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MSRA > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is the pathophysiology of acute angle closure glaucoma?

A

OPHTHALMOLOGICAL EMERGENCY

the iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining and leading to a continual increase in intraocular pressure

The pressure builds in the posterior chamber, pushing the iris forward and exacerbating the angle closure

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2
Q

What are some medications that can precipitate acute angle closure glaucoma?

A
  • Adrenergic medications (e.g., noradrenaline)
  • Anticholinergic medications (e.g., oxybutynin and solifenacin)
  • Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
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3
Q

What are some signs on examination of acute angle closure glaucoma?

A
  • Red eye
  • Hazy cornea
  • Decreased visual acuity
  • Mid-dilated pupil
  • Fixed-size pupil
  • Hard eyeball on gentle palpation
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4
Q

What is the initial management of acute angle closure glaucoma?

A

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
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5
Q

How does pilocarpine work?

A

Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent). It also causes ciliary muscle contraction.

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6
Q

How does acetazolamide work?

A

Acetazolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour.

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7
Q

What are some secondary care management in acute angle closure glaucoma?

A
  • Pilocarpine eye drops
  • Acetazolamide (PO/IV)
  • Hyperosmotic agents (e.g., IV mannitol) increase the osmotic gradient between the blood and the eye
  • Timolol is a beta blocker that reduces the production of aqueous humour
  • Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
  • Brimonidine is a sympathomimetics that reduces aqueous humour production and increases uveoscleral outflow
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8
Q

What is the definitive management in acute angle closure glaucoma?

A

Laser iridotomy

This involves making a hold in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber. This relieves the pressure pushing the iris forward against the cornea and opens the pathway for the aqueous humour to drain.

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9
Q

What is glaucoma?

A

Glaucoma refers to the optic nerve damage caused by a rise in intraocular pressure. Raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.

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10
Q

What is normal intraocular pressure?

A

10-21 mmHg

Treatment is for 24mmHg and above

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11
Q

What is the pathophysiology of open-angle glaucoma?

A

gradual increase in resistance to flow through trabecular meshwork, intraocular pressure slowly builds up within the eye

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12
Q

How does raised intraocular pressure affect the optic disc?

A

cupping of the optic disc

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13
Q

How does open-angle glaucoma usually present?

A

May be asymptomatic - Dx by routine eye testing

Affects peripheral vision first => gradual onset peripheral vision loss/tunnel vision

Also may cause:
- fluctuating pain
- headaches
- blurred vision
- halos around lights, esp at night

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14
Q

How to measure intraocular pressure? What is the gold standard?

A

Non-contact tonometry (air puff thing)

Goldmann applanation tonometry - gold-standard
:::::::device acc touches the cornea and applies pressure

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15
Q

How is open-angle glaucoma usually diagnosed?

A

Diagnosis is based on:

  • Goldmann applanation tonometry for the intraocular pressure
  • Slit lamp assessment for the cup-disk ratio and optic nerve health
  • Visual field assessment for peripheral vision loss
  • Gonioscopy to assess the angle between the iris and cornea
  • Central corneal thickness assessment
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16
Q

What is the management of open-angle glaucoma?

A

360° selective laser trabeculoplasty for all pts

1st line Rx: Prostaglandin analogue eye drops (e.g., latanoprost) - increase uveoscleral outflow

other eye drops:
- 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

Surgical: trabeculectomy

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17
Q

How do prostaglandin analogues work? What are some notable side effects?

A

e.g. latanoprost

work by increasing uveoscleral outflow

S/E: eyelash growth, eyelid pigmentation, iris pigmentation (browning)

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18
Q

What is anterior uveitis?

A

inflammation of the anterior uvea. The uvea consists of the iris, ciliary body and choroid. The choroid is the layer between the retina and the sclera. Intermediate uveitis and posterior uveitis are less common.

usually caused by autoimmune process, but can be infection, trauma, ischaemia, malignancy

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19
Q

What are some associated autoimmune conditions with anterior uveitis?

A
  • seronegative spondyloarthropathies
  • IBD
  • sarcoidosis
  • Behcet’s disease
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20
Q

What are the symptoms of anterior uveitis?

A
  • painful red eye (dull,aching pain)
  • reduced visual acuity
  • photophobia
  • excessive lacrimation
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21
Q

What are some signs/examination findings in anterior uveitis?

A
  • ciliary flush - ring of red spreading from cornea outwards
  • miosis (constricted pupils) - sphincter muscle contraction
  • abnormally shaped pupil - posterior adhesions pulling iris
  • hypopyon (inflammatory cells fluid collection)
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22
Q

What is the management of anterior uveitis?

A

urgent assessment and management by ophthalmologist

1st line: steroids (eye drops/PO/IV) and cycloplegic eye drops (cyclopentolate or atropine) ::: cycloplegics dilate pupil and reduce pain due to spasms by paralysing ciliary muscles

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23
Q

What is retinal vein occlusion?

A

thrombus in retinal veins - centra or branch retinal veins
branch veins drain into central vein, branch blockage affects that area, central vein affects whole retina

=> venous congestion in retina => blood leakage into retina => macular oedema and retinal haemorrhages => retinal damage and vision loss

classified into:
- ischaemic - leads to release of VEGF (vascular endothelial growth factor) => neovascularisation
- non-ischaemic

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24
Q

How does retinal vein occlusion present?

A
  • painless blurred vision/vision loss
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25
Q

What are the findings on fundoscopy in retinal vein occlusion?

A
  • dilated tortuous retinal veins
  • flame and blot haemorrhages
  • retinal oedema
  • cotton wool spots
  • hard exudates

“blood and thunder” appearance

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26
Q

What is the management of retinal vein occlusion?

A

immediate referral to opthalmologist

  • Anti-VEGF therapies (e.g., ranibizumab and aflibercept)
  • Dexamethasone intravitreal implant (to treat macular oedema)
  • Laser photocoagulation (to treat new vessels)
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27
Q

What are some causes of central retinal artery occlusion?

A

most common - Atherosclerosis

GCA - vasculitis affects ophthalmic or central retinal artery

28
Q

How does central retinal artery occlusion present?

A

Sudden painless loss of vision “curtains coming down”

Relative Afferent Pupillary Defect - affected pupil constricts LESS with light than other eye

29
Q

What can be seen on fundoscopy in central retinal artery occlusion?

A

Pale retina
Cherry red spot (fovea thinner showing red-coloured choroid below)

30
Q

What are some differentials for sudden painless vision loss?

A
  • Central retinal artery occlusion
  • Central retinal vein occlusion
  • Retinal detachment
  • Vitreous haemorrhage (diabetic retinopathy)
31
Q

What is the management of central retinal artery occlusion?

A

vision-threatening emergency = immediate referral

if GCA, test with ESR and temporal artery biopsy, treat with high-dose systemic steroids

Immediate management options attempt to dislodge/resolve the blockage. There is no consensus, guidelines or solid evidence base for these options:
- Ocular massage (massaging the eye)
- Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure)
- Inhaled carbogen (5% carbon dioxide and 95% oxygen) (to dilate the artery)
- Sublingual isosorbide dinitrate (to dilate the artery)
- Oral pentoxifylline (to dilate the artery)
- Intravenous acetazolamide (to reduce the intraocular pressure)
- Intravenous mannitol (to reduce the intraocular pressure)
- Topical timolol (to reduce the intraocular pressure)

32
Q

How does conjunctivitis present?

A
  • red, bloodshot eye
  • itchy, gritty sensation
  • discharge

No pain/photophobia/reduced visual acuity

33
Q

What is the difference in presentation between bacterial and viral conjunctivitis?

A

Bac - purulent discharge, worse in morning (eyes stuck together), contagious, spread to other eye

Viral - clear discharge, assoc w/ other symptoms of viral infection (dry cough, sore throat, blocked nose), may have tender pre-auricular lymph nodes, contagious

34
Q

What are some differentials of painful red eye?

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury
35
Q

What are some differentials for painless red eye?

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
36
Q

What is the management of conjunctivitis?

A

Resolves in 1-2 weeks without treatment
Hygiene to stop spreading
Cleaning eyes with cooled boiled water and cotton wool

Chloramphenicol or fusidic acid for bac

Neonates under 1 m/o need URGENT assessment - maybe gonococcal infection which can cause permanent vision loss

37
Q

What are the risk factors for developing cataracts?

A
  • Increasing age
  • Smoking
  • Alcohol use
  • Diabetes
  • Steroid use
  • Hypocalcaemia
38
Q

What are the typical symptoms of cataracts?

A
  • Slow reduction in visual acuity
  • Progressive blurring
  • Faded or yellowed colors
  • Starbursts around lights, especially at night
39
Q

What is the key examination finding for cataracts?

A

Loss of the red reflex

40
Q

What is the management of cataracts?

A

If symptoms are manageable, no intervention is needed. Cataract surgery involves removing the cloudy lens and replacing it with an artificial lens. Surgery is a day case under local anaesthetic and has good results.

41
Q

What is endophthalmitis, and why is it important?

A

Endophthalmitis is a rare but serious complication of cataract surgery, involving infection and inflammation inside the eye. It can lead to vision loss and is treated with intravitreal antibiotics (injected into the eye).

42
Q

What can be discovered after cataract surgery, and why is this important?

A

Cataracts can obscure other conditions like macular degeneration or diabetic retinopathy. After surgery, these conditions may become apparent and still contribute to reduced visual acuity.

43
Q

What are the two types of AMD?

A
  1. Wet AMD (also called neovascular), accounting for 10% of cases
  2. Dry AMD (also called non-neovascular), accounting for 90% of cases
44
Q

What are drusen and why are they important in AMD?

A

Drusen are yellow deposits of proteins and lipids found between the retinal pigment epithelium and Bruch’s membrane. While small drusen can be normal in older adults, larger or frequent drusen are an early sign of macular degeneration.

45
Q

What happens in wet AMD?

A

In wet AMD, new blood vessels grow from the choroid layer into the retina (neovascularization). These vessels can leak fluid or blood, causing oedema and faster vision loss. Vascular endothelial growth factor (VEGF) stimulates this process and is the target of treatments.

46
Q

What are some risk factors for developing AMD?

A
  • Older age
  • Smoking
  • Family history
  • Cardiovascular disease (e.g., hypertension)
  • Obesity
  • Poor diet (low in vitamins, high in fat)
47
Q

How does AMD typically present?

A
  • Gradual loss of central vision
  • Reduced visual acuity
  • Metamorphopsia (straight lines appear wavy)
  • Difficulty reading small text

Wet AMD progresses rapidly, often causing significant vision loss within days to years.

48
Q

What examination findings suggest AMD?

A
  • Reduced visual acuity (Snellen chart)
  • Scotoma (central vision loss)
  • Distortion on Amsler grid
  • Drusen visible on fundoscopy
  • OCT and fluorescein angiography to assess retinal layers and blood supply in wet AMD
49
Q

What is the management for dry AMD?

A
  • Monitoring
  • Avoiding smoking
  • Controlling blood pressure
  • Vitamin supplementation to slow progression (some evidence supports this)

There is no specific treatment for dry AMD.

50
Q

How is wet AMD treated?

A

Wet AMD is treated with anti-VEGF medications (e.g., ranibizumab, aflibercept), which block the action of VEGF to slow vessel growth. These are given as intravitreal injections, usually monthly.

51
Q

How can you differentiate AMD from glaucoma based on vision loss?

A

AMD is associated with central vision loss and wavy lines (metamorphopsia), while glaucoma is associated with peripheral vision loss and halos around lights.

52
Q

What are the key pathophysiological changes in diabetic retinopathy?

A
  • Increased vascular permeability => leaking blood vessels => blot haemorrhages and hard exudates (yellow-white lipid deposits).
  • Microaneurysms (small bulges in blood vessel walls) and venous beading (veins resemble a string of beads).
  • Cotton wool spots (fluffy white patches from nerve damage).
  • Intraretinal microvascular abnormalities (IRMA), where capillaries become tortuous and dilated.
  • Neovascularisation, the development of new, fragile blood vessels in the retina.
53
Q

What are hard exudates and how do they form in diabetic retinopathy?

A

Hard exudates are yellow-white deposits of lipids and proteins in the retina, formed due to leaking blood vessels as a result of hyperglycemia.

54
Q

How is diabetic retinopathy graded?

A

Diabetic retinopathy is graded based on fundus findings:
- Background: microaneurysms, retinal haemorrhages, hard exudates, cotton wool spots.
- Pre-proliferative: venous beading, multiple blot haemorrhages, intraretinal microvascular abnormalities (IRMA).
- Proliferative: neovascularisation, vitreous haemorrhage.

55
Q

What is the difference between non-proliferative and proliferative diabetic retinopathy?

A
  • Non-proliferative includes background and pre-proliferative stages with damage but no new blood vessels.
  • Proliferative involves neovascularisation, the formation of new blood vessels, which increases the risk of vision loss and complications.
56
Q

What is diabetic maculopathy?

A

Diabetic maculopathy involves changes in the macula, leading to:
- Exudates within the macula.
- Macular oedema, swelling that affects central vision.

57
Q

What are the complications of diabetic retinopathy?

A
  • Vision loss
  • Retinal detachment
  • Vitreous haemorrhage (bleeding into the vitreous)
  • Rubeosis iridis (new blood vessels in the iris) leading to neovascular glaucoma
  • Optic neuropathy
    Cataracts
58
Q

How is non-proliferative diabetic retinopathy managed?

A

It is managed through close monitoring and careful diabetic control to prevent progression to proliferative retinopathy.

59
Q

What are the treatment options for proliferative diabetic retinopathy?

A
  • Pan-retinal photocoagulation (PRP): laser treatment to prevent neovascularisation.
  • Anti-VEGF medications by intravitreal injection.
  • Surgery (e.g., vitrectomy) for severe cases.
60
Q

What treatment options exist for macular oedema in diabetic retinopathy?

A

An intravitreal implant containing dexamethasone may be used to reduce swelling and improve vision in cases of macular oedema.

61
Q

What is silver wiring or copper wiring in hypertensive retinopathy?

A

These terms refer to the thickened and sclerosed arterioles that reflect more light due to damage caused by chronic hypertension.

62
Q

What is arteriovenous (AV) nipping?

A

AV nipping is where the thickened and hardened arterioles compress veins at the crossing points, seen in hypertensive retinopathy.

63
Q

What causes cotton wool spots in hypertensive retinopathy?

A

Cotton wool spots are caused by ischaemia and infarction in the retina, which damages nerve fibres.

64
Q

What are hard exudates in hypertensive retinopathy?

A

Hard exudates are lipid deposits on the retina caused by leaking blood vessels due to high blood pressure.

65
Q

What are the types of retinal haemorrhages seen in hypertensive retinopathy?

A
  • Dot and blot haemorrhages: occur deeper in the inner nuclear or outer plexiform layers.
  • Flame haemorrhages: occur in the nerve fibre layer.
66
Q

What causes papilloedema in hypertensive retinopathy?

A

Papilloedema is caused by optic nerve ischaemia, leading to optic nerve swelling (oedema), often seen in severe hypertension.

67
Q

What is the Keith-Wagener Classification for hypertensive retinopathy?

A

Stage 1: Mild arteriolar narrowing.

Stage 2: Focal vessel constriction and AV nipping.

Stage 3: Cotton wool spots, haemorrhages, and hard exudates.

Stage 4: Papilloedema.

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