Eye in Systemic Disease (neurological conditions) Flashcards

1
Q

what are the main features of neuro-ophthalmic disease

A

eye movement defects- double vision

visual defects- visual acuity, field loss

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2
Q

what is the biggest cause of eye problems

A

microvascular disease

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3
Q

what is de-myelination

A

loss of myelin shealth from (optic) nerve making it inefficient

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4
Q

what are inter-nuclear ophthalmoplegia (INO)

A

lesion affects medial longitudinal fasciculus (MLF) (inter nuclear connections) resulting in cranial nerve 3 and 6 being unable to coordinate their signals

=when the patient’s gaze is directed away from the side of the lesion, the ipsilateral (adducting) eye will not adduct and the contralateral (abducting) eye demonstrates horizontal nystagmus

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5
Q

what are supra nuclear defects

A

when problem with occular motility arises from an area before the cranial nerves

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6
Q

what muscles are affected by a 6th nerve palsy

A

lateral rectus (inability to abduct eye)

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7
Q

what type of diplopia will someone with a 6th nerve palsy get

A

horizontal

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8
Q

what can cause a 6th nerve palsy

A

microvascular
raised ICP
tumour
congenital

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9
Q

why is the 6th cranial nerve susceptible to raised ICP

A

as comes up from bottom of brain stem over the petrous tip

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10
Q

what causes papilloedema

A

raised ICP

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11
Q

what nerve is affected by a fourth nerve palsy

A

superior oblique (in ability to look medially (intorsion) and down (deoression in adduction), with palsy eye will lift when look medially)

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12
Q

what nerve palsy do you get a head tilt in

A

trochlear (IV) nerve palsy as trying to lift head to match high eye

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13
Q

what are the actions of superior oblique muscle

A

intorsion (adduction)
depression in adduction
weak abduction

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14
Q

what can cause a IVth nerve palsy

A

congential decompensated (will have double vision)
microvascular
tumour
bilateral (closed head trauma)

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15
Q

what is a compensated nerve palsy

A

where brain is still able to fuse two fields of vision so wont have diplopia

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16
Q

what is the longest cranial nerve. why is this important

A

trochlear- 4th

comes out of posterior brain stem- susceptible to trauma

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17
Q

what muscles does the occulomotor nerve supply (III)

A
medial rectus
inferior rectus
superior rectus 
inferior oblique 
sphincter pupillae 
levator palpebrae superioris
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18
Q

what muscle palsy causes ptosis

A

levator palpaebrae superioris- CN III

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19
Q

what are the signs of a III nerve palsy

A

ocular position= down and out (lateral rectus and superior oblique only ones working)

droopy lid - ptosis

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20
Q

what can cause a III nerve palsy

A
microvascular
tumour 
aneurysm (close to circle of willis)
MS
congenital
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21
Q

what can cause a PAINFUL third nerve palsy

A

aneurysm

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22
Q

what causes a PUPIL SPARING III nerve palsy

A

microvascular (as parasympathetics in III nerve on the outside- more likely to be affected by an aneurysm)

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23
Q

what are the key word causes of the three palsys

A

all caused by vasculopathic/ tumour

III= aneurysm 
IV= congenital/ trauma 
VI= cranial pressure
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24
Q

what can cause inter opthalmoplegia

A

MS, vascular, lots e.g. stroke

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25
Q

what is the hallmark of MS on an MRI

A

plaque in ventricles cause by demyelination

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26
Q

what are the parts of the optic pathway

A
optic nerve 
chiasm 
optic tracts 
lateral geniculate nucleus (splits and goes to different levels of the lobes- right goes to left etc)
optic radiations 
cortex (occipital lobe)
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27
Q

what can cause visual field defects

A

vascular disease
space occupying lesion
demyelination
trauma (inc surgery)

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28
Q

why is there macular sparing in vision field loss caused by the visual cortex

A

as there is so many nerves within the macula

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29
Q

what are the pathologies of the optic nerve

A

ischaemic optic neuropathy
optic neuritis (MS)
tumours- meningioma, gliomas, haemangioma (vascular tumours)

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30
Q

will optic nerve defects present with horizontal or verticle defects

A

horizontal

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31
Q

will visual defects originating from the brain be horizontal or verticle

A

verticle

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32
Q

what are the features of optic neuritis

A
progressive visual loss (unilateral)
pain behind eye (esp on movement)
colour desaturation 
central scotoma (vision loss)
gradual recovery over weeks- months
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33
Q

what is very specific to optic nerve damage

A

colour desaturation- will see differences in the colour red between eyes

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34
Q

what can follow optic neuritis

A

optic atrophy

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35
Q

what can affect the optic chiasm

A

pituitary tumour
craniopharyngioma
meningioma

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36
Q

what reflex is seen in a chiasm pathology

A

RAPD

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37
Q

what field defect will result from an optic chiasm pathology

A

bi-temporal

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38
Q

what happens to visual loss caused by pituitary tumours after the tumour is decompressed or removed

A

commonly reversed

39
Q

how are pituitary tumours removed

A

via transsphenoidal surgery

40
Q

what can affect the optic tract and radioatoins

A

tumours (primary and secondary)
demyelination
vascular anomalies

41
Q

what visual defects arise from pathologies within the optic tracts and radiations

A

homonomous
macula not spared
quadrantanopia
incongrous

42
Q

where do you know a pathology is if it is a quadrantanopia

A

after the lateral geniculate nucleus

43
Q

why dont you get raised ICP in meningiomas

A

as grows very slowly

44
Q

what pathologies can affect the occipital cortex

A
vascular disease (infarct)
demyelination
45
Q

what visual field defects do you get from pathologies in the occipital cortex

A

homonomous
macular sparing
congruous

46
Q

what visual field defects are macular sparing

A

ones originating from the occipital cortex

47
Q

what will cause lots of whits dots in a specific pattern that are all the same size in the eye

A

laser retinopathy treatment

48
Q

what is the commonest cause of blindness in the western world

A

ARMD

49
Q

what is the pathogenesis of diabetic retinopathy

A

chronic hyperglycaemia
= glycosylation of protein/ basement membrane
= loss of pericytes (cells on outer layer of capillaries)
= microaneurysm
= leakage/ ischaemia

50
Q

what are the signs of non proliferative retinopathy

A

micro aneurysms/ dot and blot haemorrhages (red small dots)
hard exudates (yellow dots)
cotton wool patches (fluffy white patches of oedematous axons on the retina)
abnormal venous calibre (vessels not smooth)
intra-retinal microvascular abnormalities

51
Q

what does ischaemia in the eye lead to

A

production of VEGF which causes neovascularisation- fragile vessels prone to haemorrhage

fibrotic scarring- shrink= retinal detachment

52
Q

what is NVE and NVD

A

NVD= neovascularisation on optic nerve head

NVE= neovascularisation in the periphery of the retina

53
Q

when does neovascularisation show that ischaemia is severe

A

if there are new vessels growing on the iris

also by the time you have NVD you have profound loss of useful vessels

54
Q

how do you know where ischaemia is in eye

A

fine white vessels show closed arteries and venules- neovasularisation should stem from here

55
Q

what is rubeosis iridis

A

when VEGF diffuses through vitreous into iris
very severe ischaemia in the eye
causes secondary glaucoma no sight restoration
neovascularisation in the iris

56
Q

why do diabetic patients go blind

A

retinal oedema affecting the fovea
vitreous haemorrhage
scarring/ tractional retinal detachment

57
Q

what are types of retinopathy

A
non proliferative (mild, moderate and severe)
proliferative retinopathy
58
Q

how do you classifymaculopathy

A

observable (vision hast deteriorated)
referable maculopathy
clinically significant maculopathy (oedema has spread to the centre of the fovea (foveal dip)

59
Q

what happens to the foveal dip when oedema hits it

A

will pop up (like an umbrella inside out) and vision blurs

60
Q

how do you manage diabetic retinopathy

A

optimise medical management of diabetes
laser- PPR (pan retinal photocoagulation), macular grid
surgery- vitrectomy
rehab- blind/ partially sighted

61
Q

how does the laser work in diabetic retinopathy

A

kills bots of retina do reduce oxygen demand to rest of eye so centre can receive more nutrients and oxygen

62
Q

are axons below or above the photoreceptors

A

above, light has to go through them to reach the photo receptors

63
Q

why does the eye look pink

A

blood vessels in the choroid showing through

64
Q

how do you treat disc neovascularisation

A

laser

65
Q

how do you treat maculopathy

A

laser macula (less used now) or injections of VEGF antibodies

66
Q

what shows the severity of hypertension in the eye

A

how the fundus looks and the retinal arteries

67
Q

why do you people have hypertensive retinopathy

A

usually malignant hypertension

68
Q

what does hypertensive retinopathy look like

A
like diabetic 
attenuated blood vessels (look like copper or silver wire)
cotton wool spots
hard exudates 
retinal haemorrhage 
optic disc oedema
69
Q

what are the features of central retinal artery occulsion

A

cattle tracking in vessels
retinal oedema (pale)
foveal dip doesnt go white as axons over this so thin they dont go oedematous
sudden painless loss of vision (v profound)
retinal nerve fibre layer becomes swollen except the fovea (cherry red spot)
rarely recovers

70
Q

why dont you get necrosis in macula in CRAO

A

as choroid supply very good here

71
Q

what are the features of central retinal vein occlusion

A
no neovascularisation 
haemorrhages 
sudden painless visual loss 
range of visual loss 
haemorrhagic and exudative process downstream from occluded vein
72
Q

why does the CRV occlude in diaebtes

A

Anulus- limited size hole for central artery and vein. When retina becomes bigger in hypertension it occludes this hole

73
Q

what is used to image the capillary bed in CRVO

A

angiogram

74
Q

what are the features of branch vein occlusion

A

painless disturbance in vision
may be assymptomatic
may be aware of loss of part of field

75
Q

what are the features of sarcoidosis

A

uveitis- keratic precipitate
lung involvement
non caseating granulomas

76
Q

what are the infective causes of uveitis

A
TB
herpes zoster (and simplex)
toxoplasmosis 
candidiasis 
syphillis 
lyme disease
77
Q

what are the non infective causes of uveitis

A
idiopathic 
HLA-B27
juvenile arthritis (not it RA)
sarcoidosis 
behcets disease
78
Q

what is the histology of GCA

A

loss of lumen size, destruction of the lamina, multinucleated giant cell accumulation

79
Q

what are the features of GCA

A
inflammation of middle sized arteries 
associated with polymyalgia rheumatica 
headache 
jaw claudication 
malaise 
raised PV 
blinding condition
80
Q

what condition is GCA associated with

A

polymyalgia rheumatica

81
Q

what are the features of thyroid eye disease

A

extra ocular:

  • proptosis (due to muscle and fat swelling)
  • lids: retraction, chemosis (conjunctival oedema), lag, pigmentation
  • restrictive myopathy (diplopia)

ocular:

  • anterior segment: chemosis, injection, exposure (cant close eye well), glaucoma
  • posterior segment: choroidal folds, optic nerve swelling
82
Q

what is the most common cause of unilateral and bilateral proptosis

A

thyroid eye disease

83
Q

how do you treat thryoid eye disease

A

medical control- carbimazole, radioiodine, surgery

84
Q

what are the eye features of SLE

A

ocular inflammation

85
Q

what are the occular features of RA

A

dry eyes (keratoconjunctivitis sicca)
scleritis
corneal melt
(doesnt give yo intraocular inflammation- affects the surface of the eye)

86
Q

what are the features of sjogrens syndrome

A
keratoconjunctivitis sicca 
xerostomia (dry mouth) 
dry featureless tongue
RA
infiltration of lacrimal glands
87
Q

what are the features of marfans

A

Displacement of the lens (zonules) spontaneously rupture
Long fingers
high arched palate
tall

88
Q

what way does the lens always dislocate in marfans

A

upwards(m for moon)

89
Q

what dermatological features can affect the eyes

A
steven- johnson syndrome/ erythema multiforme 
drug or food hypersensitivity 
maulopapular rash
stomatitis 
conjunctivitis
90
Q

what are the features of stevens-johnsons syndrome

A

symblepharon ( partial or complete adhesion of the palpebral conjunctiva of the eyelid to the bulbar conjunctiva of the eyeball)
occlusion of lacrimal glands
corneal ulcers

91
Q

what is the medial longitudinal fasiculus

A

in grey matter

links CN VIII to eye movement nerves (CN III, IV and VI)

92
Q

what is the presentation of INO

A

inability to adduct (on side of lesion) and horizontal nystagmus on other eye

93
Q

what cranial nerves are affected in internuclear ophthalmoplegia

A

CN III and VI (3 and 6)

remember its a horizontal nystagmus