-related macular degeneration (AMD)

Question 15

Give some risk factors for AMD?

Answer 15

Older age
Family history
Smoking (x2 risk)
Cardiovascular disease (e.g., hypertension)
Obesity
Poor diet (low in vitamins and high in fat)

Question 16

How does AMD typically present?

Answer 16

Visual changes associated with AMD tend to be unilateral, with:

Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphopsia)
Worsening night vision

Patients often present with a gradually worsening ability to read small text.

Question 17

What are the key examination findings for AMD?

Answer 17

Reduced visual acuity using a Snellen chart

Scotoma (an enlarged central area of vision loss)

Amsler grid test can be used to assess for the distortion of straight lines seen in AMD

Drusen may be seen during fundoscopy

Question 18

What is the pathophysiology of diabetic retinopathy?

Answer 18

Hyperglycaemia (high blood sugar) damages the retinal small vessels and endothelial cells.

Damage to the blood vessel walls leads to microaneurysms and venous beading

Increased vascular permeability leads to leaking blood vessels, blot haemorrhages and hard exudates

Damage to nerve fibres in the retina causes fluffy white patches called cotton wool spots to form on the retina

Question 19

What are the potential complications of diabetic retinopathy?

Answer 19

Vision loss
Retinal detachment
Vitreous haemorrhage (bleeding into the vitreous humour)
Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
Optic neuropathy
Cataracts

Question 20

Give some risk factors for developing cataracts

Answer 20

Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia

Question 21

How do cataracts present?

Answer 21

Symptoms are usually asymmetrical, as both eyes are affected separately.

It presents with:
Slow reduction in visual acuity
Progressive blurring of the vision
Colours becoming more faded, brown or yellow
Starbursts can appear around lights, particularly at night

Question 22

Give a complication of cataract surgery

Answer 22

Endophthalmitis : inflammation of the inner contents of the eye, usually caused by infections

Can lead to vision loss

Treated with intravitreal antibiotics injected directly into the eye

Question 23

Give some causes of Mydriasis (Dilated Pupil)

Answer 23

Trauma
Third nerve palsy
Raised ICP
Acute angle-closure glaucoma
Stimulants (e.g., cocaine)
Anticholinergics (e.g., oxybutynin)
Holmes-Adie syndrome

Question 24

Give some causes of Miosis (Constricted Pupil)

Answer 24

Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine

Question 25

How can you test for Horner syndrome?

Answer 25

Cocaine eye drops:
acts on the eye to stop noradrenalin re-uptake at the NMJ which causes a normal eye to dilate

In Horner syndrome, the nerves are not releasing noradrenalin, so blocking re-uptake makes no difference, and there is no pupil reaction.

Alternatively, low-dose adrenalin eye drops (0.1%) will dilate the pupil in Horner syndrome but not a normal pupil.

Question 26

Causes of an acute painful red eye include:

Answer 26

Acute angle-closure glaucoma
Anterior uveitis
Scleritis
Keratitis
Corneal abrasions or ulceration
Foreign body
Traumatic or chemical injury

Question 27

Causes of an acute painless red eye include:

Answer 27

Conjunctivitis
Episcleritis
Subconjunctival haemorrhage

Question 28

What are the potential complications of Pan-retinal photocoagulation?

Answer 28

50% of patients develop reduction in their visual fields due to the scarring of peripheral retinal tissue

decrease in night vision (majority of rod cells - which are responsible for night vision - are located in the peripheral retina which is targeted by PRP)

Question 29

What type of hypersensitivity reaction is SJS?

Answer 29

Type 4 hypersensitivity reaction – unlike anaphylaxis, symptoms gradually come on as offending drug builds up in the body

Question 30

What should you ask all patients with suspected SJS?

Answer 30

Always ask about palms, soles and mucous membranes – involvement of these is the distinguishing feature

Always ask about OTC meds as well as prescribed
Ask about recent infection

Question 31

What systemic sxs may be seen in SJS?

Answer 31

Pyrexia
Sore throat
Flu like sxs
Sore red eyes, conjunctivitis
Arthralgia

Question 32

What is the difference between SJS and TENS?

Answer 32

SJS = 10% body involvement
TENS is the same as SJS but with over 30% body involvement

Question 33

How might you investigate SJS?

Answer 33

Skin biopsy
Culture – swab culture or blood culture
Blood tests for inflammatory markers
CXR for lung involvement

Question 34

What can be used to predict mortality in SJS?

Answer 34

SCORTEN score can be used to predict mortality in SJS and TENS cases:
Age >40
Presence of malignancy
HR >120
Initial epidermal detachment >10%

Question 35

How can you manage SJS?

Answer 35

Stop offending meds
IV Fluids
Wound care, Eye care
Analgesics, topical steroids, abx
IV Immunoglobulins (within 72 hours)

Question 36

What is pyoderma gangrenosum? How would you describe the lesions?

Answer 36

Autoimmune neutrophilic dermatosis
Usually on the legs because it is a common site of trauma
Well demarcated, erythematous, ulcerative nodule on a background of normal skin

Question 37

How can you manage pyoderma gangrenosum?

Answer 37

Potent topical steroid – e.g. dermovate
Can also do intralesional steroid injections
Can give doxycycline because it is a very good anti-neutrophil drug
Can give oral prednisolone if severe