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Opthalmology > 4- Ophthalmology (Transient visual symptoms) > Flashcards

4- Ophthalmology (Transient visual symptoms) Flashcards

1
Q

Transient visual symptoms last how long

A

lasts <24 hours
- Migraine
- Amaurosis fugax
- Papilledema

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2
Q

migraine background

A
  • Complex neurological condition that cause headache and other associated symptoms including aura
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3
Q

types of migraine

A
  • Migraine without aura
  • Migraine with aura
  • Silent migraine (migraine with aura but without a headache)
  • Hemiplegic migraine
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4
Q

triggers of migraine

A

Triggers
- Stress
- Bright light
- Strong smells
- Chocolate, caffeine, wine
- Dehydration
- Menstruation
- trauma

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5
Q

pathophysiology of migraine

A

No simple explanation

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6
Q

Presentation of migraine

A
  • Typical headache symptoms
    o Mod to severe
    o Pounding or throbbing
    o Usually unilateral
    o Photophobia
    o Phonophobia
    o With or without aura
    o Nausea and vomiting
  • Aura
    o Sparks in vision
    o Blurring vision
    o Lines across vision
    o Loss of different visual fields
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7
Q

Acute management of migraine

A
  • Paracetamol
  • Triptans (sumatriptans 50mg as the migraine starts)
  • NSAIDS
  • Antiemetics e.g. metoclopramide
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8
Q

Prophylactic management of migraine

A
  • Propranolol
  • Topiramate (teratogen)
  • Amitriptyline
  • Acupuncture
  • Vitamin B2 (riboflavin)
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9
Q

Amaurosis fugax
Background

A
  • Means ‘transient darkening’ -> temporary loss of vision through one eye, which returns to normal afterwards
  • Also known as retinal transient ischaemic attack
  • Due to transient ischaemia and may be a feature of embolic, thrombotic, vasospastic or haematological problems
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10
Q

amaurosis fugax risk factors

A
  • Most common in adults >50
  • Diabetes
  • Smoking
  • Tobacco
  • Cocaine use
  • Hypertension and hyperlipidaemia
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11
Q

Pathophysiology of amaurosis fugax

A
  • Most commonly associated with thrombotic vascular events originating from the internal carotid arteries -> possible warning sign for an impending stroke
  • Leads to hypoperfusion of the retina -:> most often a atherosclerotic emboli
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12
Q

Causes amaurosis fugax

A
  • Transient ischaemic attacks e.g. if a small blood clot or cholesterol plaque, which ahs broken off from a diseased blood vessel and has passed through the circulation at the back of the eye
  • Giant cell arteritis
  • Takayasu’s arteritis
  • Sickle cell disease
  • Carotid artery stenosis
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13
Q

Investigations for amaurosis fugax

A
  • Eye examination
  • Blood tests e.g. FBC< blood glucose, lipid levels
  • Doppler US and angiography
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14
Q

presentation of amaurosis fugax

A

Presentation
- Shutter coming down across vision or curtains coming acrosse eye
- Sudden
- Can last from a few minutes to a couple of hours
- Painless

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15
Q

management of amaurosis fugax

A

Management
- Control and treat underlying vascular risk factors such as hypertension, diabetes and hyperlipidaemia
- Anticoagulants e.g. aspirin and clopidogrel
- Carotid stenosis stenting/ endarterectomy

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16
Q

papilledema background

A
  • Optic disc swelling secondary to elevated intracranial pressure
  • In contrast to other causes of optic disc swelling, vision is usually well preserved with acute papilledema
  • Nearly always bilateral and may develop over hours to weeks
17
Q

Patient with suspected optic disc swelling or specifically papilledema should be considered to have an

A

intracranial mass until proven otherwise

18
Q

papilledema pathophysiology

A

The optic nerve sheath is continuous with the subarachnoid space, so that increased ICP is transmitted to the subarachnoid space surrounding the optic nerve.

The anterior end of the optic nerve stops quite abruptly at the eye. The pressure prevents axonal flow back along the nerve, causing swelling and protrusion of the optic nerve at its head into the globe.

19
Q

causes of papilledema

A

Causes- anything that increases intracranial pressure
- Malignant hypertension
- Any tumours of SoL of the CNS
- Idiopathic intracranial hypertension
- Decreased CSF reabsorption e.g. venous sinus thrombosis, subarachnoid haemorrhage
- Increase CSF production
- Obstruction of ventricular system
- Meningitis

20
Q

What is idiopathic intracranial hypertension (IIH)?

A

Raised intracranial pressure in the absence of a mass lesion or of hydrocephalus. It is often idiopathic. Idiopathic intracranial hypertension (IIH) appears to be due to impaired cerebrospinal fluid (CSF) absorption from the subarachnoid space across the arachnoid villi into the dural sinuses.

Idiopathic intracranial hypertension can lead to significant visual impairment, so prompt recognition and treatment are needed to prevent potentially permanent visual changes including partial or total loss of vision.

21
Q

IIH most commonly occurs in

A

Idiopathic intracranial hypertension most frequently occurs in obese women of childbearing age.

22
Q

presentation of papilledema

A

Presentation
- Headache that grows worse when lying down
- Nausea and vomiting
- Reduced visual field
- Short spurts of gray, blurred or double vision
- Sudden difficulty seeing colours

23
Q

ocular findings for papilledema

A
  • Optic disc swelling (usually bilateral, sometimes asymmetrical).
  • Venous engorgement (typically the first sign in papilloedema).
  • Absent venous pulsation (may be absent in papilloedema).
  • Haemorrhages over or adjacent to the optic disc.
  • Blurring of optic margins.
  • Elevation of optic disc - if the disc is significantly swollen it may be hard to focus on the whole of it at the same time.
  • Radial retinal lines (Paton’s lines) radiating out from the disc.
  • Visual field defects - eg, an enlarged blind spot.
  • VA - may remain relatively intact in mild-to-moderate papilloedema and in many other causes of optic nerve swelling.
  • Impaired colour vision, red desaturation.
  • May have an RAPD or a VI cranial nerve palsy.
24
Q

What causes a blind spot?

A

Everyone has a normal blind spot that’s about as big as a pinhead. In this spot, the optic nerve passes through the retina, where there are no photoreceptors there to detect light. No light-detecting cells means the eye can’t send signals to the brain.

25
Q

Classification of papilledema

A

Frisen Scale

26
Q

investigations for papilledema

A

Investigations
- Fundoscopy
- Check visual acquity with Snellen chart
- Assess relative afferent pupillary defect (RAPD) with flashlight test
- Check for colour impairment
- Further tests: head MRI and lumbar puncture

27
Q

management of papilledema

A

treat condition causing RICP

28
Q

prevention of papilledema

A
  • Manage high blood pressure
    o E.g. surgery to treat bleed or tumour
  • If idiopathic intracranial hypertension -> weight loss and a diuretic e.g. Acetazolamide (carbonic anhydrase inhibitor)
  • Bacterial infection – antibiotics

Opthalmology (16 decks)

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