9. OPTHALMOLOGY Flashcards

(97 cards)

1
Q

There are 6 extraocular muscles. Describe their innervation.

A

SO4LR6!

Superior Oblique = CN IV

Lateral Rectus = CN VI

Inferior oblique, sup, med, inf rectus = CN III

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2
Q

Describe the path of the optic nerve to the visual cortex.

A

Optic nerve
Optic chiasm
Lateral geniculate nucleus
Optic radiation
Visual cortex

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3
Q

How do you remember where the lesion is of a homonymous quadrantanopia?

A

PITS

Parietal lobe, Inferior optic radiations = inf.

Temporal lobe, Superior optic radiations = sup.

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4
Q

Which visual field defect does an optic chiasm lesion cause?

A

Bitemporal hemianopia

Upper quadrant defect > lower = inferior chiasm compression, commonly pituitary tumour

Lower > upper = superior chiasm compression e.g. craniopharyngioma

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5
Q

Someone is found to have an incongruous left homonymous hemianopia. Where is the lesion likely to be?

A

Right optic tract

Incongruous = incomplete or asymmetric

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6
Q

Someone is found to have a congruous right homonymous hemianopia. Where is the lesion likely to be?

A

Left optic radiation or occipital cortex.

Congruous = complete / symmetrical field loss

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7
Q

Someone has a homonymous hemianopia with macula sparing. Where is the lesion likely to be?

A

Occipital cortex

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8
Q

What range of acuity does the human eye have, both vertically and horizontally?

A

60* up
75* down

100* lateral
60* medial

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9
Q

Does the optic nerve sit nasally or temporally?

A

NASAL

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10
Q

Describe the path of the central retinal artery.

A

Internal carotid > Ophthalmic > Central Retinal

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11
Q

2 causes of CRAO:

A

Atherosclerosis

Giant cell arteritis

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12
Q

Risk factors for CV disease increase the risk of CRAO. What risk factors exist for GCA to be aware of?

A

White ethnicity
Older
Female
Polymyalgia rheumatica

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13
Q

Give 4 differentials for sudden painless loss of vision:

A

CRAO
CRVO
Retinal detachment
Vitreous haemorrhage

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14
Q

Clinical features of CRAO:

A

Sudden, painless, unilateral loss of vision.

RAPD

Pale fundus. Cherry red spot on fundoscopy: fovea. Macular has different blood supply to rest of retina?

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15
Q

CRAO can cause permanent visual loss, and is essentially a stroke event. What medication should patients be given, and where should they be referred / investigated?

A

300 mg aspirin

Stroke / TIA clinic

CPR/ESR bloods important as GCA is a potentially reversible cause - IV methylpred may be indicated.

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16
Q

Vitreous haemorrhage is one of the most common causes of PAINLESS loss of vision. Give 3 causes of a vitreous haemorrhage.

A

Diabetic retinopathy

Posterior vitreous detachment / Retinal detachment

Ocular trauma (most common in children and young people)

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17
Q

Posterior vitreous detachment is a painless condition. usually occuring due to natural changes with age. Give 3 key features a patient may present with, and discuss managment.

A

Floaters
Flashing lights
Blurred vision

Dark curtain coming down; this would indicate retinal detachment.

No management often, symptoms improve over a period of 6 months.

BUT if an associated retinal tear, then surgery will be required to fix this.

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18
Q

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24 hours to exclude:

A

Retinal tear or detachment

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19
Q

2 risk factors for vitreous detachment:

A

Aging - vitreous fluid does not hold it’s shape as well as it becomes less viscous.

Near-sightedness / myopia - longer axial length

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20
Q

Age-related macular degeneration is the most common cause of blindness in the UK. What is the % prevalence of the 2 types?

A

Dry 90%

Wet 10%

More often unilateral

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21
Q

Describe the pathology in wet AMD.

A

New blood vessels develop from the choroid layer and grow into the retina (neovascularisation). These vessels are new and weak and can leak fluid or blood, causing oedema and faster rate of decline if VA.

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22
Q

4 layers of the macula, which generates high -definition colour vision in the central visual field, from base to surface.

A

Choroid

Bruch’s membrane

Retinal pigment epithelium

Photoreceptors

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23
Q

Yellowish deposits are seen in a older patient. What do these indicate, and give 2 other features that are common to both wet and dry AMD.

A

Drusen - protein and lipid deposition between the retinal pigment epithelium and Bruch’s membrane.

Atrophy of retinal pigment epithelium

Degeneration of photoreceptors

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24
Q

Describe how AMD can present, and highlight the differences between wet and dry.

A

Gradual loss of central vision (DRY), but wet can develop within days and progress very quickly.

Reduced VA
Metamorphopsia
Gradually worsening ability to read small text

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25
Key differences between glaucoma and AMD:
Glaucoma = halos around lights and PERIPHERAL loss AMD = wavy appearance to straight lines and CENTRAL loss
26
4 examination findings in AMD:
Scotoma (enlarged central vision loss) Snellen chart reduced VA Amsler grid test - distortion of straight lines Drusen on fundoscopy OCT - xsection of layers of the retina - used for Dx and monitoring
27
Initial investigation of choice for AMD:
Slit-lamp microscopy
28
What therapy can be used in wet AMD and how is it administered?
Anti-VEGF agents e.g. bevacizumab Injection into eye, regular Fluroscein angiography used to guide
29
Management of dry AMD:
Avoid smoking Control BP Vitamin supplementation growing evidence?
30
The majority of patients with CRVO are managed conservatively. Give 2 indications for treatment.
Macular oedema; anti-VEGF agents, ?dexamethasone Retinal neovascularization; laser photocoagulation of the new vessels
31
Clinical and fundoscopy features of CRVO:
Sudden, painless loss of vision Reduced VA / blurred vision Tortuous, dilated retinal veins Flame and blot haemorrhage s Retinal oedema Cotton wool spots Hard exudates
32
RFs for CRVO:
CV risk factors Age Hypertension Polycythaemia / viscosity e.g myeloma. Glaucoma
33
Describe the blood supply and drainage to the retina.
Branch retinal veins > central retinal vein > drains into superior ophthalmic vein or cavernous sinus.
34
Blockage of the branch retinal veins can lead to a more limited area of the fundus being affected by the occlusion. Where are these blockages most likely to occur in these branch veins?
Arteriovenous crossings - compression of the veins causing occlusion is more likely.
35
The neurosensory layer of the retina can become detached from the underlying pigment epithelium, and is known as retinal detachment. It can be reversed, but if left untreated can progress to permanent visual loss. Give 5 risk factors.
Often due to tears that allow the vitreous fluid to get under the neurosensory layer and fill the space. Diabetes Myopia Age Previous cataract surgery Eye trauma e.g. boxing
36
Clinical features of retinal detachment:
New onset flashes and floaters Sudden onset, painless, progressive visual loss 'Curtain' coming down, peripheral progressing to central RAPD if optic nerve involved Red reflex lost
37
Suspicion of retinal detachment requires immediate ophthalmology referral to assess for tears or detachment. What are the options for each respectively?
Tears: Laser therapy Cryotherapy Detachment: Vitrectomy Scleral buckling Pneumatic retinopexy
38
5 clinical features of optic neuritis:
Pain, worse on eye movement Scotoma Unilateral decrease in VA / blurred vision over hours to days RAPD Red desaturation / poor discrimination of colours
39
MS is obviously associated with optic neuritis (inflammation of the optic nerve), but which 2 other conditions are associated as well?
Diabetes Syphilis
40
Investigation and management of optic neuritis episode?
MRI brain + orbit with gadolinium contrast High dose steroids, recovery usually takes 4-6 weeks
41
Keratitis describes inflammation of what?
Cornea Potentially sight threatening
42
2 typical organisms in bacterial keratitis?
Staph aureus Pseudomonas in contact lenses
43
A person presents with keratitis with a history of eye exposure to soil and contaminated water, in pain out of proportion to clinical examination. What is the most likely causative organism?
Acanthamoebic keratitis Accounts for 5% of cases
44
4 clinical features of keratitis:
Red eye, pain, erythema Photophobia Foreign body / gritty sensation Hypopyon
45
What is the most common cause of keratitis?
HSV
46
HSV keratitis can be primary or recurrent, caused by the virus travelling to the trigeminal ganglion and becoming latent. Which layer of the cornea does HSV affect?
Epithelial
47
Slit lamp examination is required to diagnose keratitis. What is used to visualise the eye properly and what might be seen in HSV keratitis?
Fluroscein stain Dendritic corneal ulcer - branching appearance
48
Treatment for HSV keratitis?
Topical +/- oral aciclovir
49
Clinical features of AACG:
severe pain; ocular or headache decreased VA symptoms worsen with mydriasis (watching tv in a dark room) hard, red eye non-reacting pupil dull/hazy cornea? halos around lights
50
AACG is a medical emergency where treatment is required to lower the IOP, and then surgery. Patients should be lain on their back without a pillow. Give 3 examples of eye drops and their mechanism for reducing IOP.
Pilocarpine, direct parasympathomimetic - contraction of ciliary muscle, increasing outflow of the aqueous humour BB e.g. timolol - decreases aqueous humour production Apraclonidine e, alpha-2 agonist - decreases humour production and increases outflow
51
Which IV drug is often given in AACG and what is the action?
IV acetazolamide (carbonic anhydrase inhibitor) Reduces aqueous secretions
52
Tonometry is used to assess for elevated IOP and gonioscopy is used to visualise the angle in AACG. What is the definitive management of AACG?
Laser peripheral iridotomy - tiny hole in the peripheral iris so aqueous humour can flow into the angle
53
Risk factors for AACG:
Increased age Family history Female Chinese and East Asian ethnicity Shallow anterior chamber / Hypermetropia (long sighted) Cataracts
54
Give 3 medication classes that can precipitate AACG:
Adrenergic e.g. noradrenaline Anticholinergic e.g. oxybutynin, solfenacin Tricyclic antidepressants e.g. amitriptyline (has anti-Ach effects)
55
Provisional diagnosis is done by an optometrist, and the patient is then referred to the ophthalmologist by the GP. What investigations can be done to confirm the diagnosis of open-angle glaucoma?
Visual field assessment Slit lamp with pupil dilatation Applnation tonometry to assess IOP Gonioscopy
56
What is normal intraocular pressure?
10-21 mmHg Created by resistance to flow through the trabecular meshwork
57
When is 360 degree selective laser trabeculoplasty (SLT) offered first line to people with glaucoma?
IOP >=24 mmHg
58
Second and third line options for open angle glaucoma:
2) Prostaglandin analogue eyedrops e.g. latanoprost 3) BB, carbonic anhydrase and sympathomimetic eye drops (timolol, dorzolamide, brimonidine respectively)
59
Risk factors for open-angle glaucoma:
Black ethnic origin Increased age First degree relatives Myopia HTN DM Corticosteroid use
60
Panretinal laser photocoagulation is used in proliferative diabetic retinopathy. Give 2 complications / side effects of this treatment and explain them.
Noticeable reduction in visual fields. Decreases in night vision. Peripheral fields are targeted in PRP to reduce / halt neovascularisation. They usually target the periphery. Rods are most abundant in the periphery and they are predominantly responsible for night vision, therefore there is a decrease in night vision.
61
Causes of mydriasis:
CN III palsy Holmes-Adie pupil Traumatic iridoplegia Phaeochromocytoma Congenital Drugs: tropicamide, atropine, amphetamines, cocaine, tricyclics
62
What is an Argyll-Robertson pupil?
Small, irregular pupil Don't respond to light but do accommodate Causes e.g. neurosyphilis, DM
63
Anything above ? on an audiogram is normal.
20 decibels
64
How to read an audiogram:
Sensorineural hearing loss; both air and bone conduction are impaired Conductive hearing loss; only air conduction is impaired
65
Presenting symptoms of vitreous haemorrhage:
Dark floaters Red hue to vision Painless loss of vision or haze
66
Which electrolyte abnormality predisposes to cataracts?
Hypocalcaemia
67
3 features that distinguish pre-septal cellulitis from orbital cellulitis.
Ophthalmoplegia / pain on eye movements Reduced VA Proptosis
68
There is an associated systemic inflammatory condition in 50% of patients presenting with scleritis. Give the 4 of the most common:
RA - scleral tissue is similar to connective tissue in joints Vasculitis esp GPA SLE Sarcoidosis
69
What are the classic associations with anterior uveitis?
HLA-B27 Seronegative spondyloarthropathies: Ankylosing spondylitis Psoriatic arthritis Reactive arthritis Enteropathic arthritis (associated with IBD) ALSO, Sarcoidosis; bilateral disease Behcet's disease - oral ulcers, genital ulcers and anterior uveitis
70
Symptoms of anterior uveitis:
Inflammation of the anterior uvea - ciliary body and the iris. Acute onset ocular discomfort and pain Small / irregular pupil Intense photophobia Blurred vision Red eye Lacrimation VA initially normal, then impaired Hypopyon = very bad
71
Management of anterior uveitis:
Urgent ophthalmology review Cycloplegics - dilate pupil to relieve pain and photophobia e.g. atropine, cyclopentolate Steroid eye drops
72
Diabetic retinopathy is often split into NPDR, PDR and maculopathy. Which is more common in T1DM, and describe the pathophysiology?
Proliferative retinopathy Retinal neovascularisation occurs, thought to be due to production of VEGF in response to the retinal ischaemia caused by endothelial dysfunction. May lead to vitreous haemorrhage, fibrous tissue forming anterior to retinal disc. 50% have profound visual impairment within 5 years.
73
NPDR describes the presence of microaneurysms, plus or minus blot haemorrhages, hard exudates and cotton wool spots. Describe the categorisation of mild, moderate and severe NPDR.
Mild = 1 or more microaneurysm. Moderate = microaneurysm, blot haemorrhage, hard exudates, cotton wool spots. Venous beading and intraretinal microvascular abnormalities (IRMA), but less than severe. Severe = blot haemorrhages and microaneurysms in 4 quadrants. Venous beading in 2 quadrants. IRMA in at least 1 quadrant.
74
Maculopathy describes any changes on the macula area e.g. hard exudates. If there is a change in visual acuity, what treatment can be initiated?
Anti-VEGF
75
What is the treatment for proliferative diabetic retinopathy?
Panretinal laser photocoagulation (PRP)
76
Differences between bacterial and viral conjunctivitis:
Bacterial = purulent discharge, 'stuck together' eyes in the morning Viral = serous discharge, recent URTI, pre-auricular lymph nodes
77
A pregnant woman presents with bacterial conjunctivitis. What should her management be?
Topical fusidic acid (NOT chloramphenicol)
78
Management of allergic conjunctivitis:
Topical / systemic antihistamines for symptom control Topical mast-cell stabilisers e.g. sodium cromoglicate / nedocromil
79
Cataracts are the leading cause of curable visual impairment. Give some causes / risk factors.
Age Smoking Long term steroids Alcohol Radiation DM Hypocalcaemia Trauma Myotonic dystrophy
80
Give 4 symptoms and 1 sign of a cataract:
Reduced VA and blurring Faded colour vision / brown / yellow Glare, lights appearing brighter than normal Haloes around lights All gradual onset ^ Defect in red reflex
81
Findings on ophthalmoscopy of a cataract:
Normal fundus and optic nerve
82
4 classifications of cataract:
Nuclear; changes lens refractive index, age related Polar; localised, ?inherited Subcapsular; steroid use Dot opacities; common in normal lenses, also DM and myotonic dystrophy
83
3 complications of cataract surgery:
Endophthalmitis = inflammation of the vitreous humour Retinal detachment Posterior capsule rupture / opacification
84
Describe the role and control of the lens.
To focus light onto the retina. It is held in place by suspensory ligaments that are attached to the ciliary body which contracts and relaxes to change the shape of the lens. Ciliary body relaxes, suspensory ligaments tense and the lens narrows. Ciliary body contracts, suspensory ligaments loosen and lens thickens.
85
Blepharitis is the inflammation of ...
Eyelid margins
86
There are two types of blepharitis; discuss them.
Most common = posterior blepharitis. Meibomian gland dysfunction. Less common = anterior blepharitis. Seborrhoiec dermatitis / staph infection. Blepharitis is more common in patients with rosacea, regardless of type.
87
What is the function of meibomian glands ? Give presenting features of blepharitis.
They secrete oil onto the eye surface to prevent rapid evaporation of tear film. Problems with these can cause dry eyes and therefore irritation. Features of blepharitis: Gritty eyes Bilateral ?Sticky eyes in the morning Swollen eyelids in staph infection Stye Secondary conjunctivitis
88
Management of blepharitis:
Hot compresses BD to soften lid margins Lid hygiene - cleaning debris from lid margins, baby shampoo or sodium bicarb Artificial tears for dry eyes
89
What is a chalazion?
Meibomian gland cyst - firm painless lump in the eyelid. Spontaneous resolvement usually, but maybe drainage.
90
Management of scleritis:
Same day ophthalmologist assessment, and review for underlying systemic conditions. Oral NSAIDs first line Severe = oral steroids Immunosuppression appropriate to the underlying systemic conditions if applicable e.g. MTX in RA.
91
Most common complication of thyroid eye disease?
Exposure keratopathy Eyelid retraction and exopthalmos causing proptosis - cornea is excessively exposed disrupting the normal tear film - dryness, irritation and corneal ulceration. Foreign body sensation, pain, photophobia.
92
Features of thyroid eye disease:
Exophthalmos Conjunctival oedema Failure to close eyelids fully Optic disc swelling Ophthalmoplegia
93
Pathophysiology of thyroid eye disease:
Autoimmune response to an autoantigen of the ?TSHr. Lead to retro-orbital inflammation. Inflammation results in glycosaminoglycan and collagen deposition in the muscles, causing the classic appearance of thyroid eye disease.
94
Prevention of thyroid eye disease:
STOP SMOKING If taking radio-iodine treatment, 15% of patients developed or had worsening of their eye disease. Prednisolone could be protective for this.
95
Most serious complication of thyroid eye disease, and when does it occur?
Optic neuropathy Enlarged extraocular muscles compress the optic nerve at the apex of the orbit. Results in reduction of VA, colour vision deficits and visual field defect. URGENT INTERVENTION to prevent permanent visual loss.
96
How does thyroid eye disease cause strabismus?
Fibrosis and enlargement of the extra-ocular muscles can result in restrictive strabismus (misalignment of the eyes) and therefore double vision.
97
For patients with established thyroid eye disease what should indicate an urgent ophthalmology review?
Unexplained vision deterioration Colour vision change Globe subluxation Obvious corneal opacity Cornea visible when eyes are closed Disc swelling