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MRCP > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is glaucoma?

A

Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP).
open angle glaucome
closed angle glaucoma

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2
Q

What is acute closed angle glaucoma?

A

In acute angle-closure glaucoma (AACG) there is a rise in IOP secondary to an impairment of aqueous outflow. Factors predisposing to AACG include:
hypermetropia (long-sightedness)
pupillary dilatation
lens growth associated with age

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3
Q

what are the features of 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

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4
Q

how do you investigate closed angle glaucoma?

A

tonometry to assess for elevated IOP
gonioscopy (literally looking, oscopy, at the angle, gonio): a special lens for the slit lamp that allows visualisation of the angle

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5
Q

Hos is closed angle glaucoma managed?

A

combo of eye drops
- 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 secretions

some guidelines also recommend the use of topical steroids to reduce inflammation

Definitive management
laser peripheral iridotomy
creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle

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6
Q

What is open angle glaucoma?

A

In primary open-angle glaucoma (POAG), 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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7
Q

What are the risk factors for open angle glaucoma?

A

increasing age
- affects < 1’5 in individuals under 55 years of age
- but up to 10% over the age of 80 years
genetics
- first degree relatives of an open-angle glaucoma patient have a 16% chance of developing the disease
Afro Caribbean ethnicity
myopia
hypertension
diabetes mellitus
corticosteroids

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8
Q

What are the features of open angle glaucoma?

A

peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
decreased visual acuity
optic disc cupping

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9
Q

what are the fundoscopy signs of open angle glaucoma?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
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10
Q

what investigations of open angle glaucoma?

A

automated perimetry to assess visual field
slit lamp examination with pupil dilatation to assess optic nerve 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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11
Q

How is open angle glaucoma managed?

A

offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg

Porstaglandin analogue (latanoprost) eyedrops should be used next line

the next line of treatments includes:
beta-blocker eye drops
carbonic anhydrase inhibitor eye drops
sympathomimetic eye drops

surgery in the form of a trabeculectomy may be considered in refractory cases.

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12
Q

What are the mechanisms of actions of primary open angle glaucoma?
prostaglandin analogue
Betal blocker
Sympathomimetics
Carbonic anhydrase inhibitors
Miotics

A

Prostaglandin analogues (e.g. latanoprost)- Increases uveoscleral outflow - Once daily administration
Adverse effects include brown pigmentation of the iris, increased eyelash length

Beta-blockers (e.g. timolol, betaxolol)- Reduces aqueous production- Should be avoided in asthmatics and patients with heart block

Sympathomimetics (e.g. brimonidine, an alpha2-adrenoceptor agonist)- Reduces aqueous production and increases outflow- Avoid if taking MAOI or tricyclic antidepressants - Adverse effects include hyperaemia

Carbonic anhydrase inhibitors (e.g. Dorzolamide) Reduces aqueous production- Systemic absorption may cause sulphonamide-like reactions

Miotics (e.g. pilocarpine, a muscarinic receptor agonist) Increases uveoscleral outflow - Adverse effects included a constricted pupil, headache and blurred vision

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13
Q

What is the Marcus-Gunn pupil?

A

a relative afferent pupillary defect is found by the ‘swinging light test’. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina

e.g. when the light is shone in the right eye both pupils constrict but when the light source moves to the left eye, both eyes appear to dilate.

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14
Q

what is a relative afferent pupillary defect?

A

the affected and normal eye appears to dilate when light is shone on the affected

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15
Q

what are the causes of relative afferent pupillary defect

A

retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis

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16
Q

what is the pathway of the pupillary light reflex?

A

afferent: retina → optic nerve → lateral geniculate body → midbrain

efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve

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17
Q

What is blepharitis?

A

Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis).

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18
Q

what is the function of the meibomian glands?

A

The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation

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19
Q

What are the features of Blepharitis?

A

symptoms are usually bilateral
grittiness and discomfort, particularly around the eyelid margins
eyes may be sticky in the morning
eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis
styes and chalazions are more common in patients with blepharitis
secondary conjunctivitis may occur

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20
Q

How is Blepharitis managed?

A

Soften lid margin with hot compresses twice a day
lid hygiene - mechanical removal of the debris from the lid margins
artificial tears may be given for symptom relief

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21
Q

what is 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.

Features
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

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22
Q

What is the management of herpes zoster ophthalmicus?

A

oral antiviral - 7-10 days
IV may be given if there is a severe infection or if patient is immunocompromised

topical corticosteroid may be used to treat any secondary inflammation of the eye
ocular involvement requires urgent ophthalmology review

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23
Q

What are the complications of herpes zoster ophthalmicus?

A

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

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24
Q

what is the difference between scleritis and episcleritis?

A

Scleritis is painful, episcleritis is not painful

Episcleritis - irritation, soreness or a gritty sensation but importantly no pain.

Scleritis - sclera become severely red and inflamed and can be very painful

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24
Q

what are the ocular manifestations of RA?

A

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

Iatrogenic
steroid-induced cataracts
chloroquine retinopathy

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25
Q

What are the features of Horner’s syndrome?

A

miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)

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26
Q

What are the causes of Horner’s syndrome?

A

Central lesions (anhidrosis of the face, arm and trunk) -
Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis

Pre-ganglionic lesions (anhidrosis of the face)
Pancoast’s tumour
Thyroidectomy
Trauma
Cervical rib

Post-ganglionic lesion (no anhidrosis)
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

Congental horners - they will have heterchromia (difference in iris colour)

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27
Q

what can be used to diagnose Horner syndrome?

A

apraclonidine drops (an alpha-adrenergic agonist) can be used: causes pupillary dilation in Horner’s syndrome due to denervation supersensitivity but produces mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft

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28
Q

what are the causes of optic neuritis?

A

multiple sclerosis: the commonest associated disease
diabetes
syphilis

29
Q

what are the features of optic neuritis?

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect
central scotoma

30
Q

what is the investigation and management of optic neuritis?

A

Investigation
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

Management
high-dose steroids
recovery usually takes 4-6 weeks

31
Q

What is Holmes-Adie pupil?

A

commonly seen in woman
it is one of the differential of a 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

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

32
Q

what is retinal detachment characterised by?

A

sudden painless loss of vusuin
characterised by a dense shadow starting peripherally and processing centrally

33
Q

wha are the causes of sudden 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

34
Q

what is ischaemic optic neuropathy?

A

due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve

35
Q

what are the causes and features on fundoscopy seen in 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

36
Q

what causes central retinal artery occlusion and what are the features?

A

due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)

features include afferent pupillary defect, ‘cherry red’ spot on a pale retina

37
Q

What causes vitreous haemorrhage and what are the features of it?

A

causes: diabetes, bleeding disorders, anticoagulants
features may include sudden visual loss, dark spots

38
Q

How can you Differentiating posterior vitreous detachment, retinal detachment and vitreous haemorrhage?

A

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

Retinal detachment
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

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

39
Q

what is posterior vitreous detachment?

A

Posterior vitreous detachment is the separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing. Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina. It is important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment, as they may result in permanent loss of vision.

40
Q

what at the risk factors for age-related macular degeneration?

A

advancing age itself is the greatest risk factor for ARMD
the risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.

smoking
current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
]family history is also a strong risk factor for developing ARMD
first degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.

other risk factors for developing the condition include those associated with an increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.

41
Q

how is macular degeneration classified?

A

dry macular degeneration
90% of cases
also known as atrophic
characterised by drusen - yellow round spots in Bruch’s membrane

wet macular degeneration
10% of cases
also known as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis

Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)

42
Q

what are the clinical features of macular degeneration?

A

subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
gradual in dry ARMD
subacute in wet ARMD

difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects
visual hallucinations may also occur resulting in Charles-Bonnet syndrome

43
Q

what are the signs of macular degeneration?

A

distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

44
Q

how would you investigate macular degeneration?

A

slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
optical coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone.

45
Q

What is the management of macular degeneration?

A

combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third

Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.

vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.

laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

46
Q

what staging system is used in the classification of hypertensive retinopathy?

A

Keith-Wagener classification of hypertensive retinopathy

I - Arteriolar narrowing and tortuosity
Increased light reflex - silver wiring
II - Arteriovenous nipping
III - Cotton-wool exudates
Flame and blot haemorrhages
These may collect around the fovea resulting in a ‘macular star’
IV- fsclePapilloedema

47
Q

How to determine the site of the lesion in Horner’s syndrome?

A

Horner’s syndrome - anhydrosis determines site of lesion:
head, arm, trunk = central lesion: stroke, syringomyelia
just face = pre-ganglionic lesion: Pancoast’s, cervical rib
absent = post-ganglionic lesion: carotid artery

48
Q

what are the features of anterior unveils?

A

acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush

49
Q

what is optic atrophy?

A

Optic atrophy is seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision

50
Q

what causes optic atrophy?

A

Acquired causes
multiple sclerosis
papilloedema (longstanding)
raised intraocular pressure (e.g. glaucoma, tumour)
retinal damage (e.g. choroiditis, retinitis pigmentosa)
ischaemia
toxins: tobacco amblyopia, quinine, methanol, arsenic, lead
nutritional: vitamin B1, B2, B6 and B12 deficiency

Congenital causes
Friedreich’s ataxia
mitochondrial disorders e.g. Leber’s optic atrophy
DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram’s syndrome)

51
Q

what is Keratitis?

A

Keratitis describes inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated.

52
Q

what are the causes of keratitis?

A

bacterial - staph aureus or pseudomonas aerguinosa in contact lens wearers
fungal
amoebic - acanthamoebic keratitis, accounts for around 5% of cases, increased incidence if eye exposure to soil or contaminated water, pain is classically out of proportion to the findings
parasitic: onchocercal keratitis (‘river blindness’)

53
Q

what are the clinical features of keratitis?

A

red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen

54
Q

how is keratitis managed?

A

stop using contact lens until the symptoms have fully resolved
topical antibiotics
typically quinolones are used first-line
cycloplegic for pain relief
e.g. cyclopentolate

55
Q

complications of keratitis?

A

corneal scarring
perforation
endophthalmitis
visual loss

56
Q

what is mydriasis ?

A

dilation of the pupil

57
Q

what are the causes of mydriasis?

A

Causes of mydriasis (large pupil)
third nerve palsy
Holmes-Adie pupil
traumatic iridoplegia
phaeochromocytoma
congenital

Drug causes of mydriasis
topical mydriatics: tropicamide, atropine
sympathomimetic drugs: amphetamines, cocaine
anticholinergic drugs: tricyclic antidepressants

58
Q

what features are observed In fundoscopy of someone with papilloedema?

A

venous engorgement: usually the first sign
loss of venous pulsation: although many normal patients do not have normal pulsation
blurring of the optic disc margin
elevation of optic disc
loss of the optic cup
Paton’s lines: concentric/radial retinal lines cascading from the optic disc

59
Q

what are the causes of papilloedema?

A

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

Rare causes include
hypoparathyroidism and hypocalcaemia
vitamin A toxicity

60
Q

how does herpes simplex keraitits present ?

A

Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer.

Features
red, painful eye
photophobia
epiphora
visual acuity may be decreased
fluorescein staining may show an epithelial ulcer

61
Q

how do you manage herpes simplex keratitis?

A

management
immediate referral to an ophthalmologist
topical aciclovir

62
Q

what is Dacryocystitis?
what are the features and management?

A

Dacryocystitis is infection of the lacrimal sac

Features
watering eye (epiphora)
swelling and erythema at the inner canthus of the eye

Management is with systemic antibiotics. Intravenous antibiotics are indicated if there is associated periorbital cellulitis

63
Q

what is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes

Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia

64
Q

how is diabetic retinopathy classified?

A

non-proliferative diabetic retinopathy (NPDR), proliferative retinopathy (PDR) and maculopathy

65
Q

How is non-proliferative diabetic retinopathy classified?

A

Mild NPDR
1 or more microaneurysm

Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
cotton wool spots (‘soft exudates’ - represent areas of retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR
blot haemorrhages and microaneurysms in 4 quadrants
venous beading in at least 2 quadrants
IRMA in at least 1 quadrant

66
Q

what are the features of proliferative diabetic retinopathy?

A

retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc
more common in Type I DM, 50% blind in 5 years

67
Q

what are the features of diabetic maculopathy?

A

based on location rather than severity, anything is potentially serious
hard exudates and other ‘background’ changes on macula
check visual acuity
more common in Type II DM

68
Q

how is maculopathy managed?

A

if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

69
Q

how is non-proliferative diabetic retinopathy managed?

A

regular observation
if severe/very severe consider panretinal laser photocoagulation

70
Q

how is proliferative retinopathy managed?

A

panretinal laser photocoagulation
following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema

intravitreal VEGF inhibitors
often now used in combination with panretinal laser photocoagulation
examples include ranibizumab
strong evidence base suggests they both slow progression of proliferative diabetic retinopathy and improve visual acuity

if severe or vitreous haemorrhage: vitreoretinal surgery

MRCP (18 decks)

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