opthalmology Flashcards

1
Q

Acute angle closure glaucoma:
1. Features
2. Investigations (2)

A
  1. Features of acute angle closure glaucoma:
    - 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
  2. Investigations:
    1- tonometry to assess for elevated IOP
    2- gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle
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2
Q

Acute angle closure glaucoma- initial management

A

combination of eye drops, for example:
- a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
- a beta-blocker (e.g. timolol, decreases aqueous humour production)
- an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
- intravenous acetazolamide- reduces aqueous secretions

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3
Q

acute angle closure glaucoma- definitive management

A

the definitive management for this condition is a peripheral iridotomy to relief the intraocular pressure.

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4
Q

What is blepharitis?
1. causal mechanisms? (2)
2. Associated condition?

A

inflammation of the eyelid margins

  1. causal mechanisms:
    - Posterior blepharitis (most common)- is due to meibomian gland dysfunction
    - Anterior blepharitis - less common, is due to staph infection or seborrheic dermatitis
  2. Associated with rosacea
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5
Q

Blepharitis
1. Features
2. Management (3)

A
  1. Features:
    - usually bilateral
    - grittiness and discomfort around eyelid margins
    - eyelids may be sticky in the morning
    - Swollen eyelids may be seen in staphylococcal blepharitis
    - styes and chalazions are more common in patients with blepharitis
    - there can be secondary conjunctivitis
  2. Management:
    1- softening of the lid margin using hot compresses twice a day
    2- ‘lid hygiene’ - mechanical removal of the debris from lid margins
    - cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used
    - an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled
    3- artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film
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6
Q

What is a cataract? what is the biggest risk factor?

A

A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision. Cataracts are the leading cause of curable blindness worldwide.

Ageing is the biggest risk factor- One study found that 30% of individuals aged 65 and over had a visually-impairing cataract in either one or both eyes

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7
Q

Cataracts:
1. Symptoms (4)
2. Sign
3. Investigations (2)

A
  1. Symptoms of a cataract:
    1 - Reduced vision
    2- Faded colour vision: making it more difficult to distinguish different colours
    3- Glare: lights appear brighter than usual
    4- Halos around lights
  2. Sign: Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
  3. Investigations:
    1- Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
    2- Slit-lamp examination. Findings: visible cataract
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8
Q

classification of cataracts (4)

A

1- Nuclear: change lens refractive index, common in old age
2- Polar: localized, commonly inherited, lie in the visual axis
3- Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
4- Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy

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9
Q

management of cataracts:
1. Early disease
2. Definitive management

A
  1. Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed
  2. Surgery is the only definitive management of cataracts. This involves removing the cloudy lens and replacing this with an artificial one. Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.
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10
Q

central retinal vein occlusion- presentation
Fundoscopy signs? (2)

A
  • sudden, painless reduction or loss of visual acuity, usually unilaterally
  • fundoscopy shows (1) widespread hyperaemia and (2) severe retinal haemorrhages - ‘stormy sunset’
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11
Q

central retinal vein occlusion- management

A
  • the majority of patients are managed conservatively
  • indications for treatment in patients with CRVO include:
    1. macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
    2. retinal neovascularization - laser photocoagulation
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12
Q

central retinal artery occlusion:
1. Causes
2. features (3)
3. Management/prognosis?

A
  1. Thromboembolism (e.g. from atherosclerosis) or arteritis (e.g. temporal arteritis)
  2. Features:
    1- sudden, painless unilateral visual loss
    2- relative afferent pupillary defect
    3- ‘cherry red’ spot on a pale retina
  3. Management is difficult and the prognosis is poor
    any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
    if a patient presents acutely then Intraarterial thrombolysis may be attempted but currently, trials show mixed results.
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13
Q

What is chronic open angle glaucoma?

A

Chronic open angle glaucoma refers to optic neuropathy with the death of optic nerve fibres, with or without raised intraocular pressure (IOP). Glaucoma leads to characteristic visual field changes over time.

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14
Q

what is the difference between open angle glaucoma and angle closure glaucoma?

A

In open-angle, eye pressure builds gradually, but in closed-angle, it’s far more sudden. Open-angle glaucoma is not a medical emergency, but can cause vision issues over time; closed-angle is a medical emergency requiring immediate medical attention.9

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15
Q

fundoscopy signs of chronic open angle glaucoma (4) and finding on tonometry?

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
  5. IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
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16
Q

chronic open angle glaucoma- management (3)

A
  1. first line: prostaglandin analogue (PGA) eyedrop e.g. Latanoprost
  2. second line: beta-blocker (e.g. timolol), carbonic anhydrase inhibitor, (e.g. Dorzolamide) or sympathomimetic eyedrops (e.g. Brimonidine, an alpha 2 agonist)
  3. if more advanced: surgery or laser treatment can be tried
17
Q

how common is infective conjunctivitis? how does it typically present?

A

it is the most common eye problem which presents to primary care
sore, red eyes associated with a sticky discharge

18
Q

management of infective conjunctivitis
1. most cases
2. antibiotics?
3. contact lense wearers
4. hygiene and school eclusion

A
  1. normally a self-limiting condition that usually settles without treatment within 1-2 weeks
  2. topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially whereas chloramphenicol ointment is given qds initially
    Topical fusidic acid is an alternative and should be used for pregnant women. Treatment is twice daily
  3. contact lens users:
    topical fluoresceins should be used to identify any corneal staining
    treatment as above
    contact lens should not be worn during an episode of conjunctivitis
  4. advice should be given not to share towels
    school exclusion is not necessary
19
Q

management of allergic conjunctivitis

A

first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil

20
Q

Diabetic retinopathy:
1. Pathophysiology
2. Changes seen in diabetic retinopathy (3)

A
  1. Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes

changes:
1. Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy.
2. Pericyte dysfunction predisposes to the formation of microaneurysms.
3. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

21
Q

associated condition:
- microaneurysms
- blot haemorrhages
- hard exudates
- cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA)

A

Moderate non-proliferative diabetic retinopathy

22
Q

associated condition:
- blot haemorrhages and microaneurysms in 4 quadrants
- venous beading in at least 2 quadrants
- IRMA in at least 1 quadrant

A

severe non-proliferative diabetic retinopathy

23
Q

Associated condition:
- retinal neovascularisation - may lead to vitrous haemorrhage
- fibrous tissue forming anterior to retinal disc
- more common in Type I DM, 50% blind in 5 years

A

proliferative diabetic retinopathy

24
Q

associated condition:
- hard exudates and other ‘background’ changes on macula
- more common in type II diabetes

A

Diabetic maculopathy

25
Q

diabetic maculopathy management

A

if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

26
Q

non-proliferative diabetic retinopathy management

A

regular observation
if severe/very severe consider panretinal laser photocoagulation

27
Q

proliferative diabetic retinopathy management (3)

A
  1. panretinal laser photocoagulation: following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
  2. intravitreal VEGF inhibitors:
    often now used in combination with panretinal laser photocoagulation
    examples include ranibizumab
    strong evidence base suggests they both slow progression of proliferative diabetic retinopathy and improve visual acuity
  3. if severe or vitreous haemorrhage: vitreoretinal surgery
28
Q
  1. most common cause of keratitis in contact lens wearers
  2. cause of acanthamoebic keratitis
  3. associated parasitic cause
  4. management (3)
A
  1. pseudomonas aeruginosa
  2. contaminated soil or water
  3. onchocercal keratitis (‘river blindness’)
  4. management:
    1- stop using contact lens until the symptoms have fully resolved
    2- topical antibiotics; typically quinolones are used first-line
    3- cycloplegic for pain relief
    e.g. cyclopentolate