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MRCP part 1 > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Causes of painless loss of vision

A

ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). This includes recognised syndromes e.g. occlusion of central retinal vein and occlusion of central retinal artery
vitreous haemorrhage
retinal detachment
retinal migraine

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2
Q

ischaemic/vascular causes of painless loss of vision

A

often referred to as ‘amaurosis fugax’
wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion
may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given
altitudinal field defects are often seen: ‘curtain coming down’
ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve

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3
Q

Central retinal vein occlusion

A

incidence increases with age, more common than arterial occlusion
causes: glaucoma, polycythaemia, hypertension
severe retinal haemorrhages are usually seen on fundoscopy

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4
Q

Central retinal artery occlusion

A

due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features include afferent pupillary defect, ‘cherry red’ spot on a pale retina

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5
Q

vitreous haemorrhage

A

causes: diabetes, bleeding disorders, anticoagulants

features may include sudden visual loss, dark spot

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6
Q

retinal detachment

A

features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters

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7
Q

Posterior vitreous detachment

A

Flashes of light (photopsia) - in the peripheral field of vision
Floaters, often on the temporal side of the central vision

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8
Q

Retinal Detachment

A

Dense shadow that starts peripherally progresses towards the central vision
A veil or curtain over the field of vision
Straight lines appear curved
Central visual loss

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9
Q

Vitreous Haemorrhage

A

Large bleeds cause sudden visual loss
Moderate bleeds may be described as numerous dark spots
Small bleeds may cause floaters

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10
Q

Rheumatoid arthritis: ocular presentations

ocular manifestations

A 
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
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11
Q

Rheumatoid arthritis: ocular presentations

Iatrogenic

A

steroid-induced cataracts

chloroquine retinopathy

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12
Q

What is Retinitis pigmentosa?

A

Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision

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13
Q

Features of retinitis pigmentosa

A

night blindness is often the initial sign
tunnel vision due to loss of the peripheral retina (occasionally referred to as funnel vision)
fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

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14
Q

Conditions associated with retinitis pigmentosa

A 
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport's syndrome
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15
Q

Pilocarpine - what is it

A

muscarinic receptor agonist - increases uveoscleral outflow

adverse effects - constricted pupil, headache and blurred vision.

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16
Q

What is glaucoma

A

optic neuropathies associated with raised intraocular pressure (IOP). They can be classified based on whether the peripheral iris is covering the trabecular meshwork, which is important in the drainage of aqueous humour from the anterior chamber of the eye. In open-angle glaucoma, the iris is clear of the meshwork. The trabecular network functionally offers an increased resistance to aqueous outflow, causing increased IOP.

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17
Q

Open angle glaucoma

Symptoms

A

characterised by a slow rise in intraocular pressure: symptomless for a long period
typically present following an ocular pressure measurement during a routine examination by an optometrist

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18
Q

Open angle glaucoma

Signs

A

increased intraocular pressure
visual field defect
pathological cupping of the optic disc1

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19
Q

Open angle glaucoma

Case finding

A

optic nerve head damage visible under the slit lamp
visual field defect
IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
if suspected full investigations are performed

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20
Q

investigations for open angle glaucoma

A

automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
applanation tonometry to measure IOP
central corneal thickness measurement
gonioscopy to assess peripheral anterior chamber configuration and depth
Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy

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21
Q

management of open angle glaucoma

A

first line: prostaglandin analogue (PGA) eyedrop
second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
if more advanced: surgery or laser treatment can be tried2

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22
Q

Prostaglandin analogues (e.g. latanoprost)

A

Increases uveoscleral outflow Once daily administration

Adverse effects include brown pigmentation of the iris, increased eyelash length

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23
Q

Beta-blockers (e.g. timolol, betaxolol)

A

Reduces aqueous production Should be avoided in asthmatics and patients with heart block

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24
Q

Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)

A

Reduces aqueous production and increases outflow Avoid if taking MAOI or tricyclic antidepressants

Adverse effects include hyperaemia

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25
Q

Carbonic anhydrase inhibitors (e.g. Dorzolamide)

A

Reduces aqueous production Systemic absorption may cause sulphonamide-like reactions

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26
Q

Herpes simplex keratitis

Features

A 
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer- dendritic corneal ulcer
27
Q

herpes simplex keratitis

management

A

immediate referral to an ophthalmologist

topical aciclovir

28
Q

What is Argyll-Robertson Pupil

A

Argyll-Robertson pupil is one of the classic pupillary syndrome. It is sometimes seen in neurosyphilis. A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

29
Q

Features of Argyll-Roberston Pupil

A

small, irregular pupils

no response to light but there is a response to accommodate

30
Q

Causes of Argyll-Robertson pupil

A

diabetes mellitus

syphilis

31
Q

Herpes zoster ophthalmicus

A

Herpes zoster ophthalmicus (HZO) 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.

32
Q

Features of herpes zoster ophthalmicus

A

vesicular rash around the eye, which may or may not involve the actual eye itself
Hutchinson’s sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement

33
Q

Management of herpes zoster ophthalmicus

A

oral antiviral treatment for 7-10 days
ideally started within 72 hours
intravenous antivirals may be given for very severe infection or if the patient is immunocompromised
topical antiviral treatment is not given in HZO
topical corticosteroids may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review

34
Q

Complications of herpes zoster opthalmicus

A

ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia

35
Q

Holmes Adie pupil - what is it

A

pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil.

36
Q

Holmes-Adie pupil overview

A

unilateral in 80% of cases
dilated pupil
once the pupil has constricted it remains small for an abnormally long time
slowly reactive to accommodation but very poorly (if at all) to light

37
Q

Homes-Adie syndrome

A

association of Holmes-Adie pupil with absent ankle/knee reflexes

38
Q

typical history of scleritis

A

a woman with a history of rheumatoid arthritis presents with severe, constant pain in her right eye. On examination the right eye is red and there is a degree of photophobia. Visual acuity is normal

39
Q

Fundoscopy findings in retinitis pigmentosa

A

Black bone spicule- shaped pigmentation in the peripheral retina

40
Q

Retinal detachment

A

Painless loss of vision

Dense shadow moving from periphery to central

41
Q

Bevacizumab

A

Monoclonal antibody against vascular endothelial growth factor
Used in treatment of age related macular degeneration

42
Q

Fluocinolone

A

orticosteroid used via intraocular injection in some eye conditions as an anti-inflammatory. Corticosteroids are used in conditions such as diabetic macular oedema, vasculo-occlusive macular oedema, posterior uveitis

43
Q

Laser photocoagulation

A

used in the management of several eye conditions, normally to finely cauterise ocular blood vessels
Mainly used in diabetic retinopathy

44
Q

Verteporfin

A

photosensitiser prior to photodynamic therapy. Verteporfin can be used in eye conditions with ocular vessel proliferation where it accumulates in the abnormal vessels. When exposed to a specific red light wavelength in phototherapy there is a resulting local damage to these vessels endothelium, blocking and destroying them.

45
Q

Zinc supplementation

A

slow the progression of AMD however it has not been associated with an anti-VEGF effect and is instead thought to work by increasing autophagy, the orderly degradation and recycling of cellular components, something that is decreased in AMD.

46
Q

Marcus Gunn pupil (relative afferent pupillary defect)

A

diagnosed during the swinging light test. If there is damage to the afferent pathway (retina or optic nerve) of one eye, the pupil of that affected eye will abnormally dilate when a light is shone into it. This is because the consensual pupillary relaxation response from the healthy eye will dominate. Marcus Gunn pupil can be found in patients with multiple sclerosis

47
Q

Causes of tunnel vision

A 
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
48
Q

Acute closed angle glaucoma

A

ise in IOP secondary to an impairment of aqueous outflow. Factors predisposing to AACG include:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

49
Q

Features of Acute closed angle glaucoma

A

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

50
Q

Acute management of acute closed angle glaucoma

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 secretio

51
Q

Definitive management of acute closed angle glaucoma

A

laser peripheral iridotomy

creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

52
Q

Cause of primary open angle glaucoma

A

gradual rise in intraocular pressure in the eyes due to reduced drainage within the trabecular meshwork of the eye. This presents as a gradual vision loss. Examination findings include increased cupping and raised intraocular pressure on examination.

53
Q

1st line treatment of primary open-angle glaucoma

A

β-blockers (timolol), prostaglandin analogues (latanoprost), carbonic anhydrase inhibitors (brinzolamide) and alpha-2-agonist (brimonidine)

54
Q

Mechanism of action: B- Blockers (timolol)

A

reducing the aqueous humour production of the eye.

55
Q

Mechanism of action Carbonic anhydrase inhibitors (acetazolamide/dorzolamide/brinzolamide)

A

Reduce aqueous humour production

56
Q

Mechanism of action: Prostaglandin analogues (latanoprost)

A

acts by increasing the uveoscleral outflow

57
Q

Mechanism of action: Alpha-2-agonists ( brimonidine)

A

improves symptoms by having a dual action (reducing humour production and increased outflow).

58
Q

Conditions associated with retinitis pigmentosa

A 
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport's syndrome
59
Q

Causes of mydriatic (dilated) pupil

A 
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital
60
Q

Argyll-Roberts Pupil

A

Typically the pupil accommodates but doesn’t react. A mnemonic used for the Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)

Features
small, irregular pupils
no response to light but there is a response to accommodate

Causes
diabetes mellitus
syphilis

61
Q

Enophthalmus

A

the posterior displacement of the globe in an anteroposterior plane within the orbit.

62
Q

anisocoria

A

unequal pupil size.

63
Q

Horner’s syndrome - anhydrosis (determines site of lesion)

A

head, arm, chest - central: stoke or syringomelia
Just face- pre-ganglionic lesion- Pancoast, cervical rib
Absent anhydrosis - carotid artery dissection

MRCP part 1 (15 decks)

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