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Finals Revision > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is Glaucoma?

A

Optic nerve damage from rise in intraocular pressure

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2
Q

What causes increased intraocular pressure?

A

Blockage in aqueous humour trying to escape the eye

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3
Q

What parts of the eye have aqueous humour in them?

A

Anterior and posterior chamber (from lens to cornea)
NOT the vitreous chamber

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4
Q

Where is aqueous humour produced?

A

Ciliary body

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5
Q

What is the normal flow of aqueous humour in the eye?

A

From the ciliary body, around the lens and under the iris, through the anterior cancer, through the trabecular meshwork in to the canal of Schlemm, where it eventually enters the general circulation

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6
Q

What is normal intraocular pressure?

A

10-21 mmHg

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7
Q

What creates intraocular pressure normally?

A

Resistance to flow through the trabecular meshwork

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8
Q

What happens in open-angle glaucoma?

A

Gradual increase in resistance through the trabecular meshwork

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9
Q

What happens in acute angle-closure glaucoma?

A

Iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing any drainage
Ophthalmology emergency

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10
Q

What effect does increased pressure have on the optic disc?

A

Cupping of the optic disc (cup of more than 0.5 the size of the optic disc is abnormal)

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11
Q

What are risk factors for open angle glaucoma?

A

Increasing age
Family history
Black ethnic origin
Near sightedness (myopia)

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12
Q

How does open angle glaucoma present?

A

Asymptomatic
Peripheral vision first -> tunnel vision
Fluctuating pain, headaches, blurred vision, halos around lights, particularly at night time

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13
Q

How do you measure intraocular pressure?

A

Non-contact tonometry (puff of air to the cornea and measure the corneal response)
Gold standard is Goldmann application tonometry

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14
Q

What is the management of open-angle glaucoma?

A

Treat if pressure is above 24 mmHg
Prostaglandin analogue eye drops (e.g. latanoprost) - these increase uveoscleral outflow
Also: beta-blockers/carbonic anhydrase inhibitors/Sympathomimetics to reduce production of aqueous humour

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15
Q

What surgery may be required in open-angle glaucoma?

A

Trabeculectomy - creates a new channel from the anterior chamber, through the sclera to a location under the conjunctiva. Causes a bleb under the conjunctiva where the aqueous humour drains

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16
Q

What are the risk factors for acute angle-closure glaucoma?

A

Increasing age
Females affected 4 times more
Family history
Chinese and East Asian ethnic origin
Shallow anterior chamber

Medications: adrenergic medications, anticholinergic medications, TCAs

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17
Q

What is the presentation of acute angle-closure glaucoma?

A

Generally unwell
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

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18
Q

What do you see on examination of acute angle-closure glaucoma?

A

Red-eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation

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19
Q

What is the management for acute angle-closure glaucoma?

A

Same day assessment by an ophthalmologist
Lie patient on back without a pillow
Pilocarpine eye drops (2% for blue, 4% for brown eyes)
Acetazolamide 500 mg orally
Analgesia and antiemetic if required.

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20
Q

How does pilocarpine eye drops work?

A

Acts on the muscarinic receptors in the sphincter muscles in the iris. Constricts the pupil and contracts the ciliary muscle.

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21
Q

How does acetozolamide work?

A

Carbonic anhydrase inhibitor - reduces the production of aqueous humour

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22
Q

What is the definitive treatment for acute angle-closure glaucoma?

A

Laser iridotomy - makes a hole in the iris for the aqueous humour to flow from the posterior chamber into the anterior chamber

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23
Q

What are the two types of macular degeneration?

A

90% dry
10% wet - worse prognosis

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24
Q

What are the four layers of the macula?

A

Bottom - choroid layer, providing blood supply
Next - Bruch’s membrane
Next - Retinal pigment epithelium
Top - photoreceptors

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25
Q

What are drusen?

A

Yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane (normal to have some small ones)

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26
Q

What is the pathophysiology of wet AMD?

A

New vessels growing from the choroid layer into the retina - these leak and cause oedema and rapid loss of vision. Key chemical is vascular endothelial growth factor - target of medications

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27
Q

What is the macula of the eye?

A

Part of the retina at the back of the eye
5mm of pigmented retina, responsible for our central vision, much of our colour vision, and fine detail. Lots of photoreceptors

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28
Q

What are risk factors for AMD?

A

Age
Smoking
White or Chinese ethnic origin
Family history
Cardiovascular disease

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29
Q

What are key visual changes that are key for spotting AMD?

A

Gradual worsening central visual field loss
Reduced visual acuity
Crooked or wavy appearance to straight lines

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30
Q

What is used to diagnose AMD?

A

Snellen chart, Scotia, Amsler grid test, fudoscopy
Slit-lamp biomicroscopic fundus examination by a specialist
Optical coherence tomography to diagnose wet AMD (or fluorescein angiography)

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31
Q

What is used to treat dry AMD

A

Lifestyle measures that slow progression:
Stop smoking
Control BP
Vitamin supplementation

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32
Q

What is used to treat wet AMD?

A

Anti-VEGF medications - e.g. ranibizumab, bevacizumab, pegaptanib. Injected directly into the vitreous chamber once a month. Need to be started within 3 months

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33
Q

What is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia damages retinal small vessels and endothelial cells
Increased vascular permeability - leakage, blot haemorrhages, hard exudate deposits
Microaneurysms
Venous beading
Damage to nerve fibres - cotton wool spots
Intraretinal microvascular abnormalities - dilated and tortuous capillaries in the retina
Neovascularisation

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34
Q

What are the two categories of diabetic retinopathy?

A

Non-proliferative - more microaneurysms, blot haemorrhages, venous beading
Proliferative - neovascularisation, vitreous haemorrhage

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35
Q

What happens in diabetic maculopathy?

A

Macular oedema
Ischaemic maculopathy

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36
Q

What are some complications of diabetic retinopathy?

A

Retinal detachment
Vitreous haemorrhage
Rebeosis iridis (new blood vessel formation in the iris)
Optic neuropathy
Cataracts

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37
Q

What is the management of diabetic retinopathy?

A

Laser photocoagulation
Anti-VEGF medications
Vitreoretinal surgery

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38
Q

What are some features of hypertensive retinopathy?

A

Silver wiring (arterioles sclerosed causing increased reflection of the light)
Arteriovenous nipping - due to sclerosis, compress veins that they cross
Cotton wool spots (ischaemia and infarction of nerve fibres)
Hard exudates
Retinal haemorrhages
Papilloedema

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39
Q

What is the classification of hypertensive retinopathy?

A

Keith-Wagener
Stage 1: Mild narrowing of the arterioles
Stage 2: Focal constriction of blood vessels and AV nicking
Stage 3: Cotton wool patches, exudates and haemorrhages
Stage 4: Papilloedema

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40
Q

What is the job of the lens in the eye?

A

To focus light onto the retina

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41
Q

What is the lens held in place by?

A

Suspensory ligaments which are attached to the ciliary body (contracts and relaxes to focus the lens)
When the ciliary body contracts - tension is released, when it relaxes tension is increased.
No blood supply - nourished by the surrounding fluid

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42
Q

What are risk factors for cataracts?

A

Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia

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43
Q

How do cataracts present?

A

Asymmetrical
Very slow reduction in vision
Progressive blurring of vision
Change of colour of vision - become more brown or yellow
Starbursts can appear around lights, particularly at night time

KEY: loss of red reflex

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44
Q

What causes pupil constriction?

A

Circular muscles in the iris
Parasympathetic nervous system
Acetylcholine as the neurotransmitter
Oculomotor nerve

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45
Q

What causes pupil dilation?

A

Dilator muscles like spokes of a bicycle wheel in the iris
Sympathetic nervous system
Adrenalin

46
Q

What can cause an abnormal pupil shape?

A

Trauma to the sphincter muscles
Anterior uveitis with adhesions
Acute angle closure glaucoma - ischaemic damage to the muscles causing a vertical oval
Rubeosis iridis (neovascularisation)
Coloboma - congenital
Tadpole pupil - temporary spasm associated with migraines

47
Q

What can cause mydriasis (dilated pupil)?

A

Third nerve palsy
Holmes-Adie syndrome
Raised ICP
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics

48
Q

What can cause miosis (constricted pupil)?

A

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

49
Q

What does a third nerve palsy cause?

A

Ptosis
Dilated non-reactive pupil
Divergent strabismus (down and out)

50
Q

What does the third nerve travel through?

A

Carvers sinus and close to the posterior communicating artery - therefore cavernous sinus thrombosis or posterior communicating artery aneurysm can cause compression

51
Q

What can cause a Third Nerve Palsy?

A

Idiopathic
With sparing of the pupil - suggests a microvascular cause (diabetes, hypertension, ischaemia)
Full = compression (idiopathic, tumour, trauma, cavernous sinus thrombosis, PCA aneurysm, raised ICP)

52
Q

What is the triad in Horner’s syndrome?

A

Ptosis
Miosis
Anhidrosis
(damage to sympathetic nervous system supplying the face)

53
Q

What is the journey of sympathetic nerves to the head (relevant for Horner syndrome)?

A

From spinal cord, alongside the internal carotid artery, entering the sympathetic ganglion at the base of the neck
Location of Horner syndrome can be determined by the anhidrosis:
- Central lesions cause anhidrosis of the arm, trunk and face
- Pre-ganglionic lesions cause anhidrosis of the face
- Post-ganglionic lesions do not cause anhidoriss

54
Q

Central lesion causes of Horner syndrome

A

Central lesions = 4 S
Stroke
MS
Swelling (tumours)
Syringomyelia (cyst in the spinal cord)

55
Q

What are the pre-gangiolic lesions for Horner’s?

A

4Ts for Torso
Tumour (Pancoast tumour)
Trauma
Thyroidectomy
Top rib

56
Q

What are the post-ganglionic lesions in Horner’s syndrome?

A

4Cs for cervical
Carotid aneurysm
Carotid artery dissection
Cavernous sinus thrombosis
Cluster headache

57
Q

What is congenital Horner syndrome associated with?

A

Heterochromia - difference in the colour of the iris on the affected side

58
Q

How do you test for Horner syndrome?

A

Cocaine eye drops - stop noradrenalin re-uptake at the neuromuscular junction
Normal eyes dilate
Horner’s = no reaction

59
Q

What is a Holmes Adie Pupil?

A

Unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction
Damage to the post-ganglionic parasympathetic fibres

60
Q

What is an Argyll-Robertson Pupil?

A

Specific finding in neurosyphilis
Constricted pupil that accommodates when focusing on a near object but does not react to light
Often irregularly shaped

61
Q

What is blepharitis?

A

Inflammation of the eyelid margins

62
Q

What is blepharitis associated with?

A

Dysfunction of the Meibomian glands
Can lead to styes and chalazions

63
Q

What is used in management of blepharitis

A

Hot compresses and gentle cleaning of eyelid margins
Lubricating eye drops: hypromellose, polyvinyl alcohol, carbomer (each have varying viscosities)

64
Q

What is a stye?

A

Hordeolum externum: infection of the glands of Zeis (sebaceous) or glands of Moll (sweat glands)
Hordeolum internum: infection of the Meibomian glands

65
Q

What is a chalazion?

A

When a Meibomian gland becomes blocked and swells up to form a cyst
Swelling that is usually not tender
Consider chloramphenicol antibiotics

66
Q

What is an entropion?

A

Where the eyelid turns inwards with the lashes against the eyeball
Can cause corneal damage and ulceration

67
Q

What is an ectropion

A

Eyelid turns outwards
Can cause exposure keratopathy

68
Q

What is trichiasis?

A

Inward growth of eyelashes
Pain, corneal damage, ulceration
Requires epilation (removal of eyelash)
May require electrolysis, cryotherapy or laser treatment to prevent reoccurence

69
Q

What is periorbital cellulitis?

A

Eyelid and skin infection
Swelling, redness and hot skin around the eyelids and eye
Systemic antibiotics

70
Q

What differentiates orbital cellulitis from periorbital cellulitis?

A

Orbital has: pain on eye movement, reduced eye movements, changes in vision, abnormal pupil reactions, forward movement of the eyeball
IV antibiotics +/- surgical drainage

71
Q

What are the three types of conjunctivitis?

A

Bacterial
Viral
Allergic

72
Q

What does conjunctivitis not cause?

A

Pain/photophobia/reduced visual acuity

73
Q

What are the differential diagnosis of painless red eye?

A

Cnjunctivitis
Episcleritis
Subconjunctival haemorrhage

74
Q

What are the differential diagnosis of painful red eye?

A

Glaucoma
Anterior uveitis
Scleritis
Corneal abrasions or ulceration
Keratitis
Foreign body
Traumatic or chemical injury

75
Q

What can you use in the management of bacterial conjunctivitis?

A

Chloramphenicol eye drops
Fuscidic acid eye drops

76
Q

What patients with conjunctivitis require urgent ophthalmology review?

A

Under 1 month old - can be associated with gonococcal infection and cause loss of sight and more severe complications such as pneumonia

77
Q

What happens in anterior uveitis?

A

Immune cells infiltrate the anterior chamber - usually autoimmune but can be due to infection, trauma, ischaemia, malignancy.
Causes floaters

78
Q

What conditions is acute anterior uveitis associated with?

A

HLA B27 conditions:
Ankylosing spondylitis
IBD
Reactive arthritis

79
Q

What conditions is chronic anterior uveitis associated with?

A

Sarcoidosis
Syphilis
Lyme disease
Tuberculosis
Herpes virus

80
Q

How does anterior uveitis present?

A

Unilateral
Spontaneous
Dull, aching, painful red eye
Ciliary flush
Reduced visual acuity
Floaters
Constricted pupil
Photophobia
Pain on movement
Excessive lacrimation
Abnormally shaped pupil due to adhesions
Hypopyon (collection of WBC in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level)

81
Q

What is the management of anterior uveitis?

A

Same day ophthalmology review to rule out sight threatening conditions - need full slit lamp assessment
Steroids
Cycloplegic-mydriatic medications - cyclopentolate or atropine eye drops ( paralyses the ciliary muscles, dilate the pupils)
Immunosuppressants such as DMARDS and TNF inhibitors

81
Q

What is the management of anterior uveitis?

A

Same day ophthalmology review to rule out sight threatening conditions - need full slit lamp assessment
Steroids
Cycloplegic-mydriatic medications - cyclopentolate or atropine eye drops ( paralyses the ciliary muscles, dilate the pupils)
Immunosuppressants such as DMARDS and TNF inhibitors

82
Q

What is episcleritis?

A

Benign and self-limiting inflammation of the episclera (just below the conjunctiva)
Associated with Rheumatoid arthritis and IBD

83
Q

How does episcleritis present?

A

Non painful patch of redness on lateral sclera
Foreign body sensation
Dilated episcleral vessels
Watering of eye
No discharge

Usually caused by infection
Self-limiting, analgesia and cold compresses

84
Q

What is scleritis?

A

Inflammation of the full thickness of the sclera
Worst case is necrotising scleritis

85
Q

What conditions are associated with scleritis?

A

Rheumatoid arthritis
SLE
IBD
Sarcoidosis
Granulomatosis with polyagiitis

86
Q

How does scleritis present?

A

Severe pain
Pain with movement
Photophobia
Eye watering
Reduced visual acuity
Abnormal pupil reaction to light
Tenderness to palpation

87
Q

Management of scleritis

A

Same day assessment
NSAIDs
Steroids
Immunosuppression

88
Q

What is keratitis?

A

Inflammation of the cornea

89
Q

What can cause keratitis?

A

Viral infection - herpes simplex - most common
Bacterial - pseudomonas or staph
Fungal - candida or aspergillus
Contact lens acute red eye
Exposure keratitis - ectropion

90
Q

What is stroll keratitis?

A

When there is inflammation of the stroma as well as the epithelium
Complications: stromal necrosis, vascularisation, scarring, corneal blindness

91
Q

How does keratitis present?

A

Painful red eye
Photophobia
Vesicles around the eye
Foreign body sensation
Watering eye
Reduced visual acuity

92
Q

How do you diagnose keratitis?

A

Staining with fluorescein - dendritic corneal ulcer
Slit lamp examination
Corneal swabs or scrapings - PCR

93
Q

What is the management of keratitis?

A

Same day ophthalmology assessment
Aciclovir or Ganciclovir
Topical steroids if stromal
Cornal transplant may be required if there is corneal scarring

94
Q

What bacteria is associated with corneal abrasions secondary to contact lenses?

A

Pseudomonas

95
Q

How do corneal abrasions present?

A

History of contact lenses or foreign body
Painful red eye
Foreign body sensation
Watering eye
Blurring vision
Photophobia

96
Q

How do you diagnose a corneal abrasion?

A

Fluorescein stain - corneal abrasion is a yellow-orange colour
Slit lamp examination

97
Q

Management of corneal abrasion

A

Same day ophthalmology assessment
Removing foreign bodies
Simple analgesia
Lubricating eye drops
Antibiotic eye drops - chloramphenicol
Follow up after 24 hrs

98
Q

What does the vitreous body do?

A

Maintains structure and keeps the retina pressed on the choroid

99
Q

What is the vitreous body made of?

A

Collagen and water - with age it becomes less firm

100
Q

How does posterior vitreous detachment present?

A

Painless
Spots of vision loss
Floaters
Flashing lights

101
Q

What is the management for posterior vitreous detachment?

A

None - brain will adjust over time
Can predispose them to retinal tears and retinal detachment - need to exclude this by a thorough assessment of the retina

102
Q

What happens in retinal vein occlusion?

A

Pooling of blood in the retina - leakage, macular oedema, retinal haemorrhages
This damages the tissue and loss vision
Leads to the release of VEGF - stimulates neovascularisation

103
Q

How does retinal vein occlusion present?

A

Sudden painless loss of vision

104
Q

What are the risk factors for retinal vein occlusion

A

Hypertension
High cholesterol
Diabetes
Smoking
Glaucoma
SLE

105
Q

What do you see on fundoscopy in retinal vein occlusion?

A

Flame and blot haemorrhages
Optic disc oedema
Macula oedema

106
Q

What associated conditions should you check for in retinal vein occlusion?

A

FBC for leukaemia
ESR for inflammatory disorders
BP for hypertension
Serum glucose for diabetes

107
Q

What is the management of retinal vein occlusion?

A

Immediate referral to secondary care ophthalmology - amino treat macular oedema and prevent neovascularisation
Laser photocoagulation
Intravitreal steroids
Anti-VEGF therapies

108
Q

How does central retinal artery occlusion present?

A

Sudden painless loss of vision
Relative afferent pupillary defect (constricts more when light is shone at the other eye than itself)

109
Q

What do you see on fundoscopy of central retinal artery occlusion?

A

Pale retina with a cherry-red spot

110
Q

What is a reversible cause of central retinal artery occlusion?

A

GCA - test ESR and temporal artery biopsy

111
Q

What are some ways to try to dislodge the thrombus in central retinal artery occlusion?

A

Ocular massage
Removing fluid from the anterior chamber to reduce intraocular pressure
Inhaling carbogen - to dilate the artery
Sublingual isosorbide dinitrate - to dilate the artery

Finals Revision (20 decks)

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