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MRCP > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

What are the main symptoms of Horner’s syndrome?

A

Ptosis
Miosis
Anhidrosis (loss of sweating on one side)
Pseudo-enophthalmos (looks like eye has sunken back into the skull)

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2
Q

What are the main causes of Horner’s syndrome?

A

Central – stroke, MS, Syringomyelia
Pre-ganglionic – Pancoast tumour (apex of the lung), thyroidectomy, cervical rib
Post-ganglionic – carotid artery dissection (sympathetic nerve plexus formed around the carotid artery), cavernous sinus thrombosis, cluster headaches

Anhydrosis:
(first order neurone): Central - head, arm trunk
(second order neurone): Pre-ganglionic - just on face
(third order neurone): Post-ganglionic - no anhydrosis

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3
Q

What is the normal route for the passage of fluid through the eye (that does not function correctly in glaucoma)?

A
  • The ciliary epithelium produce aqueous humour into the posterior chamber which provides nutrition for the lens
  • This then passes through a narrow passage to the anterior chamber and reabsorbed by the trabecular meshwork
  • When this drainage system is blocked pressure builds in all chambers of the eye and causes intraocular HTN
  • The optic nerve may become damaged, leading to vision loss
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4
Q

What is the normal interocular pressure range?

A

11-21mmHg

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5
Q

What are the three characteristic examination findings in Glaucoma?

A

1) High IOP
2) Enlargement of the optic disc cup (cup should be less than half the diameter of the optic disc)
3) Progressive loss of visual fields

1 + 2 + 3 = glaucoma
1 only = ocular hypertension
2 + 3 only = normal pressure glaucoma

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6
Q

How does tunnel vision develop in Glaucoma?

A

Arcuate scotomas (semi-circles) begin
These join up to produce ring scotomas
These extend to produce tunnel vision
Eventually central vision is lost (visual acuity remains good until very late)

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7
Q

What are the three main investigations for Glaucoma?

A
  • Screening by IOP – tonometry
  • Visual fields testing
  • Identification by cupping – slit-lamp fundoscopy
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8
Q

What are the medical treatment options in Glaucoma?

A

Observation (mainly just for ocular hypertension)
Medical: eye drops
• Prostaglandin analogues (latanoprost)
• B-blockers (timolol)
• Carbonic anhydrase inhibitors (dorzolamide)
• Alpha agonists (brimonidine)

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9
Q

What do prostaglandin analogues do and what is the main SE?

A

o Increase uveoscleral outflow

o SE: increased eyelash length

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10
Q

What do B blockers do in Glaucoma and in who do you need to be careful of prescribing them?

A

o Reduce aqueous production

o SE: careful in asthmatics + heart block

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11
Q

What are the surgical options for Glaucoma?

A
  • Create a drainage route for aqueous humour, end up with a cystic structure above cornea called a ‘bleb’
  • Other: Laser surgery – e.g. laser trabeculoplasty, ciliary body laser, laser iridotomy
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12
Q

In who should you consider screening for Glaucoma and from when?

A

Those with a positive family history should be screened annually from aged 40 years

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13
Q

RFs for Glaucoma?

A

age, black, hypertension, FH, myopia

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14
Q

What are the symptoms of a sudden rise in IOP in acute glaucoma?

A
  • Acute loss of vision/blurred (classically with haloes around lights) -> Occurs d/t corneal oedema
  • Severe periocular pain
  • Nausea + vomiting
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15
Q

What would the pupil look like in acute glaucoma and what would the IOP be?

A

Fixed and dilated

IOP: 40-80

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16
Q

Would findings would you see on inspection of the eye in glaucoma?

A

Oval pupil
Loss of the red light reflex
Inability to visualise the fundus (back of the eye)

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17
Q

What is the management of acute angle glaucoma?

A

Urgent referral to ophthalmology
Analgesics + anti-emetics
Reduce aqueous secretion (acetazolamide PO – carbonic anhydrase inhibitor) and induce pupillary constriction (topical pilocarpine)

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18
Q

What are you at risk of if acute glaucoma is left untreated?

A

central retinal artery occlusion

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19
Q

Causes of papiloedema?

A 
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
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20
Q

What is episcleritis and what are the main symptoms?

A

Uncommon but not that serious cause of red eye
• Inflammation of episclera (outermost layer of the sclera)
• Often seen with a nodule
• Wedge shape of engorged vessels seen on sclera that can be moved over the sclera
• May get dull ache, NO PAIN
• Acuity usually okay

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21
Q

What causes episcleritis?

A

No cause found in 70% - complication of a systemic disease in a small proportion

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22
Q

How to treat episcleritis?

A

Rx symptomatic relief with artificial tears and topical/systemic NSAIDs

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23
Q

What are the symptoms of optic neuritis?

A

Unilateral vision loss over hrs -> days (central scotoma)
Poor discrimination of colours, red seems ‘washed-out’
Pain worse on eye movements
Relative afferent pupillary defect

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24
Q

What is the treatment of optic neuritis?

A

high-dose steroids, usually recover in 4-6 weeks

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25
Q

What is the macula for and where in the eye is it found?

A

part of the retina where visual acuity is at its highest

Found 3mm temporal to the optic disc (2 disc diameters)

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26
Q

What is found in the centre of the macula?

A

fovea centralis (containing only cone photoreceptors)

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27
Q

RFs for macular degeneration?

A

AGE ++ , DM, smoking, CVD, FH, cataracts surgery

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28
Q

What does good visual acuity rely on?

A
  • Functioning photoreceptors
  • Healthy retinal pigment epithelium (RPE)
  • Choroid perfusion by capillaries
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29
Q

What occurs in and are the symptoms of dry macular degeneration?

A

ATROPHY of RPE, choroid and retina

Patient develops central scotoma
Patient retains good peripheral vision

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30
Q

What occurs in wet macular degeneration?

A 
Choroidal neo-vascularisation
Leaking vessels below retina
Localised retinal detachment which leads to distorted central vision and eventually a central scotoma
Exudates and haemorrhage
Retinal scarring
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31
Q

What are the symptoms of wet macular degeneration?

A

Patients notice a more rapid change in vision – objects become distorted or smalling in size (micropsia). Patients are given a grid in clinic to take home + keep looking at and to return if the grid changes at all. Amsler grid.

Also poor night time vision
May notice flickering lights/halos
Symptoms fluctuate day to day

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32
Q

Investigations in macular degeneration?

A

Slit-lamp - to look at back of eye

Fluorescein angiography - to see if new vessels

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33
Q

What is the management of wet macular degeneration?

A

Reversible if you act promptly, but carries a worse prognosis than dry
Intravitreal injections (monthly) of anti-VEGF are now standard treatment for wet AMD
Laser photodynamic therapy can be used by caries risks
Provide glasses etc

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34
Q

Treatment for dry macular degeneration?

A

For dry: stop smoking, balanced diet, beta carotene, Vit C + E, zinc
GP: ‘Stop smoking, BCEZ you’ll be seeing the specialist in a week’
Beta-carotine in smokers increases your risk of lung cancer

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35
Q

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

A

Age-related macular degeneration

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36
Q

What causes retinal detachment and what occurs when the retina detaches?

A

When the retina detaches it takes its blood supply with it

Most retinal breaks are caused by posterior vitreous detachment, or trauma

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37
Q

What are the symptoms of retinal detachment?

A

Symptoms of vitreous detachment often occur first –
• Flashing lights
• Floaters (fine dots, cobwebs, veils)
When the retina detaches, patients usually describe a dark “curtain” coming across
- Can take hours-weeks for curtain to cover full vision
- Painless
May also see retinal tears on fundoscopy (holes with bright red choroid shining through)

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38
Q

What would you see on examination of the eye in retinal detachment?

A
  • Loss of red reflex
  • Retinal detachment near the macula can be seen
  • Detached retina may be pale, opaque + wrinkled with absent normal choroidal pattern
    May see relative afferent pupillary defect
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39
Q

What is the management of retinal detachment?

A

Immediate referral

Surgical repair is the only Tx option: laser photocoagulation or cryotherapy

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40
Q

Three most common causes of vitreous haemorrhage?

A

Proliferative diabetic retinopathy
Posterior vitreous detachment
Ocular trauma (most © cause in children)

41
Q

What are the symptoms of vitreous haemorrhage?

A

Painless vision loss or haze
Red hue in the vision
Floaters or shadows/dark spots

42
Q

How to investigate a vitreous haemorrhage?

A

Dilated fundoscopy – may be able to visualise the haemorrhage
Slit-lamp exam – RBCs in the anterior vitreous
USS – useful to rule out retinal tear/detachment
Fluorescein angiography – to identify neovascularisation
Orbital CT – used if open global injury

43
Q

Treatment of vitreous haemorrhage?

A

Can spontaneously resolve, but if large may need surgery – photocoagulation

44
Q

Symptoms specific to posterior vitreous detachment?

A

Sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light
Blurred vision
Cobweb across vision

45
Q

Management of posterior vitreous detachment?

A

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment

Mx – symptoms will improve over 6m
No permanent vision loss
If there are retinal tears/detachment, need Tx

46
Q

What is Holmes-Adie pupil?

A

Benign condition, more common in women

Causes one dilated pupil

47
Q

Symptoms of Holmes-Adie pupil?

A

unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slow to accommodation
very poorly (if at all) reactive to light
Affected pupil is initially larger -> then becomes smaller over time and remains constricted

48
Q

What other clinical finding on examination is associated with Holmes-Adie pupil?

A

absent ankle/knee reflexes

49
Q

What are the possible causes of conjunctivitis?

A

Viral –
• Adenovirus ©, HSV, Herpes zoster ophthalmicus, molluscum contagiosum
Bacterial –
• Staphlococcus, strep. Pneumoniae, H. influenzae, Chlamydial
Allergic © –
• Seasonal allergic conjunctivitis (recurring at the same time of the year)
• Perennial allergic conjunctivitis (daily, often on waking)
• Giant papillary conjunctivitis (often in those wearing contact lenses or following eye surgery)
• Contact dermatoconjunctivitis (associated with use of eye drops)
Infestation – E.g. Lice

50
Q

What are the symptoms of conjunctivitis?

A

• Red eye (often bilateral, usually generalised)
• Irritation, grittiness and discomfort
• Discharge
(Photophobia: suggests corneal involvement)

51
Q

What are the causes of anterior uveitis?

A
  • Idiopathic
  • Autoimmune – HLA B27, chronic Reiter’s disease, sarcoidosis, UC, crohns, juvenile rheumatoid arthritis
  • Infections – syphilis, TB, herpes simplex
  • Malignancy – retinoblastoma, leukaemia, lymphoma
  • Other – trauma, retinal detachment
52
Q

What are the symptoms of anterior uveitis?

A
  • Unilateral red eye
  • Pain/photophobia
  • POORLY REACTIVE pupil (d/t iris adhesion to the anterior lens)

Hypophon may be seen

53
Q

Horner’s syndrome - which are first, second and third order neurones?

A

First - travels from the brain to the spinal cord
Second - from the spinal cord to the ganglion
Third - from the ganglion to the eye

54
Q

What eye drops are used and what will happen in first, second and third order neurone dysfunction causing corners syndrome?

A

A normal pupil is dilated by cocaine and hydroxyamphetamine
In Horner’s:
4% cocaine eyedrops fail to dilate the pupil
Central + pre-ganglionic lesions (first and second order) hydroxyamphetamines cause dilation
Post-ganglionic lesions (third order) adrenaline causes dilation

55
Q

Symptoms of central retinal vein occlusion?

A

Sudden painless vision loss

56
Q

Treatment of central retinal vein occlusion?

A

Anti-VEGF, then dexamethasone implants (to treat the swelling)
Photocoagulation to prevent/treat neovascularisation

57
Q

Symptoms of central retinal artery occlusion?

A

Cherry red spots in the macula

Sudden complete loss of vision

58
Q

Treatment of central retinal artery occlusion?

A

drop IOP with acetazolamide
vigorous ocular massage
Manage with stroke protocols

59
Q

What is seen on fundoscopy in optic atrophy?

A

pale, well demarcated disc

60
Q

Usual symptom of optic atrophy?

A

usually bilateral and causes a gradual loss of vision

61
Q

Which conditions are associated with optic atrophy?

A 
MS
papilloedema (longstanding)
raised IOP (e.g. glaucoma, tumour)
retinal damage
ischaemia
toxins: tobacco amblyopia, quinine, methanol, arsenic, lead
nutritional: vitamin B1, B2, B6 and B12 deficiency
B+Q MALT
62
Q

What is a Marcus-Gunn pupil?

A

Relative afferent pupillary defect

When light is shone into the affected size (and the normal side is in the dark) - both pupils dilate

63
Q

What will you see in an Argyll-Robinson pupil and what are the two main causes?

A

Will accommodate but not react

caused by neurosyphilis and DM

64
Q

What is the mode of the action of pilocarpine and what type of receptor does it work at?

A

Muscarinic receptor agonist

Constricts the pupil - increased uveoscleral flow

65
Q

Name two examples of anti-VEGF?

A

Bevacizumab, ranibizumab

66
Q

What is the journey of the afferent nerve used in pupillary light reflex?

A

retina → optic nerve → lateral geniculate body → midbrain

67
Q

What is the journey of the efferent nerve used in pupillary light reflex?

A

Edinger-Westphal nucleus (midbrain) → oculomotor nerve to the pupil

68
Q

Two main symptoms of retinitis pigmentosa?

A

Night blindness

Tunnel vision

69
Q

What causes blepharitis?

A

Meibomian gland dysfunction
Seborrheic dermatitis
Staph infection

70
Q

What are the symptoms for blepharitis?

A

Bilateral
Grittiness and discomfort
Red eyelid margins
Eyes may be sticky in the morning

71
Q

Management of blepharitis?

A

Lid hygiene
Warm compress
Artificial tears

72
Q

What is the role of VEGF?

A

promotes new vessel growth + proliferation, also makes them leaky
Therefore anti-VEGF works to prevent this

73
Q

Causes of cataracts?

A
  • Increasing age (usual onset from 5th decade)
  • Sunlight
  • Diabetes, Downs
  • Smoking/alcohol, steroid-use, hypocalcaemia
74
Q

Visual symptoms experienced with cataracts?

A
  • Reduced vision
  • Faded colour vison
  • Glare – bright lights
  • Haloes around lights
75
Q

Complications and prognosis of cataracts?

A

sight-threatening = endophthalmitis (inflammation within the eye), retinal detachment/tear, choroidal haemorrhage
© intra-operative complication = posterior capsule rupture with vitreous loss
© post-operative complication = posterior capsule opacification, intraocular lens dislocation
• Outcome: 92% pts attain best-corrected visual acuity (BCVA) >6/12 within 3 months

76
Q

What is a hypophon?

A

Seen in the anterior of the eye

Collection of WBCs

77
Q

Symptoms of keratitis?

A

Painful, red eye
Foreign body sensation
Photophobia
Hypophon may be seen

78
Q

Treatment of keratitis?

A

Don’t wear your contacts

Topical abx

79
Q

Complications of keratitis?

A

Corneal scarring
Perforation
Endophthalmitis
Visual loss

80
Q

What might you see on inspection in herpetic keratitis?

A

Dendritic pattern under blue light

81
Q

RFs for central retinal vein occlusion?

A

increasing age
glaucoma
polycythaemia

82
Q

Two drug classes/types that may precipitate acute angle glaucoma?

A

anticholinergics and tricyclic antidepressants

83
Q

What is Herpes zoster ophthalmicus (HZO)?

A

describes the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles.

84
Q

What is Hutchinson’s sign?

A

Rash on the tip or side of the nose seen in herpes zoster ophthalmicus. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

85
Q

Management of Herpes zoster ophthalmicus (HZO)?

A

PO antiviral

Topical steroids may be used if eye involvement and needs urgent ophthalmology review

86
Q

What is herpes zoster oticus?

A

Ramsay Hunt syndrome (herpes zoster oticus) is caused by the reactivation of the varicella zoster virus in the geniculate ganglion of the seventh cranial nerve.

87
Q

Symptoms of Ramsay Hunt syndrome?

A

auricular pain is often the first feature
facial nerve palsy
vesicular rash around the ear
other features include vertigo and tinnitus

88
Q

Treatment of Ramsay Hunt syndrome?

A

oral aciclovir and corticosteroids are usually given

89
Q

What causes diabetic retinopathy?

A

a multifocal disease of the retinal microvasculature – multiple abnormalities occur in small retinal arteries (haemorrhages/new vessel formation)

90
Q

What is the prevalence of diabetic retinopathy in T1 and T2?

A

In T1, retinopathy is rare at Dx but present in >90% after 15yrs
In T2, retinopathy is present in 20% at Dx but only 60% after 15yrs

91
Q

What might you see on fundoscopy?

A

Microaneurysms, exudates, cotton wool spots, haemorrhages
Neovascularisation
Macular oedema

92
Q

What is the main case of severe sight loss in diabetic retinopathy?

A

Diabetic maculopathy (damage to macula)

93
Q

What might be seen in non-proliferative diabetic retinopathy and how to treat?

A
  • Microaneurysms
  • Small haemorrhages (flame shaped)
  • Hard exudates
  • Cotton wool spots
  • Microinfarcts – interrupted axon flow at site of microvascular occlusion
  • Venous beading/loops

Ranges from mild -> severe

Tx: Regular review
if severe/very severe consider panretinal laser photocoagulation

94
Q

What might be seen in proliferative diabetic retinopathy and how to treat?

A

• Retinal neovascularisation

Tx:
Anti-VEGF therapies intravitreal
For oedema = steroids
Laser photocoagulation

95
Q

Causes of sudden vision loss?

A 
Ischaemic/vascular – often amaurosis fugax (vision disappears and then returns)
Central retinal artery occlusion
Central retinal vein occlusion
Vitreous haemorrhage
Retinal detachment
96
Q

Hypertensive retinopathy stages 1-4?

A

1 – arteriolar narrowing + tortuous vessels, increased light reflex (silver wiring)
2 – arteriovenous nipping (a small artery crosses a small vein -> compression of the vein and bulging either side)
3 – cotton-wool exudates (when axons become damaged and leak fluid), flame and blot haemorrhages
4 – papilledema

97
Q

Treatment of conjunctivitis?

A

Viral – most cases are self-limiting and resolve in 1-2 weeks
• Chloramphenicol eye drops – may be used to prevent secondary bacterial infections
• Oral aciclovir – in herpes simplex + varicella zoster
Bacterial – often self-limiting
• General measures – personal hygiene, saline irrigation
• Antibiotics – chloramphenicol, bd for 5 days
Allergic –
• Avoid allergen if known
• Topical antihistamines (not oral) – e.g. antazoline
• Oral corticosteroid therapy – in severe cases with no diagnostic uncertainty

98
Q

Difference between acute vs chronic anterior uveitis?

A

Acute – often non-granulomatous
• Characterised by pain, photophobia, redness, lacrimation
Chronic – characterised by granulomata (can get acute exacerbations on top)
• Often white (Alice’s friends Ellie has this)

99
Q

Treatment of anterior uveitis?

A

Needs an urgent ophthalmology review
Symptom relief: Systemic analgesics + dark glasses for photophobia
Infectious causes – Tx with antiviral or antimicrobial agents
Non-infectious causes – corticosteroids
Mydriatic (dilating)/cycloplegic agents – can be used to relieve pain and prevent adhesion
Immunosuppressants may be recommended if not responding to above

MRCP (14 decks)

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