DIS - Optic Nerve IV - Week 10 Flashcards
List two ways in which build up of toxic substances can lead to dysfunction.
Can interfere with ATP bioavailability
Can lead to ion channel dysfunction
Are toxic and nutritional neuropathies acute or chronic?
Slow, chronic progressive loss
-takes months eather than days/weeks
List 6 aggravating factors for toxic and nutritional neuropathies.
Heavy alcohol use Heavy smoking Recreational and illicit drug use Exposure to workplace chemicals Dietary intake Use of systemic medications
What kinds of workplace chemicals can potentially aggravate toxic/nutritional neuropathies (7)?
Glues Lead Pesticide Radiators Paints Solvents Plastics
What two aspects of dietary intake can potentially aggravate toxic/nutritional neuropathy?
Malnutrition
Ingestion of food containing toxins
List three vitamin and mineral deficiencies that can aggravate toxic/nutritional neuropathy.
Vitamin B12
Folate
Copper
List four systemic medications that can aggravate toxic/nutritional neuropathy.
Digitalis
Chloramphenicol
Chloroquine
Phenothiazine
If affected by toxic/nutritional neuropathy, would you expect it to be uni- or bilateral? Would pain be involved? What happens to the RNFL? What is a consequence of this (include what section of the ONH involved)?
Bilateral and painless
Papillomacula RNFL loss
Temporal optical atrophy
-due to injured papillomacular bundle
What may be one of the first signs of toxic/nutritional neuropathy and is it proportionate to VA loss?
Dyschromatopsia
-disproportionate to VA loss
How are visual fields typically affected with toxic/nutritional neuropathy (2)? What VF test would you consider doing?
Central or cecocentral scotoma
-consider 10-2
What eventually happens to the ONH with toxic/nutritional neuropathy? What happens initially?
Diffuse optic disc pallor
Begins temporally initially
What ocular motility problems may occur with toxic/nutritional neuropathy?
Nystagmus
What may be seen at the macula with toxic/nutritional neuropathy?
Crystal deposits
What kind of haemorrhages may be seen with toxic/nutritional neuropathy?
Flame haemorrhages
What may happen to the RPE with toxic/nutritional neuropathy (appearance)?
Salt and pepper fundus
What corneal changes may occur with toxic/nutritional neuropathy?
Corneal pigment deposits
What may happen to the retinal blood vessels with toxic/nutritional neuropathy?
Small retinal vessel tortuosity - telangiectasia
What should you do if you suspect toxic/nutritional neuropathy (4)? What referral can be made?
Dilated fundus exam -rule out other retinal causes Extensive history taking Check VA Patient education -need to stay clean of drugs Referral to GP for serological testing and treatment
What are two possible treatment options for toxic/nutritional neuropathy?
Zinc and vitamin B supplements
Would you expect ischaemic neuropathy to occur following closure of the short posterior ciliary artery? Explain why. Mention what generally occurs with young patients regarding ischaemic insult and what happens with age.
Doesnt lead to ischaemic neuropathy due to many anastamoses
May explain why young patients are resistant to ischaemic insult
Ageing reduces autoregulatory capacity or collateral systems, increasing ischaemic potential
What are two general causes of acute blood flow compromise? Explain.
Generally embolic
-blood clot or something else (gas bubble) becomes stuck in a blood vessel and obstructs flow
Thrombic
-inflammation > sticky platelets > blood clot develops > reduces flow
What is generally the cause of chronic blood flow compromise? Explain (4).
Hypoperfusive
-low arterial pressure reduces blood flow
List three possible causes of reduced or slowed down blood flow.
Compromised metabolism
Local inflammatory response
Blood vessel wall damage
List the two types of ischaemic neuropathy, and note which is more common. For this type, note what structure it affects and what main vascular supply is involved.
Anterior and posterior
Anterior is more common
-affects the ONH
-main vascular supply - posterior ciliary arteries
Is posterior ischaemic neurpathy commonly seen? What kind of diagnosis is it? What two regions does it involve and what is the main vascular supply involved?
Not often seen
Diagnosis of exclusion
Retrobulbar/intraorbital region affected
Main vascular supply - pial vascular plexus
List the two types of anterior ischaemic optic neuropathy.
Arteritic
Non-arteritic
What is the general cause of arteritic AION? What can it lead to (3)?
Generalised arterial inflammation affecting local arterial walls
Leads to thrombus formation
-can give embolus
SPCA occlusion
What is the general cause of non-arteritic AION (3)? What can it lead to?
Low perfusion pressure at the ONH
Local slowing down of blood
Arterial ischaemia/wall compromise
Leads to thrombus formation
List two possible mechanisms for arteritic AION.
Inflammation of arteries supplying the ONH leading to possible occlusion
Inflammation due to giant cell (temporal) arteritis
What is rumbolds disease also known as? What is it and what is damaged? Why is it called giant cell arteritis?
Giant cell arteritis
Degeneration of arterial smooth muscle
Damage to elastic lamina
Macrophages form giant cells, coalesce and ingest material
List 10 medium and large sized arteries that may be inflammed with giant cell arteritis, listing four of those with ocular involvement first.
SPCA LPCA CRA Cilioretinal artery (if present) Facial Temporal Carotid Verebral Renal Aorta
List 5 symptoms of giant cell arteritis due to cranial vessel involvement.
Headache Jaw claudication Scalp tenderness Loss of vision Abnormalities of the temporal artery