Ophthalmology Flashcards

1
Q

List the differentials for painless red eye

A

Episcleritis
Subconjunctival haemorrhage
conjunctivitis

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2
Q

List differential causes of a painful red eye

A
Acute angle closure glaucoma
Anterior Uveitis
Scleritis
Keratitis
Corneal ulcers/abrasions
Foreign body
Trauma
Chemical injury
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3
Q

Describe cataract and it’s risk factors

A

Opacification and clouding of the lens (which is avascular)

Older age
Congenital (TORCH infections)
Smoking
Alcohol (dehydration)
Iatrogenic -> steroids, vitrectomy, IV injections
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4
Q

What are the S/S of cataract?

A

Change in colour vision (becomes more brown/yellow)
Vision worse at night -> glare and starbursts around lights
Myopic shift (become short sighted i.e. cannot see things far away)
Protein aggregation and lens opacification
Reduced VA
Loss of red reflex

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5
Q

Define phakic, aphakic and pseudophakic

A

Phakic = natural lens
Aphakic - eye has no lens
Pseudophakic - lens has been artificially replaced

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6
Q

What is the treatment for cataracts?

A

Conservative - do nothing if not severe

Phacoemulsification (uses USS) to emulsify lens and then replace with new one

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7
Q

Describe complications of cataract surgery

A

Endophthalmitis = inflammation of inner eye, 3-5 days post op, needs treated with intravitreal antibiotics

Retinal detachment

Acute angle closure glaucoma (cataract proteins can leak into the anterior chamber)

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8
Q

Define glaucoma

A

Group of eye diseases resulting in damage to the optic nerve, often due to increased IOP

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9
Q

Describe the production and flow of aqueous humour in the eye

A

Produced by the ciliary body, flows from the posterior chamber around the iris to the anterior chamber, drains through trabecular meshwork (through Canal of Schlemm) into general circulation

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10
Q

Describe the classifications of glaucoma and describe the pathophys behind each

A

Open or closed angle
Acure or chronic
Primary or secondary

Open = there is resistance to flow of aqueous humour through the trabecular network

Closed = Iris pushed forwards against the cornea and blocks flow of aqueous humour into the trabecular mesh

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11
Q

What are the risk factors for acute angle closure glaucoma?

A
Age
Hypermetropia (long-sighted and having a smaller eye)
FHx
East Asian/Chinese
Shallow anterior chamber
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12
Q

What are the risk factors for open angle glaucoma?

A
Age
Black
Myopic (short-sighted i.e. bigger eye)
Smoking
Diabetes
HTN
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13
Q

What is the classical S/Sx of glaucoma?

How is glaucoma investigated?

A

Halos around lights at night
Peripheral vision affected
Increased cup:disc ratio >0.5

(Goldmann applanation) tonometry = measuring pressure
Fundoscopy - assess for disc cupping
Visual fields

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14
Q

How is open angle vs closed angle glaucoma treated?

A

Open angle:
- prostaglandins (latanoprost) to increase outflow of fluid
- beta blocker (timolol) to reduce fluid production
- carbonic anhydrase (dorzolamide) - reduce aqueous humour production
- Sympathomimetics (brimonidine) - increase outflow and reduce fluid production
(surgical = trabeculectomy)

Closed angle:

  • pilocarpine (muscarinic receptor agonist which constrict pupil to open up the pathway for aqueous humour to flow)
  • acetazolamide 500mg oral (carbonic anhydrase inhibitor) to reduce fluid production
  • then same drugs as open ^^^
    (surgical: Iridotomy, trabeculectomy)
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15
Q

Describe AMD and its subtypes

A

Age related macular degeneration
Progressive degenerative disease involving macula
Dry (atrophic) or wet (exudative - caused by choroidal neovascularisation)

Dry = 90%, Wet = 10%

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16
Q

What are the presenting features of macular degeneration?

Describe pathophysiology

A

Reduced VA
Central vision lost / metamorphopsia
Normal peripheral vision

Pathophysiology:
- Disruption of Bruch’s layer and RPE cells

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17
Q

What are the risk factors for AMD?

A
Smoking
Increasing age
HTN
CVD
FH
Female
Hypermetropia
Caucasian
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18
Q

What are the fundoscopy findings in wet vs dry AMD?

A

Dry: macula drusen, RPE hyperpigmentation
Wet: haemorrhages, lipid exudates, neovascularisation…

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19
Q

How is AMD investigated?

What is the treatment for AMD?

A

VA
Fundoscopy (look for drusen vs neovascularisation)
Amsler chart (look for metamorphopsia)
Fluoroscein angiogram - to show neovascularisation

Dry - no treatment (reduce RFx e.g. stop smoking)
Wet - Intravitreal injections (Anti-VEGF)

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20
Q

Differentiate scleritis and episcleritis

A

Episclera = between conjunctiva and sclera

Sclera = the white outer coating of the eye (under the episclera)

Episcleritis = mild pain and self-limiting, blanches with phenylephrine

Scleritis = acute red eye, pain on movement and keeps awake at night, associated with RA and GPA, does not blanch with phenylephrine

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21
Q

What is Charles Bonnet syndrome?

A

Where visual hallucinations occur as a result of visual loss
Not related to psychosis/dementia
The patient is very aware that their hallucinations are not real

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22
Q

What are the S/Sx of acute angle closure glaucoma

A
Sudden onset painful red eye
Blurry vision
Photophobia
Headache
Halos around lights
N&V
Hazy cornea (oedema)
Mid-dilated fixed pupil
Iris bombe
Reduced VA
Closed angle on gonioscopy
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23
Q

Describe endophthalmitis and how it may present

A

Infection of the aqueous +/- vitreous humour which causes inflammation in the eye
Most commonly occurs post-op from cataract surgery

Onset 1-7 days post-surgery 
Disproportionate/increasing post-operative inflammation
Hypopyon 
Pain 
Worsening vision 
Posterior segment inflammation 
RAPD 
Lid swelling
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24
Q

Define central retinal artery occlusion and its risk factors

A
= blockage of the retinal artery which carried oxygen to the nerve fibres in the retina
RFx:
- HTN
- ageing
- glaucoma
- DM
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25
Q

How is CRAO caused?

A

Atherosclerosis
Suggestive if: HTN, diabetes, hypercholesterolaemia, smoking
Embolism: Carotid artery disease, valvular disease
Inflammatory: GCA
Medications: OCP, cocaine
Sickle cell disease

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26
Q

What are the clinical features of CRAO?

A
Sudden onset, unilateral, 
PAINLESS vision loss 
White swollen retina with a
 ‘cherry red spot’
RAPD
Visible emboli (25%)
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27
Q

How is CRAO investigated and treated?

A
Fundoscopy 
ESR/CRP – rule out GCA
OCT: inner retinal atrophy with outer retinal preservation 
Fluorescein angiography 
Carotid artery US 

Mgx: depends on cause

28
Q

Distinguish between pre-septal and orbital cellulitis

A

Pre-septal cellulitis: Inflammation of eyelid/ soft tissues, ANTERIOR to the orbital septum
Usually from Trauma/ bacteraemia (e.g. bite, penetrating injury, foreign body)

Orbital cellulitis: inflammation of the soft tissue within the orbit POSTERIOR to the orbital septum (i.e. muscles, fat and connective tissue)
Often secondary to paranasal sinusitis (as sinuses surround orbit)

Orbital septum = membranous sheath which acts as the anterior boundary of the orbit, connecting orbital rims to eyelids

29
Q

How do pre-septal and orbital cellulitis present

A

Pre-septal: Lid erythema, inflammation, tenderness, warmth, rarely fever, NO VISUAL CHANGE

Orbital: same as above + fever, conjunctival swelling (chemosis), proptosis, painful/ limited eye movement + diplopia (due to inflammation of muscles/ cranial nerves), reduced VA/ RAPD (due to optic nerve involvement)

30
Q

What are the complications of orbital cellulitis

A
Sepsis
Orbital compartment syndrome
Central spread of infection
Meningitis – Spread to meninges
Cavernous sinus thrombosis
Cerebral abscess
Blindness – due to pressure on optic nerve/ thrombotic ischemia of optic nerve vessels
31
Q

When the eyeball is looking medially, which muscle controls upwards gaze?

A

Inferior oblique

32
Q

What is the most common cause of a 3rd nerve palsy?

A

ANEURYSM - vasculopathic patient

33
Q

What is the most common cause of a 4th nerve palsy?

A

Congenital or trauma

34
Q

What is the most common cause of a 6th nerve palsy?

A

Raised ICP

35
Q

What is the most common type of retinal detachment?

A

Rhegmatogenous = separation of the vitreous from the retina -> retinal tear then occurs -> wallpaper theory -> separation of neurosensory retina from RPE

36
Q

What are the risk factors for a retinal tear

A

Cataract surgery
Trauma
DM
Myopia (larger eyes when short sighted, increased stretching of retina)

37
Q

What are the signs/symptoms of retinal detachment

A

4F’s

  • flashes
  • floaters
  • field loss (corresponding to area of detachment)
  • fall in VA
38
Q

List the differentials for ‘flashing lights’

A
Posterior vitreous detachment
Retinal tear
Retinal detachment
Occular migraine
Postural hypotension
TIA etc...
39
Q

List the differentials for ‘sudden painless visual loss’

A
Vitreous haemorrhage
Retinal vein occlusion
Retinal artery occlusion
Retinal detachment
Amaurosis fugax
CVA
Anterior ischaemic optic neuropathy
40
Q

Describe the pathophysiology of diabetic retinopathy

A

Microvascular changes
Basement membrane thickening
VEGF response
Neovascularisation and leaky vessels

41
Q

How is diabetic eye disease classified?

A

Can get retinopathy (non-proliferative or proliferative)
Can get maculopathy

Non-proliferative retinopathy can be:
- mild = microaneurysms
- moderate = hard exudates and cotton wool spots
- severe = dot haemorrhages in 4 quadrants
Proliferative retinopathy = neovascularisation

42
Q

Describe the treatment of DR

A

Non-invasive:

  • BP, lipid and BM control
  • smoking cessation

Invasive (once neovascularisation has occurred):

  • anti-VEGF injections
  • laser treatment
  • vitrectomy
43
Q

What are the complications of DR

A
Retinal detachment
Vitreous haemorrhage
Cataracts
Optic neuropathy
Rebeosis iridis
44
Q

Describe the types of conjunctivitis, how they present and their treatment

A

Bacterial - usually unilateral, green discharge, good hygiene and self limiting or treat with topical Abx

Viral - bilateral, pre-auricular LNs often involved, clear discharge, self-limiting/use lubricating drops

Allergic - bilateral, swollen, itchy eyes. No LN. Treat with antihistamines/anti-inflammatories

45
Q

What is keratitis

A

Inflammation of the cornea

46
Q

Compare and contrast bacterial vs viral vs fungal keratitis

A

Bacterial

  • caused by staph/strep/pseudomonas
  • rapid onset, photophobia, reduced VA, hypopyon sometimes
  • treat with Abx
  • circular on fluoroscein staining

Viral

  • insidious onset
  • pain, reduced VA, vesicles around eye
  • commonly caused by herpes simplex ( = herpes keratitis) or VZV
  • look for Huchinson’s sign = nose vesicles are a predictor of optic ZOSTER involvement
  • Treat with PO aciclovir
  • will see dentritic spiky ulcers on fluoroscein staining

Fungal -> shows cloudy, white, spreading fluffy lesions, caused by vegetative matter getting into the eye

47
Q

Compare and contrast scleritis vs episcleritis

A

The coverings of the eye from outer to inner are:

  • conjunctiva
  • episcleritis
  • scleritis

Scleritis

  • painful, severe, awake at night
  • diffuse red eye
  • associated with RA/SLE/granulomatosis + PA
  • does NOT blanch with phenylephrine
  • treat with NSAIDs/steroids

Episcleritis

  • mild pain
  • sectoral red eye
  • DOES blanch with phenylephrine
  • usually self-limiting but NSAIDs/steroids may be required
48
Q

Describe uveitis and the features of anterior uveitis

A

Uveitis = inflammation of uveal tract = iris + ciliary body + choroid

Anterior uveitis = mainly inflammation of iris. Associated with HLA-B27 diseases.
Fts:
- painful red eye
- photophobia
- small fixed pupil (synechiae form and pupil may be abnormal shape)
- hypopyon in anterior chamber
Treatment:
- steroids
- mydriatics (dilating drops)
49
Q

What are the complications of anterior uveitis

A

Cataract
Glaucoma
Macular oedema

50
Q

Describe a retrobulbar haemorrhage and the signs/symptoms

A
Emergency
Bleeding within the orbit
Causes orbital compartment syndrome
Fts:
- pain
- reduced VA
- RAPD
- increased IOP
- proptosis
- reduced eye mobility
51
Q

How is retrobulbar haemorrhage treated?

A

Lateral canthotomy procedure -> emergency decompression by cutting open eyelid

52
Q

Describe the nerve control and neurotransmitters behind

a) pupil constriction
b) pupil dilation

A

a) constriction = parasympathetic, CN3, uses ACh

b) dilation = sympathetic, uses NA/A

53
Q

List causes of abnormal pupil shape

A

Anterior uveitis and synechiae formation
Acute angle closure glaucoma (causes ischaemic damage to iris muscles)
Coloboma (congenital malformation)
Tadpole pupil (temporary spasm of segment of pupil seen in migraine)

54
Q

List causes of mydriasis

A

Dilated pupil

  • Holmes Ades pupil
  • 3rd nerve palsy
  • anticholinergics (oppose ACh in the parasympathetic system)
  • cocaine
  • raised ICP
55
Q

List causes of miosis

A
  • Horners syndrome
  • Argyll-Robertson pupil
  • Pilocarpine (muscarinic receptor agonist used to treat acute angle closure glaucoma)
56
Q

Describe features of a 3rd nv palsy

A

ptosis
dilated, non-reactive pupil
down and out position of the eye

57
Q

Describe the differences between medical and surgical 3rd nv palsy

A

Medical = pupil sparing, as outer parasympathetic fibres are spared. Usually a microvascular cause e.g. diabetes, HTN, ischaemia

Surgical = pupil affected, usually a physical compressive cause which affects the outer parasympathetic fibres e.g. tumour, trauma, raised ICP, cavernous sinus thrombosis, posterior communicating artery aneurysm

58
Q

What are the features of Horner’s syndrome and list causes based on the 3 regions of the sympathetic tract which can be affected

A
= ptosis, miosis, anhidrosis
- damage to the sympathetic supply to the eye which can be:
CENTRAL - S
- cyst in spinal cord (syringomyelia)
- Stroke
- MS
- Swelling (tumour)

Pre-ganglionic = THORACIC - T

  • Tumour (pancoast)
  • Trauma
  • Thyroidectomy
  • Top (cervical) rib

Post-ganglionic (CERVICAL) - C

  • carotid aneurysm
  • carotid artery dissection
  • cavernous sinus thrombosis
  • cluster headache
59
Q

How can the site of the sympathetic lesion be worked out?

A

Based on the presence of anhidrosis!
Central lesion - anhidrosis of face, arms and trunk
Pre-ganglionic - anhidrosis of face
Post-ganglionic - no anhidrosis

60
Q

How can you test for Horner’s syndrome

A

Cocaine eye drops
Stop noradrenaline reuptake at the NMJ and make it hand around for longer
This would cause a normal eye to DILATE as more NA stimulates iris dilator muscles

In Horner’s syndrome, there is no NA in the first place, so cocaine eye drops DO NOT CAUSE DILATION

61
Q

Describe a Holmes-Adie pupil and what is Holmes-Adie syndrome

A
  • unilateral dilated pupil
  • cause unclear ?viral
  • damage of post-ganglionic sympathetic fibres

Holmes-Adie syndrome = HA pupil + absent knee and ankle reflexes

62
Q

Describe an Argyll-Robertson pupil

A
  • specific finding in neurosyphilis
  • constricted pupil
  • accommodates but does not react to light
63
Q

Describe the cause and presentation of central retinal vein occlusion

A

*Central retinal artery vs vein occlusion cannot be distinguished from history -> both present with sudden painless visual loss!

Cause - usually atherosclerotic
Features on examination:
- tortuous vessels
- disc swelling/oedema
- flame haemorrhages on the retina
- macular oedema
64
Q

Describe the presentation of posterior vitreous detachment

A

Vitreous humour detached from retina
PAINLESS
Spot of visual loss
Flashing and floaters

No treatment needed, brain adjusts to areas of visual loss over time

65
Q

Describe what can progress from posterior vitreous detachment

A

Posterior vitreous detachment -> retinal tears (where vitreous fluid can travel under the retina) -> retinal detachment

66
Q

Describe the presentation of retinal detachment

A

SIGHT THREATENING as the retina is detached from the choroid, and the retina gets its blood supply via diffusion from the choroid

Fts:

  • painless
  • peripheral visual loss (like a curtain coming)
  • blurred/distorted vision
  • flashes and floaters