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MD2 Opthalmology > Eye Review > Flashcards

Eye Review Flashcards

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1
Q

Label the illustration

A
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2
Q

How should an eye review Hx be structured?

A

HOPC (unilateral or bilateral eye problem)

PMHx

Past ocular Hx

FHx

SHx

Rx

Allergies

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3
Q

Outline the structure of the eye exam

A

VISION, PUPILS, PRESSURE

1) Visual acuity + further examinations according to suspected Dx (e.g. pin hole, contrast sensitivity, colour saturation, Ishihara colour vision test, visual fields by confrontation, light saturation)
2) Pupil reactions: direct, consensual, swinging
3) IOP + additional tests (e.g. corneal reflections, EOMs, cover testing, corneal sensation, red reflex)
4) Slit lamp/fundus examination

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4
Q

How is visual acuity measured?

A

Using a Snellen chart

Patient is positioned at a predetermined distance from the chart (classically 6 metres) in well illuminated room and covers one eye at a time

Try pinhole if VA is 6/9 or worse

NB Leave distance glasses/bifocals/multifocals on for the test but take reading glasses off

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5
Q

How is contrast sensitivity assessed?

A

Using a Pelli-Robson contrast sensitivity chart

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6
Q

How can colour saturation be tested?

A

Ask patient to cover one eye (start by covering “bad eye” if you already know which this is) and look at something red

Then ask them to swap eyes and report any change

“If the intensity of the colour in one eye is worth $1, how much is it worth in the other eye?” E.g. 30 cents in this example

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7
Q

How can colour vision/differentiation be assessed?

A

Using Ishihara colour plates

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8
Q

How can light saturation be tested?

A
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9
Q

How is the swinging light test performed and how are the findings interpreted? What does it assess for?

A

Assesses for RAPD

Swing the light between the two eyes; the pupil with the poorer, functioning anterior visual pathway will dilate despite light stimulus

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10
Q

Describe the light reflex pathway

A
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11
Q

What is the Marcus Gunn pupil?

A

RAPD

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12
Q

What is the Argyll Robertson pupil?

A

Pupil constricts on accommodation (when focussed on an object close-up) but NOT to light

Highly specific sign of neurosyphilis, and may also be a sign of diabetic neuropathy

In general, pupils that “accommodate but do not react” are said to show light-near dissociation - i.e., it is the absence of a miotic reaction to light, both direct and consensual, with the preservation of a miotic reaction to near stimulus (accommodation-convergence)

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13
Q

What is the Holmes Adie pupil?

A

Tonically dilated pupil that does not react to light

Associated with damage to parasympathetic pupillary fibres

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14
Q

How is IOP measured?

A

By applying pressure to the cornea using a tono-pen or Goldmann applanation tonometry; IOP is inferred from the force required to “flatten” (applanate) the cornea

Topical anaesthetic should be applied to the eye first to reduce discomfort caused by probe making contact with the cornea

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15
Q

What influences IOP? What is its normal range?

A

Measurement is influenced by corneal thickness (i.e. a thicker cornea will have more resistance and produce a higher IOP reading)

Normal IOP: 6-21mmHg (mean 15mmHg)

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16
Q

How may visual fields be tested?

A

By confrontation

By automated perimetry (uses a mobile stimulus moved by a perimetry machine; patient indicates whether he sees the light by pushing a button)

Using an Amsler grid (used to detect visual field defects within the centremost region of the visual field)

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17
Q

How are results of visual field testing recorded?

A

Documentation is from the patient’s point of view

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18
Q

What do positive findings on Amsler grid testing usually indicate?

A

Macular pathology

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19
Q

What might abnormal EOMs indicates?

A

Cranial nerve palsy (III, IV, VI)

Muscle entrapment (e.g. in orbital #)

Muscle infiltrate (e.g. thyroid eye disease)

Muscle weakness (i.e Guillain-Barre Miller-Fisher variant)

Gaze centre dysfunction (e.g. horizontal gaze palsy, internuclear opthalmoplegia)

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20
Q

Internuclear opthalmoplegia

A

Disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction

Caused by injury or dysfunction in the medial longitudinal fasciculus (MLF); in young patients with bilateral INO, multiple sclerosis is often the cause and in older patients with one-sided lesions a stroke is a distinct possibility

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21
Q

Miller Fisher variant of GBS

A

Rare, acquired nerve disease characterised by abnormal muscle coordination, paralysis of the eye muscles, and absence of the tendon reflexes; like Guillain-Barré syndrome, symptoms may be preceded by a viral illness

Majority of individuals with Miller Fisher syndrome have a unique antibody that characterises the disorder

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22
Q

How is corneal reflection testing (Hirschberg test) performed?

A

By shining a light in the person’s eyes and observing where the light reflects off the corneas

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23
Q

6 causes of leukocoria

A

Cataract

Retinoblastoma

Coats’ disease

Retinal detachment

Retinopathy of prematurity

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24
Q

How is the red reflex tested?

A

The red reflex refers to the reddish-orange reflection of light from the eye’s retina that is observed when using an ophthalmoscope or retinoscope from approximately 30 cm / 1 foot; examination is usually performed in a dimly lit or dark room

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25
How is cover testing performed and how are results interpreted?
Unilateral cover test is performed by having the patient focus on an object then covering the fixating eye and observing the movement of the other eye; if the eye was exotropic, covering the fixating eye will cause an inwards movement, and esotropic if covering the fixating eye will cause an outwards movement Dominant fixating eye being covered prompts the other eye to take up fixation (see image)
26
What is the purpose of cover testing?
Used to determine both the type of ocular deviation and measure the amount of deviation; two primary types of ocular deviations are the tropia and the phoria Tropia is a misalignment of the two eyes when a patient is looking with both eyes uncovered; a phoria (or latent deviation) only appears when binocular viewing is broken and the two eyes are no longer looking at the same object
27
What is leukocoria?
An abnormal white reflection from the retina of the eye (seen in place of the normal red reflex)
28
What is Coats' disease?
Coats’ disease (AKA exudative retinitis or retinal telangiectasis) is a rare congenital, nonhereditary eye disorder, causing full or partial blindness, characterized by abnormal development of blood vessels behind the retina
29
How should the slit lamp examination be approached?
Examine from superficial to deep structures: Lids Tear film Conjuctiva Episclera and sclera Cornea Anterior chamber Iris Pupil Lens Fundus examination
30
Explain how a fundal assessment should be performed
Dark room, comfortable position for the patient Ask patient to look into the distance (accommodation constricts the pupil) Use your R eye for the patient's R eye and your L eye for the patient's L eye Hand on the patient's forehead allows you to stabilise the distance between the patient's fundus and fundoscope Using the dial: green numbers (+) shortens the focal length of the fundoscope and red numbers (-) increase Once you have the retina in focus, try following a blood vessel to the optic disc Disc is on nasal side of retina
31
Revise your fundal anatomy!
32
What do each of these illustrations demonstrate?
33
How can myopia and hypermetropia be corrected?
34
What is astigmatism? What is regular vs irregular astigmatism and what are the implications for Mx?
Normal cornea is curved like a sphere Regular astigmatic cornea has 2 different curves at 90 degrees to each other and is correctable with glasses or contact lenses Irregular astigmatic cornea has variable degrees of curvature along each axis and is not easily corrected with glasses-
35
What is the fastest way to detect a refractive error and how does this work?
Pinhole; obscures the light which has been inappropriately focussed onto the retina
36
What is presbyopia and how is it managed?
Long-sightedness caused by loss of elasticity of the lens of the eye, occurring typically in middle and old age (lens loses its flexibility with age) Mx: reading glasses/bifocals
37
Main causes of cataracts
Age-related Drugs (e.g. steroids) Trauma (including intra-ocular surgery) Systemic diseases (e.g. DM, myotonic dystrophy, Wilson's disease, atopic dermatitis) Ocular diseases (e.g. uveitis, retinitis pigmentosa)
38
Sx of cataracts
Gradual decrease in visual acuity and increase in glare Sx over weeks to years
39
How is cataract surgery performed? What is the success rate?
Patients often admitted as day case Usually performed under topical or local anaesthesia Patient must be able to lie flat and still Approach: phacoemulsification (emulsification and aspiration of the lens) with insertion of intra-ocular lens Post-op Abx and steroid eye drops prescribed over 4 weeks Post-op r/vs at 1 day, week and month Success rates: visual improvement in \>95% of operations performed
40
What is a cataract?
Clouding of the lens in the eye leading to a decrease in vision
41
Describe the movement of aqueous humor through the anterior chamber
42
What are the 3 major clinical features of POAG?
Progressive visual field loss Progressive increase in cup-to-disc ratio of optic disc Elevated IOP NB Some people have high IOP but no evidence of glaucoma (ocular HTN), some people have features of glaucoma despite normal IOP (normal tension glaucoma)
43
How does visual loss progress in glaucoma?
44
If the L image is a normal optic disc, what is the pathology on the R?
Increased cup to disc ratio seen in glaucoma
45
What is the aim of medical Mx for POAG?
To lower IOP and slow disease progression by increasing aqueous outflow or decreasing aqueous production Lowering IOP slows disease progression, even when IOP is already in normal range
46
Eye drops for POAG; give an example of each
Prostaglandin inhibitors: latanoprost (Xalatan) Beta blockers: timolol (timoptic) Alpha agonists: brimonidine (Alphagan) Miotics: pilocarpine Carbonic anhydrase inhibitors: brizolamide (Azopt)
47
Tablets for treatment of POAG
Carbonic anhydrase inhibitors: acetazolamide (Diamox)
48
Mechanism of action of prostaglandin inhibitors for Mx of POAG
Increase aqueous outflow
49
Mechanism of action of B blockers for Mx of POAG
Decrease aqueous production
50
Mechanism of action of alpha agonists for Mx of POAG
Increase aqueous outflow AND decrease production
51
Mechanism of action of miotics for Mx of POAG
Increase aqueous outflow
52
Mechanism of action of carbonic anyhydrase inhibitors for Mx of POAG
Decrease aqueous production
53
Mx of POAG
Medical: eye drops, tablets Laser: selective laser trabeculoplasty (SLT; this is a good alternative for pts who do not tolerate or comply with daily eye drops) Surgical: trabeculectomy (creation of an alternative drainage path for aqueous through the formation of a subconjunctival bleb)
54
Describe the pathophysiology of uveitic glaucoma
Synechiae ("adhesions") and inflammatory cells effect fluid dynamics within the anterior chamber
55
Describe the pathophysiology of neovascular glaucoma
Neovascularisation of angle leads to reduced drainage of aqueous humor and increased IOP Neovascularisation occurs secondary to ischaemia in the eye (e.g. in setting of central retinal vein occlusion, CRVO, or proliferative diabetic retinopathy) Leads to characteristic "rubeosis iridis" appearance (new blood vessels seen on surface of iris
56
How is non-proliferative diabetic retinopathy graded? What findings are seen with each grading?
Mild NPDR: microaneurysms Moderate NDPR: microaneurysms, intra-retinal haemorrhages, hard exudates, cotton wool spots Severe NPDR (any one feature of the "4-2-1 rule"): intra-retinal haemorrhages in 4 quadrants, OR venous beading in 2 quadrants, OR IRMA (intra-retinal vascular abnormalities) in 1 quadrant) Very severe NPDR: 2 features from the 4-2-1 rule
57
How can retinal microaneurysms be better visualised?
Using fluorescain angiography
58
Features of mild NPDR
Microaneurysms
59
Features of moderate NPDR
Microaneurysms Intra-retinal haemorrhages Hard exudates Cotton wool spots
60
Severe NPDR
Any one of: Intra-retinal haemorrhages in 4 quadrants Venous beading in 2 quadrants IRMA in 1 quadrant NB If 2 features, this is classified as very severe NPDR
61
What is proliferative diabetic retinopathy?
Advanced form of diabetic eye disease that occurs when blood vessels in the retina disappear and are replaced by new fragile vessels that bleed easily; can result in sudden loss of vision
62
Distinguish between low- and high-risk PDR
Low: \<1/3 of disc neovascularised (NVD) High: NVD plus vitreous haemorrhage, OR NVD \>1/3 of disc, OR NVE (neovascularisation everywhere!)
63
How is PDR managed?
Pan-retinal photocoagulation; burns away areas of peripheral retina, decreases drive of VEGF production (leading to reduced neovascularisation), with sacrifice of peripheral vision
64
What processes can cause diavetic maculopathy?
Macular oedema Macular ischaemia
65
Mechanism of macular oedema in diabetic maculopathy
Leakage of fluid into foveal tissue Lipid exudates adjacent to fovea
66
Mechanism of macular ischaemia in diabetic maculopathy
Capillary non-perfusion at fovea
67
What sign on fluorescein angiography indicates macular ischaemia?
Enlarged foveal avascular zone and capillary drop-out
68
How can macular oedema be visualised?
Using optical coherence tomography (OCT), a non-invasive imaging test that uses light waves to take cross-section pictures of your retina, the light-sensitive tissue lining the back of the eye Shows fluid leakage and lipid exudates adjacent to fovea
69
Mx of diabetic macular oedema
Macular (grid) laser Intra-vitreal anti-VEGF agents
70
Mx of macular ischaemia
No specific treatment: BSL control, BP control, cholesterol control
71
What is the most common cause of blindness in people \>50 in the developed world?
Dry age-related macular degeneration
72
Major risk factors for dry macular degeneration
Increasing age Smoking
73
Mx for dry macular degeneration
Amsler grid: frequent use allows patient to detect changes/new distortion of vision Cessation of smoking Low vision aids
74
Appearance of dry macular degeneration on fundoscopy and OCT What is drusen? What is geographic atrophy?
Drusen are yellow lipid deposits under the retina; while drusen likely do not cause age-related macular degeneration (AMD), their presence increases a person's risk of developing AMD Geographic atrophy is the advanced (late) form of dry AMD; atrophy refers to the degeneration of the deepest cells of the retina (retinal pigment epithelium; RPE), which normally helps maintain the photoreceptor cells
75
What is the classic feature of wet (neovascular) age-related macular degeneration?
Choroidal neovascularisation (CNV): abnormal new vessels grow from choroid to RPE (process linked to increased VEGF levels), and these vessels bleed/leak, leading to macular scarring
76
Mx of wet macular degeneration
Anti-VEGF agents via (typically monthly) intra-ocular injection: ranbizumab, bevacizumab Photodynamic therapy Macular laser
77
Photodynamic therapy (PDT)
Photodynamic therapy (PDT) is a treatment that uses a drug, called a photosensitizer or photosensitizing agent, and a particular type of light; when photosensitizers are exposed to a specific wavelength of light, they produce a form of oxygen that kills nearby cells
78
What is the classical appearance of a 3rd nerve palsy?
"Down and out"
79
What are the major causes of CN III palsy?
Compressive: from tumour, haemorrhage or aneurysm (commonly pupil involving) Vascular: HTN, DM (commonly pupil sparing) Trauma Vasculitis (i.e. GCA) Demyelinating disease Idiopathic
80
Ix of CN III palsy
MRI/MRA urgently if compressive lesion suspected BP and blood tests for vascular risk factors (including glucose, lipid profile)
81
Mx and prognosis of CN III palsy
According to the cause Prognosis is variable
82
Classic appearance of a CN IV palsy
Tip, turn and tilt
83
Causes of CN IV palsy
Trauma (can cause bilateral CN IV involvement) Microvascular disease Tumour Demyelination Vasculitis (GCA) Idiopathic Can be congenital
84
Ix for CN IV palsy
Old photos (if congenital palsy suspected) Bloods for vascular risk factors Consider neuro-imaging
85
Mx of CN IV palsy
According to cause Prisms in glasses +/- strabismus surgery to re-align the visual axis if not improving
86
Strabismus
Abnormal alignment of the eyes
87
What kind of difficulties are experienced by the patient with CN IV palsy and why?
SO allows eye to look down, inwards and provides intortion A CN IV palsy can cause difficulty reading and walking down stairs
88
Classic appearance of a CN VI palsy
Abduction deficit
89
What Sx will a patient complain of with a CN VI palsy?
Horizontal diplopia (binocular)
90
Causes of CN VI palsy
Vascular Raised ICP Tumours Trauma Demyelinating disease Vasculitis (GCA) Idiopathic
91
DDx for underlying cause in CN VI palsy
Thyroid eye disease Medial wall blow-out # Myaesthenia gravis
92
Ix of CN VI palsy
Assess vascular RFs MRI if other associated pathology present, if palsy does not resolve in 3/12 or if patient \<40
93
Mx of CN VI palsy
According to cause Prisms +/- strabismus surgery Botox to ipsilateral MR
94
Interpretation of visual fields

MD2 Opthalmology (3 decks)

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