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Finals > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What does the conjunctiva line?

A

The inner eyelids and sclera

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2
Q

What does the cornea cover?

A

The anterior chamber, iris, and pupil

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3
Q

Cause of a cloudy aqueous humor

A

Anterior uveitis

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4
Q

Cause of sterile pus in the aqueous humor?

A

Corneal ulcer

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5
Q

What is the anterior chamber of the eye?

A

Small cavity lying behind the cornea and in front of the iris
0.2ml

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6
Q

Outline the normal production and flow of aqueous humor

A

Produced by the ciliary body and flows through the pupil and empties out at the drainage angle.

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7
Q

Describe the boundaries of the posterior chamber of the eye

A

Anteriorly by the iris
Peripherally by the ciliary processes
Posteriorly by the lend and sinuses

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8
Q

Define visual acuity and how you’d assess it

A

Measure of the clarity or sharpness of vision
Sit pt 6m from Snellen chart and cover one eye (use glasses if worn!)
Ask them to read as many lines as they can - the last line completed indicates the acuity (6/6 is normal)
If pt sees less than 6/6 examine with pinhole in front of the eye

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9
Q

Define visual field

A

Area seen with both eyes without shifting gaze

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10
Q

If a pt has diplopia, how might you distinguish which eye has the pathology?

A

Assess extraocular movements and ask which movement provokes the most diplopia
Hold gaze in that direction, cover each eye in turn and ask which one sees the outer image - this is the eye with pathology

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11
Q

Briefly outline how you’d conduct ophthalmoscopy

A

Examine lens and vitreous - 1m away, focus beam of light at pupil. Should see the red reflex (absent in dense cataracts and intraocular bleeding)
Move closer to pt and follow the vessels until the optic disc is seen - examine the precise boundaries and central cup
Examine radiating vessels and macula

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12
Q

What is a stye?

A

Mainly used by pts to describe inflammatory lid swelling in.
Usually and abscess or infection (staph) in a lash follicle
They point outwards and can be treated with warm compresses for 5-10min several times each day

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13
Q

What is a chalazion?

A

Left behind after an abscess of Meibomian gland

Point inwards

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14
Q

What is blepharitis? How would you treat it?

A

Lid inflammation - staph, seborrhoeic dermatitis, or rosacea
Eyes have burning itching red margins, with scales on lashes

Treat with good eyelid hygiene. In kids, condenser oral erythromycin

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15
Q

What is entropion?

A

Lid inturning due to degeneration of the lower lid fascial attachments and their muscles.

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16
Q

What is ectopion?

A

Lower lid eversion causing irritation, watering +/- keratitis

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17
Q

Causes of ptosis

A

Congenital - absent nerve to levator muscle, poorly developed levator
Mechanical - oedema, xanthelasma, upper lid tumour
Myogenic - muscular dystrophy, myasthenia
CNS - CNIII palsy, Horner’s

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18
Q

What is lagophthalmos? Give causes and treatment

A

Difficulty in lid closure

Causes - exophthalmus, mechanical impairment of lid movement, leprosy
Treat - lubricate eyes and treat any corneal ulcers

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19
Q

Outline the three categories of watery eye

A
  1. Dec drainage - punctal stenosis
  2. Inc lacrimation - environmental, corneal injury, FB
  3. Pump failure
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20
Q

Causes of dry eyes

A

Dec tear production - old age, Sjogren’s, mumps, sarcoidosis, amyloidsis, lymphoma, haemochromatosis

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21
Q

Signs of retinoblastoma

A

White pupil

Absent red reflex in a child

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22
Q

Presentation of ophthalmic shingles. How would you treat it?

A

Pain and neuralgia in the distribution of cranial nerve V1 dermatome
Then blistering inflammed rash

Treat - oral antivirals improve symptoms if given within 72hrs of rash onset

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23
Q

How do orbital swellings typically present?

A

Proptosis- may be deviated +/- diplopia

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24
Q

Describe orbital cellulitis ad how it usually presents

A

Severe sight- and life-threatening emergency
There’s infection of the soft tissues posterior to the orbital septum (typically via sinus infection)

Typically seen in kids with inflammation of orbit, fever, lid swelling, dec eye movements +/- diplopia, painful eye movements

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25
Q

Complications and treatment of orbital cellulitis

A

Complications = subperiosteal and orbital abscesses, extra-orbital extension, visual loss

Treat = admit for CT, get ENT + ophthalmic opinion, antibiotics
Rule out rhabdomyosarcoma, Grave’s disease, or cavernous sinus thrombosis

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26
Q

Describe periorbital cellulitis and its management

A

Infection of soft tissues anterior to the orbital septum
Commonly caused by sinusitis or facial skin lesions
Characterised by acute erythematous swelling of eyelid

Treat = empirical treatment for cellulitis (amoxicillin)

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27
Q

What is a squint?

A

Aka strabismus

Abnormality of the co-ordinated movement of both eyes to maintain single vision

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28
Q

Management of squints

A

Optical - exclude eye pathology, give glasses
Orthoptic - patching good eye
Operations - help alignments, can use botulinum toxin

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29
Q

Presentation of 3rd nerve palsy

A

Oculomotor nerve

  • ptosis
  • proptosis (dec recti tone)
  • fixed dilatation
  • eye looks down and out
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30
Q

Presentation of a 4th nerve palsy

A

Trochlear nerve:

  • diplopia
  • pt may hold head tilted (ocular torticollis)
  • eye looks upward in adduction -> can’t look down and in (SO paralysed)
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31
Q

Presentation of 6th nerve palsy

A

Abducens:

  • diplopia in horizontal plane
  • eye is medially deviated and can’t move laterally from midline (LR is paralysed)
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32
Q

Action of superior rectus

A

Moves gaze upwards

Particularly in abduction

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33
Q

Action of superior oblique

A

In adduction, looks down

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34
Q

Action of medial rectus

A

Adduction

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35
Q

Action of lateral rectus

A

Abduction

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36
Q

Action of inferior rectus

A

Looks Down (particularly in abduction)

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37
Q

Action of inferior oblique

A

In adduction, looks up

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38
Q

Briefly describe the mechanisms behind the pupil reflexes

A

Light detected by retina -> signal via optic nerve to brain (afferent) -> signal via oculomotor nerve to pupillary muscles (efferent) -> pupil constriction

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39
Q

How would you establish if abnormal pupil reflexes are due to afferent defects? What are some causes of this?

A

Pupil won’t respond to light, but constricts to beam in the other eye (consensual response).

Causes = optic neuritis, optic atrophy, retinal disease

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40
Q

How would you establish if abnormal pupil reflexes are due to efferent defects? What are some causes of this?

A

Absence of pupil constriction on direct and consensual

Causes = 3rd nerve palsy, cavernous sinus lesion, DM, posterior communicating artery aneurysm

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41
Q

Other causes of a fixed dilated pupil (not afferent or efferent defect specifically)

A

Mydriatics
Trauma
Acute glaucoma
Coning (uncal herniation)

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42
Q

Presentation and causes of Horner’s

A

Pupil is miotic (small) with no dilatation in dark
Partial ptosis
Unilateral facial anhydrosis

Causes = post inf cerebellar artery or basilar artery occlusion, MS, cavernous sinus thrombosis, Pancoast’s tumour, hypothalamic lesion, aortic aneurysm

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43
Q

What is Argyll Robertson pupil?

A

Occurs in neurosyphilis and DM

Bilateral miosis, poor pupillary dilation, pupil irregularity

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44
Q

Define myopia

A

Eyeball is too long - only close objects focus on the retina

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45
Q

Define astigmatism

A

Common, occurs when cornea doesn’t have same degree of curvature (becomes an irregular surface)
Usually one half if flatter or steeper than the other half
Light rays don’t focus together and so produce a blurred image

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46
Q

Define hypermetropia

A

Long sighted

Eye is too short - distant objects are focused behind retina

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47
Q

What is presbyopia?

A

With age, the lens stiffens as the ciliary muscles are unable to reduce tension in the lens for close focusing.

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48
Q

Describe the presentation of optic nerve lesions

A

Total blindness of the eye

Direct pupillary reflex is absent, indirect remains intact

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49
Q

Describe the presentation of lesions in the optic chiasma

A

Bitemporal hemianopia

Normal direct, indirect, and accommodation reflexes

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50
Q

Describe the presentation of lesions in the optic tract

A

Contralateral homonymous hemianopia (R sided optic tract lesion causes L temporal hemianopia + R nasal hemianopia)
Normal direct, indirect, and accommodation reflexes

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51
Q

Describe the presentation of lesions in the optic radiation

A

Contralateral homonymous hemianopia

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52
Q

Describe the presentation of lesions in the visual cortex

A

Contralateral homonymous hemianopia
Pupils react normally to reflex stimulation
Macula is often spared due to anastomoses between post and middle cerebral arteries

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53
Q

General causes of visual cortex field defects

A 
Ischaemia (TIA, migraine, stroke)
Glioma
Meningioma
Abscess
AV malformation
Drugs (ciclosporin)
54
Q

How might you differentiate between scleritis and episcleritis clinically?

A

Episclera lies superficially and so episcleral vessels will move when probed with cotton bud and will blanch
Deeper sclera vessels don’t move or blanch

55
Q

Describe episcleritis

A 
Inflammation below the conjunctiva
30% are bilateral
Acute onset
Eye aches dully and is tender
Acuity is usually ok
Cause = 70% unknown, may complicate rheumatic fever, PAN, SLE
56
Q

Describe scleritis

A

Generalised inflammation of sclera with oedema of conjunctiva, scleral thinning, and vasculitic changes.
50% have systemic disease (RA, or GwP)
Constant, severe dull ache
Ocular movements are painful
May present with headache and photophobia

57
Q

Management of scleritis

A

Urgent referral!

Specific management depends on subtype and severity - ranges from oral NSAIDs +/- pred, to systemic immunosuppression

58
Q

Name the 4 conditions that prompt an urgent referral to ophthalmology

A

Acute glaucoma
Acute iritis
Corneal ulcers
Scleritis

59
Q

Causes of anterior uveitis

A 
Ankylosing spondylitis
Sarcoid
Behcet’s
IBD
Reactive arthritis
Herpes, TB, syphilis, HIV
60
Q

Causes of posterior uveitis

A 
Herpes simplex
TB
CMV
Lymphoma
Sarcoidosis
Behcet’s
61
Q

Describe the typical presentation of anterior uveitis. How is it diagnosed?

A

Pain, blurred vision, and photophobia
Inc lacrimation
Onset over hours/days

Diagnosis = slit lamp with dilated pupils to determine location (if truly ant then you’ll see leucocytes in the ant chamber)

62
Q

Management of anterior uveitis

A 
Urgent referral to eye clinic
Treatment depends on cause
Drops:
- pred -> dec inflammation
- cyclopentolate -> prevent adhesions and relieve spasm of ciliary body
63
Q

Describe acute closed-angle glaucoma. How does it present?

A

Form of glaucoma where the angle of ant chamber narrows acutely causing a sudden rise in intraocular pressure to >30mmHg
Pupil becomes fixed and dilated, and axonal death occurs
Often generally unwell - N+V, headache, painful red eye, blurred vision

64
Q

What’s the difference between 1’ and 2’ angle-closure in acute closed-angle glaucoma?

A 
1’ = pts with anatomical predisposition
2’ = due to pathological processes
65
Q

Management of acute closed-angle glaucoma

A

Start triad of:
- B-blockers (suppress aqueous humour production)
- pilocarpine (causes miosis which can open the blocked drainage angle)
- acetazolamide (dec aqueous humour formation)
Antiemetics and analgesia may be used
Admit to monitor IOP
Once IOP controlled, consider iridectomy (removal of part of iris)

66
Q

Non-infective causes of conjunctivitis

A

Allergic
Toxic
AI
Neoplastic

67
Q

Infective causes of conjunctivitis

A

Non-herpetic viral (serous discharge)
- 80% adenoviruses

Bacterial (purulent discharge)
- gonococcal infection

68
Q

Define corneal abrasion. What are some common causes? Treatment?

A

Epithelial breach causing pain, photophobia, +/- dec vision

Causes = accidental scratches, contact lenses, trauma, chemical injury, prev corneal disease

Treat = chloramphenicol ointment

69
Q

What are corneal ulcers? How would you manage them?

A

Epithelial breach caused by bacterial, herpetic, fungal, or protozoal infections, or vasculitis.

Treat = urgent referral, liaise with micro. Give chloramphenicol with ofloxacin drops (admit if DM/immunosuppressed, or if pt can’t manage drops)

70
Q

Describe the pattern of features associated with damage to the optic nerve

A

Monocular vision loss with central scotoma
Afferent pupillary defects
Dyschromatopsia (colour blindness)
Papillitis on fundoscopy

71
Q

Causes of optic neuropathy

A

Anterior ischaemic optic neuropathy
Giant cell arteritis
Non-arteritic
Optic neuritis

72
Q

Describe anterior ischaemic optic neuropathy and what you’d see on fundoscopy

A

Optic nerve is damaged if post vascular supply to optic nerve is blocked by inflammation or atheroma.
Two main type:
- arteritic (GCA most common)
- non-arteritic

Fundoscopy shows a pale/swollen disc

73
Q

Symptoms, investigations, and management of GCA

A

Symptoms = new-onset headache, malaise, jaw claudication, tender scalp + temporal arteries, neck pain, monocular vision loss (may be transient)

Investigations = ESR + CRP, temporal artery biopsy

Treat = prednisolone 60mg/d PO

74
Q

Describe non-arteritic anterior ischaemic optic neuropathy

A

Visual loss is typically painless and noticed upon awakening
Affects pts <50
Associated with HTN, inc lipids, DM, smoking

75
Q

Describe the symptoms and management of optic neuritis

A

Subacute loss of vision - unilateral, over hours or days, colour vision affected, painful eye movements, pupil has afferent defect

Treat = high-dose methyl-pred for 72h, then pred for 11d

76
Q

Causes of transient vision loss

A

Vascular - TIA, migraine
MS
Subacute glaucoma
Papilloedema

77
Q

Presentation and management of central retinal artery occlusion

A

Dramatic vision loss within seconds of occlusion
Afferent pupil defect
Retina appears white, with cherry red spot at macula
Considered a form of stroke (occlusion is often thromboembolic)

Treat = according to stroke protocols

78
Q

Describe retinal vein occlusion and give the causes/associations of it

A

Much more common than arterial occlusion
2nd most common cause of blindness (diabetic neuropathy is first)
Can affect the central or branching veins

Causes/associations = atherosclerosis, HTN, DM, polycythaemia, glaucoma

79
Q

Describe vitreous haemorrhage including some causes and investigations

A

Arise from retinal neovascularisation (DM, BRVO, CRVO), retinal tears, retinal detachment, trauma
Small extravasations of blood produce vitreous floaters

Check = acuity, pupil reactions, fundoscopy

80
Q

Common causes of gradual loss of vision

A 
Cataract
Macular degeneration
Glaucoma
Diabetic retinopathy
HTN
Optic atrophy
Slow retinal detachment
81
Q

Describe age-related macular degeneration, including the pathogenesis

A

Occurs in the elderly who present with deteriorating central vision

Pathogenesis = pigment, drusen, sometimes bleeding at the macula. Over time it progresses to retinal atrophy and central retinal degeneration causing loss of central vision

82
Q

Symptoms of macular degeneration

A

Initially no change in acuity, but difficulty making out images
Difficulty with reading and faces
Difficulty with night vision and changing light conditions
Visual fluctuation
Metamorphopsia- distortion of visual images

83
Q

Outline the two types of age-related macular degeneration

A

Wet (exudative) - pathologic membranes develop under retina leaking fluid and blood -> scar. Vision deteriorates rapidly. O/E there’s fluid exudation and detachment of pigment. Treatment available

Dry (non-exudative) - much slower progressive visual loss. No satisfactory method to treat it

84
Q

Risk factors for age-related macular degeneration

A 
Inc age
Smoking
CV disease
FHx
Cataract surgery
85
Q

Describe optic atrophy and give some cause

A

Discs are pale
May be from inc IOP (glaucoma), or retinal damage, or ischaemia
Others = MS, syphilis, intraorbital/IC tumours

86
Q

Criteria for partial sighted registration

A

Acuity is <6/60 (or >6/60 with visual field restrictions)

87
Q

Criteria for registering as blind

A

Acuity <3/60, or >3/60 but with substantial visual field loss

88
Q

Main causes of blindness in developed countries

A

Cataract
Age-related macular degeneration
Glaucoma
Diabetic retinopathy

89
Q

Define chronic simple (open-angle) glaucoma

A

Optic neuropathy with death of many retinal ganglion cells and their optic revenue axons
May be optic disc cupping
IOP may be raised (but not necessary)
May be asymptomatic until visual fields are impaired

90
Q

Management of chronic simple glaucoma

A

Prostaglandin analogues (latanoprost) - inc uveoscleral outflow
B-blockers (timolol) - dec production of aqueous humor
A-adrenergic agonists - inc uveoscleral outflow and dec aqueous
Carbonic anhydrase inhibitors - dec production

Surgery is possible if medical management fails

91
Q

Describe optic disc cupping

A

Characterised by loss of disc substance which makes cup look larger
Normal cups occupy <50% of the disc
Disc begins to atrophy (appears pale), and cup widens and deepens
Disc vessels are displaced nasally

92
Q

Define cataract

A

Any opacity in the lens

93
Q

Risk factors for cataract development

A

Most are age-related
Occur early in DM
Others - alcohol, smoking, sunlight exposure, trauma, radiotherapy

94
Q

Typical presentation of cataracts

A

Blurred vision - gradual and painless +/- dazzle (in sunlight) +/- monocular diplopia
Pts often describe difficulties driving at night and haloes around street lights

95
Q

Briefly outline surgery for cataract removals, including complications

A

Under LA a small incision is made and lens is removed by phacoemulsion (US breaks it up).
Artificial lens is implanted
Day case surgery

Complications = capsule thickening, astigmatism may be more noticed, infection

96
Q

Describe the anatomy of the retina

A

Outer pigmented layer (in contact with choroid)
Inner sensory layer (in contact with vitreous)
At the centre of the posterior part lies the macula

97
Q

Describe retinal detachment and how it often presents

A

Holes/tears in the retina allow fluid to separate the two layers

Presents with 4 ‘F’s -> floaters, flashes, field loss, fall in acuity

  • painless and may be as sudden as a curtain falling
  • field defects will indicate position and extent of detachment

O/E - grey retina that balloons forwards

98
Q

Differential diagnoses of retinal detachment

A

Migraine
Retinal artery occlusion
Posterior vitreous detachement
Vitreous haemorrhage

99
Q

Management of retinal detachment

A

Rest

  • if superior detachment, lie flat
  • if inferior detachment, lie at 30 degrees

Treat with laser photocoagulation therapy

100
Q

Describe retinitis pigmentosa

A

Most prevalent inherited degeneration in the retina

Night blindness -> peripheral -> central daytime vision loss

101
Q

Common causes of floaters

A

Often caused by RBCs (anything that causes new vessels to form on retina can cause vitreous haemorrhage)
Trauma/retinal detachment
WBCs - from inflammatory/infective cause
Sudden onset of large floaters = posterior vitreous detachment

102
Q

Causes of flashing lights (photopsia)

A

Either intraocular or cerebral pathology (migraine)

103
Q

Describe posterior vitreous detachment

A

Degenerative changes in the vitreous leads to separation from retina -> normal part of ageing
Monochomatic photopsia in the peripheral temporal field (more obvious in dim light and with eye movements

104
Q

Describe the anatomy of the macula

A

Area of 5.5mm diameter, just lateral to the optic disc
In the middle is a pit - the fovea
In the middle of the fovea is the foveola

105
Q

Describe a macular hole. How does it present?

A

Small break in the macular region of the retinal tissue involving the fovea (and therefore affects visual acuity) -> blurred and distorted central vision

106
Q

Describe vascular retinopathy

A

May be arteriopathic (arteriovenous nipping) or HTNsive (arteriolar vasoconstriction and leakage)
Producing hard exudates, macular oedema, haemorrhages, and (rarely) papilloedema
Thick, shiny arterial walls look like wiring

107
Q

Structural eye changes caused by diabetes

A

DM causes ocular ischaemia which can cause new blood vessels to form on the iris -> if these block the drainage of aqueous fluid -> glaucoma

Formation of age-related cataract is accelerated

108
Q

Pathogenesis of diabetic eye disease

A

Microangiopathy in capillaries causes:

  • vascular occlusion causes ischaemia +/- new vessel formation (ie proliferative retinopathy) which bleed. Inc risk of retinal detachment. Occlusion also causes cotton wool spots (ischaemic nerve fibres)
  • vascular leakage -> as pericytes are lost, capillaries bulge (microaneurysms) and there’s oedema and hard exudates. Rupture of microaneurysms at the nerve fibre level causes flame-shaped haemorrhages, when deep in the retina, blot haemorrhages form
109
Q

What are the two types of diabetic retinopathy (DR)?

A

Non-proliferative DR -> micro-aneurysms, haemorrhages, hard exudates, engorged tortuous veins, cotton wool spots, large blot haemorrhages
Proliferative DR -> presence of new vessels on retina (neovascularisation), can cause vitreous haemorrhage

110
Q

Management of diabetic retinopathy

A

Ensure target BP is <140/80
Good control of DM prevents new vessels forming
Photocoagulation by laser is used to treat maculopathy and proliferative DR

111
Q

Describe the normal examination findings of the optic disc

A

Contour - borders should be well-defined
Colour - pink/yellow with pale centre
Cup - should occupy 1/3 of the disc diameter

112
Q

Causes of optic disc swelling

A 
Papilloedema
Malignant HTN
Cavernous sinus thrombosis
Optic neuritis
Cranial SOL
Optic neuropathy
Central v occlusion
Disorders of nerve sheath
113
Q

Define papilloedema. What investigations would you do?

A

Swelling of the optic disc due to raised ICP
Always bilateral, but not always symmetrical

Investigations - MRI/CT, BP, LP (if neuroimaging is normal(=)

114
Q

What is pseudopapilloedema?

A

May mimic papilloedema - disc margins are blurred, disc appears elevated
Usually benign and associated with hypermetropia +/- astigmatism
No true oedema, veins are of normal size
Usually bilateral and symmetrical, and doesn’t change over time
Treat as papilloedema until proven otherwise

115
Q

Action of mydriatic drugs

A

Dilate pupil

116
Q

Action of miotic drugs

A

Constrict the pupil

117
Q

Drug causes of drug eye

A

B-blockers

Anticholinergics

118
Q

Drug causes of corneal deposits

A

Amiodarone
Chloroquine
Chlorpromazine

119
Q

Drug causes of lens opacities

A

Steroids

120
Q

Drug causes of glaucoma

A

Steroid drops
Mydriatics
Anticholinergics

121
Q

Drug causes of papilloedema

A

Tetracyclines
Steroids
COCP

122
Q

Drug causes of retinopathy

A

Ethambutol
Chloroquine
Vigabatrin

123
Q

Which type of macular degeneration carries the worst prognosis?

A

Wet

124
Q

How would you differentiate between glaucoma and uveitis?

A

Glaucoma - severe pain, haloes, semi-dilated pupil

Uveitis - small, fixed oval pupil, ciliary flush

125
Q

Investigations in age related macular degeneration

A

Slit-lamp microscopy
Fluorescein angiography if neovascular ARMD suspected
Ocular coherence tomography

126
Q

Management of macular degeneration

A 
Dry = zinc + anti-oxidants
Wet = anti-VEGF injections (within 2m of diagnosis)
127
Q

Outline the classification for hypertensive retinopathy

A 
I = arteriolar narrowing + tortuosity, inc light reflex (silver wiring)
II = arteriovenous nipping
III = cotton-wool exudates, flame and blot haemorrhages
IV = papilloedema
128
Q

Outline the new classification for non-proliferative DR

A 
Mild = 1 or more microaneurysm
Mod = microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading and intraretinal microvascular abnormalities (less severe than severe NPDR)
Severe = blot haemorrhages and micraneurysms in 4 quadrants, venous bleeding in at lease 2 quadrants, IRMA in at least 1 quadrant
129
Q

Outline the traditional classification of background and pre-proliferative DR

A 
Background = microaneurysms, =<3 blot haemorrhages, hard exudates
Pre-proliferative = cotton wool spots (soft exudates), >3 blot haemorrhages, venous beading
130
Q

Describe how proliferative DR appears

A

Retinal neovascularisation - may lead to vitreous haemorrhage
Fibrous tissue forming ant to retinal disc

131
Q

Describe the features of retinitis pigmentosa

A

Primarily affects the peripheral retina leading to tunnel vision
Features:
- night blindness
- tunnel vision

On fundoscopy = blocks bone spicule-shaped pigmentation on peripheral retina

Finals (25 decks)

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