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Ophthamology > Approah to Visual Loss > Flashcards

Approah to Visual Loss Flashcards

1
Q

Conditions than can cause acute loss of vision and other ‘red flag’ conditions presenting with visual loss

A 
Acute angle closure glaucoma
Central Retinal artery occlusion
Retinal detachment 
Giant Cell Arteritis 
Papilloedema - raised ICP
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2
Q

Causes of Ptosis

A
  • Neurogenic Causes
    • Eg: CNIII Palsy, Horner’s Syndrome
  • Myogenic Causes
    • Eg: Myaesthenia Gravis, Myotonic Dystrophy
  • Aponeurotic Causes
    • Eg: Involutional
  • Mechanical Causes
    • Eg: Orbital tumors, oedema, scarring
  • Pseudoptosis
    • Eg: contralateral lid retraction
  • Mitochondrial Disease
    • Eg: Chronic Progressive External Ophthalmoplegia
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3
Q

What is a test on examination can differentiate myasthenia gravis as a cause of ptosis?

A

Ice - test. Ptosis will improve with application of cold. Note, the ptosis will also be bilateral.

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4
Q

Horner’s Syndrome - what are the three features and the clinical correlation

A

Partial Ptosis, miosis, anhidrosis (lack of sweating).
Due to interruption of the sympathetic nervous system supply to the eye.
Miosis = constricted pupil (i.e. lose dilation)

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5
Q

What are some causes of Horner’s Syndrome?

A

Interruption of the SYMPATHETIC nerve supply to the eye:

  • brainstem stroke/lesion
  • brachial plexus lesion
  • tumour of lung apex (Pancoast’s tumour)
  • lesion of the post-ganglionic neuron
  • dissecting carotid aneurysm, carotid artery ischaemia
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6
Q

Pattern of vision loss in Retinitis pigmentosa

A

annular scotoma
+ typically affects rods = poor night vision.
Presents in young adults

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7
Q

Fundus examination in retinal vein occlusion

A

hemorrhages
cotton wool spots
macular oedema
+ RAPD and reduced visual acuity on examination

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8
Q

Clinical Presentation of Giant Cell Arteritis

A

○ Scalp tenderness
○ Headache
○ Jaw claudication

- Acute, unilateral vision loss
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9
Q

Which rheumatological condition is associated with GCA?

A

Polymylagia rheumatica

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10
Q

How is GCA diagnosed and treated

A

Requires temporal artery biopsy (+ look for raised ESR).

Mx = high dose steroids

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11
Q

What is the presentation of Optic Neuritis

A
  • reduced colour saturation - often red desaturation
  • RAPD
  • swollen optic disc (though fundus can look normal in some)
  • pain on eye movement
  • visual field defect
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12
Q

Causes of Optic Neuritis

A
  • MS = most common cause
  • Infection e.g. syphilis, HSV
  • autoimmune conditions - SLE, neurosarcoidosis
  • IBD
  • drug induced - ethambutol, isoniazid
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13
Q

Causes of Optic Neuropathy

A

Optic Neuropathy = damage to the optic nerve due to any cause.

  • GCA/AION
  • NAION - patients 50+ at risk, + systemic vascular disease (see small cup-to-disc ratio and altidunal visual field defect)
  • compression (e.g. tumour pressing on optic nerve) - slowly progressive. See optic atrophy or oedema, often central scotoma.
    other
  • inflammatory (e.g. SLE, IBD)
  • infiltrative (e.g. malignancies such as lymphoma)
  • toxic - ethambutol
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14
Q

Causes of cataracts

A
  • Congenital cataract - dx often at birth
    • Drugs (steroids, amiodarone)
    • Trauma (including intra-ocular surgery)
    • Systemic disease
    • Diabetes Mellitus, myotonic dystrophy, Wilson’s disease, atopic dermatitis.
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15
Q

Clinical presentation of cataracts

A

Progressively more blurry - may need to change glasses prescription.
General/diffuse visual decline
Glares, colour less bright
Halos around lights

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16
Q

Opacity of the lens, cloudy, discoloured seen on slit-lamp examination.
Decreased red reflex
Improvement of visual acuity with pin hole

NO distortion of image on Amsler grid
What is the likely condition?

A

Cataracts

17
Q

Risk Factors for Macular degeneration

A 
Age related - genetic + environmental.
Risk factors
	- Age
	- FHx
	- Smoking
	- HTN, obesity, hypercholesterol
18
Q

What is Macular Degeneration?

A

Painless, irreversible, degenerative eye condition. Associated with the damage and ultimately death of photoreceptors.

19
Q

What is the appearance of the fundus in a patient with macular degeneration

A

early - see drusen and/or pigment changes
may see atrophy
exudates, haemorrages

20
Q

Clinical Presentation of macular degeneration

A

Central vision loss
Limited vision - particularly at night
Metamorphopsia (grid of straight lines appear wavy) may be present in severe cases.
WET MACULAR DEGENERATION - can occur rapidly over weeks-months

21
Q

What is a key examination finding in macular degeneration that differentiate it from cataracts?

A
  • distortion of image on Amsler grid

- NO improvement with pin hole

22
Q

What is the treatment approach in macular degeneration

A

aim is to detect early and slow progression.
in dry macular degeneration - dietary (antioxidants, lueitin, vitamins) + manage HTN + smoking cessation. However, still progressive with no cure.

Wet macular degeneration

  • photodynamic therapy (coagulate leaky vessels)
  • anti-VEGF intra-vitreal injections
23
Q

Painful loss of vision + fixed and mid-dilated pupil. DDx?

A

This presentation is suspicious for acute-angle closure glaucoma.
Vision may also be blurry
Will also see increased IOP on examination.

24
Q

What is the clinical presentation of acute-angle closure glaucoma.
Compare this to primary angle closure glaucoma

A
  • painful loss of vision, may have N&V
  • blurring of vision
  • redness of the eye
  • may report halo around lights

POAG = often silent, more chronic. But may have headache, halos, previous ocular disease, FHx

25
Q

How is acute angle closure glaucoma treated?

A
  • Acetazolamide (IV stat dose then PO) → Carbonic anydrase Inhibitor
    • Topical beta blocker e.g. timolol
    • Topical steroid
    • Can add alpha agonist
      +
    • Analgesia and anti-emetics to provide comfort and therefore reduce IOP.
      Then 1 hour after beginning treatment
    • Pilocarpine (a miotic) to open the angle
      Definitive treatment → Laser peripheral iridotmoy (and can also be done prophetically).
26
Q

What classes of drugs are used in treating primary open angle glaucoma?

A
  • beta-blockers
  • carbonic anhydrase inhibitors
  • alpha-2 adrenoceptor antagonists
  • prostaglandin analogues

Ophthamology (2 decks)

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