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FINALS > OPTHALMOLOGY > Flashcards

OPTHALMOLOGY Flashcards

1
Q

What is the difference between Episcleritis and scleritis?

A 
Scleritis = painful
Episcleritis = not painful
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2
Q

What is a key cause of corneal abrasions?

A

Herpes simplex

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3
Q

What is the most common cause of Episcleritis?

A

idiopathic

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4
Q

What are the four slit lamp signs seen in anterior uveitis?

A

conjunctival injection
keratin precipitates
anterior chamber cells
posterior synechiae

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5
Q

What is glaucoma?

A

Glaucoma refers to the optic nerve damage that is caused by a significant rise in intraocular pressure.

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6
Q

What causes the raised intraocular pressure in gluacoma?

A

The drainage of aqueous fluid is blocked.

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7
Q

What is the normal intraocular pressure?

A

10-21 mmHg

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8
Q

How is normal intraocular pressure maintained?

A

Trabecular mesh

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9
Q

What is the pathophysiology of open angle glaucoma?

A

Thickening of the trabecular mesh slows the drainage of aqueous fluid.

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10
Q

What is cupping?

A

Cup (small indent in the centre of the optic disc) becomes more than 0.5x the diameter of the optic disc.

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11
Q

What are risk factors for open angle glaucoma?

A

Black ethnicity
Age
Family history
Near sightedness (myopia)

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12
Q

When should you receive screening if you have a positive family history of glaucoma?

A

Annual screening from the age of 40

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13
Q

What is the presentation of open angle glaucoma?

A

Often asymptomatic

Visual field changes (tunnel vision)
Headaches
Pain
Halos appearing around lights (worse at night)

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14
Q

How is vision affected?

A

Peripheral vision is affected first

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15
Q

How is open angle glaucoma usually picked up?

A

Optometrist (incidental)

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16
Q

How is intraocular pressure measured?

A
  1. Non-contact tonometry

2. Goldmann applanation tonometry

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17
Q

What is the gold standard way to measure intraocular pressure?

A

Goldmann applanation tonometry (using a slit lamp)

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18
Q

How can cupping be visualised?

A

Fundoscopy

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19
Q

Which three tests are used to make the diagnosis of open angle glaucoma?

A
  1. Goldmann applanation tonometry
  2. Fundoscopy
  3. Visual fields assessment
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20
Q

At what intraocular pressure is treatment commenced for open angle glaucoma?

A

24 mmHg

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21
Q

What is the first-line treatment for open-angle glaucoma?

A

Prostaglandin analogue eye drops (Latanoprost)

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22
Q

Name some side-effects of prostaglandin analogue eye drops.

A

Browning of the iris
Pigmentation of the eyelid
Lengthening of the eyelashes

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23
Q

Name three other medical options for treating open angle glaucoma.

A
  1. Beta-blockers - Timolol
  2. Carbonic anhydrase inhibitors - Dorzolamide
  3. Sympathomimetics - Brimonidine
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24
Q

What is tried if eyedrops are ineffective?

A

Surgery - Trabeculectomy

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25
Q

What is the pathophysiology of acute closed angle glaucoma?

A

Acute angle-closure glaucoma occurs 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. The pressure builds up particularly in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle.

Ophthalmology emergency

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26
Q

What are the risk factors for closed angle glaucoma?

A 
Age
Family history
Chinese/Asian ethnicity
Female
Shallow anterior chamber
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27
Q

Which medications can precipitate acute closed angle glaucoma?

A

Adrenergic medications - noradrenaline
Anticholinergic medications - oxybutynin and solifenacin
Tricyclic antidepressants - amitriptyline

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28
Q

How does acute closed angle glaucoma present?

A

Painful, red eye
Blurred vision
Halos around lights
Headache, nausea, vomiting

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29
Q

What can be seen on examination in closed angle glaucoma?

A 
Red-eye
Teary
Hazy cornea
Dilated pupil
Decreased visual acuity
Firm eyeball on palpation
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30
Q

What can be done in primary care for acute closed angle glaucoma?

A

Lie down
Pilocarpine eye drops (2% for blue, 4% for brown)
Give acetazolamide 500mg PO
Give analgesia and an antiemetic if required

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31
Q

How does pilocarpine act?

A

Acts on muscarinic receptors
Causes sphincter muscles in the iris to contract
Pupil constricts which allows aqueous humour to drain

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32
Q

What are the side effects of pilocarpine?

A

Headaches
Blurred vision
Constricted pupil

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33
Q

What does miotic mean?

A

Constricts the pupil

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34
Q

What is the management of acute closed angle glaucoma in secondary care?

A 
Pilocarpine
Acetazolamide
Hyperosmotic agents - glycerol/mannitol
Timolol
Dorzolamide
Brimonidine
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35
Q

What is the definitive treatment of acute closed angle glaucoma?

A

Laser iridotomy

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36
Q

What is anterior uveitis?

A

inflammation in the anterior part of the uvea

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37
Q

What conditions are associated with acute anterior uveitis?

A

HLA B27
• Ankylosing spondylitis
• Inflammatory bowel disease
Reactive arthritis

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38
Q

What conditions are associated with chronic anterior uveitis?

A 
• Sarcoidosis
• Syphilis
• Lyme disease
• Tuberculosis
Herpes virus
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39
Q

How does anterior uveitis present?

A 
Painful red eye
Reduced visiual acuity
Floaters and flashes
Miosis
Photophobia (ciliary muscle spasm)
Pain on eye movement
Lacrimation
Abnormally shaped pupil
Hypopyon
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40
Q

What is the management of anterior uveitis?

A

Referral for same day assessment

Steroids
Cycloplegic-mydriatic eye drops
Immunosuppressants

41
Q

Name 4 eyelid disorders.

A

Blepharitis

Styes

Chalazion

Entropion

Ectropion

Trichiasis

Periorbital cellulitis

Orbital cellulitis

42
Q

Which eyelid disorders require same day referral to ophthalmology?

A 
Entropion
Ectropion (if concern over eyesight)
Trichiasis
Periorbital cellulitis
Orbital cellulitis (A&E)
43
Q

How can you distinguish between a chalazion and a stye?

A 
Stye = tender
Chalazion = non-tender
44
Q

What is the management of trichiasis?

A

Epilation
Electrolysis
Cryotherapy
Laser treatment

45
Q

What is the management of periorbital cellulitis?

A

IV or PO Abx

46
Q

How can you distinguish between periorbital and orbital cellulitis?

A

CT head

47
Q

Describe the anatomical origin of the central retinal artery

A

central retinal artery supplies the blood to the retina. It is a branch of the ophthalmic artery, which is a branch of the internal carotid artery.

48
Q

What is the most common cause of occlusion of the retinal artery?

A

Atherosclerosis

49
Q

Give two causes for central retinal artery occlusion

A

Atherosclerosis

Giant cell arteritis

50
Q

What are the risk factors for central retinal artery occlusion?

A 
• Older age
• Family history
• Smoking 
• Alcohol consumption
• Hypertension
• Diabetes
• Poor diet
• Inactivity
Obesity
51
Q

How does central retinal artery occlusion present?

A

sudden painless loss of vision

RAPD

52
Q

Why does central retinal artery occlusion cause an RAPD?

A

input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex.

53
Q

What is shown on fundoscopy in central retinal artery occlusion?

A

pale retina with a cherry-red spot

54
Q

What is the management of central retinal artery occlusion?

A

Same-day assessment by opthalmologist

55
Q

Describe the immediate management of central retinal artery occlusion

A
  • Ocular massage
  • Removing fluid from the anterior chamber to reduce intraocular pressure.
  • Inhaling carbogen (a mixture of 5% carbon dioxide and 95% oxygen) to dilate the artery
  • Sublingual isosorbide dinitrate to dilate the artery

(^aims to dislodge the thrombus)

56
Q

What is the long-term management of central retinal artery occlusion?

A

Treating reversible risk factors

Prevent CVS disease

57
Q

What is the pathophysiology of CRVO?

A

Blockage of a retinal vein causes pooling of blood in the retina. This results in leakage of fluid and blood causing macular oedema and retinal haemorrhages. This results in damage to the tissue in the retina and loss of vision. It also leads to the release of VEGF, which stimulates the development of new blood vessels (neovascularisation).

58
Q

What are the risk factors for CVRO?

A 
• Hypertension
• High cholesterol
• Diabetes
• Smoking
• Glaucoma
Systemic inflammatory conditions such as systemic lupus erythematosus
59
Q

What is the presentation of CVRO?

A

Sudden painless loss of vision

60
Q

What is the presentation of CVRO?

A

Sudden painless loss of vision

61
Q

How do you diagnose CRVO?

A

Ophthalmoscopy

62
Q

What are the findings on fundoscopy in CRVO?

A

Flame and blot haemorrhages
Optic disc oedema
Macula oedema

63
Q

What other tests should be done to check for associated conditions in CRVO?

A 
• Full medical history
• FBC for leukaemia
• ESR for inflammatory disorders
• Blood pressure for hypertension
Serum glucose for diabetes
64
Q

What is the management of CRVO?

A

Same-day assessment by ophthalmologist

65
Q

What are the treatment options for CRVO?

A

• Laser photocoagulation
• Intravitreal steroids (e.g. a dexamethasone intravitreal implant)
Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)

66
Q

What is keratitis?

A

Keratitis is inflammation of the cornea.

67
Q

Give 5 causes of keratitis.

A

• Viral infection with herpes simplex
• Bacterial infection with pseudomonas or staphylococcus
• Fungal infection with candida or aspergillus
• Contact lens acute red eye (CLARE)
Exposure keratitis is caused by inadequate eyelid coverage (e.g. eyelid ectropion)

68
Q

What is the most common cause of keratitis?

A

Herpes simplex

69
Q

What is the presentation of keratits?

A 
• Painful red eye
• Photophobia
• Vesicles around the eye 
• Foreign body sensation
• Watering eye
Reduced visual acuity. This can vary from subtle to significant.
70
Q

How is herpes keratitis diagnosed?

A

Staining with flourescein = dendritic ulcer
Slit-lamp examination
Swabs/scrapings & viral culture/PCR

71
Q

What is the management of herpes keratiits?

A

• Aciclovir (topical or oral)
• Ganciclovir eye gel
Topical steroids may be used alongside antivirals to treat stromal keratitis

72
Q

What are the complications of herpes keratitis?

A

stromal necrosis
vascularisation
Scarring
corneal blindness.

73
Q

What are the two types of macular degeneration?

A

Dry

Wet

74
Q

Which type of macular degeneration is more common?

A

Dry

75
Q

Which type of macular degeneration carries the worst prognosis?

A

Wet

76
Q

What are the four layers of the macula?

A

Choroid layer
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors

77
Q

What are Drusen?

A

Yellow deposits of protein and lipids (some drusen are normal, but larger amounts are a feature of macular degeneration)

78
Q

What features are common in wet and dry AMD?

A

Atrophy of the retinal pigment epithelium
Degeneration of the photoreceptors
Drusen

79
Q

Why is wet AMD described as “wet”?

A

Associated oedema due to the development of new vessels growing from the choroid layer into the retina.
New vessels are stimulated by VEGF

80
Q

Which chemical stimulates the growth of new vessels in wet AMD?

A

VEGF

81
Q

What are the risk factors?

A 
Age
Smoking
White or Chinese ethnic origin
Family hx
Cardiovascular disease
82
Q

How does AMD present?

A

Scotoma (gradual, central vision loss)

83
Q

How are drusen detected?

A

Fundoscopy

84
Q

How is wet AMD diagnosed?

A

Optical coherence tomography
OR
Fluorescein angiography

85
Q

What is the treatment of dry AMD?

A

No treatment

Avoid smoking
Control BP
Vitamin supplementation

86
Q

What is the treatment of wet AMD?

A

Anti-VEGF medications

87
Q

Which medications block VEGF? When do they need to be started?

A
  • Ranibizumab
  • Bevacizumab

Start within 3 months to be beneficial.

87
Q

Which medications block VEGF? When do they need to be started?

A
  • Ranibizumab
  • Bevacizumab

Start within 3 months to be beneficial.

88
Q

What is posterior vitreous detachment?

A

Separation of the vitreous membrane from the retina

89
Q

What should be ruled-out in suspected posterior vitreous detachment?

A

Retinal tears

Retinal detachment

90
Q

What are the risk factors for posterior vitreous detachment?

A

Age

Near-sighted (myopic patients)

91
Q

How does posterior vitreous detachment present?

A 
Flashes
Floaters
Blurred vision
Cobweb across vision
Dark curtain descending downwards (retinal detachment)
92
Q

What is seen on ophthalmoscopy in posterior vitreous detachment?

A

Weiss ring (he detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater)

93
Q

What is the management of PVD?

A

Ophthalmology referral within 24 hours

94
Q

What is the treatment for PVD?

A

Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If associated retinal tear/detachment = surgery

95
Q

What are the risk factors for cataracts?

A 
• Increasing age
• Smoking
• Alcohol
• Diabetes
• Steroids
Hypocalcaemia
96
Q

How do cataracts present?

A
  • Very slow reduction in vision
  • Progressive blurring of vision
  • Change of colour of vision with colours becoming more brown or yellow
  • “Starbursts” can appear around lights, particularly at night time

Asymmetrical changes

97
Q

What is the management of cataracts?

A

Cataract surgery

98
Q

Name a complication of cataract surgery

A

Endophthalmitis

Inflammation of the inner contents of the eye, usually caused by infection. It can be treated with intravitreal antibiotics injected into the eye. This can lead to loss of vision and loss of the eye itself.

FINALS (26 decks)

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