Ophthalmology Passmedicine 2024

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Question 1 of 90
A 39-year-old woman with a history of rheumatoid arthritis presents with a two day history of a
red right eye. There is no itch or pain. Pupils are 3mm, equal and reactive to light. Visual acuity is
6/5 in both eyes. What is the most likely diagnosis?
Keratoconjunctivitis sicca 13%
Scleritis 10%
Glaucoma 1%
Episcleritis 65%
Anterior uveitis 10%
Scleritis is painful, episcleritis is not painful

Important for me Less important
The most likely diagnosis in this case is episcleritis. Episcleritis is an inflammation of the episclera,
which is a thin layer of tissue between the conjunctiva and sclera. It typically presents with a red
eye, but without significant pain or visual disturbance. The patient's history of rheumatoid arthritis
increases her risk for episcleritis, as it can be associated with systemic inflammatory conditions.
Keratoconjunctivitis sicca, also known as dry eye syndrome, occurs when there is insufficient tear
production or poor quality tears to lubricate and nourish the eye. Symptoms include dryness,
burning sensation, and grittiness in the eyes. However, in this case, the patient does not report
any itch or pain that would suggest dry eye syndrome.
Scleritis refers to inflammation of the sclera and can be associated with autoimmune diseases like
rheumatoid arthritis. However, scleritis usually presents with severe ocular pain that worsens with
eye movement and can cause decreased vision if left untreated. The absence of pain and normal
visual acuity make this diagnosis less likely.
Glaucoma is a group of eye conditions characterized by optic nerve damage due to increased
intraocular pressure (IOP). Acute angle-closure glaucoma can present with a red eye alongside
other symptoms such as severe ocular pain, headache, nausea, vomiting, and blurred vision.
However, the patient's lack of pain and normal visual acuity do not support this diagnosis.
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Finally, anterior uveitis involves inflammation of the iris and ciliary body within the uveal tract. It
typically presents with unilateral eye pain, photophobia (light sensitivity), tearing, and potentially
decreased vision. While anterior uveitis could also be associated with rheumatoid arthritis, the lack
of pain and normal visual acuity, in this case, make it less likely.
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Rheumatoid arthritis: ocular manifestations
Ocular manifestations of rheumatoid arthritis are common, with 25% of patients having eye
problems
Ocular manifestations
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis
Iatrogenic
steroid-induced cataracts
chloroquine retinopathy
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Question 2 of 90
A 76-year-old man attends the diabetic eye clinic. He has proliferative retinopathy without vitreous
haemorrhage and is being consented to the first-line procedure.
What should he be told occurs in up to 50% of patients who have this procedure?
A reduction in visual fields 67%
Brown pigmentation of the iris 8%
Corneal scarring 12%
Increased intraocular pressure 3%
Vitreous detachment 9%
Following panretinal laser photocoagulation up to 50% of patients have a noticeable

reduction in their visual field
Panretinal laser photocoagulation is the first-line procedure for proliferative retinopathy. Due to
the retinal scarring caused by this procedure, there is a 50% chance of a reduction in visual fields
. This procedure is often used in combination with intravitreal VEGF.
Brown pigmentation of the iris is incorrect. This is a side effect of prostaglandin analogues,
given for open-angle glaucoma.
Corneal scarring is incorrect. This is a complication of keratitis.
There is a high chance of rising intraocular pressure is incorrect. This is a common

complication of laser peripheral iridotomy, the definitive management for acute angle-closure
glaucoma.
Vitreous detachment is incorrect. This is a condition associated with near-sightedness and

ageing.
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Diabetic retinopathy
Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old.
Pathophysiology
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
Classification
Patients are typically classified into those with non-proliferative diabetic retinopathy (NPDR),
proliferative retinopathy (PDR) and maculopathy.
Non-proliferative diabetic retinopathy
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
Proliferative diabetic retinopathy
Key features
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
Maculopathy
Key features
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
Management
All patients
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology
Maculopathy
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF)
inhibitors
Non-proliferative retinopathy
regular observation
if severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy
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
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Question 3 of 90
A 34-year-old female presents with fatigue and frequent headaches. On examination of her eyes,
you notice an abnormality during the swinging light test. As the light is moved from the left to the
right eye both pupils appear to dilate. The pupillary response to accommodation is normal
bilaterally. Fundoscopy is also normal bilaterally. Her past medical history includes type one
diabetes and hypertension. What is the most likely explanation for this patients' signs?
Raised intracranial pressure 3%
Diabetic eye disease 2%
Holmes-Adie's pupil on the right 12%
Marcus-Gunn Pupil (relative afferent pupillary defect) on the right 72%
Argyll Robertson pupil on the right 12%
Marcus Gunn pupil (relative afferent pupillary defect) is 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. Therefore, given the history, this should be ruled out in this
patient.
The history and examination findings in the question are not typical of raised intracranial pressure.
Raised intracranial pressure may present with symptoms such as a headache, vomiting, bilateral
blurred vision and seizures. Patients with increased intracranial pressure often have bilateral
papilloedema on fundoscopy.
Although the history states the female is diabetic, there are typically normal pupillary light
responses in patients with diabetic eye disease. Furthermore, with diabetic eye disease, you would
expect to see some abnormality on fundoscopy.
Holmes-Aide's pupil is a dilated pupil which poorly (if at all) reacts to direct light, however, slowly
reacts to accommodation. This does not correlate to the history.
The information given in the question above does not suggest Argyll Robertson pupil. This is
characterised by a constricted pupil that does not respond to light but responds to
accommodation. It is usually bilateral and is often associated with neurosyphilis.
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Relative afferent pupillary defect
Also known as the Marcus-Gunn pupil, 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
Finding
the affected and normal eye appears to dilate when light is shone on the affected
Causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis
Pathway of pupillary light reflex

afferent: retina → optic nerve → lateral geniculate body → midbrain
efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve
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Question 4 of 90
A 78-year-old woman presents to the emergency department after having a car accident. She
describes that her vision has been deteriorating with some line distortion and loss of her central
vision. Her vision was particularly bad this evening.
On examination of her eyes, you see drusen and new vessel formation around the macula.
Before discharge, you organise follow-up with the ophthalmologist as you think they may need to
start monoclonal antibody treatment directed against vascular endothelial growth factor (VEGF).
What monoclonal antibody has this mechanism of action?
Abciximab 5%
Adalimumab 8%
Bevacizumab 78%
Omalizumab 5%
Rituximab 5%
Bevacizumab is a monoclonal antibody directed against vascular endothelial growth factor

(VEGF)
Bevacizumab is the correct answer, it is a monoclonal antibody directed against vascular

endothelial growth factor (VEGF). It can be used to limit the progression of wet age-related
macular degeneration (ARMD) which is described in this case. It should be instituted within the
first two months of diagnosis of wet ARMD.
Abciximab is a monoclonal antibody directed against platelet IIb/IIIa receptors and hence
prevents platelet aggregation. It can be used to prevent clots in unstable angina or post coronary
artery stenting.
Adalimumab is a monoclonal antibody that targets tumor necrosis factor (TNF) and is mainly
used to treat inflammatory arthritis.
Omalizumab is a monoclonal antibody that targets the IgE receptor, which decreases an IgE
response. It can be used for severe allergic asthma.
Rituximab is a monoclonal antibody that targets CD20 receptors on B cells causing the lysis of B
lymphocytes. It can be used in the treatment of lymphoma.
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Age-related macular degeneration
Age-related macular degeneration is the most common cause of blindness in the UK.
Degeneration of the central retina (macula) is the key feature with changes usually bilateral. ARMD
is characterised by degeneration of retinal photoreceptors that results in the formation of drusen
which can be seen on fundoscopy and retinal photography. It is more common with advancing
age and is more common in females.
Risk factors
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.
Classification
Traditionally two forms of macular degeneration are seen:

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)
Clinical features
Patients typically present with 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
Signs:
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.
Investigations:
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.
Management
Treatment
the AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that 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.
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Question 5 of 90
Each one of the following is a cause of a mydriatic pupil, except:
Third nerve palsy 12%
Atropine 12%
Holmes-Adie pupil 15%
Argyll-Robertson pupil 51%
Traumatic iridoplegia 10%
Argyll-Robertson pupil is one of the classic pupillary syndromes. It is sometimes seen in

neurosyphilis. 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
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Mydriasis
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
Anisocoria may result in apparent mydriasis, due to the difference with the other pupil.
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Question 6 of 90
A 71-year-old with a history of type 2 diabetes mellitus and hypertension presents due to the
sensation of light flashes in his right eye. These symptoms have been present for the past 2 days
and seem to occur more at the peripheral part of vision. There is no redness or pain in the
affected eye. Corrected visual acuity is measured as 6/9 in both eyes. What is the most likely
diagnosis?
Change in shape of eye secondary to variations in blood sugar 3%
Primary open angle glaucoma 8%
Normal phenomenon in diabetic retinopathy 10%
Normal phenomenon in healthy eyes 2%
Flashes and floaters - vitreous/retinal detachment

Flashes and floaters are symptoms of vitreous detachment. The patient is at risk of retinal
detachment and should be referred urgently to an ophthalmologist
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Sudden loss of vision
Sudden loss is a frightening symptom for patients. It may represent an ongoing issue or only be
temporary. The term transient monocular visual loss (TMVL) describes a sudden, transient loss of
vision that lasts less than 24 hours.
The most common causes of a sudden painless loss of vision are as follows:
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
Ischaemic/vascular
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
Central retinal vein occlusion

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

due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
features include afferent pupillary defect, 'cherry red' spot on a pale retina
Vitreous haemorrhage
causes: diabetes, bleeding disorders, anticoagulants
features may include sudden visual loss, dark spots
Retinal detachment
features of vitreous detachment, which may precede retinal detachment, include flashes of
light or floaters (see below)
Differentiating posterior vitreous detachment, retinal detachment and

Posterior vitreous
detachment Retinal detachment Vitreous haemorrhage
Flashes of light (photopsia) Dense shadow that starts Large bleeds cause sudden
- in the peripheral field of peripherally progresses towards visual loss
vision the central vision Moderate bleeds may be
Floaters, often on the A veil or curtain over the field of described as numerous dark
temporal side of the central vision spots
vision Straight lines appear curved Small bleeds may cause
Central visual loss floaters
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Central Retinal Vein Occlusion
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Question 7 of 90
A 25-year-old woman attends the emergency department with a gradual loss of vision in her left
eye. She explains this has been progressing over the last couple of days. She is not experiencing
any black spots or curtain-like sensations in her vision.
On examination, there is pain in eye movement, with a relative afferent pupillary defect and
central scotoma.
Given the likely diagnosis, what else would be expected in her presentation?
Jaw claudication 8%
Optic disc cupping 23%
Poor discrimination of colour 55%
Ptosis 4%
Symptoms worse in the dark 10%
Colour vision ('red desaturation') is affected in optic neuritis

Poor discrimination of colour is the correct answer. The diagnosis described in this patient is
optic neuritis. This is inflammation of the optic nerve due to multiple sclerosis, diabetes or syphilis.
As described optic neuritis will present with gradual loss of visual acuity, painful eye movements, a
relative afferent pupillary defect and evidence of a central scotoma. Another important feature of
optic neuritis is affected colour vision and red desaturation of images.
Jaw claudication is incorrect. This would be seen classically in a diagnosis of temporal arteritis.
Although this would also present with visual loss and a relative afferent pupillary defect due to an
affected optic nerve as described in this vignette, patients typically do not describe a central
scotoma. They also may describe a severe unilateral headache over the temporal region which is
not seen in this patient, and patients are often older on initial presentation.
Optic disc cupping is incorrect. This can be seen in a diagnosis of primary open-angle glaucoma.
Although patients can also describe a gradual visual loss as seen in this patient, they typically have
a loss of the peripheral fields of vision, as opposed to the development of a central scotoma that
is described in this vignette.
Ptosis is incorrect. This is seen in a variety of conditions some of which include a third nerve palsy
and myasthenia gravis. Given the most likely diagnosis in this vignette is optic neuritis due to this
patient's presentation, ptosis is not the most appropriate answer as this is not seen in cases of
optic neuritis.
Symptoms worse in the dark is incorrect. Although symptoms may be worse in the dark this is
not a characteristic feature seen in optic neuritis. This presenting feature can be seen in retinitis
pigmentosum, a genetic disorder that leads to loss of night vision and peripheral vision.
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Optic neuritis
Causes
multiple sclerosis: the commonest associated disease
diabetes
syphilis
Features
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
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
Prognosis
MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%
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Question 8 of 90
A 67-year-old woman presents for review. She has recently been diagnosed with dry age-related
macular degeneration. Which one of the following is the strongest risk factor for developing this
condition?
Hypertension 9%
Poor diet 2%
Smoking 70%
Diabetes mellitus 17%
Alcohol excess 1%
Macular degeneration - smoking is risk factor

Having a balanced diet, with plenty of fresh fruits and vegetables may also slow the progression of
macular degeneration. There is still ongoing research looking at the role of supplementary
antioxidants
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Risk factors

aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases

Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
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Question 9 of 90
An 84-year-old man presents with loss of vision in his left eye since the morning. He is otherwise
asymptomatic and of note has had no associated eye pain or headaches. His past medical history
includes ischaemic heart disease but he is otherwise well. On examination he has no vision in his
left eye. The left pupil responds poorly to light but the consensual light reaction is normal.
Fundoscopy reveals a red spot over a pale and opaque retina. What is the most likely diagnosis?
Vitreous haemorrhage 3%
Retinal detachment 3%
Ischaemic optic neuropathy 7%
Central retinal vein occlusion 11%
Central retinal artery occlusion 76%
The correct answer is Central retinal artery occlusion. The patient's presentation of sudden,
painless vision loss in one eye, poor direct pupillary light response, normal consensual light
reaction, and fundoscopic findings of a pale and opaque retina with a cherry-red spot are classic
features of central retinal artery occlusion (CRAO). CRAO occurs when the central retinal artery
becomes blocked, typically by an embolus, leading to ischemia and infarction of the inner retina. It
is considered an ophthalmic emergency requiring immediate evaluation and treatment.
The first incorrect option is Vitreous haemorrhage. This condition presents with sudden, painless
vision loss or floaters in the affected eye. However, the fundoscopic examination would reveal
blood within the vitreous humour rather than a pale and opaque retina with a cherry-red spot.
The second incorrect option is Retinal detachment. Although this condition can also present with
sudden, painless vision loss or floaters in the affected eye, it is often accompanied by flashes of
light or a curtain-like shadow over the visual field. Fundoscopy would reveal an elevated retina
separated from the underlying choroid layer.
The third incorrect option is Ischaemic optic neuropathy. This condition typically presents as
sudden, painless vision loss that may be associated with optic disc swelling on fundoscopy.
However, it does not cause a pale and opaque retina with a cherry-red spot.
Lastly, the fourth incorrect option is Central retinal vein occlusion. Central retinal vein occlusion
(CRVO) presents as sudden-onset, painless vision loss in one eye similar to CRAO. However, a
fundoscopic examination would reveal diffuse retinal haemorrhages ('blood and thunder'
appearance), venous dilation and tortuosity rather than the pale and opaque retina with a cherry-
red spot seen in CRAO.
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Central retinal artery occlusion is a relatively rare cause of sudden unilateral visual loss. It is due to
thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
Features
sudden, painless unilateral visual loss
'cherry red' spot on a pale retina
Management is difficult and the prognosis is poor

any underlying conditions should be identified and treated (e.g. intravenous steroids for
temporal arteritis)
if a patient presents acutely then Intraarterial thrombolysis may be attempted but currently,
trials show mixed results.
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Question 10 of 90
A 74-year-old man presents to the emergency department with sudden, painless loss of vision in
his right eye. He denies headache, photophobia, flashers/floaters or painful eye movements. He
has a past medical history of hypertension and ischaemic heart disease.
On examination, the acuity in the right eye is reduced to finger counting. The acuity in the left eye
is normal. On fundoscopy, retinal haemorrhages are evident. Eye movements are normal in all
directions. The red reflex is present.
What is the most likely diagnosis?
Amaurosis fugax 7%
Temporal arteritis 1%
Central retinal vein occlusion - sudden painless loss of vision, severe retinal haemorrhages on
fundoscopy
Central retinal vein occlusion is correct. Central retinal vein occlusion presents as a sudden
painless reduction in visual acuity. Common risk factors include chronic glaucoma, hypertension
and increasing age. Fundoscopy findings are described as looking like a stormy sunset, with retinal
haemorrhages and engorged veins visible.
Amaurosis fugax is incorrect. In amaurosis fugax, a transient loss of vision occurs progressively,
classically like a curtain coming down. There are multiple causes, with some of the more common
including internal carotid or ophthalmic artery atherosclerosis, acute closed-angle glaucoma,
vasospasm, giant cell arteritis and hyperviscosity of the blood. The presentation described above
could fit with amaurosis fugax; however, amaurosis fugax would not explain the fundoscopy
findings, making this answer less likely.
Central retinal artery occlusion is incorrect. This is usually due to a thromboembolic occlusion. It
would also present as a sudden painless loss of vision; however, fundoscopy would show a pale
retina with a cherry-red spot at the macula.
Temporal arteritis is incorrect. This can present as a sudden painless loss of vision; however, the
patient does not describe a headache, which makes this diagnosis less likely. Additionally, the
retinal haemorrhages on fundoscopy are not seen in temporal arteritis.
Vitreous haemorrhage is incorrect. This would be caused by bleeding, usually from new vessels
formed as part of diabetic retinopathy. On fundoscopy, the red reflex may be absent and the
retina may be obscured by the bleeding.
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Central retinal vein occlusion (CRVO) is a differential for sudden painless loss of vision.
Risk factors
increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia
Features
sudden, painless reduction or loss of visual acuity, usually unilaterally
fundoscopy
widespread hyperaemia
severe retinal haemorrhages - 'stormy sunset'
A key differential is branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal
retinal venous system is occluded and is thought to occur due to blockage of retinal veins at
arteriovenous crossings. It results in a more limited area of the fundus being affected.
Management
the majority of patients are managed conservatively
indications for treatment in patients with CRVO include:
macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
retinal neovascularization - laser photocoagulation
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Question 11 of 90
A 43-year-old man attends his GP with pain and facial swelling after an upper respiratory tract
infection. On examination, erythema and swelling surround the right eye and there is pain on eye
movements. Visual acuity is 6/6 on the left and 6/24 on the right.
What is the most appropriate course of action?
Admit to hospital for IV antibiotics 81%
Prescribe high-dose oral steroids and check thyroid function 3%
Prescribe high-dose oral steroids and refer urgently to Rheumatology 8%
Supportive management and nasal decongestants 3%
Urgent referral to maxillofacial surgeons for debridement 6%
Patients with orbital cellulitis require admission to hospital for IV antibiotics due to the risk of
cavernous sinus thrombosis and intracranial spread
The correct answer is admit to hospital for IV antibiotics. The symptoms described are
suggestive of orbital cellulitis. This usually results from the spread of organisms from the upper
respiratory tract. Admission for IV antibiotics is recommended as under-treatment can lead to
cavernous sinus thrombosis.
Prescribe high-dose oral steroids and check thyroid function is incorrect. Thyroid eye disease
could cause orbital pain and painful eye movements and should be in the differential here.
However, the recent upper respiratory tract symptoms and facial pain/swelling are more
suggestive of orbital cellulitis, which often results from the spread of infection from the upper
respiratory tract.
Prescribe high-dose oral steroids and refer to Rheumatology is incorrect. This would be the
appropriate choice for suspected giant cell arteritis. This condition is extremely unusual under the
age of 65. It can cause headache and visual loss but this is usually in the form of monocular
blindness rather than reduced acuity.
Supportive management and nasal decongestants is incorrect. This would be appropriate for
conditions such as sinusitis that may lead to orbital cellulitis. However, the facial pain and swelling
with painful eye movements suggest orbital cellulitis has now developed. At this stage, supportive
therapy would not be appropriate and IV antibiotics are required.
Urgent referral to maxillofacial surgeons for debridement is incorrect. Orbital cellulitis is

generally managed with IV antibiotics rather than operative intervention. This may be required if
there were suspicion of necrotising infection but there is nothing to suggest this is a concern here.
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Orbital cellulitis
Orbital cellulitis is the result of an infection affecting the fat and muscles posterior to the orbital
septum, within the orbit but not involving the globe. It is usually caused by a spreading upper
respiratory tract infection from the sinuses and carries a high mortality rate. Orbital cellulitis is a
medical emergency requiring hospital admission and urgent senior review.
Periorbital (preseptal) cellulitis is a less serious superficial infection anterior to the orbital septum,
resulting from a superficial tissue injury (chalazion, insect bite etc...). Periorbital cellulitis can
progress to orbital cellulitis.
Risk factors
Childhood
Mean age of hospitalisation 7-12 years
Previous sinus infection
Lack of Haemophilus influenzae type b (Hib) vaccination
Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
Ear or facial infection
Presentation
Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Ophthalmoplegia/pain with eye movements
Eyelid oedema and ptosis
Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare)
Differentiating orbital from preseptal cellulitis

reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT
consistent with preseptal cellulitis
Investigations
Full blood count - WBC elevated, raised inflammatory markers.
Clinical examination involving complete ophthalmological assessment - Decreased vision,
afferent pupillary defect, proptosis, dysmotility, oedema, erythema.
CT with contrast - Inflammation of the orbital tissues deep to the septum, sinusitis.
Blood culture and microbiological swab to determine the organism. Most common bacterial
causes - Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.
Management
admission to hospital for IV antibiotics
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Question 12 of 90
Which one of the following causes of Horner's syndrome is due to a lesion in the post-ganglionic
part of the nerve supply?
Internal carotid aneurysm 70%
Stroke 3%
Syringomyelia 5%
Pancoast's tumour 18%
Thyroidectomy 4%
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
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Horner's syndrome
Features
miosis (small pupil)
ptosis
enophthalmos* (sunken eye)
anhidrosis (loss of sweating one side)
Distinguishing between causes

heterochromia (difference in iris colour) is seen in congenital Horner's
anhidrosis: see below
pharmacologic tests
can be useful to confirm the diagnosis of Horner syndrome and localise the lesion
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
Central lesions Pre-ganglionic lesions Post-ganglionic lesions
Anhidrosis of the face, arm and trunk Anhidrosis of the face No anhidrosis
Stroke Pancoast's tumour Carotid artery dissection

Syringomyelia Thyroidectomy Carotid aneurysm
Multiple sclerosis Trauma Cavernous sinus thrombosis
Tumour Cervical rib Cluster headache
Encephalitis
*in reality the appearance is due to a narrow palpebral aperture rather than true enophthalmos
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Pancoast tumors
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Question 13 of 90
A 32-year-old man presents with night sweats and a cervical lymph node. Aspirate of the node
reveals many acid-fast bacilli and PCR confirms the presence of Mycobacterium tuberculosis. He is
started on quadruple therapy.
As part of the counselling, you warn him of potential side effects including optic neuritis.
What symptom should he be warned about?
Diplopia 11%
Pain relieved by eye movements 5%
Peripheral visual loss 20%
Red desaturation 47%
Sudden monocular blindness 17%
Colour vision ('red desaturation') is affected in optic neuritis

The correct answer is red desaturation. The anti-tuberculous agent ethambutol can be associated
with optic neuritis. This often presents first with deficits in colour vision, particularly red
desaturation. In one study, abnormal colour vision was recognised in 94% of patients with optic
neuritis.
Diplopia is incorrect. This would be an unusual feature with optic neuritis. It generally occurs with
problems of the nerves controlling the extra-ocular muscles, namely III, IV and VI.
Pain relieved by eye movements is incorrect. The opposite is true with optic neuritis, with pain
generally exacerbated by eye movements.
Peripheral visual loss is incorrect. Visual loss in optic neuritis usually represents a central scotoma
rather than a peripheral defect.
Sudden monocular blindness is incorrect. Complete monocular blindness is unusual in optic

neuritis. Where it does occur, the onset is generally gradual rather than sudden.
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Optic neuritis
Causes
diabetes
syphilis
Features
central scotoma
Investigation
Management
high-dose steroids
Prognosis
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Question 14 of 90
A 71-year-old man who has recently been diagnosed with macular degeneration asks for advice
regarding antioxidant dietary supplements. Which one of the following may contraindicate the
prescription of such supplements?
Current smoker 52%
Pernicious anaemia 22%
Treated hypertension 3%
History of depression 11%
Previous episodes of tendonitis 11%
Beta-carotene has been found to increase the risk of lung cancer and hence antioxidant dietary
supplements are not recommended for smokers.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases

Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
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Question 15 of 90
Which one of the following is not a risk factor for primary open-angle glaucoma?
Diabetes mellitus 9%
Family history 5%
Hypertension 9%
Afro-Caribbean ethnicity 21%
Hypermetropia 56%
Acute angle closure glaucoma is associated with hypermetropia, where as primary open-
angle glaucoma is associated with myopia
The correct answer is Hypermetropia. Primary open-angle glaucoma (POAG) is a complex,

multifactorial eye disease with an unknown etiopathogenesis. It is known that hypermetropia
(farsightedness) does not increase the risk for POAG. In fact, myopia (nearsightedness), rather than
hypermetropia, has been associated with an increased risk of developing glaucoma.
Now let's discuss each of the other options:
Diabetes mellitus has been linked to an increased risk of primary open-angle glaucoma. Studies
have shown that diabetic patients are nearly twice as likely to develop POAG compared to non-
diabetic individuals. The exact mechanism by which diabetes increases the risk of POAG remains
unclear but it may be related to changes in blood flow and metabolism within the optic nerve
head.
Family history is a well-established risk factor for primary open-angle glaucoma. First-degree
relatives of individuals with POAG have a significantly higher risk of developing the disease
themselves compared to those without a family history.
Hypertension, or high blood pressure, also increases the risk for primary open-angle glaucoma.
Chronic hypertension can lead to vascular changes and damage in the optic nerve, contributing to
the pathogenesis of POAG.
Lastly, Afro-Caribbean ethnicity is associated with a higher prevalence and severity of primary
open-angle glaucoma. People of African descent are up to six times more likely to develop this
disease than Caucasians and they tend to experience more severe visual field loss at diagnosis.
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Primary open-angle glaucoma: presentation and diagnosis
Glaucomas are 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 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. It is now
recognised that a minority of patients with raised IOP do not have glaucoma and vice versa.
Risk factors:
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
POAG may present insidiously and for this reason is often detected during routine optometry
appointments. Features may include
peripheral visual field loss - nasal scotomas progressing to 'tunnel vision'
decreased visual acuity
optic disc cupping
Fundoscopy signs of POAG
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
Diagnosis:
Case finding and provisional diagnosis is done by an optometrist
Referral to the ophthalmologist is done via the GP
Final diagnosis is done by investigations as below
Investigations:
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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2 0
2017 Glaucoma guidelines
Clinical Knowledge Summaries 0 0
Glaucoma guidelines
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Understanding Open Angle Glaucoma
Zero To Finals - YouTube 10 0
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Question 16 of 90
A 60-year-old man presents to his GP with a progressive dry, itchy right eye and associated
blurring of his vision. The patient and his family have also noticed he has difficulty fully closing his
eyelid. The patient is known to have hypertension and type 2 diabetes but has no previous
hospital admission or eye issues in the past.
On examination, the patient has evidence of miosis, partial ptosis, anhidrosis of the face and
enophthalmos.
What is the most likely cause of this patient's presentation?
Carotid artery dissection 9%
Cavernous sinus thrombosis 8%
Cerebral vascular event 7%
Pancoast tumour 68%
Syringomyelia 7%

This patient has presented with a collection of signs and symptoms in keeping with Horner's
syndrome. Horner's symptoms arise from a lesion to the sympathetic nerve trunk and result in
miosis, partial ptosis, enophthalmos and varying degrees of anhidrosis on the same side as the
patient's lesion. Lesions can occur anywhere along the sympathetic nerve trunk and the site of
these lesions can be determined by the presence and location of anhidrosis. Pre-ganglionic
lesions result in anhidrosis of the face only. They are due to causes such as Pancoast tumours,
cervical rib and thyroid issues (e.g. thyroid carcinoma, thyroidectomy and goiter).
Carotid artery dissection results in a post-ganglionic lesion. In Horner's syndrome secondary to
post-ganglionic lesion patients normally present without anhidrosis.
Cavernous sinus thrombosis also results in a post-ganglionic lesion and like carotid artery
dissections, anhidrosis is absent and sweating is unaffected in these patients.
Cerebral vascular events (i.e stroke) result in central lesions. In Horner's syndrome due to central
lesions patients generally present with anhidrosis of the face, arm and trunks.
In syringomyelia a cysts or cavity forms within the spinal cord resulting in a central lesion. As with
strokes these patients present with Horner's syndrome and anhidrosis of the face, arm and trunk
on the affected side.
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Horner's syndrome
Features
ptosis

pharmacologic tests

synaptic cleft

Encephalitis
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Question 17 of 90
A 24-year-old man who has a family history of retinitis pigmentosa is reviewed in the
ophthalmology clinic. He reports worsening vision over the past few months. During fundoscopy,
which of the following findings with most support a diagnosis of retinitis pigmentosa?
Pigmented scrambled egg appearance concentrated around the macula 6%
Central irregular pigmentation with bull's eye maculopathy 8%
Black bone spicule-shaped pigmentation in the peripheral retina 67%
Drusen with haemorrhagic atrophic changes concentrated at the periphery of the retina 7%
Pigmented choroidal neovascularisation throughout the retina 12%
The correct answer is black bone spicule-shaped pigmentation in the peripheral retina.
Retinitis pigmentosa (RP) is a group of inherited retinal disorders characterized by progressive
degeneration of the photoreceptors, leading to vision loss. The classic fundoscopic finding in RP is
black bone spicule-shaped pigmentation in the peripheral retina, which occurs due to the
migration and proliferation of retinal pigment epithelial cells into the outer retina. This finding is
highly suggestive of RP and supports the diagnosis in this patient with a family history and
worsening vision.
The option pigmented scrambled egg appearance concentrated around the macula describes
a pattern seen in Stargardt disease, an inherited macular dystrophy that causes central vision loss.
It is characterized by yellow-white flecks with a scrambled egg appearance at the level of the
retinal pigment epithelium (RPE) around the macula.
Central irregular pigmentation with bull's eye maculopathy is a characteristic finding in

chloroquine or hydroxychloroquine toxicity. Bull's eye maculopathy refers to a circular band of RPE
atrophy surrounding the fovea, which can cause central vision loss. This pattern is not typically
seen in retinitis pigmentosa.
The option Drusen with haemorrhagic atrophic changes concentrated at the periphery of the
retina describes findings more consistent with age-related macular degeneration (AMD). Drusen
are extracellular deposits located between Bruch's membrane and RPE, commonly associated with
AMD. Haemorrhagic atrophic changes are also observed in advanced stages of AMD but are not
typical for RP.
Finally, pigmented choroidal neovascularisation throughout the retina refers to abnormal

blood vessel growth from the choroid into subretinal space or RPE, which can be seen in
conditions such as wet age-related macular degeneration, high myopia, or choroidal rupture.
Choroidal neovascularisation is not a typical finding in retinitis pigmentosa.
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Retinitis pigmentosa
Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision
Features
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
Associated diseases
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport's syndrome
Image sourced from Wikipedia
Fundus showing changes secondary to retinitis pigmentosa
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Question 18 of 90
A 70-year-old man is investigated for blurred vision. Fundoscopy reveals drusen, retinal epithelial
and macular neovascularisation. A diagnosis of age related macular degeneration is suspected.
What is the most appropriate next investigation?
Vitreous fluid sampling 4%
MRI orbits 5%
Ocular tonometry 20%
Fluorescein angiography 65%
Kinetic perimetry 7%
The correct answer is Fluorescein angiography. This is because fluorescein angiography is a key
investigation in assessing the extent of neovascularisation, which is a feature of wet or exudative
age-related macular degeneration (AMD). In this procedure, a fluorescent dye is injected into the
bloodstream and pictures are taken as the dye passes through the blood vessels in the retina. This
allows for the visualisation of any abnormal blood vessels, leaks or blockages.
Discussing the incorrect answers:
Vitreous fluid sampling is not routinely performed in AMD. It may be used in cases where there's
suspicion of intraocular infection or inflammation, such as uveitis or endophthalmitis, conditions
that present differently from AMD.
An MRI orbits would not provide detailed enough information about the retinal vasculature to
diagnose AMD. While MRI can provide useful information about larger structures within and
around the eye, it does not have sufficient resolution to assess small structures such as drusen or
macular neovascularisation.
Ocular tonometry measures intraocular pressure and is primarily used in the diagnosis and
monitoring of glaucoma. While raised intraocular pressure can cause vision problems, it does not
cause drusen or macular neovascularisation seen in AMD.
Finally, Kinetic perimetry tests visual fields but would not help determine whether a patient has
wet or dry AMD. Visual field testing might show central vision loss associated with advanced AMD
but it would not give information about neovascularisation which is critical for management
decisions.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases

Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
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Question 19 of 90
A 65-year-old man with a history of primary open-angle glaucoma presents with sudden painless
loss of vision in his right eye. On examination of the right eye the optic disc is swollen with
multiple flame-shaped and blot haemorrhages. What is the most likely diagnosis?
Diabetic retinopathy 13%
Occlusion of central retinal vein 58%
Occlusion of central retinal artery 8%
fundoscopy
The most likely diagnosis in this case is occlusion of the central retinal vein. The patient's
presentation of sudden painless vision loss, optic disc swelling, and multiple flame-shaped and
blot haemorrhages are all characteristic features of central retinal vein occlusion (CRVO). CRVO
occurs when there is a blockage in the central retinal vein, leading to impaired venous drainage
from the retina. This results in increased pressure within the blood vessels, causing them to leak
blood and fluid into the surrounding tissues.
Diabetic retinopathy is an incorrect option because it typically presents with microaneurysms,

dot and blot haemorrhages, hard exudates, and cotton wool spots rather than optic disc swelling.
Diabetic retinopathy is a common complication of diabetes mellitus and affects the small blood
vessels of the retina. While it may cause vision loss over time, it does not usually present as
sudden painless vision loss.
Vitreous haemorrhage is also an incorrect option. While vitreous haemorrhage can cause sudden
painless vision loss, it would not be associated with optic disc swelling or multiple flame-shaped
and blot haemorrhages on examination. Vitreous haemorrhage occurs when blood leaks into the
vitreous humour from damaged blood vessels in conditions such as diabetic retinopathy or retinal
tears.
The diagnosis of ischaemic optic neuropathy is less likely given the presence of multiple flame-
shaped and blot haemorrhages. Ischaemic optic neuropathy typically presents with sudden
painless vision loss along with pallid swelling of the optic disc due to impaired blood supply to the
optic nerve head. However, it does not usually present with retinal haemorrhages.
Finally, occlusion of central retinal artery is an incorrect option as well. Central retinal artery
occlusion presents with sudden painless vision loss and a pale retina with a cherry-red spot at the
fovea on examination. This condition occurs when blood flow to the retina is obstructed, leading
to ischemia and subsequent infarction of the retina. It would not present with optic disc swelling
or multiple flame-shaped and blot haemorrhages.
In summary, the most likely diagnosis for this patient is occlusion of the central retinal vein due to
his presentation of sudden painless vision loss, optic disc swelling, and multiple flame-shaped and
blot haemorrhages.
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Risk factors
increasing age
hypertension
glaucoma
polycythaemia
Features
fundoscopy
Management
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Question 20 of 90
A 66-year-old male is referred to ophthalmology by his general practitioner with a complaint of

gradual deterioration of peripheral vision bilaterally. His past medical history includes
hypertension and a left knee replacement. He is on regular amlodipine. He does not smoke or
drink and is retired and lives alone.
On examination, there is clinical evidence of a mild reduction in the peripheral vision bilaterally.
Formal tonometry demonstrates a raised intraocular pressure of 25 mmHg.
Based on the likely diagnosis, the treating ophthalmologist prescribes a medication that works by
reducing aqueous production without increasing uveoscleral outflow.
Which class of medication has this mechanism of action?
Brimonidine 7%
Ciclosporin 1%
Latanoprost 15%
Pilocarpine 9%
Timolol 68%
Beta blockers such as timolol work in primary open-angle glaucoma by reducing aqueous
production
Timolol is correct. The diagnosis is open-angle glaucoma is evidenced by the impaired peripheral
vision and raised intraocular pressure. Beta-blockers such as timolol work in primary open-angle
glaucoma by reducing aqueous production.
Brimonidine is incorrect. The diagnosis is open-angle glaucoma as evidenced by impaired

peripheral vision and raised intraocular pressure. Sympathomimetics (e.g. brimonidine, an alpha2-
adrenoceptor agonist) work in open-angle glaucoma by both increasing uveoscleral outflow and
reducing aqueous production rather than reducing aqueous production, alone.
Ciclosporin is incorrect. This is not a treatment for open-angle glaucoma but is used topically in
severe keratitis in dry eye disease that has not responded to treatment with tear substitutes. It
works by inhibiting the production and release of cytokines.
Latanoprost is incorrect. Prostaglandin analogues are the first-line treatment of open-angle

glaucoma but they work by increasing uveoscleral outflow.
Pilocarpine is incorrect. Miotics (e.g. pilocarpine, a muscarinic receptor agonist) work in open-
angle glaucoma by increasing uveoscleral outflow.
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Primary open-angle glaucoma: management
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.
The aim of treatment is to lower intra-ocular pressure which in turn has been shown to prevent
progressive loss of visual field.
NICE guidelines
offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg
NICE
360° SLT can delay the need for eye drops and can reduce but does not remove the
chance they will be needed at all
a second 360° SLT procedure may be needed at a later date
prostaglandin analogue (PGA) eyedrops should be used next-line NICE
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.
Medication Mode of action Notes
Prostaglandin analogues (e.g. Increases uveoscleral Once daily administration

latanoprost) outflow
Adverse effects include brown
pigmentation of the iris, increased
eyelash length
Beta-blockers (e.g. timolol, Reduces aqueous Should be avoided in asthmatics

betaxolol) production and patients with heart block
Sympathomimetics (e.g. Reduces aqueous Avoid if taking MAOI or tricyclic

brimonidine, an alpha2- production and antidepressants
adrenoceptor agonist) increases outflow
Adverse effects include
hyperaemia
Carbonic anhydrase inhibitors Reduces aqueous Systemic absorption may cause

(e.g. Dorzolamide) production sulphonamide-like reactions
Miotics (e.g. pilocarpine, a Increases uveoscleral Adverse effects included a

muscarinic receptor agonist) outflow constricted pupil, headache and
blurred vision
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Question 21 of 90
Which one of the following statements regarding the Holmes-Adie pupil is incorrect?
May be associated with absent ankle/knee reflexes 8%
Bilateral in 80% of cases 49%
It is a benign condition 9%
Slowly reactive to accommodation but very poorly (if at all) to light 21%
Causes a dilated pupil 13%
The incorrect statement about Holmes-Adie pupil is that it is 'Bilateral in 80% of cases'. In
reality, the Holmes-Adie syndrome, which includes Adie's pupil, along with absent deep tendon
reflexes (typically the Achilles reflex), is bilateral in only about 20% of cases. Thus, this statement is
incorrect.
Now let's discuss each of the other options:
'May be associated with absent ankle/knee reflexes' - This statement is correct. The absence of
deep tendon reflexes, especially at the ankle (Achilles reflex), is a common feature of Holmes-Adie
syndrome. The loss of these reflexes may not be apparent immediately but becomes more evident
over time.
'It is a benign condition' - This statement is also correct. Although Holmes-Adie pupil can cause
some visual disturbances and discomfort due to light sensitivity and difficulty focusing on close
objects, it does not lead to blindness or any serious health problems. It's a benign neurological
condition and doesn't progress to become life-threatening.
'Slowly reactive to accommodation but very poorly (if at all) to light' - This statement
accurately describes one of the key features of Holmes-Adie pupil. The affected pupils are typically
large and react slowly or not at all when exposed to light. However, they do constrict slowly when
focusing on near objects (accommodation).
'Causes a dilated pupil' - This too is correct. The defining characteristic of an Adie's pupil is that
it's larger (dilated) than normal because it doesn't respond well to light stimulation due to damage
to the postganglionic fibres of the parasympathetic innervation.
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Holmes-Adie pupil
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the
differentials of a dilated pupil.
Overview
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
Holmes-Adie syndrome
association of Holmes-Adie pupil with absent ankle/knee reflexes
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Question 22 of 90
A 71-year-old female with dry age-related macular degeneration is reviewed. Unfortunately her
eyesight has deteriorated over the past six months. She has never smoked and is taking
antioxidant supplements. What is the most appropriate next step?
Retinal transplant 3%
Intravitreal ranibizumab 30%
Explain no other medical therapies currently available 40%
Photodynamic therapy 9%
Photocoagulation 18%
The correct answer is Explain no other medical therapies currently available. Dry age-related
macular degeneration (AMD) is a chronic, progressive disease that primarily affects the central
vision. There is currently no cure for dry AMD according to UK guidelines, and management
mainly involves monitoring for conversion to wet AMD and supportive measures such as low
vision aids and antioxidant supplements in certain cases.
Retinal transplant is not a feasible option for AMD. While theoretically it may seem like replacing
the damaged retina could restore vision, in practice this is not currently possible due to technical
difficulties with integrating a transplanted retina into the existing retinal circuitry.
Intravitreal ranibizumab is an anti-VEGF therapy used in the treatment of wet AMD, but not dry
AMD. Wet AMD involves abnormal blood vessel growth under the retina which can leak fluid or
blood, damaging the macula and causing rapid central vision loss. Ranibizumab works by
inhibiting VEGF, a protein that promotes new blood vessel formation. However, this would not be
effective in dry AMD where there are no abnormal blood vessels to target.
Photodynamic therapy also targets abnormal blood vessels and thus has its place in treating wet
AMD but not dry AMD. It involves injecting a light-sensitive drug into the bloodstream which
accumulates in the abnormal vessels under the retina, then activating it with laser light via an
intravenous line which damages these vessels.
Finally, photocoagulation, which uses laser energy to seal leaking blood vessels in the eye, was
previously used as a treatment for wet AMD but has largely been replaced by anti-VEGF therapies
like ranibizumab because they have better outcomes. Again photocoagulation would not help in
dry AMD where there are no leaking vessels present.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases


Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
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Question 23 of 90
A 67-year-old man presents as he has developed a painful blistering rash around his right eye. On
examination a vesicular rash covering the right trigeminal nerve dermatome is seen. Currently he
has no eye symptoms or signs. Which one of the following is most likely to predict future eye
involvement?
Presence of the rash on the tip of his nose 68%
Smoking history 6%
Increasing age 4%
Previous courses of corticosteroids 6%
Presence of the rash in the ear canal 16%
This is Hutchinson's sign which is strongly predictive for ocular involvement.
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Herpes zoster ophthalmicus
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.
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
Management
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
Complications
ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
ptosis
post-herpetic neuralgia
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Question 24 of 90
A 24-year-old woman presents with visual disturbance. On examination, you swing the penlight
from eye to eye quickly and note that the right pupil and left pupil dilate when light is shone into
the right eye.
Where is the most likely site of the lesion?
CN III 10%
CN IV 2%
Left retina or optic nerve 10%
Right retina or optic nerve 72%
Sympathetic nerve fibers 7%
A relative afferent pupillary defect is when the affected and normal eye appears to dilate
when light is shone on the affected eye
Right retina or optic nerve is correct, During the 'swinging light test' the right and left pupil
dilate when shining light into the right eye. This indicates a problem with the right-sided afferent
pathway (e.g. right sided retina or optic nerve).
CN III is incorrect, In compressive CN III palsy, the pupil becomes fixed and dilated due to
paralysis of sphincter pupillae.
CN IV is incorrect, This cranial nerve plays no role in pupil physiology.
Left retina or optic nerve is incorrect, A left-sided RAPD would be characterised by bilateral pupil
dilation when shining light into the left eye.
Sympathetic nerve fibres is incorrect, Horner syndrome is caused by damage to a certain

pathway in the sympathetic nervous system. The sympathetic nervous system acts to dilate the
pupils, and thus lesions of this pathway are characterised by pupil constriction.
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Finding
Causes
retina: detachment

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Question 25 of 90
A 35-year-old man presents with visual problems. He has had very poor vision in the dark for a
long time but is now worried as he is developing 'tunnel vision'. He states his grandfather had a
similar problem and was registered blind in his 50's. What is the most likely diagnosis?
Leber's congenital amaurosis 7%
Vitelliform macular dystrophy 5%
Central serous retinopathy 3%
Primary open angle glaucoma 12%
Retinitis pigmentosa 73%
Retinitis pigmentosa - night blindness + tunnel vision

The most likely diagnosis, in this case, is retinitis pigmentosa. Retinitis pigmentosa is a group of
inherited retinal disorders characterized by progressive degeneration of the retina, leading to
night blindness and peripheral vision loss. The patient's symptoms of poor night vision and
developing 'tunnel vision', as well as a family history of visual problems leading to blindness, are
classic features of retinitis pigmentosa.
Leber's congenital amaurosis is an incorrect answer because it presents as severe visual impairment
or blindness at birth or within the first few months of life. This condition does not match the
patient's age and presentation.
Vitelliform macular dystrophy is also an incorrect option. This disorder typically affects central
vision due to the accumulation of yellow deposits under the macula, causing distortion or loss of
central vision. However, it does not cause night blindness or tunnel vision as described by the
patient.
Central serous retinopathy is another incorrect choice. It usually presents with sudden onset
blurred central vision, often affecting only one eye. This condition may resolve spontaneously but
can recur in some individuals. It does not cause night blindness or tunnel vision and has no known
familial association.
Finally, primary open-angle glaucoma is incorrect as well. Although it can cause tunnel vision
due to gradual loss of peripheral vision, primary open-angle glaucoma typically does not cause
night blindness. Additionally, this condition usually affects people over 40 years old and has a
more insidious onset compared to the patient's presentation.
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Features
Associated diseases
Usher syndrome
Alport's syndrome
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Question 26 of 90
A 65-year-old man presents with a sudden loss of vision in his right eye upon waking up this
morning. He has no pain in his eye. Past medical history is notable for diabetes mellitus and
hypertension. Fundoscopic examination of the left eye reveals no abnormalities. Fundoscopic
examination of the right eye reveals multiple retinal haemorrhages.
Amaurosis fugax 8%
Hypertensive retinopathy 11%
Optic neuritis 1%
fundoscopy
This patient's sudden painless loss of vision, coupled with the fundoscopy finding of retinal
haemorrhages in the affected eye, is consistent with central retinal vein occlusion.
Amaurosis fugax causes temporary vision loss that resolves in a few minutes. It is caused by
atheroembolism from the carotid arteries. This patient has persistent vision loss.
Central retinal artery occlusion presents with acute painless vision loss. However, the patient
would have a loss of relative afferent pupillary defect, and the fundoscopy would reveal a cherry-
red macula and a white/pale retina.
Hypertensive retinopathy may cause flame-shaped haemorrhages and cotton wool spots on the
retina, but it does not cause a sudden vision loss.
Optic neuritis presents with a sudden loss of vision associated with severe pain and an afferent
pupillary defect. This patient's painless loss of vision makes this diagnosis unlikely.
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Risk factors
increasing age
hypertension
glaucoma
polycythaemia
Features
fundoscopy
Management
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Question 27 of 90
A 66-year-old man presents to his GP complaining of 'funny symptoms' in his eyes. He describes
having flashes of light in his eyes for several days. In addition to this, he has been noticing darker
'bits' floating around in his vision. He denies any pain. He is short-sighted and wears glasses but
otherwise has no significant past medical history.
On examination, the visual acuity and fields are normal.
What is the most likely cause of his symptoms?
Migraine 3%
Optic neuritis 3%
Posterior vitreous detachment 74%
Retinal tear 4%
Flashes + floaters are most commonly caused by a posterior vitreous detachment

The most common cause of flashers and floaters is posterior vitreous detachment (PVD), occurring
in over 75% of people over the age of 65. This is the separation of the vitreous membrane from
the retina, which occurs over time with ageing. It does not cause any pain, nor loss of vision.
Highly myopic patients are also at increased risk. Referral to an ophthalmologist should take place
within 24 hours to rule out retinal tears or detachment.
Migraine is incorrect - there is no headache described here and so this is unlikely. For some
people, migraine auras can mimic flashes and floaters - they may experience strange ocular
sensations - but the most likely cause here is posterior vitreous detachment.
Optic neuritis is also unlikely - there is no pain, nor any history of any previous disease to suggest
this. In this patient, posterior vitreous detachment remains by far the most likely cause of his
flashers and floaters.
Retinal detachment may be a complication of PVD, but again not as common as the PVD itself -
this would present with sudden visual loss (whereas here, the fields and acuity are normal), often
as a 'veil' covering the visual field. This requires urgent intervention from an ophthalmologist.
A retinal tear may also occur, without progressing to detachment. This would present with similar
symptoms as the detachment but, on detailed examination, a tear would be visualised rather than
complete detachment. This, again, requires intervention from an ophthalmologist.
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Posterior vitreous detachment
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.
Epidemiology:
Occur in over 75% of people over the age of 65
More common in females
Risk factors:
As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its
shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the
centre of the eye.
Highly myopic (near-sighted) patients are also at increased risk of developing posterior
vitreous detachment earlier in life. This is because the myopic eye has a longer axial length
than an emmetropic eye.
Symptoms:
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal
detachment)
Signs:
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic
nerve to form a ring-shaped floater).
Investigations:
All patients with suspected vitreous detachment should be examined by an ophthalmologist
within 24hours to rule out retinal tears or detachment.
Management:
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms
gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
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Question 28 of 90
Which one of the following is least recognised as a cause of tunnel vision?
Papilloedema 29%
Choroidoretinitis 8%
Angioid retinal streaks 38%
Glaucoma 16%
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Tunnel vision
Tunnel vision is the concentric diminution of the visual fields
Causes
papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria
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Question 29 of 90
A 74-year-old man presents to ophthalmology clinic after seeing his optician. They have noticed
raised intra-ocular pressure and decreased peripheral vision. His past medical history includes
asthma and type 2 diabetes mellitus. What is the most appropriate treatment given the likely
diagnosis?
Latanoprost 57%
Pilocarpine 19%
Timolol 9%
Dorzolamide 11%
Brimonidine 4%
The correct answer is Latanoprost. This patient's presentation of raised intraocular pressure and
decreased peripheral vision suggests a diagnosis of open-angle glaucoma, which is the most
common form of glaucoma. Latanoprost is a prostaglandin analogue and it works by increasing
the outflow of aqueous humour from the eye, thereby reducing intraocular pressure.
Prostaglandin analogues such as latanoprost are first-line treatments for open-angle glaucoma.
Pilocarpine is incorrect because it is not a first-line treatment for open-angle glaucoma in the UK.
Pilocarpine is a muscarinic receptor agonist that increases the outflow of aqueous humour but has
more side effects than latanoprost, including miosis (pupil constriction) and potential worsening
of presbyopia.
Timolol would not be an appropriate choice for this patient due to his past medical history of
asthma. Timolol is a non-selective beta-blocker which can cause bronchoconstriction and
potentially exacerbate asthma symptoms.
Dorzolamide is also incorrect. Dorzolamide is a carbonic anhydrase inhibitor used as adjunctive

therapy in patients with inadequate response to first-line treatments or if they are intolerant to
them. It works by reducing production of aqueous humour but it's less effective than latanoprost.
Lastly, Brimonidine would not be the best choice either. Brimonidine is an alpha-2 adrenergic
receptor agonist that reduces the production of aqueous humour and increases its outflow.
However, it has more systemic side effects compared to latanoprost and like dorzolamide,
brimonidine would only be considered if first-line treatments were ineffective or not tolerated.
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NICE guidelines
NICE

eyelash length


hyperaemia


blurred vision
Next question
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Question 30 of 90
A 32-year-old woman presents with visual disturbance. On examination, you swing the penlight
from eye to eye quickly and note that the right and left pupils dilate when light is shone into the
right eye.
Where is the most likely site of the lesion?
CN III 10%
CN IV 2%
Left retina or optic nerve 9%
Right retina or optic nerve 71%
Sympathetic nerve fibres 8%
Relative afferent pupillary defect indicates an optic nerve lesion or severe retinal disease
Right retina or optic nerve is correct. During the 'swinging light test' the right and left pupils
dilate when shining light into the right eye. This indicates a problem with the right-sided afferent
pathway (e.g. right-sided retina or optic nerve).
CN III is incorrect. In compressive CN III palsy, the pupil becomes fixed and dilated due to
paralysis of sphincter pupillae.
CN IV is incorrect. This cranial nerve plays no role in pupil physiology.
Left retina or optic nerve is incorrect. A left-sided RAPD would be characterised by bilateral pupil
dilation when shining light into the left eye.
Sympathetic nerve fibres is incorrect. Horner syndrome is caused by damage to a certain

pathway in the sympathetic nervous system. The sympathetic nervous system acts to dilate the
pupils, and thus lesions of this pathway are characterised by pupil constriction.
Discuss Improve
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Finding
Causes
retina: detachment

Next question
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Question 31 of 90
Which one of the following features is not characteristic of optic neuritis?
Eye pain worse on movement 13%
Relative afferent pupillary defect 7%
Poor discrimination of colours, 'red desaturation' 11%
Sudden onset of visual loss 51%
Central scotoma 17%
Visual loss typically occurs over days rather than hours. Sudden visual loss due to optic neuritis is
very unusual.
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Optic neuritis
Causes
diabetes
syphilis
Features
central scotoma
Investigation
Management
high-dose steroids
Prognosis
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Question 32 of 90
A 24-year-old man presents to the emergency department complaining of left eye pain. He has
not been able to wear his contact lenses for the past 24 hours due to the pain. He describes the
pain as severe and wonders whether he has 'got something stuck in his eye'. On examination there
is diffuse hyperaemia of the left eye. The left cornea appears hazy and pupillary reaction is normal.
Visual acuity is reduced on the left side and a degree of photophobia is noted. A hypopyon is also
seen. What is the most likely diagnosis?
Acute angle closure glaucoma 12%
Viral conjunctivitis 5%
Keratitis 37%
Episcleritis 5%
Whilst a hypopyon can of course be seen in anterior uveitis the combination of a normal pupillary
reaction and contact lens use make a diagnosis of keratitis more likely.
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Keratitis
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.
Aetiology
Causes
bacterial
typically Staphylococcus aureus

Pseudomonas aeruginosa is seen 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')
Remember, other factors may causes keratitis:

viral: herpes simplex keratitis
environmental
photokeratitis: e.g. welder's arc eye
exposure keratitis
contact lens acute red eye (CLARE)
Clinical features
Features
red eye: pain and erythema
photophobia
foreign body, gritty sensation
hypopyon may be seen
Evaluation and management
Referral
contact lens wearers
assessing contact lens wearers who present with a painful red eye is difficult
an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day
referral to an eye specialist is usually required to rule out microbial keratitis
Management
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
Complications may include:

corneal scarring
perforation
endophthalmitis
visual loss
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Question 33 of 90
An 80-year-old man presented to his general practitioner with sudden, painless loss of vision in his
right eye 2 hours ago. He is an insulin-dependant type 2 diabetic, with a history of hypertension
and dyslipidaemia. On further questioning, he reports brief flashing of lights before a dense
shadow that started peripherally and progressed centrally.
Pre-proliferative retinopathy 1%
Retinal detachment is a cause of sudden painless loss of vision. It is characterised by a dense

shadow starting peripherally and progressing centrally
Retinal detachment is a disorder of the eye in which the retina peels away from its underlying
layer of support tissue causing flashes of light, increased floaters and a dense shadow that starts
in the peripheral vision and slowly progresses towards the central vision.
Central retinal artery occlusion is the blockage of blood to the retina of one eye. It usually causes
a sudden loss of eyesight in one eye usually from an embolus. It rarely gives floaters, flashing
lights or dense shadows seen in this case.
Central retinal vein occlusion will often be described as the blurry or distorted vision in one eye
that began suddenly, these symptoms are not seen here.
Vitreous haemorrhage results in the sudden appearance of spots or floaters in your vision to cause
a sudden blurring of vision but does not cause flashing lights seen in retinal detachment.
Pre-proliferative retinopathy causes the sudden appearance of floaters in your vision with
distortion of object shapes and visual loss as a result.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Question 34 of 90
A 53-year-old male who presents to the emergency department with a painful red eye. He has
vomited once since the pain started. He reports seeing haloes around lights.
His immediate management includes latanoprost and pilocarpine, and he requires an urgent
ophthalmology referral.
What is the mode of the action of pilocarpine?
Muscarinic receptor agonist 58%
Muscarinic receptor antagonist 34%
Nicotinic receptor agonist 2%
Nicotinic receptor antagonist 2%
Adrenergic receptor agonist 4%
Pilocarpine is a muscarinic receptor agonist

Pilocarpine is a muscarinic receptor agonist - it increases uveoscleral outflow by constricting the

pupil.
Examples of muscarinic receptor antagonists include atropine and hyoscine (scopolamine) - these
are not used in the management of glaucoma.
Nicotinic receptor agonists include nicotine and acetylcholine, therefore this answer is incorrect.
Nicotinic receptor antagonists include succinylcholine, atracurium, vecuronium and bupropion.
Adrenergic receptor agonists include norepinephrine and epinephrine.
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Acute angle-closure glaucoma
Glaucoma is a group of disorders characterised by optic neuropathy due, in the majority of

patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with
raised IOP do not have glaucoma and vice versa.
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
Features
severe pain: may be ocular or headache
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
Investigations
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
Management
The management of AACG is an emergency and should prompt urgent referral to an

ophthalmologist. Emergency medical treatment is required to lower the IOP with more definitive
surgical treatment given once the acute attack has settled.
There are no guidelines for the initial medical treatment emergency treatment. An example regime
would be:
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 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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Question 35 of 90
During routine follow-up at renal clinic a man is noted to have corpuscular pigmentation of the
left retina. Which one of the following conditions is associated with retinitis pigmentosa?
Autosomal dominant polycystic kidney disease 10%
Tuberous sclerosis 15%
Von Hippel-Lindau syndrome 21%
Alport's syndrome 50%
Medullary sponge kidney 5%
The correct answer to this question is Alport's syndrome. Alport's syndrome is a genetic disorder
characterized by glomerulonephritis, end-stage kidney disease, and hearing loss. It can also
sometimes affect the eyes, with changes such as anterior lenticonus and retinitis pigmentosa.
Retinitis pigmentosa refers to a group of inherited diseases causing retinal degeneration where
patients experience night blindness and a loss of peripheral vision.
Autosomal dominant polycystic kidney disease (ADPKD) is not typically associated with
retinitis pigmentosa. ADPKD is a genetic disorder characterised by the growth of numerous cysts
in the kidneys which can lead to kidney failure over time. The most common extrarenal
manifestations are hepatic cysts, but it does not typically involve the eye.
Tuberous sclerosis is an autosomal dominant condition that causes non-malignant tumours to

grow in the brain and on other vital organs like the kidneys, heart, liver, eyes, lungs and skin.
Ocular abnormalities may occur in tuberous sclerosis but these are usually retinal astrocytic
hamartomas rather than retinitis pigmentosa.
Von Hippel-Lindau syndrome is an inherited disorder characterized by the formation of tumours

and fluid-filled sacs (cysts) in many different parts of the body. Eye involvement can occur in Von
Hippel-Lindau syndrome however this usually manifests as retinal haemangioblastomas rather
than retinitis pigmentosa.
Finally, Medullary sponge kidney is a congenital disorder where cysts form in the urine-
collecting ducts and tubules of one or both kidneys but it does not have any known associations
with ocular conditions including retinitis pigmentosa.
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Features
Associated diseases
Usher syndrome
Alport's syndrome
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Question 36 of 90
Which one of the following is least associated with the development of optic atrophy?
Tobacco 16%
Methanol 13%
Vitamin B12 deficiency 20%
Lead 19%
Zinc deficiency 32%
The correct answer is Zinc deficiency. Optic atrophy, a condition characterised by the
degeneration of the optic nerve, can be caused by several factors. However, zinc deficiency is the
least associated with its development. Zinc plays a crucial role in maintaining the health of the eye
and its deficiency can cause symptoms like night blindness or slow wound healing but it doesn't
typically lead to optic atrophy.
Tobacco use has been linked to optic atrophy. Tobacco-alcohol amblyopia, also known as toxic
amblyopia, is a form of optic neuropathy that can result from tobacco use. It's thought that the
toxins in tobacco damage the mitochondria in cells of the optic nerve leading to their dysfunction
and subsequent death.
Methanol is another substance strongly associated with optic atrophy. Methanol poisoning can
cause severe metabolic acidosis and visual disturbances due to its metabolites which are toxic to
the retina and optic nerve.
A Vitamin B12 deficiency can also lead to optic atrophy. Vitamin B12 plays an essential role in
maintaining the health of nerve cells and the myelin sheath around them. Its deficiency may lead
to subacute combined degeneration (SCD) of the spinal cord, peripheral neuropathy and also
optic neuropathy causing progressive vision loss leading eventually to optic atrophy if left
untreated.
Similarly, exposure to Lead has been found to cause optic atrophy. Lead toxicity can affect many
organs including the nervous system where it causes demyelination and axonal damage leading
eventually to conditions like peripheral neuropathy or rarely optic atrophy.
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Optic atrophy
Optic atrophy is seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and
causes a gradual loss of vision*. Causes may be acquired or congenital
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)
*strictly speaking optic atrophy is a descriptive term, it is the optic neuropathy that results in visual
loss
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Question 37 of 90
Which one of the following is associated with the Holmes-Adie pupil?
Decreased ankle reflexes 49%
Pupillary constriction 14%
Ptosis in 10-20% of cases 8%
An increased of developing multiple sclerosis 7%
Neurosyphilis 22%
Holmes ADIe = DIlated pupil, females, absent leg reflexes

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Holmes-Adie pupil
Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the
differentials of a dilated pupil.
Overview
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
Holmes-Adie syndrome
association of Holmes-Adie pupil with absent ankle/knee reflexes
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Question 38 of 90
A 52-year-old woman is referred to the ophthalmology clinic by her optician. The optician
detected raised intraocular pressure (IOP) in both eyes. The patient is currently asymptomatic but
describes a family history of glaucoma. She has no other past medical history of note.
On examination, the IOP is currently 23 mmHg bilaterally. The ophthalmologist prescribes

latanoprost eye drops to be used daily in both eyes.
What is the mechanism of action of this drug?
Increases choroidal blood flow 1%
Increases intravascular osmolarity 1%
Increases uveoscleral outflow 69%
Reduces aqueous production 11%
Reduces aqueous production and increases uveoscleral outflow 17%
Latanoprost is a prostaglandin analog used in glaucoma. It works by increasing uveoscleral

outflow
Latanoprost is a prostaglandin analogue and is commonly used first-line in patients with open-
angle glaucoma. It acts by increasing uveoscleral outflow. It is typically administered once daily.
Side effects include brown pigmentation of the iris and increased eyelash length.
Carbonic anhydrase inhibitors are an alternative to be given topically, but may also be given orally.
Oral acetazolamide appears to increase choroidal blood flow in some studies. Latanoprost does
not cause this effect.
Oral hyperosmotic drugs such as mannitol may be given in emergencies relating to acute IOP
increases. These act by increasing intravascular osmolarity and drawing fluid out of the vitreous
humour of the eye. Latanoprost does not act by this mechanism.
Beta-blockers, such as timolol, are often used in the treatment of glaucoma. They act by reducing
aqueous production. Latanoprost does not work via this mechanism.
Sympathomimetics, such as brimonidine, act by both increasing uveoscleral outflow and

reducing aqueous production. Latanoprost only acts via the former mechanism, not the latter.
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NICE guidelines
NICE


eyelash length


hyperaemia


blurred vision
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Question 39 of 90
A 54-year-old woman presents with a persistent watery left eye for the past 4 days. On
examination there is erythema and swelling of the inner canthus of the left eye. What is the most
likely diagnosis?
Blepharitis 20%
Meibomian cyst 17%
Dacryocystitis 57%
Pinguecula 4%
The correct answer is Dacryocystitis. This condition is an infection of the lacrimal sac, secondary
to obstruction of the nasolacrimal duct. The symptoms typically include persistent watering of the
eye (epiphora) and inflammation at the inner canthus, which are both present in this patient's
case. Moreover, it often occurs in middle-aged and older adults, fitting this patient's demographic.
Blepharitis is a chronic inflammatory condition affecting the eyelid margins. It presents with
symptoms such as gritty sensation, burning, itching and redness of the eyelid margin. Crusting
may be seen around the base of eyelashes especially on waking up in the morning. While this
patient does have erythema (redness), it is localized to the inner canthus rather than along the
eyelid margin which makes blepharitis less likely.
Acute angle closure glaucoma typically presents with a painful red eye accompanied by reduced
vision, haloes around lights, headache and sometimes nausea or vomiting. Intraocular pressure
would be elevated on examination. This patient's presentation lacks these key features making
acute angle closure glaucoma unlikely.
A Meibomian cyst, also known as a chalazion, is a granulomatous inflammation of a Meibomian

gland in the tarsal plate of either upper or lower eyelid. It usually presents as a painless swelling
on an eyelid without any associated watering or redness unless secondarily infected or inflamed
which again does not fit with this clinical scenario.
Finally, a Pinguecula is a common degenerative condition characterised by yellowish patch or

bump on conjunctiva near cornea (usually on nasal side). It tends to be asymptomatic but may
cause discomfort or foreign body sensation particularly in dry conditions. Given that our patient
has presented with persistent watery eyes and erythema at inner canthus rather than any
discomfort or foreign body sensation makes pinguecula unlikely diagnosis here.
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Lacrimal duct problems
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
Congenital lacrimal duct obstruction affects around 5-10% of newborns. It is bilateral in around
20% of cases
Features
watering eye (even if not crying)
secondary infection may occur
Symptoms resolve in 99% of cases by 12 months of age
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Question 40 of 90
A 56-year-old female with longstanding rheumatoid arthritis presented to her general practitioner
with redness of her right eye. She reports feeling slight discomfort and being irritating with
occasional watering of the eye. She denied any dryness or pain as such. Assessment of her pupils
was normal and light did not cause her any discomfort.
Corneal ulceration 2%
Episcleritis 63%
Keratitis 5%
Scleritis 8%

Episcleritis is one of the many ocular manifestations of rheumatoid arthritis. In episcleritis, the
episclera becomes inflamed and red. It often causes irritation, soreness or a gritty sensation but
importantly no pain.
Keratitis is marked by moderate to intense pain and usually involves impaired eyesight,
photophobia, redness of the eye with a gritty sensation.
Scleritis is a disorder in which the sclera becomes severely inflamed and red. It can be very painful.
Given the absence of pain, in this case, scleritis is unlikely.
Keratoconjunctivitis sicca is dryness of the conjunctiva and cornea. Too few tears may be
produced, or tears may evaporate too quickly. There is no evidence to suggest this occurring here.
Corneal ulceration is a painful sore that develops on the outer surface of your eye. They're more
common in contact lens wearers.
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problems
corneal ulceration
keratitis
Iatrogenic
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Question 41 of 90
A 40-year-old man presents with bilateral dry, gritty eyes. A diagnosis of blepharitis is considered.
Which one of the following is least likely to be associated with blepharitis?
Meibomian gland dysfunction 11%
Seborrhoeic dermatitis 10%
Staphylococcal infection 12%
Acne rosacea 24%
Viral upper respiratory tract infection 43%
The correct answer is Viral upper respiratory tract infection. Blepharitis, an inflammation of the
eyelid margins, is typically associated with a number of conditions but not commonly linked to
viral upper respiratory tract infections. The main causes are often related to skin disorders or
bacterial infections.
Meibomian gland dysfunction is indeed associated with blepharitis. These glands produce oil
that forms part of the tear film on our eyes, and when they're not functioning properly, it can lead
to dryness and irritation - symptoms synonymous with blepharitis.
Similarly, Seborrheic dermatitis, a common skin condition affecting areas rich in sebaceous
glands (including the eyelids), can cause flaky skin (dandruff) and redness around the eyes - both
signs of blepharitis.
A Staphylococcal infection caused by the bacterium Staphylococcus aureus, is also closely linked
with blepharitis. This bacterium often lives harmlessly on our skin but can cause infection if it
enters deeper into tissue - in this case leading to inflammation along the eyelid margin.
Acne rosacea, a long-term skin condition characterised by reddening and pimples primarily on
facial skin, can also affect the eye causing ocular rosacea. This can manifest as blepharitis
alongside other eye symptoms such as dryness and redness.
In contrast, while a viral upper respiratory tract infection may cause conjunctivitis due to
spread of virus through nasolacrimal duct, it's not commonly associated directly with blepharitis.
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Blepharitis
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). Blepharitis is also more common in patients with rosacea
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
Features
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
Management
softening of the lid margin using hot compresses twice a day
'lid hygiene' - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often
used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has
recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear
film
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Question 42 of 90
A 45-year-old man presents to the Emergency Department following the sudden onset of pain in
the right side of his face whilst hammering a nail into the wall. The pain is described as severe and
constant. On examination he has a mild right ptosis and small right pupil. What is the most likely
diagnosis?
Trigeminal neuralgia 23%
Glaucoma 6%
Syringomyelia 8%
Migraine 5%
This patient has Horner's syndrome caused by a carotid artery dissection. This may be caused by
relatively benign trauma to the neck such as hyperextension whilst doing DIY. Cluster headache
would be a differential diagnosis
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Horner's syndrome
Features
ptosis

pharmacologic tests
synaptic cleft

Encephalitis
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Horner's syndrome
Pancoast tumors
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Question 43 of 90
An 83-year-old female presented to her GP with complete loss of vision in her right eye which
occurred suddenly. The episode lasted for 10 minutes and she denies any pain in her eye. Her past
medical history includes hypercholesterolaemia, diet controlled, and hypertension for which she
takes amlodipine.
Eye examination and fundoscopy are normal. Her blood pressure is 145/80 mmHg.
What medication are you going to give first?
Aspirin 300mg 83%
Aspirin 75mg 9%
Simvastatin 20mg 3%
Apixaban 5mg BD 2%
Enoxaparin 40mg 3%
Monocular transient painless loss of vision (amaurosis fugax) should be treated as a TIA
Sudden painless loss of vision with a normal fundoscopy examination is an amaurosis fugax and
thus treated as a transient ischaemic attack (TIA). NICE guidance states that 300mg of aspirin
should be given immediately and admission if ABCD2 score >3 or crescendo TIA, otherwise an
immediate TIA clinic referral is required.
Option 2 is the correct medication but incorrect dose.
Option 3 is likely to be added later but aspirin is the first initial plan.
Apixaban is usually given for cardiovascular disease and enoxaparin 40mg is the dose given for
deep vein thrombosis prophylaxis with normal renal function.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Score: 18.6%
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Question 44 of 90
A 55-year-old woman attends the clinic with worsening vision. She has a past medical history of
poorly controlled diabetes mellitus. A slit lamp examination confirms proliferative diabetic
retinopathy.
You counsel the patient for panretinal laser photocoagulation.
What complication is this patient most at risk of?
Endophthalmitis 5%
Macular oedema 10%
Myopia 3%
Reduction of the visual field 68%

Reduction of the visual field is correct. This is a common complication following panretinal laser
photocoagulation with up to 50% of patients having a noticeable reduction in their visual field.
Endophthalmitis is incorrect. Endophthalmitis is not a recognised complication of panretinal laser

photocoagulation.
Macular oedema is incorrect. Whilst this can occur, it is a rare complication.
Myopia is incorrect. Myopia is not a recognised complication of panretinal laser

photocoagulation.
Vitreous haemorrhage is incorrect. Whilst this can occur, it is a rare complication.
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Pathophysiology
Classification
Mild NPDR
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
severe NPDR
Severe NPDR
Key features
Maculopathy
Key features
check visual acuity
Management
All patients
Maculopathy
inhibitors
regular observation
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Question 45 of 90
A 65-year-old male who has a new diagnosis of giant cell arteritis has had a positive relative
afferent pupillary defect (RAPD) in his left eye on examination.
Which of the following describes the finding of RAPD in this man?
The right eye appears to dilate when light is shone on the right eye 5%
The left eye appears to dilate when light is shone on the left eye 19%
The left and right eye appears to dilate when light is shone on the left eye 58%
The left and right eye appears to dilate when light is shone on the right eye 11%
The left and right eye appears to constrict when light is shone on the left eye 7%
A relative afferent pupillary defect is when the affected and normal eye appears to dilate
when light is shone on the affected eye
A RAPD is caused by differences between the two eyes in the afferent pathway due to retinal or
optic nerve disease. This leads to reduced constriction, hence appears as dilation, of both pupils
when light is shone from the unaffected eye to the affected eye.
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Finding
Causes
retina: detachment

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Score: 17.8%
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Question 46 of 90
A 74-year-old myopic woman with known hypertension presents with a sudden, painless
reduction in her vision. She describes a dense shadow obscuring her right eye, this started
peripherally and has progressed towards the central vision.
On examination, she can only see hand movements in her right eye and has 6/6 visual acuity in
her left eye.
What is the most likely cause of the loss of vision?
Optic neuritis 2%
Vitreous hemorrhage 8%

Central retinal artery occlusion occurs due to a blockage of blood flow from thromboembolism for
arteritis. It can cause a partial or complete sudden, painless loss of vision. However, this doesn't
tend to occur peripherally and move centrally as described here. Typical features include afferent
pupillary defect, 'cherry red' spot on a pale retina.
Central retinal vein occlusion is more common than arterial occlusion and occurs with increasing
age, but unlike here is more common in patients with glaucoma. It can cause sudden painless loss
of vision in any venous territory and the ophthalmoscope shows severe retinal haemorrhages.
This case is typical of retinal detachment. It occurs more commonly in people with myopia. It can
be preceded by flashes and floaters and tends to present with a shadow to the vision beginning
peripherally and progressing centrally.
Optic neuritis can cause sudden visual loss but this is often transient and associated with painful
eye movement.
The vitreous hemorrhage causes a dark spot to a vision where the hemorrhage is rather than a
shadow to the vision.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Score: 17.4%
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Question 47 of 90
A 68-year-old man with a history of type 2 diabetes mellitus presents with worsening eye sight.
Mydriatic drops are applied and fundoscopy reveals pre-proliferative diabetic retinopathy. A
referral to ophthalmology is made. Later in the evening whilst driving home he develops pain in
his left eye associated with decreased visual acuity. What is the most likely diagnosis?
Keratitis secondary to mydriatic drops 9%
Proliferative diabetic retinopathy 4%
Mydriatic drops are a known precipitant of acute angle closure glaucoma. This scenario is more
common in exams than clinical practice.
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Features
hard, red-eye
Investigations
Management

would be:

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Score: 19.1%
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Question 48 of 90
A 24-year-old man self-presents to the eye casualty department. He admits to being persuaded to
attend by his girlfriend as he is not normally keen on seeing doctors. The patient has a past
medical history of ulcerative colitis.
The doctor performs a preliminary examination of the eyes and decides that either the episclera or
the sclera are inflamed. He subsequently performs a slit lamp examination.
Which key feature of the history or examination classically differentiates between the two
diagnoses?
Association with autoimmune disease 9%
Fluorescein staining 10%
Laterality 3%
Pain 75%
Redness of eyes 3%

The correct answer is the presence of pain. Classically, episcleritis is a milder condition without any
pain (although occasionally may be uncomfortable). Scleritis is almost always painful and is a
more serious condition. Whilst episcleritis is usually self-limiting, scleritis requires intervention.
Association with autoimmune disease would not particularly help to differentiate between
episcleritis and scleritis. Both are commonly associated with a number of autoimmune and
rheumatological diseases, including rheumatoid arthritis, ulcerative colitis and granulomatosis
with polyangiitis.
Fluorescein staining would not help to differentiate between the two. This is used to detect
corneal abnormalities; as such, it does not help with regards to episcleritis and scleritis.
Laterality is not a particularly useful discriminator between the two conditions either - episcleritis
is bilateral in about 40% of cases and, similarly, scleritis is bilateral in approximately 50% of cases.
The redness of the eyes would not help to differentiate between scleritis and episcleritis - in both
conditions, the eyes will be visibly red.
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problems
corneal ulceration
keratitis
Iatrogenic
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Score: 18.8%
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Question 49 of 90
A 78-year-old gentleman presents to the emergency department complaining of a severe

headache. His only medical condition is hypertension, for which he take Ramipril 10 mg and
Amlodipine 10 mg. As part of the full work up fundoscopy is performed, with the following results
bilaterally: Scattered cotton wool spots, tortuous vessels throughout, and AV nipping.
What stage of hypertensive retinopathy according the Keith-Wagener classification does this
patient have?
Stage 1 2%
Stage 2 21%
Stage 3 66%
Stage 4 11%
No retinopathy present 1%
Fundoscopy reveals end organ damage in hypertension

This describes stage 3 hypertensive retinopathy, as there are features of stages 1 to 3 described.
Hypertensive and diabetic retinopathy are both common finals questions.
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Hypertensive retinopathy
The table below shows the Keith-Wagener classification of hypertensive retinopathy
Stage Features
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 Papilloedema
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Score: 18.4%
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Question 50 of 90
A 40-year-old woman presents to the emergency department with a two-day history of worsening
blurry vision and painful movements of the right eye. She also has reduced oral intake with
persistent fever. She denies any headaches. The patient was last seen by her general practitioner a
week ago for acute sinusitis.
On examination, there is right eye proptosis, right eyelid oedema, erythema and tenderness. The
best-corrected visual acuity is 6/12 in the right eye, 12/12 in the left eye. Colour vision is reduced
in the right eye.
Given the most likely diagnosis, what should be the next step in management?
Admit and administer IV antibiotics 76%
Admit and arrange for computed tomography (CT) brain 8%
Admit and arrange for urgent ophthalmology review 15%
Discharge with a course of oral antibiotics 0%
Discharge with ophthalmology follow up in 24 hours 0%
The presence of right eye proptosis, painful eye movements, reduced visual acuity, and systemic
symptoms strongly suggest orbital cellulitis. The patient recently had acute sinusitis, which is a
common risk factor, as the bacterial infection spreads from the paranasal sinuses into the orbit.
Patients require urgent admission and intravenous antibiotics as soon as possible to minimize the
risk of complications such as cavernous sinus thrombosis.
Although CT brain should also be performed to look for the presence of sinusitis, subperiosteal
abscess, stranding of orbital fat, and intracranial involvement, it is not the most appropriate next
step. There is a high clinical suspicion of orbital cellulitis in this case and antibiotics should not be
delayed to wait for CT confirmation.
Similarly, the patient should have an ophthalmology review, but it should not take precedence
over antibiotics administration. Given the high clinical suspicion here, waiting for ophthalmology
review would only delay antibiotic treatment, putting the patient at greater risk of fatal
complications.
Discharging the patient with oral antibiotics or ophthalmology follow up is dangerous and puts
her at risk of fatal complications such as abscess and cavernous sinus thrombosis.
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Orbital cellulitis
Risk factors
Childhood
Presentation
Severe ocular pain
Visual disturbance
Proptosis

Investigations
Management
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Score: 18%
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Question 51 of 90
A 64-year-old woman presents with bilateral sore eyelids. She also complains of her eyes being
dry all the time. On examination her eyelid margins are erythematous at the margins but are not
swollen. Of the given options, what is the most appropriate initial management?
Topical chloramphenicol + mechanical removal of lid debris 7%
Hot compresses + topical steroids 14%
Topical chloramphenicol + topical steroids 5%
Hot compresses + mechanical removal of lid debris 59%
Topical chloramphenicol + hot compresses 15%
1st line of treatment for blepharitis is hot compresses

The correct answer is Hot compresses + mechanical removal of lid debris. The patient's
symptoms and signs are suggestive of blepharitis, a common chronic bilateral inflammatory
condition of the eyelid margins. Initial management should involve a combination of eyelid
hygiene measures such as warm compresses to loosen crusts, mechanical removal of lid debris
with cotton-tipped applicators or clean washcloth, and lid massage to express meibomian
secretions. This approach can help control symptoms and prevent complications.
Topical chloramphenicol + mechanical removal of lid debris is not the most appropriate initial
management. While it includes the important step of removing lid debris, topical antibiotics like
chloramphenicol are typically reserved for cases where there is an associated bacterial infection
(such as staphylococcal anterior blepharitis) or in severe cases that do not respond to conservative
management.
Hot compresses + topical steroids is also incorrect. Although hot compresses are beneficial in
managing blepharitis, topical steroids are generally not recommended for long-term use due to
potential side effects such as glaucoma and cataract formation. They may be used short-term in
severe cases under specialist supervision.
Topical chloramphenicol + topical steroids would be inappropriate as first-line treatment for
this patient's presentation. As mentioned earlier, both these medications have specific indications
and potential side effects that make them unsuitable for the initial management of uncomplicated
blepharitis.
Finally, Topical chloramphenicol + hot compresses doesn't include the crucial step of
mechanically removing lid debris which contributes significantly to symptom relief in blepharitis.
Additionally, as stated above, using topical antibiotics like chloramphenicol should be reserved for
more severe or refractory cases.
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Blepharitis
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). Blepharitis is also more common in patients with rosacea
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
Features
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
Management
softening of the lid margin using hot compresses twice a day
'lid hygiene' - mechanical removal of the debris from lid margins
cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often
used
an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has
recently been boiled
artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear
film
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Question 52 of 90
Which one of the following is the most common ocular manifestation of rheumatoid arthritis?
Scleritis 16%
Episcleritis 29%
Keratitis 5%
Keratoconjunctivitis sicca is characterised by dry, burning and gritty eyes caused by decreased tear
production
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problems
corneal ulceration
keratitis
Iatrogenic
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Score: 19.2%
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Question 53 of 90
A 67-year-old man who is known to have raised intraocular pressure is prescribed dorzolamide
eye drops. What is the mechanism of action of this drug?
Prostaglandin analogue 5%
Alpha2-adrenoceptor agonist 5%
Carbonic anhydrase inhibitor 83%
Muscarinic receptor agonist 5%
Beta-blocker 1%
Dorzolamide - carbonic anhydrase inhibitor

The correct answer is Carbonic anhydrase inhibitor. Dorzolamide is a carbonic anhydrase

inhibitor which works by decreasing the production of aqueous humour in the eye, thereby
reducing intraocular pressure. This makes it useful in the management of conditions such as
glaucoma where there is raised intraocular pressure.
Prostaglandin analogue is incorrect. Prostaglandin analogues like latanoprost increase

uveoscleral outflow, which reduces intraocular pressure. They do not act by inhibiting carbonic
anhydrase.
The option Alpha2-adrenoceptor agonist is also incorrect. Drugs such as brimonidine are
alpha2-adrenoceptor agonists that reduce the production of aqueous humour and increase its
outflow, thus lowering intraocular pressure. However, they do not work by inhibiting carbonic
anhydrase.
Muscarinic receptor agonist is another incorrect choice. Muscarinic receptor agonists like
pilocarpine work by constricting the ciliary muscle which opens up the trabecular meshwork and
increases the outflow of aqueous humour from the eye, thereby reducing intraocular pressure.
They do not inhibit carbonic anhydrase.
Finally, Beta-blocker is also incorrect. Beta-blockers such as timolol decrease aqueous humour
production but their mechanism does not involve carbonic anhydrase inhibition.
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NICE guidelines
NICE

eyelash length


hyperaemia


blurred vision
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Question 54 of 90
A 22-year-old woman presented with a history of a sudden loss of vision of her left eye for 4 days
in duration. It was associated with pain in eye movement.
Ocular examination revealed visual acuity of the left eye was only counting fingers with a positive
afferent pupillary defect. Visual acuity of the right eye was 6/6. Anterior segments of both eyes
showed normal ocular findings. The contrast sensitivity and colour vision test were severely
impaired. The visual field showed unilateral central scotoma.
What is the underlying diagnosis?
Episcleritis 3%
Glaucoma 7%
Macular degeneration 9%
Optic neuritis 77%
A central scotoma is a feature of optic neuritis

Optic neuritis is an inflammation of the eye's optic nerve. The two most common symptoms of
optic neuritis are vision loss and eye pain. Central scotoma is recognised as a characteristic visual
field defect pattern of optic neuritis. It may be associated with demyelinating diseases or
infectious or inflammatory processes. The signs include decreased visual acuity, decreased colour
vision (red desaturation) and relative afferent pupillary defect (RAPD).
Episcleritis is a common condition affecting the episclera, the layer of tissue between the surface
membrane (conjunctiva) and the firm white part of the eye (the sclera). In episcleritis, the episclera
becomes inflamed and red. It often causes irritation, soreness or a gritty sensation. However, it
typically does not cause visual loss which makes this incorrect.
Glaucoma is an eye condition that is often associated with elevated intraocular pressure, in which
damage to the optic nerve can lead to loss of vision and even blindness. The visual field loss
(scotoma) in glaucoma has a distinctive pattern that differs from visual loss due to other causes
and includes para-central scotoma, nasal step, and arcuate defect.
Corneal ulceration is an erosion or open sore on the surface of the cornea which causes sudden
painful visual loss. A corneal ulcer usually results from an eye infection, but severe dry eye or other
eye disorders can cause it. The absence of tearing and redness make this diagnosis unlikely.
Macular degeneration produces a scotoma which most often appears in the central visual field
resulting in its being called a central scotoma. In dry macular degeneration, the light-sensing cells
(called rods and cones) in the centre of the retina degenerate along with their supporting cells.
This diagnosis is unlikely as it is typically painless and also age-related.
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Optic neuritis
Causes
diabetes
syphilis
Features
central scotoma
Investigation
Management
high-dose steroids
Prognosis
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Score: 20.4%
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Question 55 of 90
An 80-year-old woman presents with 'funny spots' affecting her vision. Over the past week she has
noticed a number of flashes and floaters in the visual field of the right eye. What is the most likely
diagnosis?
Optic neuritis 2%
Depression 1%
Posterior vitreous detachment is thought to occur in up to 50-75% of the population over 65 years
and is the most likely diagnosis here. Such patients are normally reviewed by an ophthalmologist
to assess the risk of progressing to retinal detachment.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
Posterior vitreous
Next question
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Score: 21.8%
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Question 56 of 90
A 71-year-old man is under the ophthalmology clinic for bilateral primary open-angle glaucoma.
He has been using latanoprost eye drops but despite this, his intraocular pressures remain
elevated.
The ophthalmologist has to add in a second topical agent to try to reduce intraocular pressure
further by decreasing the rate of aqueous humour production.
Which class of drug should be offered next?
Antimuscarinic 8%
Beta-blocker 67%
Carbonic anhydrase analogue 20%
Corticosteroids 0%
Prostaglandin analogue 5%
production
Topical beta-blockers are commonly used in the management of primary open-angle glaucoma.
They reduce intraocular pressure (IOP) by decreasing the rate of production of aqueous humour.
Examples include timolol, betaxolol and levobunolol.
It is sometimes used as first-line pharmacological therapy or may be added to a prostaglandin

analogue (as in this patient) as second-line treatment if monotherapy is unsuccessful.
Topical antimuscarinics have no role in the management of primary open-angle glaucoma. In fact,
they can obstruct the outflow of aqueous humour and raise IOP further. Conversely, pilocarpine (a
muscarinic agonist) can be used to reduce IOP in primary open-angle glaucoma.
Carbonic anhydrase inhibitors (e.g. brinzolamide, dorzolamide) are available to treat glaucoma,
rather than carbonic anhydrase analogues.
Topical corticosteroids are used in other eye conditions such as uveitis and post-cataract surgery,
but not for glaucoma.
This patient is already using latanoprost with insufficient benefit, so it would be incorrect to
combine with a second prostaglandin analogue. Patients are sometimes tried on a different drug
in the same class if one is poorly tolerated. However, guidelines recommend that a drug from
another therapeutic class should be used if current treatment is not sufficiently reducing IOP.
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NICE

eyelash length


hyperaemia


blurred vision
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Question 57 of 90
Which one of the following is associated with heterochromia in congenital disease?
Holmes-Adie pupil 30%
Third nerve palsy 5%
Sixth nerve palsy 3%
Argyll-Robertson pupil 23%
Horner's syndrome 39%
The correct answer to this question is Horner's syndrome. Heterochromia, a condition where the
two eyes are different colours, can be associated with Horner's syndrome. This is a neurological
disorder that results from damage to the sympathetic nerves supplying the eye. Symptoms of
Horner's syndrome include ptosis (drooping of the upper eyelid), miosis (constriction of the pupil),
anhidrosis (lack of sweating), and heterochromia. The heterochromia in Horner's syndrome is
usually partial and more commonly seen in patients who acquire the condition at a young age.
Discussing each incorrect option:
Holmes-Adie pupil is not associated with heterochromia. This condition, also known as Adie's
tonic pupil, is characterised by a dilated pupil that reacts slowly to light but has a normal or near-
normal response to accommodation. It often presents unilaterally and may be accompanied by
absent tendon reflexes.
Third nerve palsy, also known as oculomotor nerve palsy, causes drooping of the eyelid (ptosis)
and outward deviation of the eye due to paralysis of the medial rectus muscle. There might be
dilation of the pupil due to parasympathetic fibres involvement but it does not cause
heterochromia.
Sixth nerve palsy, or abducens nerve palsy, leads to horizontal double vision as it primarily
affects lateral rectus muscle responsible for eye abduction. It does not have any association with
heterochromia.
The Argyll-Robertson pupil is a small, irregular pupil that constricts normally with
accommodation but does not react to light. It is typically bilateral and associated with
neurosyphilis, specifically tertiary syphilis. However, it doesn't cause heterochromia.
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Horner's syndrome
Features
ptosis

pharmacologic tests
synaptic cleft

Multiple sclerosis
Tumour Trauma Cavernous sinus thrombosis

Encephalitis Cervical rib Cluster headache
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Question 58 of 90
A 65-year-old woman presents to the Emergency Department with visual problems. She has
rheumatoid arthritis, depression and takes medication to control her blood pressure. Over the past
few days she has been getting troublesome headaches and blurred vision but today has noted a
marked reduction in vision in the right eye. On examination her right eye is red, has a sluggish
pupil and a corrected visual acuity 6/30. Her medication has recently been changed. Which one of
the following drugs is most likely to have precipitated this event?
Methotrexate 21%
Doxazosin 16%
Amitriptyline 39%
Atenolol 14%
Bendroflumethiazide 11%
Drugs which may precipitate acute glaucoma include anticholinergics and tricyclic antidepressants
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Features
hard, red-eye
Investigations
Management

would be:

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Question 59 of 90
A 25-year-old woman presents to the emergency department with periorbital oedema, erythema,
and drainage that is worsening in her left eye. Mild proptosis is seen on examination.
A point of care ultrasound is performed to investigate her symptoms further. The modified ocular
ultrasound of her left eye demonstrates prominence and oedema of the retro-orbital soft tissue
with echogenic fat.
What is the management for this patient given the underlying diagnosis?
Intravenous antimicrobial 80%
No antimicrobial 4%
Oral antimicrobial 4%
Topical antimicrobial 3%
Topical corticosteroids 10%
Intravenous antimicrobial is required in hospitals for patients with orbital cellulitis due to the risk
of cavernous sinus thrombosis and intracranial spread. All patients with a clinical diagnosis of
orbital cellulitis MUST be admitted with an ophthalmic opinion sought as soon as possible.
Oral antimicrobial is not sufficient in this situation. Orbital cellulitis is conventionally managed by
intravenous antibiotic therapy and is a medical emergency that, if not treated urgently, may lead
to blindness and even death.
No antimicrobial is inappropriate in this situation given that orbital cellulitis is a medical

emergency that, if not treated urgently, may lead to blindness and even death. It necessitates
prompt treatment with intravenous antibiotics.
Topical antimicrobial is not sufficient in this situation. Orbital cellulitis is conventionally managed
by intravenous antibiotic therapy and is a medical emergency that, if not treated urgently, may
lead to blindness and even death.
Topical corticosteroids are unlikely to be that effective. The use of oral corticosteroids however
can help in reducing inflammation with less residual proptosis and restrictions in extraocular
movement during recovery. Intravenous antibiotic therapy remains first-line and must be initiated
promptly in this medical emergency.
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Orbital cellulitis
Risk factors
Childhood
Presentation
Severe ocular pain
Visual disturbance
Proptosis

Investigations
Management
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Question 60 of 90
A 75-year-old is referred to the ophthalmology clinic with a progressive reduction in visual acuity,
reduced night vision, and occasional floaters.
Fundoscopy shows the presents of yellow pigment deposits in the macular area as well as
demarcated red patches in keeping with fluid leakage and haemorrhage. She is otherwise well and
has no significant past medical history. Given the patient's like diagnosis her ophthalmologist
suggests a treatment that directly inhibits vascular endothelial growth factors.
What management is the patient to be commenced on?
Bevacizumab 81%
Fluocinolone 1%
Laser photocoagulation 11%
Verteporfin 3%
Zinc supplementation 3%
Bevacizumab is a monoclonal antibody directed against vascular endothelial growth factor

(VEGF)
The patient has presented with the classic signs and symptoms of age-related macular
degeneration (AMD), specifically the neovascular or exudative (also known as 'wet') form of the
condition. Vision loss is due to the proliferation of abnormal blood vessels (neovascularisation)
within the eye that are fragile, leaking blood and protein below the macula, damaging the
photoreceptors. This abnormal vessel growth is stimulated by vascular endothelial growth factor
(VEGF) which is specifically targeted and blocked by the monoclonal antibody bevacizumab.
Bevacizumab and other anti-VEGF treatments (e.g. ranibizumab and pegaptanib) are now used as
first-line treatment for AMD via direct intraocular injection.
Fluocinolone is a corticosteroid 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 and, on rare occasions, for AMD however they do not
affect VEGF and working as anti-inflammatories only.
Laser photocoagulation is used in the management of several eye conditions, normally to finely
cauterise ocular blood vessels; it does not affect VEGF. It is mainly used to close blood vessels in
diabetic retinopathy and is rarely used now AMD, in favour of anti-VEGF drugs.
Verteporfin is a medication used as 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. Although
used in AMD, again verteporfin is not an anti-VEGF drug.
Zinc supplementation can 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.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases

Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
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Question 61 of 90
Michael is a 65-year-old man who had presented with a gradual onset of visual changes over the
past 1.5 years. More recently, he has found that his peripheral vision has been deteriorating and
he has been bumping into objects.
On examination, his eye does not appear erythematous. Ophthalmoscopy reveals bilateral
cupping with a cup to disc ratio of 0.7. Tonometry reveals a pressure of 25mmHg in his left eye
and 27mmHg in his right eye.
He was trialled on brinzolamide, latanoprost and brimonidine subsequently but these were not
tolerated well due to side effects.
What is the mechanism of action of the best alternative medication?
Decrease aqueous humour production 45%
Decrease uveoscleral outflow 4%
Dual action ( increase uveoscleral outflow + decrease aqueous humour production) 35%
Increase aqueous humour production 2%
Increase uveoscleral outflow 14%
production
Primary open-angle glaucoma is caused by 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.
The common 1st line treatment of primary open-angle glaucoma includes β-blockers,
prostaglandin analogues, carbonic anhydrase inhibitors and alpha-2-agonists. We are told in the
stem that the patient is unable to tolerate brinzolamide (carbonic anhydrase inhibitors),
latanoprost (prostaglandin analogues) and brimonidine (alpha-2-agonist). This leaves beta-
blockers like timolol as the remaining choice. This acts by reducing the aqueous humour
production of the eye.
Carbonic anhydrase inhibitors (acetazolamide/dorzolamide/brinzolamide) also act by reducing

aqueous humour production.
Prostaglandin analogues (latanoprost) acts by increasing the uveoscleral outflow.
Alpha-2-agonists ( brimonidine) improves symptoms by having a dual action (reducing humour

production and increased outflow).
Increasing aqueous humour production will not help treat glaucoma and reduction in uveoscleral
outflow is seen in the use of mydriatic agents as they dilate the pupils.
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eyelash length


hyperaemia


blurred vision
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PassMedicine
Question 62 of 90
A 45-year-old female known to have rheumatoid arthritis presents to the hospital's emergency
department with a red, swollen painful right eye.
The patient is currently on hydroxychloroquine, with good drug compliance. She has had 3
arthritic flares in the past year, all responding to the IV steroids.
She frequently takes artificial teardrops, with good effect, as she often experiences foreign body
sensation. However, her current ocular symptoms are not in keeping with previous episodes and
are not responding to artificial teardrops.
Which of the following is the most likely diagnosis?
Allergic conjunctivitis 2%
Episcleritis 16%
Keratitis 13%
Retinopathy 8%
Scleritis 61%

Approximately 25% of patients with rheumatoid arthritis have ocular manifestations of the
disease. These range from episcleritis (inflammation of the outermost covering of the eye) to the
drug (chloroquine) induced retinopathy. Scleritis is characterised by a red, swollen, and painful eye
as described in this patient.
Episcleritis is commonly mistaken for scleritis however, episcleritis is painless.
As there is no clear history of stimuli exposure (i.e. pollen, dust) or increased lacrimation allergic
conjunctivitis is least likely in this case.
Keratitis is usually associated with eye discharge.
Retinopathy can occur due to hydroxychloroquine use in rheumatoid arthritis therefore, annual
eye exams are advised for rheumatoid patients. Retinopathy results in a painless reduction in
visual acuity which is not in keeping with this patient's presentation.
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problems
corneal ulceration
keratitis
Iatrogenic
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PassMedicine
Question 63 of 90
An 80-year-old male presents to the Neurology clinic with double vision and unsteadiness whilst
walking. He has a past medical history of hypertension, hypercholesterolaemia and type 2
diabetes.
On examination, you notice a right partial ptosis and miosis. The patient also has notable right
facial loss of pain and temperature sensation with left sided truncal sensory loss contralateral to
the face.
In the clinic, apraclonidine eye drops are added to the affected eye, which causes a dilatation,
whilst in the opposite eye, a pupil constriction occurs. After the eye drops have been eliminated
from the body, 1% hydroxyamphetamine eye drops are then instilled. One hour after instillation,
both pupils dilate.
What neurone order is likely affected in the sympathetic pathway?
First order 34%
Second order 34%
Third order 28%
Fourth order 3%
Fifth order 1%
The answer is the first order neurone.
Apraclonidine eye drops are initially used to confirm a Horner's pupil. Apraclonidine stimulates
both alpha-1 and alpha-2 receptors. When added to the affected eye, it causes pupil dilation by
>2mm because of the relative supersensitivity of this pupil to alpha-1 receptor activity. In a normal
pupil, however, it causes constriction due to the more potent activity at the alpha-2 receptor
which triggers reuptake of noradrenaline in the synaptic cleft.
Hydroxyamphetamine is then used to distinguish between first/second or third order neurones. In

other words, it will distinguish either a lesion in the brainstem, cervical cord, chest or neck and
one affecting above the superior cervical ganglion at the carotid bifurcation. In a normal pupil or a
first/second order Horner's, the pupil will dilate secondary to increased levels of noradrenaline
released from the post-synaptic neurones. In a third order neurone, this will not occur.
There is no fourth or fifth order neurone.
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Horner's syndrome
Features
ptosis

pharmacologic tests
synaptic cleft


Encephalitis
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Question 64 of 90
A 64-year-old woman with type 2 diabetes mellitus presents as she has started to bump into
things since the morning. Over the previous two days she had noticed some 'floating spots in her
eyes'. Examination reveals she has no vision in her right eye. The red reflex on the right side is
difficult to elicit and you are unable to visualise the retina on the right side during fundoscopy.
Examination of the left fundus reveals changes consistent with pre-proliferative diabetic
retinopathy. What is the most likely diagnosis?
Occlusion of central retinal vein 6%
Proliferative retinopathy 5%
Cataract 6%
The history of diabetes, complete loss of vision in the affected eye and inability to visualise the
retina point towards a diagnosis of vitreous haemorrhage. Please see the table below for help in
differentiating retinal detachment from vitreous haemorrhage.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Question 65 of 90
Which one of the following statements regarding macular degeneration is true?
Drusen are characteristic of wet macular degeneration 8%
Photodynamic therapy is useful in dry macular degeneration 4%
Asian ethnicity is a risk factor 5%
Male sex is a risk factor 6%
Wet macular degeneration carries the worst prognosis 77%
The correct answer is Wet macular degeneration carries the worst prognosis. Wet macular
degeneration, also known as neovascular or exudative macular degeneration, is less common but
more severe than its dry counterpart. It is characterised by choroidal neovascularisation leading to
rapid and severe vision loss. The prognosis is generally worse due to the potential for significant
central vision loss.
Drusen are characteristic of wet macular degeneration is incorrect. Drusen are small yellow
deposits under the retina, which are hallmark findings in dry (non-neovascular) age-related
macular degeneration (AMD), not wet AMD. They are composed of lipids and proteins and their
presence increases the risk of developing both forms of AMD.
The statement Photodynamic therapy is useful in dry macular degeneration is also false.
Photodynamic therapy involves injecting a drug into the bloodstream that sensitises abnormal
blood vessels in the eye to light. A special light is then shone into the eye to activate the drug,
which damages these abnormal vessels. However, this treatment method has been used primarily
for certain cases of wet AMD where anti-VEGF injections are ineffective or contraindicated, not dry
AMD.
Asian ethnicity is a risk factor for macular degeneration is not entirely accurate either. While it's
true that race can influence susceptibility to AMD, Caucasian individuals have been found to be at
higher risk compared to other racial groups including Asians according to various epidemiological
studies.
Finally, Male sex is a risk factor, this statement too isn't correct regarding AMD. According to
current evidence from multiple population-based studies, there appears to be no significant
association between gender and the prevalence of AMD; both sexes seem equally affected by this
condition.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases


Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:
Management
Treatment
category dry ARMD.
ARMD
Next question
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PassMedicine
Question 66 of 90
Which one of the following best describes the action of latanoprost in the management of
primary open-angle glaucoma?
Carbonic anhydrase inhibitor 5%
Reduces aqueous production + increases outflow 16%
Opens up drainage pores 3%
Latanoprost is a prostaglandin analog used in glaucoma. It works by increasing uveoscleral

outflow
The correct answer is Increases uveoscleral outflow. Latanoprost is a prostaglandin analogue

that works by increasing the uveoscleral outflow of aqueous humour, thereby lowering intraocular
pressure. This mechanism of action is particularly effective in the management of primary open-
angle glaucoma, where there is an imbalance between aqueous production and drainage.
Moving on to the incorrect answers, let's start with Carbonic anhydrase inhibitor. Carbonic
anhydrase inhibitors such as acetazolamide and dorzolamide are indeed used in the management
of glaucoma, but their mechanism of action differs from that of latanoprost. They work by
inhibiting carbonic anhydrase in the ciliary body, which reduces the rate of aqueous humour
production and thus decreases intraocular pressure.
Reduces aqueous production + increases outflow is another incorrect option. This describes
the combined actions of two different classes of drugs: beta-blockers (e.g., timolol) which reduce
aqueous humour production, and prostaglandin analogues like latanoprost which increase
uveoscleral outflow. However, latanoprost does not have any significant effect on aqueous
production.
The option Opens up drainage pores may be misleading as it suggests a mechanical action
rather than a pharmacological one. This could describe trabeculoplasty, a laser treatment for
open-angle glaucoma that aims to improve drainage through the trabecular meshwork (the
'drainage pores'). But this does not apply to latanoprost or any other ocular hypotensive
medication.
Finally, Reduces aqueous production would be correct for medications such as beta-blockers or
carbonic anhydrase inhibitors but not for latanoprost. As stated earlier, latanoprost works by
increasing uveoscleral outflow rather than decreasing aqueous production.
Discuss (2) Improve
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NICE guidelines
NICE


eyelash length


hyperaemia


blurred vision
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Score: 19.7%
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Question 67 of 90
A 33-year-old man presents to the emergency department with a one-day history of redness and
pain in his left eye, accompanied by blurred vision and photophobia. He has no significant past
medical history and reports no known drug allergies.
Ophthalmic examination reveals a small, fixed oval pupil with a ciliary flush in the affected eye.
Anterior ischaemic optic neuropathy 5%
Endophthalmitis 4%
Scleritis 8%
Red eye - glaucoma or uveitis?

glaucoma: severe pain, haloes, 'semi-dilated' pupil
uveitis: small, fixed oval pupil, ciliary flush
Anterior uveitis typically presents with acute onset redness, pain and blurred vision. It is
associated with ankylosing spondylitis, amongst other autoimmune diseases. The examination
findings are typical of anterior uveitis, with a small, fixed pupil and ciliary flush. A hypopyon may
also be present. Topical corticosteroids are the first line of treatment, and cycloplegic agents are
often given concomitantly.
Acute angle closure glaucoma also causes acute onset of red eye and pain. However, on
examination, the findings would differ because the pupil is fixed and semi-dilated with a hazy
cornea. Patients typically complain of reduced visual acuity and seeing haloes.
Anterior ischaemic optic neuropathy results from occlusion of the posterior ciliary artery, often
occurring in patients with temporal arteritis. It usually presents in patients over the age of 50 and
is unlikely in a patient who is only 33. Visual loss may be present, and associated symptoms such
as jaw claudication, scalp tenderness, or symptoms of polymyalgia rheumatica.
Endophthalmitis is inflammation of the inner eye that usually occurs as a result of eye injury or as
a complication from eye surgery. Red eye, pain and blurred vision may all also be present;
however, the pupil changes in this case are seen in anterior uveitis, not endophthalmitis.
Scleritis is associated with rheumatoid arthritis rather than ankylosing spondylitis. Features also
include pain and redness. Epiphora and photophobia may also be present. The pupils are not
small and fixed in scleritis, as with anterior uveitis.
Discuss (1) Improve
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Red eye
There are many possible causes of a red eye. It is important to be able to recognise the causes
which require urgent referral to an ophthalmologist. Below is a brief summary of the key
distinguishing features

severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea
Anterior uveitis
acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush
Scleritis
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
Conjunctivitis
purulent discharge if bacterial, clear discharge if viral
Subconjunctival haemorrhage
history of trauma or coughing bouts
Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery
Next question
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Score: 19.4%
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Question 68 of 90
A 34-year-old woman presents complaining of headaches. Examination of her pupils using a light
shone alternately in each eye reveals that when the light is shone in the right eye both pupils
constrict but when the light source immediately moves to the left eye both eyes appear to dilate.
Right optic neuritis 5%
Left sided Horner's syndrome 8%
Craniopharyngioma 3%
Left optic neuritis 64%
Right Holmes-Adie pupil 19%
This is the 'swinging light test' and reveals a relative afferent pupillary defect. As there is a defect
in the afferent nerve on the left side the pupils constrict less than normal, giving the impression of
dilation.
Given her age, multiple sclerosis causing optic neuritis is the likely underlying diagnosis. Optic
neuritis typically causes a dull ache in the region of the eye which is aggravated by movement
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Finding
Causes
retina: detachment

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Score: 19.1%
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Question 69 of 90
Which one of the following causes of Horner's syndrome is due to a central lesion?
Cavernous sinus thrombosis 19%
Internal carotid aneurysm 7%
Syringomyelia 67%
Cervical rib 1%

The correct answer is Syringomyelia. Horner's syndrome results from a disruption of the
oculosympathetic pathway. The central causes include brainstem stroke, demyelinating diseases
such as multiple sclerosis, and syringomyelia. Syringomyelia is a chronic condition characterised
by the development of fluid-filled cavities or syrinxes within the spinal cord. It disrupts the
descending sympathetic fibres that originate in the hypothalamus and travel down the brainstem
and cervical spinal cord before exiting at T1-T2 level to form part of the oculosympathetic
pathway.
Cavernous sinus thrombosis is an incorrect option because it is not a central cause of Horner's
syndrome. It can cause Horner's syndrome due to involvement of sympathetic fibres running
along the wall of cavernous sinus but this would be considered a pre-ganglionic lesion rather than
a central one.
Internal carotid aneurysm is another incorrect option. While it can cause Horner's syndrome due
to its proximity to the oculosympathetic pathway, this would also be considered pre-ganglionic
rather than central.
The fourth option, Pancoast's tumour, represents another peripheral cause of Horner's syndrome.
Pancoast's tumours are apical lung tumours that can invade local structures including the brachial
plexus and sympathetic chain, causing symptoms such as shoulder pain, arm weakness and
Horner's syndrome (ptosis, miosis, anhidrosis).
Finally, cervical rib is also incorrect because while it can cause compression on brachial plexus or
subclavian artery leading to thoracic outlet syndrome, it does not typically affect the
oculosympathetic pathway to result in Horner's Syndrome unless there is extensive involvement or
anomalous anatomy.
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Horner's syndrome
Features
ptosis

pharmacologic tests
synaptic cleft

Encephalitis
Next question
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Pancoast tumors
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Score: 18.8%
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Question 70 of 90
A 72-year-old man is admitted to the acute medical ward with shortness of breath. He is normally
well. His only past medical history is of primary open-angle glaucoma for which he takes timolol.
What is the mechanism of action for this medication?
Pupil constriction 3%
Pupil dilatation 3%
Reduce aqueous production and increase uveoscleral outflow 15%
production
Timolol is a beta-blocker and works to decrease intraocular pressure by reducing production of

aqueous humour.
Prostaglandin analogues such as latanoprost are first-line agents in primary open-angle glaucoma
and these work by increasing uveoscleral outflow, but they do not reduce aqueous production.
Miotics such as pilocarpine work on the muscarinic receptor causing pupil constriction and
therefore increase uveoscleral outflow.
Pupil dilatation actually decreases uveoscleral outflow and can exacerbate glaucoma.
Sympathomimetics such as brimonidine have a dual-action and reduce the ocular pressure by
reducing aqueous production and increases outflow.
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NICE


eyelash length



hyperaemia


blurred vision
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Score: 18.6%
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Question 71 of 90
A 72-year-old woman presents with a vesicular rash around her left eye. The left eye is red and
there is a degree of photophobia. A presumptive diagnosis of herpes zoster ophthalmicus is made
and an urgent referral to ophthalmology is made.
What treatment is she most likely to be given?
Topical aciclovir + topical chloramphenicol 4%
Topical aciclovir + topical corticosteroids 13%
Oral prednisolone + topical aciclovir 23%
Topical aciclovir 10%
Oral aciclovir 49%
There is no role for topical antivirals if systemic therapy is given. Topical corticosteroids are
sometimes given to treat secondary inflammation.
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case of shingles.
Features
Management
immunocompromised
Complications
ptosis
Next question
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Score: 18.3%
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Question 72 of 90
A 41-year-old woman with a history of type 1 diabetes attends a routine eye screening
appointment. She is found to have retinal neovascularisation, fibrous tissue anterior to the retinal
disc.
She is advised she will require treatment and counselled that following this treatment up to 50%
of patients have a noticeable reduction in their visual field.
What treatment will she be offered?
IV acetazolamide 1%
Intravitreal VEGF inhibitors 17%
Panretinal laser photocoagulation 80%
Topical cycloplegics 1%
Vitreoretinal surgery 2%

Panretinal laser photocoagulation is correct. The findings described are in keeping with
proliferative retinopathy, which is more common in type 1 diabetics and 50% are blind within 5
years. Following treatment around 50% of patients develop a noticeable reduction in their visual
fields due to the scarring of peripheral retinal tissue.
IV acetazolamide is incorrect. This is a carbonic anhydrase inhibitor that is used for acute angle
closure glaucoma and is not used for diabetic retinopathy. It results in an accumulation of
carbonic acid, which reduces the secretion of aqueous humour, and reduced intraocular pressure.
Intravitreal VEGF inhibitors is incorrect. These are often used in combination with pan-retinal
laser photocoagulation, but they do not cause the same reduction in the visual field. They block
VEGF which slows the growth of blood vessels within the eye.
Topical cycloplegics is incorrect. These result in paralysis of the ciliary muscle of the eye and loss
of lens accommodation, they are used for eye examinations and some ophthalmological
procedures.
Vitreoretinal surgery is incorrect. This may be used if there is severe or vitreous haemorrhage
present.
Discuss Improve
Next question
Pathophysiology
Classification
Mild NPDR
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
severe NPDR
Severe NPDR
Key features
Maculopathy
Key features
check visual acuity
Management
All patients
Maculopathy
inhibitors
regular observation
Next question
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Score: 18.1%
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Question 73 of 90
A 62-year-old man presents with sudden visual loss in his right eye. He is otherwise asymptomatic.
Which one of the following conditions is least likely to be responsible?
Occlusion of the central retinal vein 9%
Occlusion of the central retinal artery 7%
Optic neuritis 64%
Whilst optic neuritis can present with sudden loss, in this 62-year-old man it is the least likely
option. Typically there is a unilateral decrease in visual acuity over hours or days. There may be
poor discrimination of colours and eye pain on movement
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
Posterior vitreous

Next question
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Patient.info 2 4
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Score: 17.8%
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Question 74 of 90
A 12-year-old boy is taken to see his GP by his mother. She has noticed small, yellow, papular
lesions and that his skin has become 'lax'. Given these findings, the GP refers onwards to a
paediatric specialist, who ultimately makes a diagnosis of pseudoxanthoma elasticum.
Given this underlying condition, which of the following ophthalmological findings is most likely?
Drusen 14%
Open-angle glaucoma 3%
Retinal tear 4%
Angioid retinal streaks are a feature of pseudoxanthoma elasticum

The correct answer is angioid retinal streaks. Pseudoxanthoma elasticum is a rare disorder which
causes the effects described above on the skin. It also very commonly affects the eyes -
mineralisation of the elastic fibres in the Bruch membrane ultimately leads to angioid streaks that
radiate out from the optic nerve. The streaks themselves do not generally lead to loss/distortion
of vision, but may lead to retinal haemorrhages.
Drusen is incorrect. This substance builds up in age-related macular degeneration, causing

progressive visual loss. There are some studies which associate drusen with pseudoxanthoma
elasticum, although not to the same extent as angioid streaks.
Open-angle glaucoma is incorrect. There are some links between pseudoxanthoma elasticum and
acute closed-angle glaucoma, but not open-angle.
Posterior vitreous detachment is incredibly common with progressing age, but there is no known
link between this and pseudoxanthoma elasticum.
A retinal tear may occur due to posterior vitreous detachment, or severe myopia; it is not linked to
pseudoxanthoma elasticum.
Discuss (3) Improve
Next question
Angioid retinal streaks
Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from the
optic nerve head. They are caused by degeneration, calcification and breaks in Bruch's membrane .
Causes
pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget's disease
sickle-cell anaemia
acromegaly
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Score: 17.6%
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Question 75 of 90
A 54-year-old man with type 2 diabetes mellitus is found on annual review to have new vessel
formation at the optic disc. Visual acuity in both eyes is not affected (6/9). Blood pressure is155/84
mmHg.
HbA1c 68 mmol/mol (8.4%)
What is the most important intervention in this patient?
Follow-up ophthalmoscopy in 3 months 4%
Add aspirin 1%
Blood pressure control 10%
Tight glycaemic control 52%
Laser therapy 32%
This patient has proliferative diabetic retinopathy and urgent referral to an ophthalmologist for
panretinal photocoagulation is indicated
Discuss (1) Improve
Next question
Pathophysiology
Classification
Mild NPDR
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
severe NPDR
Severe NPDR
Key features

Maculopathy
Key features
check visual acuity
Management
All patients
Maculopathy
inhibitors
regular observation

Next question
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Question 76 of 90
A 66-year-old woman attends a diabetic eye screening clinic for her annual review. She has a
history of poorly controlled type 2 diabetes mellitus and the previous appointment showed some
evidence of diabetic retinopathy.
On examination, numerous microaneurysms, blot haemorrhages and hard exudates are noted
across the retina, as well as significant venous beading. She is urgently referred for panretinal laser
photocoagulation.
What complication is most strongly associated with this treatment?
Chronic pain in the eye 3%
Decrease in central vision 36%
Decrease in colour vision 17%
Decrease in night vision 43%
Temporary worsening of blood glucose control 2%
A decrease in night vision is a potential complication of panretinal photocoagulation

Panretinal photocoagulation (PRP) is a commonly used technique in the treatment of diabetic

retinopathy. It involves the use of a laser to make small burns across the peripheral retina,
halting/reducing neovascularisation. As the peripheral fields are targeted, patients often notice a
decrease in night vision, as rods are predominantly responsible for this, and the majority of rod
cells are found in the peripheral retina. This correlates with a reduction in the peripheral field of
vision.
Chronic pain in the eye is not commonly associated with PRP. Patients often experience
temporary pain in the eye following the procedure, but this does not typically last more than 24-
48 hours.
A decrease in central vision is not typically associated with PRP. The procedure targets the
peripheral retina and so central vision is usually spared.
A decrease in colour vision is sometimes associated with PRP. However, this is not as common as
a decrease in night vision, as rod cells are affected disproportionately greater than cone cells.
A temporary worsening of blood glucose control is not associated with PRP. The procedure acts
locally on the affected eye and is not known to systemically alter blood glucose levels.
Discuss (1) Improve
Next question
Pathophysiology
Classification
Mild NPDR
Moderate NPDR
microaneurysms
blot haemorrhages
hard exudates
severe NPDR
Severe NPDR
Key features
Maculopathy
Key features
check visual acuity
Management
All patients
Maculopathy
inhibitors
regular observation
Next question
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Textbooks
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Extended textbook
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PassMedicine
Question 77 of 90
A 52-year-old male is admitted to the acute medical admissions unit with a 1-day history of a left-
sided headache, retro-orbital pain, and dull left-sided facial pain. He has a history of hypertension
and migraine and takes ramipril 2.5mg.
On examination, he has a partial ptosis and enophthalmos of the left eye. Pupil examination
demonstrates anisocoria with miosis of the left eye. His visual acuity is 6/6 bilaterally and the
remainder of neurological examination is normal with normal sweating bilaterally.
What is the single most likely cause of these symptoms?
Cervical rib 4%
Stroke 7%
Syringomyelia 6%

This case represents a partial horner's syndrome. Horner's syndrome classically presents with
ipsilateral ptosis, miosis, and anhidrosis. The degree of anhidrosis helps determine the location of
the lesion along the sympathetic pathway.
Carotid artery dissection typically presents with ipsilateral pain and in this case, it was the cause of
a partial horner's syndrome with ipsilateral ptosis and miosis, in the absence of anhidrosis.
Although horners syndrome is an uncommon presentation of carotid artery dissection it is
documented in case reports and important to recognise to avoid further neurological
consequences such as an ischaemic stroke.
A cervical rib or Pancoast tumour cause pre-ganglionic interruption of the sympathetic chain. In
addition to ptosis and miosis, they would cause anhidrosis of just the face.
A stroke or syringomyelia are central lesions. If they caused a horner's syndrome then in addition
to ptosis and miosis, there would be anhidrosis of the head, arm ad trunk.
Discuss (4) Improve
Next question
Horner's syndrome
Features
ptosis

pharmacologic tests
synaptic cleft

Encephalitis
Next question
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Media
Horner's syndrome
Horner's syndrome
Pancoast tumors
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Score: 16.9%
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Question 78 of 90
A 65-year-old man with a known history of Paget's disease is noted to have irregular dark red lines
radiating from the optic nerve. What is the likely diagnosis?
Optic neuritis 4%
Choroidoretinitis 8%
Malignant hypertension 2%
This is a typical description of angioid retinal streaks which are associated with Paget's disease
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Angioid retinal streaks
Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from the
optic nerve head. They are caused by degeneration, calcification and breaks in Bruch's membrane .
Causes
pseudoxanthoma elasticum
Ehler-Danlos syndrome
Paget's disease
sickle-cell anaemia
acromegaly
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Question 79 of 90
A 65-year-old man with a 16 year history of type 2 diabetes mellitus presents complaining of poor
eye sight and blurred vision. Visual acuity measured using a Snellen chart is reduced to 6/12 in the
right eye and 6/18 in the left eye. Fundoscopy reveals a number of yellow deposits in the left eye
consistent with drusen formation. Similar changes but to a lesser extent are seen in the right eye.
Wet age-related macular degeneration 13%
Pre-proliferative diabetic retinopathy 9%
Chronic open angle glaucoma 1%
Proliferative diabetic retinopathy 9%
Dry age-related macular degeneration 68%
Drusen = Dry macular degeneration

The most likely diagnosis in this case is dry age-related macular degeneration. The patient's
symptoms of reduced visual acuity and blurred vision, along with the presence of drusen on
fundoscopy, are characteristic features of dry age-related macular degeneration (AMD). Drusen
are yellow deposits that accumulate under the retina and can lead to gradual loss of central vision.
Dry AMD is more common than wet AMD and tends to progress more slowly.
Wet age-related macular degeneration is less likely in this case because it typically presents
with more rapid onset of symptoms and a greater degree of visual impairment. Wet AMD is
characterized by the growth of abnormal blood vessels under the retina, which can leak fluid or
blood, causing sudden and severe vision loss. Fundoscopy would usually reveal haemorrhages or
exudates associated with these abnormal vessels.
Pre-proliferative diabetic retinopathy could potentially cause visual disturbances; however, the
presence of drusen makes this diagnosis less likely. Pre-proliferative retinopathy is characterized
by microaneurysms, intraretinal haemorrhages, cotton wool spots, venous beading or looping, but
not drusen formation.
Chronic open angle glaucoma is an unlikely diagnosis based on the clinical findings described.
While it can cause visual disturbances and reduced visual acuity, glaucoma typically affects
peripheral vision first before progressing to involve central vision. Additionally, fundoscopy would
typically reveal optic disc cupping rather than drusen formation.
Finally, proliferative diabetic retinopathy also seems unlikely in this case due to the absence of
its characteristic features on fundoscopy. Proliferative diabetic retinopathy involves
neovascularization - the growth of new blood vessels on the retina or optic disc - which can lead
to vitreous haemorrhage, retinal detachment, and severe vision loss. The presence of drusen in
this case is more indicative of AMD rather than diabetic retinopathy.
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Risk factors
aged 65-74.
smoking
mellitus.
Classification

90% of cases
10% of cases

Clinical features

gradual in dry ARMD
around objects
Signs:
Investigations:

Management
Treatment
category dry ARMD.
ARMD
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Question 80 of 90
A 56-year-old woman presents with a sudden loss of vision in the left eye. She denies any pain
associated with the loss of vision. The patient describes the loss of vision initially starting as a
dense shadow that started at the edges of her vision and progressed towards the centre. She has
no significant past medical history except for myopia, for which she wears corrective glasses.

The history is most suggestive of retinal detachment. The description of a dense shadow
progressing towards the centre is classic of this condition. The history of myopia is also a big risk
factor for retinal detachment. This condition requires urgent corrective surgery.
Central retinal artery occlusion is less likely to be the diagnosis here. This is due to
thromboembolism or arteritis; no risk factors are given for either. Again, the description of a
shadow progressing towards the centre of the vision, along with myopia, are more suspicious of
retinal detachment.
Central retinal vein occlusion is another possibility; its incidence increases with age and it is more
common than arterial occlusion. Again, however, no risk factors are mentioned and, given the
history, retinal detachment is more likely.
Vitreous detachment is not a cause of loss of vision. It may precede retinal detachment - but its
symptoms (if any) are typically floaters/flashes of light which do not usually interfere with daily
activities.
Vitreous haemorrhage is a reasonable differential diagnosis. Again, though, there are no risk
factors (diabetes, anticoagulants) mentioned. Whilst it would also cause sudden vision loss, the
description of centrally progressive loss and myopia is much more suggestive of retinal
detachment.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Question 81 of 90
A 34-year-old female patient is brought into the emergency department by her husband. Husband
reports that she has been confused in the last 3 days. She has a long-standing history of severe
psoriasis but no other past medical history. Basic observations are all within normal range and a
CT head is unremarkable. A fundoscopy reveals bilateral papilloedema.
What is the likely cause?
Encephalitis 18%
Brain abscess 4%
Primary brain tumour 5%
Vitamin A toxicity 53%
Hydrocephalus 20%
Vitamin A toxicity is a rare cause of papilloedema

Vitamin A toxicity is a rare cause of papilloedema. In this case, she is likely to have been taking
retinoids for psoriasis.
Encephalitis does not usually present with papilloedema.
Brain abscess, brain tumour and hydrocephalus are all less likely with a normal CT head.
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Papilloedema
Papilloedema describes optic disc swelling that is caused by increased intracranial pressure. It is
almost always bilateral.
The following features may be observed during fundoscopy:

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
Causes of papilloedema
space-occupying lesion: neoplastic, vascular
malignant hypertension
idiopathic intracranial hypertension
hydrocephalus
hypercapnia
Rare causes include

hypoparathyroidism and hypocalcaemia
vitamin A toxicity
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Question 82 of 90
A 23-year-old man presents to the emergency department with pain in his right eye. He has a past
medical history of recurrent sinusitis and ankylosing spondylitis.
On examination, there is erythema and swelling around the right eye. There is pain on testing of
eye movements. The pupils are normal.
What is the appropriate management?
IV acetazolamide 6%
IV antibiotics 64%
Oral antibiotics 4%
Oral steroids 21%
Topical antibiotics 6%
IV antibiotics is the correct answer. The combination of ocular pain and pain on eye movements
associated with redness and swelling around the eye suggests orbital cellulitis. This is a medical
emergency requiring admission to the hospital for IV antibiotics due to the risk of cavernous sinus
thrombosis and intracranial spread. Sinusitis is a risk factor for the development of this condition.
IV acetazolamide is incorrect. This is a treatment for acute glaucoma. Acute glaucoma may cause
ocular pain. However, the eye itself will be red rather than the surrounding structures and
therefore this is not a likely diagnosis.
Oral antibiotics is incorrect. This may be suitable for a very mild case of periorbital cellulitis but
would not be sufficient to treat orbital cellulitis. Patients with periorbital cellulitis do not have pain
on eye movements.
Oral steroids is incorrect. This is an option for treating uveitis, which is associated with ankylosing
spondylitis. However, like glaucoma, this is a case of acute red eye. The eye itself is red rather than
the surrounding structures and therefore this is not the correct diagnosis.
Topical antibiotics is incorrect. This might be useful in the treatment of bacterial conjunctivitis
but not orbital cellulitis.
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Orbital cellulitis
Risk factors
Childhood
Presentation
Severe ocular pain
Visual disturbance
Proptosis
Investigations
Management
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Question 83 of 90
A 49-year-old male patient presents with acute onset loss of vision in the right eye preceded by a
2-hour history of progressively enlarging dark spots in his vision. He has type-1 diabetes mellitus
for over 15 years and has been poorly controlled.
What is the most likely diagnosis
Ocular migraine 1%
Retinal artery occlusion 9%
Vitreous haemorrhage is a cause of sudden painless loss of vision in the context of diabetic
retinopathy
Vitreous haemorrhage is a cause of sudden painless loss of vision in the context of diabetic
retinopathy. It usually presents with dark spots (scotoma) in the vision initially. This man is likely to
have diabetic retinopathy.
Ocular migraine does not usually cause visual loss.
Retinal detachment usually presents with dense shadow over vision progressing centrally.
Even though this man has ischaemic risk factors, ischaemic optic neuropathy does not usually
present with dark spots.
Retinal artery occlusion does not usually present with dark spots.
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artery
retinal detachment
retinal migraine
Ischaemic/vascular


Retinal detachment

Posterior vitreous
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Score: 15.7%
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Question 84 of 90
A 75-year-old man presents with sudden onset of flashes and floaters in his right eye. A systematic
enquiry was otherwise unremarkable. He has a past medical history of hypertension. His drug
history includes amlodipine. On examination, there is no evidence of visual loss.
Ophthalmoscopy is performed:
Ophthalmoscopy Features are suggestive of Weiss ring
Acute angle-closure glaucoma 4%
Chorioretinitis 7%
Flashes + floaters are most commonly caused by a posterior vitreous detachment

Posterior vitreous detachment is correct. The sudden onset of flashers and floaters is most
commonly due to a posterior vitreous detachment. It would, of course, be important to consider
more serious causes such as retinal detachment. The ophthalmoscopy features of a Weiss ring
(peripapillary glial tissue that remains attached to the posterior vitreous cortex following posterior
vitreous detachment) adds weight to the diagnosis.
Acute angle-closure glaucoma is incorrect. This condition presents with sudden onset of severe
unilateral eye pain or a headache associated with blurred vision, rainbow-coloured halos around
bright lights, nausea, and vomiting. The absence of any of these features, and the presence of
flashes and floaters make acute glaucoma an unlikely diagnosis.
Chorioretinitis is incorrect. This condition usually presents with the sudden onset of flashes,
floaters, blurred vision, loss of vision, and scotomas. Chorioretinitis is most commonly infective in
origin with toxoplasmosis and cytomegalovirus being the commonest organisms predominantly in
immune-deficient patients. The relative rarity of this condition and the absence of
immunodeficiency makes this a less likely diagnosis.
Retinal detachment is incorrect. This condition presents with sudden onset visual loss, flashers,
floaters, and a 'dark curtain'. Flashers and floaters may precede visual loss early in the disease
process. The relative rarity of this condition, the absence of visual loss, and the ophthalmoscopy
findings make this a less likely diagnosis.
Vitreous haemorrhage is incorrect. Although vitreous haemorrhage can also present with
flashers and floaters, the ophthalmoscopy findings make this an unlikely diagnosis. A vitreous
haemorrhage should be directly observed in the majority of cases.
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Posterior vitreous detachment
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.
Epidemiology:
Occur in over 75% of people over the age of 65
More common in females
Risk factors:
As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its
shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the
centre of the eye.
Highly myopic (near-sighted) patients are also at increased risk of developing posterior
vitreous detachment earlier in life. This is because the myopic eye has a longer axial length
than an emmetropic eye.
Symptoms:
The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal
detachment)
Signs:
Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic
nerve to form a ring-shaped floater).
Investigations:
All patients with suspected vitreous detachment should be examined by an ophthalmologist
within 24hours to rule out retinal tears or detachment.
Management:
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms
gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.
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Question 85 of 90
A 71-year-old man presents with a burning sensation around his right eye. On examination an
erythematous blistering rash can be seen in the right trigeminal distribution. What is the most
likely diagnosis?
Ramsay Hunt syndrome 11%
Cluster headache 0%
Fungal keratitis 0%
Herpes zoster ophthalmicus 86%
Trigeminal neuralgia 3%
The correct answer is Herpes zoster ophthalmicus. This condition presents with a painful,
blistering rash in the distribution of the ophthalmic division of the trigeminal nerve. It is caused by
reactivation of latent varicella-zoster virus (the same virus that causes chickenpox) within the
sensory ganglion. The patient's age and presentation with a burning sensation around his right
eye followed by an erythematous blistering rash are typical features of this condition.
Ramsay Hunt syndrome, also known as herpes zoster oticus, is an incorrect option here. This
condition involves reactivation of varicella-zoster virus in the geniculate ganglion, resulting in a
characteristic triad of ipsilateral facial paralysis, ear pain and vesicles in the auditory canal and/or
on the tympanic membrane. Although it can cause facial pain due to involvement of cranial nerves
VII and VIII, it does not typically present with ocular symptoms or a rash in the trigeminal
distribution.
Cluster headache is another incorrect option. These are severe unilateral headaches often
accompanied by autonomic symptoms such as lacrimation, nasal congestion or ptosis. Although
they may cause significant periorbital discomfort, they do not cause an erythematous blistering
rash.
Fungal keratitis is also not likely given this presentation. Fungal keratitis would typically present
with eye redness, reduced vision, photophobia and a corneal ulcer visible on slit-lamp examination
rather than a dermatomal rash.
Finally, Trigeminal neuralgia is characterised by severe episodic facial pain but does not cause a
skin rash. The pain in trigeminal neuralgia tends to be electric shock-like and lasts from seconds to
minutes rather than being a persistent burning sensation as our patient has reported.
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case of shingles.
Features
Management
immunocompromised
Complications
ptosis
Next question
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Question 86 of 90
A 25-year-old woman presents with a one-day history of a painful and red left eye. She describes
how her eye is continually streaming tears. On examination she exhibits a degree of photophobia
in the affected eye and application of fluorescein demonstrates a dendritic pattern of staining.
Visual acuity is 6/6 in both eyes. What is the most appropriate management?
Topical steroid 20%
Perform a lumbar puncture 2%
Treat with subcutaneous sumatriptan 5%
Topical aciclovir 57%
Topical chloramphenicol 16%
This patient has a dendritic corneal ulcer. Topical aciclovir and ophthalmology review is required.
Giving a topical steroid in this situation could be disastrous as it may worsen the infection.
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Herpes simplex keratitis
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
Management
immediate referral to an ophthalmologist

topical aciclovir
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Question 87 of 90
A 63-year-old man presents to his GP complaining of pain in his right eye. On examination the
sclera is red and the pupil is dilated with a hazy cornea. What is the most likely diagnosis?
Scleritis 24%
Conjunctivitis 2%
Subconjunctival haemorrhage 2%
Red eye - glaucoma or uveitis?

glaucoma: severe pain, haloes, 'semi-dilated' pupil
uveitis: small, fixed oval pupil, ciliary flush
The correct answer is Acute angle closure glaucoma. This condition presents with a red eye,
dilated pupil, and a hazy cornea due to increased intraocular pressure. The patient may also
experience severe ocular pain, nausea and vomiting, blurred vision, and seeing halos around
lights. It is an ophthalmic emergency that requires immediate treatment to prevent permanent
vision loss.
Scleritis is incorrect because it typically presents with severe ocular pain that can radiate to the
forehead or jaw. The eye appears red, particularly in the area of the sclera. While this inflammation
can cause some changes in vision, it does not typically cause a hazy cornea or a dilated pupil.
Conjunctivitis is also incorrect as it usually presents with a red eye and discharge but not with
pain, hazy cornea or dilated pupil. Conjunctivitis often affects both eyes whereas acute angle
closure glaucoma generally starts in one eye.
Anterior uveitis, or inflammation of the iris and ciliary body within the uvea of the eye, is another
incorrect choice. While anterior uveitis can cause redness of the eye and pain, it typically causes
photophobia rather than a hazy cornea. The pupil in anterior uveitis would be small (miotic) rather
than dilated.
Finally, Subconjunctival haemorrhage is incorrect as this condition presents with a bright red
patch on the white part of the eye (sclera). It's often asymptomatic but may cause a sensation of
fullness under the lid or mild irritation. It does not present with pain or visual changes such as
hazy cornea or dilated pupils.
Discuss (6) Improve
Next question
Red eye
There are many possible causes of a red eye. It is important to be able to recognise the causes
which require urgent referral to an ophthalmologist. Below is a brief summary of the key
distinguishing features

severe pain (may be ocular or headache)
decreased visual acuity, patient sees haloes
semi-dilated pupil
hazy cornea
Anterior uveitis
acute onset
pain
blurred vision and photophobia
small, fixed oval pupil, ciliary flush
Scleritis
severe pain (may be worse on movement) and tenderness
may be underlying autoimmune disease e.g. rheumatoid arthritis
Conjunctivitis
purulent discharge if bacterial, clear discharge if viral
Subconjunctival haemorrhage
history of trauma or coughing bouts
Endophthalmitis
typically red eye, pain and visual loss following intraocular surgery
Next question
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PassMedicine
Question 88 of 90
A 71-year-old man presents with severe pain around his right eye and vomiting. On examination
the right eye is red and decreased visual acuity is noted. Which one of the following options is the
most appropriate initial treatment?
Topical pilocarpine + oral prednisolone 10%
Topical pilocarpine + topical steroids 11%
Topical steroids 3%
Topical pilocarpine + intravenous acetazolamide 69%
Topical steroids + intravenous acetazolamide 7%
Alongside eye drops, IV acetazolamide is used in the initial emergency medical management
of acute angle-closure glaucoma
The correct answer is Topical pilocarpine + intravenous acetazolamide. This patient's

presentation of severe ocular pain, redness, nausea, vomiting and decreased visual acuity is
suggestive of acute angle-closure glaucoma (AACG). The initial management of AACG in the UK
involves reducing intraocular pressure rapidly. Topical pilocarpine constricts the pupil and widens
the anterior chamber angle, allowing for improved aqueous humour drainage. Intravenous
acetazolamide, a carbonic anhydrase inhibitor, reduces the production of aqueous humour in the
ciliary body thereby decreasing intraocular pressure.
Topical pilocarpine + oral prednisolone is not the best option as oral prednisolone does not
have a role in the initial treatment of AACG. While it can reduce inflammation associated with
other eye conditions such as uveitis or optic neuritis, it does not contribute to lowering intraocular
pressure.
Topical pilocarpine + topical steroids is also incorrect for similar reasons. Topical steroids may
be used to treat inflammatory conditions of the eye but do not significantly lower intraocular
pressure and are therefore not useful in this setting.
Topical steroids, again, would not be beneficial in this case as they do not contribute to lowering
intraocular pressure which is crucial in managing AACG.
Finally, Topical steroids + intravenous acetazolamide would partially help by reducing

intraocular pressure through IV acetazolamide; however, without topical pilocarpine to constrict
the pupil and widen the anterior chamber angle, this combination would be less effective than
using both pilocarpine and acetazolamide together.
Discuss (2) Improve
Next question


Features
hard, red-eye
Investigations
Management

would be:
Next question
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PassMedicine
Question 89 of 90
A 32-year-old woman presents to her GP with ongoing headaches. The GP performs a cranial
nerve examination; during this, he notes normal direct and consensual reflexes when shining light
into the left eye. When shining light into the right eye, direct and consensual reflexes are present,
although neither eye constricts as much. He then swings a pen torch from one eye to the other.
When swung to the left eye, both pupils constrict. When swung from the left eye to the right eye,
both pupils appear to dilate slightly, although not back to normal.
Given this finding, where is the likely lesion?
Lateral geniculate nucleus 18%
Oculomotor nucleus 9%
Optic chiasm 9%
Optic nerve 59%
Optic radiation 5%
Relative afferent pupillary defect indicates an optic nerve lesion or severe retinal disease
The correct answer is the optic nerve.
The patient has a relative afferent pupillary defect (RAPD). This is caused by a lesion in the optic
nerve or retina. In the swinging light test, when light is shone in the unaffected eye, both pupils
constrict. When the light is swung to the affected eye, less light is detected so both pupils appear
to dilate.
'Lateral geniculate nucleus' is incorrect. This is a relay centre in the thalamus for the visual
pathway, where the optic tract connects. Lesions here are not associated with an RAPD.
'Oculomotor nucleus' is also incorrect. The oculomotor nucleus is the midbrain origin of the
oculomotor nerve. A lesion here would cause ophthalmoplegia, mydriasis and ptosis.
'Optic chiasm' is incorrect. Lesions here usually result in bitemporal hemianopia and are not
associated with RAPD.
'Optic radiation' is also incorrect. These carry information from the lateral geniculate nucleus to
the primary visual cortex. Lesions here lead to a quadrantanopia and are not associated with
RAPD.
Discuss (1) Improve
Next question
Finding
Causes
retina: detachment

Next question
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How to examine RAPD
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PassMedicine
Question 90 of 90
A 24-year-old man attends the emergency department with left eye swelling and painful eye
movements.
He is usually fit and well with a past medical history of chronic sinusitis only.
On examination, his left eye is swollen shut with marked eyelid oedema and erythema that
extends from the maxilla up to the eyebrow. When the eye is manually opened there is chemosis.
What would the most appropriate initial treatment be for this patient?
Immediate CT head 11%
Intravenous antibiotics 80%
Ophthalmology review 6%
Oral antibiotics 1%
Topical chloramphenicol 2%
This patient has evidence of orbital cellulitis which necessitates urgent treatment with intravenous
antibiotics due to the risk to sight and risk of spread.
Orbital swellings are classified by 'Chandler's classification':
I. Pre-septal cellulitis
II. Orbital cellulitis without abscess
III. Orbital cellulitis with subperiosteal abscess
IV. Intra-orbital abscess
V. Cavernous sinus thrombosis
Pre-septal cellulitis involves tissues anterior to the orbital septum i.e. the eyelids. Orbital cellulitis
involves tissues behind the orbital septum and can progress to cavernous sinus thrombosis.
Signs that point to orbital cellulitis rather the pre-septal cellulitis include:
Painful eye movements

Restricted eye movements
Reduction in colour vision
Abnormal pupillary responses to light
Reduced visual acuity
Reduced visual fields
Presence of chemosis
Presence of proptosis
Intravenous antibiotics are the most important part of the initial treatment for orbital cellulitis to
treat the underlying infection. If there is evidence of intracranial spread or abscess on CT scan the
patient may also require external drainage or neurosurgical intervention. Do not delay starting
antibiotics whilst awaiting specialist review.
Immediate CT head does form part of the management for orbital cellulitis but it is not the initial
priority, treatment with antibiotics takes precedence. The reasoning behind doing a CT head is to
assess the extent of spread. For pre-septal cellulitis, a CT head is not usually required but may be
completed if the diagnosis is uncertain or examination is difficult e.g. due to extreme swelling.
Ophthalmology review is important in the management of orbital cellulitis, these patients are
usually managed under the joint care of ENT and ophthalmology. Waiting for or requesting a
specialist review, however, should not delay the administration of antibiotics and so is not the
priority.
Oral antibiotics wouldn't be appropriate due to the potential severity of this infection. It is
recommended that antibiotics are administered via the IV route rather than oral.
Topical chloramphenicol would not be sufficient to treat orbital cellulitis, systemic therapy is
required to deliver sufficient antibiotics to the area of infection.
Discuss Improve
Orbital cellulitis
Risk factors
Childhood
Presentation
Severe ocular pain
Visual disturbance
Proptosis

Investigations
Management
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Textbooks
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3/29/24, 5:19 PM PassMedicine

Keratoconjunctivitis sicca 13%

Anterior uveitis 10%

Scleritis is painful, episcleritis is not painful

Discuss (8) Improve

Rheumatoid arthritis: ocular manifestations

Report broken media

A reduction in visual fields 67%

Brown pigmentation of the iris 8%

Corneal scarring 12%

Increased intraocular pressure 3%

Following panretinal laser photocoagulation up to 50% of patients have a noticeable

Corneal scarring is incorrect. This is a complication of keratitis.

There is a high chance of rising intraocular pressure is incorrect. This is a common

Vitreous detachment is incorrect. This is a condition associated with near-sightedness and

Non-proliferative diabetic retinopathy

Proliferative diabetic retinopathy

regular review by ophthalmology

Raised intracranial pressure 3%

Diabetic eye disease 2%

Holmes-Adie's pupil on the right 12%

Marcus-Gunn Pupil (relative afferent pupillary defect) on the right 72%

Argyll Robertson pupil on the right 12%

accommodation. It is usually bilateral and is often associated with neurosyphilis.

Discuss (7) Improve

Relative afferent pupillary defect

Pathway of pupillary light reflex

Relative afferent pupillary defect tutorial

Report broken link

Relative Afferent Pupillary Defect

U-M Kellogg Eye Center - YouTube 75 1

How to examine RAPD

Report broken media

What monoclonal antibody has this mechanism of action?

Bevacizumab is a monoclonal antibody directed against vascular endothelial growth factor

Bevacizumab is the correct answer, it is a monoclonal antibody directed against vascular

Discuss (1) Improve

Age-related macular degeneration

Traditionally two forms of macular degeneration are seen:

also known as atrophic

Recently there has been a move to a more updated classification:

Patients typically present with a subacute onset of visual loss with:

angiography to visualise any changes in the choroidal circulation.

Age related macular degeneration fundoscopy findings

Report broken link

Each one of the following is a cause of a mydriatic pupil, except:

Third nerve palsy 12%

Holmes-Adie pupil 15%

Argyll-Robertson pupil 51%

Traumatic iridoplegia 10%

Argyll-Robertson pupil is one of the classic pupillary syndromes. It is sometimes seen in

Discuss (3) Improve

Causes of mydriasis (large pupil)

third nerve palsy

Drug causes of mydriasis

Change in shape of eye secondary to variations in blood sugar 3%

Primary open angle glaucoma 8%

Vitreous detachment 77%

Normal phenomenon in diabetic retinopathy 10%

Normal phenomenon in healthy eyes 2%