Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Core clinical problems > 24. Visual disturbance/impairment > Flashcards

24. Visual disturbance/impairment Flashcards

1
Q

differentials for sudden vision loss

A

ischaemic/vascular
- retinal vein occlusion
- retinal artery occlusion: TIA/stroke/giant cell arteritis
- anterior ischaemic optic neuropathy: TIA/stroke/giant cell arteritis

  • vitreous haemorrhage
  • retinal detachment
  • acute angle closure glaucoma
  • optic neuritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

differential for gradual vision loss?

A

Refractive error
Cataracts
Macular degeneration
Chronic (open angle) glaucoma
Diabetic retinopathy
Hypertensice retinopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

differentials for diplopia

A

eye muscle problem:
- myasthenia gravis
- graves
- strabismus

neurological:
- head injury
- stroke
- migraine
- tumour
- wernikes

Nerve problem (eg 3rd CN, 4th CN or 6th CN)
- diabetes
- congenital
- raised ICP
- MS
- guilian barre

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

examination vision loss

A

Inspection: is it RED (acute angle closure)

Optic nerve: acuity, visual fields, attention, accommodation, pupils, colour vision
- Pupil unreactive/not responding/ well to light/RAPD suggests optic nerve dysfunction therefore could be due to anterior optic neuropathy (GCA or TIA), optic neuritis etc

Eye movements: H test, any double vision? any pain on movement? (any CN palsys?)

To complete…
Opthalmoscopy
HbA1c, BP
Referral for slit lamp examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what should you be able to label on fundoscopy

A

optic disc
optic cup

macula
fovea

retinal vein
retinal artery (thinner than veins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

history taking vision loss/disturbance

A

PC: onset? sudden? is the vision loss in one portion of your vision? eg the sides or the middle etc. floaters/flashes?

HoPC: PAIN?? - suggests acute angle closure glaucoma. pain on eye movement? (optic neuritis), do colours look the same? (loss of red in optic neurtis)

Associated symptoms: headache especially near temples?(GCA) weakness?

SHx:
eye trauma e.g. boxing, ask about occupation and hobbies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is amaurosis fugax? causes

A

Amaurosis fugax describes a temporary loss of vision caused by a temporary interruption to the blood supply - like a curtain coming down…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

causes of amaurosis fugax?

A

ischaemic/vascualr causes of sudden vision loss eg

Retinal vein occlusion
Retinal artery occlusion: TIA/stroke/GCA
Anterior ischaemic optic neuropathy: TIA/stroke/GCA
Giant-cell arteritis

As this may represent a TIA, 300mg aspirin is given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

central retinal vein occlusion

presentation
causes
examination
fundoscopy
management

A

presentation: sudden, painless, reduction or loss in visual acuity, unilateral

causes:
Risk factors
increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia

examination: reduced visual acuity

fundoscopy:
“stormy sunset” multiple haemorrhages

management:
majority conservative
if macualr oedema, consider VGEF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

central retinal artery occlusion

presentation
examination
fundoscopy
management

A

presentation:
sudden, painless, unilateral vision loss

examiantion: RAPD

causes:
TIA/stroke/GCA

fundoscopy
‘cherry red’ spot on a pale retina

management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Anterior ischaemic optic neuropathy

presentation
causes
examination
fundoscopy
management

A

presentation: loss of vision

causes: TIA/stroke/GCA

examination: RAPD

fundoscopy: swollen pale disc and blurred margins

management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

vessel occluded in AION

A

posterior ciliary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cherry red spot

A

central retinal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

blood supply optic nerve

A

central retinal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

“stormy sunset” multiple haemorrhages

A

central retinal vein occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Giant cell arteritis causing visual symptoms

presentation
examination
fundoscopy
management

A

PC: decreased visual acuity, temporal headache

examination: reduced visual acuity, tenderness over temple

fundoscopy: Retinal splinter haemorrhages or disc oedema. AION swollen pale disc and blurred margins.

management:
medical emergency due to risk of
- stroke
- blindness (a strple affecting the retinal vessels, optic nerve) - 90% AION (Anterior Ischemic Optic Neuropathy)

phone rheum on-call

Should have confirmatory test: USS halo sign or temporal artery biopsy

Initial
1. High dose oral glucocorticoids eg oral methylprednisolone

With visual loss:
1. IV methylprednisolone
+ Urgent ophthalmology review
+ Bone protection for steroids

refractory/relapsing : tocilizumab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

vitreous haemorrhage

presentation
causes
examination
fundoscopy
management

A

presentation: painless vision loss, dark spots obscuring vision with a red hue

causes:
- DIABETES, bleeding disorders, anticoagulants

examination: decreased visual acuity, visual field defect if severe haemorrhage

dilated fundoscopy: may show haemorrhage in the vitreous cavity

if new onset rf urgently (<24hrs) for slit-lamp examination,
other stuff may be used eg:
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

retinal detachment

presentation
causes
examination
fundoscopy
management

A

PC: vision loss, curtain or shaddow progressing to the centre from the periphery, floaters or flashes,

risk factors
diabetes mellitus
myopia
age
previous surgery for cataracts
eye trauma e.g. boxing

examination

fundoscopy
the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
if the break is small, however, it may appear normal.

It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.

rf urgently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

plan pt with new onset flashes and floaters

A

Arrange immediate referral to an ophthalmologist with retinal surgery expertise to be seen on the same day, if there are signs of sight-threatening disease, such as:
- Visual field loss or changes in visual acuity.
- Fundoscopic signs of retinal detachment or vitreous haemorrhage.

any patients with new onset flashes and floaters WITHOUT VISUAL/FUNDOSCOPY CHANGES should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for:

pigment cells

vitreous haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

posterior vitreous detachment

presentation
causes
examination
fundoscopy
management

A

presentation: no vision loss, floaters, flashes, blurred vision, cobwebs

causes:
ageing
myopia

fundoscopy: weiss ring

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

optic neuritis

presentation
causes
examination
fundoscopy
management

A

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

causes:
multiple sclerosis: the commonest associated disease
diabetes
syphilis

examiantion: relative afferent pupillary defect

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

high-dose steroids
recovery usually takes 4-6 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

most common cause of blindness in the UK

A

Age-related macular degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is age related macualr degenertaion

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

fundoscopy how is wet AMD different to dry? pathophysiology

A

In wet AMD, new vessels develop from the choroid layer and grow into the retina (neovascularisation). These vessels can leak fluid or blood, causing oedema and faster vision loss. A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF). This is the target of medications to treat wet AMD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
which is more common wet or dry AMD?
dry = 90%
26
risk factors macualr degeneration
Older age Smoking Family history Cardiovascular disease (e.g., hypertension) Obesity Poor diet (low in vitamins and high in fat)
27
dry and wet AMD compare presentation
Presentation: both: - vision loss- reduction in visual acuity particualrly for close objects - difficulties in dark adaptation - fluctuations in visual disturbance - visual hallucinations may also occur resulting in Charles-Bonnet syndrome - photopsia, (a perception of flickering or flashing lights), and glare around objects gradual in dry ARMD subacute in wet ARMD Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years. It often progresses to bilateral disease.
28
differentiating AMD and glaucoma presentation
Glaucoma is associated with peripheral vision loss and halos around lights. AMD is associated with central vision loss and a wavy appearance to straight lines. This helps you tell them apart in exams
29
examination and fundoscopy ARMD
Reduced visual acuity using a Snellen chart Scotoma (an enlarged central area of vision loss) Amsler grid test can be used to assess for the distortion of straight lines seen in AMD Drusen may be seen during fundoscopy
30
what invetsigation is useful for wet ARMD
Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
31
management wet ARMD
Anti-VEGF medications laser photocoagulation but is more risky
32
management dry ARMD
Management involves monitoring and reducing the risk of progression by: Avoiding smoking Controlling blood pressure Vitamin supplementation has some evidence in slowing progression
33
what are cataracts
A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision
34
causes of cataracts
Normal ageing process: most common cause Other possible causes Smoking Increased alcohol consumption Trauma Diabetes mellitus Long-term corticosteroids Radiation exposure Myotonic dystrophy Metabolic disorders: HYPOCALCAEMIA
35
presentation cataracts
Reduced vision Faded colour vision: making it more difficult to distinguish different colours Glare: lights appear brighter than usual Halos around lights
36
o/e cataracts
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
37
invetsigations catracts
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve Slit-lamp examination. Findings: visible cataract
38
management cataracts
conservative: stronger glassess, use brighter lights surgical This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice
39
complications post-cataracts surgery
Posterior capsule opacification: thickening of the lens capsule Retinal detachment Posterior capsule rupture Endophthalmitis: inflammation of aqueous and/or vitreous humour
40
define glaucoma
Glaucoma refers to the optic nerve damage caused by a rise in intraocular pressure.
41
risk factors for open-angle glaucoma
Increasing age Family history Black ethnic origin Myopia (nearsightedness)
42
presentation open angle glaucoma
Glaucoma affects the peripheral vision first, resulting in a gradual onset of peripheral vision loss (tunnel vision). It can also cause: Fluctuating pain Headaches Blurred vision Halos around lights, particularly at night
43
gold standard way to measure intraocualr pressure
Goldmann applanation tonometry It involves a device mounted on a slip lamp that makes contact with the cornea and applies various pressures.
44
investgations open angle glacuoma
Goldmann applanation tonometry for the intraocular pressure Slit lamp assessment for the cup-disk ratio and optic nerve health Visual field assessment for peripheral vision loss Gonioscopy to assess the angle between the iris and cornea Central corneal thickness assessment
45
when is treatment indicated for open angle closure glaucoma
intraocular pressure of 24 mmHg or above.
46
management open angle closure glaucoma
1. 360° selective laser trabeculoplasty (lazer hole to improve drainage of aqueous humour...delays need for eye drops) 2. Prostaglandin analogue eyedrops (e.g., latanoprost) are the first-line medical treatment. They increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning). 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.
47
adverse effects of miotics such as pilocarpine
constricted pupil, headache and blurred vision
48
adverse effects of prostaglandin analogues eg latanoprost
brown pigmentation of the iris, increased eyelash length
49
who shouldn't get beta blocker eye drops (e.g. timolol, betaxolol)
Should be avoided in asthmatics and patients with heart block
50
most common cause of blindness in adults adults aged 35-65 years-old?
diabetic retinopathy
51
types ofclassification of dianetic retinopathy
non-proliferative diabetic retinopathy (NPDR) proliferative retinopathy (PDR) Maculopathy.
52
characteristics of non-proliferative diabetic retinopathy - fundoscopy
microaneurysms blot haemorrhages hard exudates cotton wool spots venous bleeding Intraretinal microvascular abnormalities (precursor to neovascularisation)
53
characteristics of proliferative diabetic retinopathy - fundoscopy
retinal neovascularisation - may lead to vitrous haemorrhage fibrous tissue forming anterior to retinal disc
54
what type of diabetic retinopathy is more common in type 1 DM
PROLIFERATIVE more common in Type I DM, 50% blind in 5 years
55
characteristics of maculopathy in diabetic retinopathy
hard exudates and other 'background' changes on macula check visual acuity
56
management diabetic retinopathy for all patients
All patients: optimise glycaemic control, blood pressure and hyperlipidemia regular review by ophthalmology
57
managemet maculopathy diabetic retinopathy
if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors
58
management non-prolifertaive diabetic retinopathy
non-prolifertive: regular observation if severe/very severe consider panretinal laser photocoagulation
59
management prolifertaive dianetoc retinopathy
prolifertaive: panretinal laser photocoagulation +/- intravitreal VEGF inhibitors
60
complications 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
61
example of intravitreal VGEF inhibitor
ranibizumab
62
stages of hypertensive retinopathy
SAC papilloedema Stages: 1. S = silver wiring (increased light reflex) and arteriolar narrowing 2. A = arteriovenous nipping 3. C = cotton wool exudates and flame and blot haemorrhages 4. Papilloedema
63
Contralateral hemiparesis and sensory loss, upper extremity > lower, Contralateral homonymous hemianopia, Aphasia
Middle cerebral artery
64
Contralateral homonymous hemianopia with macular sparing, Visual agnosia
Posterior cerebral artery
65
contralateral hemiparesis/hemisensory loss of face arma dn leg, higher cog dysfunction such as aphasia, homonymous hemianopia
total anteroir ciruclation infact, if only 2 = partial
66
Bitemporal hemianopia
Midline lesion at chiasm upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
67
Right nasal hemianopia
Lesion involving right perichaismal area
68
Left homonymous hemianopia
Lesion or pressure on right optic tract (posterior to chiasm, before optic radiations) Lesion or pressure across all right optic radiations
69
Left homonymous hemianopia with macular sparing
Lesion in right occipital lobe (both banks of calcarine fissure) posterior cerebral artery
70
Left superior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore; Temporal as superior Right sided tract Lesion to the right inferior optic radiations in the temporal lobe (meyer's loop)
71
Right inferior homonymous quadrantanopia
PITS = parietal inferior, temporal superior therefore; Parietal as inferior Right visual field so left optic tract Lesion to the left superior optic radiations in the parietal lobe
72
How do patients with pituitary adenoma present?
Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion. Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.
73
Most common paediatric supratentorial tumour? how does it present?
Craniopharyngioma hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.
74
features of third nerve palsy
eye is deviated 'down and out' ptosis if surgical: pupil may be dilated (sometimes called a 'surgical' third nerve palsy) painful
75
causes of third nerve palsy
consider surgical : eg posterior communicating artery aneurysm other serious: - false localizing sign* due to uncal herniation through tentorium if raised ICP - Weber's syndrome stroke other: diabetes mellitus vasculitis e.g. temporal arteritis, SLE
76
features of fourth nereve palsy
Trochlear nerve LR6SO4 Defective downward gaze --> vertical diplopia Nasal upshoot is how it looks!!!! head tilted to the other side
77
causes of 4th nerve palsy
- CONGENITAL (esp if head tilted) Vasculopathy (htn, diabetes) Tumour Congenital (esp if head tilt) Trauma
78
features of 6th nerve palsy
defective lateral gaze appear cross-eyed
79
causes of 6th nerve palsy
think RAISED ICP eg IIH Vasculopathic Tumour
80
types of strabismus
Manifest strabismus = there all the time Latent = underlying - picked up with cover test - may be symptomatic Intermittent exotropia = strabismus when looking far Esotropia - inwards towards nose Exotropia - outwards Hypertropia - upwards Hypotropia - downwards
81
causes strabismus
non-paralytic squint (excess tone in one muscle compared to other) - Hereditary - Refractive error - most common is long sighted - associated with esophoria -need glasses Paralytic squint - disease of the III, IV and VI cranial nerves
82
pseudostrabismus cuases
Broad epicanthus as not much sleral showing medially Narrow or wide interpupillary distance Facial asymmetry Unilateral ptosis
83
examination ?diplopia ?strabismus
Cover/uncover : shows manifest strabismus (when other eye is covered, the squint corrects itself) Alternate cover test : shows latent strabismus (squint present when covers so when uncovered it moves in opposite direction) Fundoscopy (or red reflex) to rule out retinoblastoma, cataracts and other retinal pathology Visual acuity
84
differentiating features non-paryltic vs paryltic squint
non-paralytic - usually congenital - no diplopia - full movement in both eyes if tested separately - extraocular muscles and nerves are grossly normal
85
what is amblyopia
Defective visual acuity which persists after correction of the refractive error and removal of any pathology the brain will cope with this misalignment by reducing the signal from the less dominant eye. This results in one eye they use to see (the dominant eye) and one eye they ignore (the “lazy eye”). If this is not treated, this “lazy eye” becomes progressively more disconnected from the brain and over time the problem becomes worse. This is called amblyopia.
86
management of ambylopia
1. Wear appropriate glasses for 16-18 weeks 2. Occlusion of better seeing eye (patching/atropine)
87
management of strabismus
Aim: - To restore comfortable binocular single vision (BSV) - To achieve good alignment - To eliminate diplopia Conservative: Optical - glasses/contact lenses Prisms Orthoptic exercise Surgery: Resection of muscles to shorten Botulinum toxin Injecting into muscle to temporarily paralyse muscle
88
why should you always check red reflex in children especially with strabismus
RETINOBLASTOMA absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom
89
pathophysiology retinoblastoma
autosomal dominant caused by a loss of function of the retinoblastoma tumour suppressor gene on chromosome 13 around 10% of cases are hereditary
90
presentation retinoblastoma
absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom strabismus visual problems
91
management of retinoblastoma
classically enucleation other options now available: external beam radiation therapy, chemotherapy and photocoagulation
92
how to interpret snellen chart?
6/6 is normal eg 20/20 in america 1st number is what pt can see 2nd number is average number 6 metres from snellen chart therefore 9/6 is rly good 2/6 is bad
93
how to use a snellen chart
pt stood at 6 metres the whole time. cover one eye and test separetly interpret it off the chart which metre they land on is first number

Core clinical problems (94 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions