theory Flashcards

1
Q

afferent and efferent pupillary pathways are

A

Afferent pathway
Optic nerve – chiasm – optic tract – pretectal nucleus (dorsal midbrain)
Efferent
Parasympathetic and sympathetic input to iris muscles

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2
Q

light reflex what nucleus is involved

A

pretectal nucleus

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3
Q

what are the pupillary light reflexes

A

Control of pupil diameter based on light intensity
Increased light intensity leads to a reflex pupillary constriction (miosis)
Direct reflex – pupillary constriction in response to light entering the ipsilateral eye
I.e. Light shone in right eye leads to miosis in right eye
Consensual reflex – pupillary constriction in response to light entering the contralateral eye
I.e. Light shone in right eye leads to miosis in left eye

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4
Q

what are the afferent and efferent light reflex pathways

A

Control of pupil diameter based on light intensity
Increased light intensity leads to a reflex pupillary constriction (miosis)
Direct reflex – pupillary constriction in response to light entering the ipsilateral eye
I.e. Light shone in right eye leads to miosis in right eye
Consensual reflex – pupillary constriction in response to light entering the contralateral eye
I.e. Light shone in right eye leads to miosis in left eye

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5
Q

what is the near reflex

A

Pupillary constriction when fixating on near target (i.e. accommodation)
Less clearly defined pathway than light reflex

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6
Q

describe the near reflex

A

Convergence
Increased thickness of lens
Pupillary constriction for better focus (allows less peripheral ”distracting” light surrounding object of interest from entering the eye)

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7
Q

describe the oculosympathetic pathway

A

Pain, fear, excitatory inputs in general lead to pupillary dilation through the sympathetic innervation of the dilator pupillae muscle
3-neuron arc
1st order – from posterior hypothalamus, down the spinal cord, and synapse at the ciliospinal centre of Budge (at level C8-T2)
2nd order (preganglionic) – from ciliospinal centre of Budge, leaving spinal cord via ventral spinal roots, passing over apex of lung and joining the paravertebral cervical sympathetic chain to ascend and finally synapse at the superior cervical ganglion
3rd order (postganglionic) – from superior cervical ganglion, travelling up along the internal carotid artery, entering cranial cavity (via carotid canal), joining CN V1, and reaching the ciliary muscle and dilator pupillae via the nasociliary nerve and long posterior ciliary nerves

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8
Q

how to examine the pupils

A

General observation – size, shape, position, colour of iris
Start with ambient light
If anisocoria, check if anisocoria worse in dim or bright conditions
Assess light reflex – both direct and consensual responses
Swinging light test – ?RAPD
Check near reflex

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9
Q

how to assess aniosocoria

A

worse in dim light , implies failure of dilation and small pupil is therefore abnormal

worse in bright light

implies failure of constriction and large pupil is therefore abnormal

same regardless of light conditions - physiological anisocoria

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10
Q

components of the parasympathetic pathway

A

Efferent preganglionic parasympathetic fibers travel from the Edinger Westphal nucleus of CN III along the oculomotor nerve before synapsing in the ciliary ganglion
Postganglionic fibers then travel from the ciliary ganglion to the ciliary muscles and sphincter pupillae via the short ciliary nerves

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11
Q

cranial nerve 3rd palsy characteristics

A

LR (CN VI) and SO (CN IV) only left working
Eye therefore down (SO) and out (LR and SO)
Complete ptosis (loss of levator palpebrae superioris action)
Diplopia due to eye misalignment
Pupil involvement usually indicates a surgical cause
Causes include:
Microvascular disease (e.g. diabetes, hypertension)
Compression from mass effect (tumours, posterior communicating artery aneurysm)

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12
Q

surgical third nerve palsy

A

B. Microvascular disease (medical CN III palsy) – affects blood supply in vasa nervorum, but tends to spare the outer parasympathetic fibers hence pupil not affected

External compression of CN III affects those parasympathetics, leading to failure of pupillary constriction. Hence a fixed dilated pupil is seen

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13
Q

what is a relative afferent pupillary defect

A

Light intensity perceived differently by each eye (i.e. the intensity of light relative to the other eye is different)
Only the afferent limb of the light reflex is affected (i.e. sensory perception of light)
Efferent limb normal, i.e. normal pupillary constriction in response to light
However, because one eye is perceiving less light relative to the other, when light is shone in that eye, there is pupillary dilation

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14
Q

what is RAPD due to

A

Asymmetrical retinal or optic nerve pathology

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15
Q

causes of an RAPD

A

Optic nerve disease

Multiple sclerosis (demyelinating disease)
Ischaemic optic neuropathy (e.g. due to giant cell arteritis)
Glaucoma
Optic nerve compression (e.g. idiopathic intracranial hypertension)

Retinal disease

Ischaemia – e.g. retinal artery occlusion, ischaemic retinal vein occlusion
Ocular ischaemic syndrome
Retinal detachment

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16
Q

how do media opacities cause RAPD

A

Media opacities include cataracts, vitreous haemorrhage, corneal opacities

Media opacities lead to a scattering of light on the retina, leading to unfocused/blurred images…
However TOTAL light intensity detected by retina is unaffected

Therefore in the absence of optic nerve or retinal pathology, media opacities (almost) NEVER lead to an RAPD

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17
Q

what is Horners syndrome and what is the Triad ie.e what would you expect

A

Disruption along the sympathetic chain
Classic triad of
Miosis – dilator pupillae affected
Partial ptosis – Muller’s muscle affected (but levator muscle still working)
Ipsilateral anhydrosis – inability to sweat

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18
Q

causes of horners

A

Preganglionic causes
Pancoast tumour – lung apex tumour
Neck lesions

central causes: Stroke
Tumour
Cervical spinal cord lesion

Postganglionic causes
Internal carotid artery dissection (PAINFUL)
Cavernous sinus lesion

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19
Q

what are the pharmacological tests caused Horners syndrome

A

10% cocaine eyedrops
Blocks reuptake of norepinephrine (sympathetic)
Normal pupil will dilate
If sympathetic pathway is disrupted – norepinephrine is not released anyway and therefore no effect seen
Therefore in Horner’s there is no dilation with cocaine drops

0.5% apraclonidine (alpha1 agonist – sympathetic)
Very dilute and has no effect on a normal pupil
In sympathetic lesions, the iris dilator muscles develop denervation hypersensitivity (i.e. they become extremely sensitive to whatever stimulation they can get in an effort to work normally)
Therefore in Horner’s there is pupil dilation with dilute apraclonidine drops

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20
Q

what is adies tonic pupil

A

Denervation of postganglionic parasympathetic supply to ciliary muscle and sphincter pupillae
May follow viral illness
May be inherited
Sluggish response to light, but better response to accommodation (light-near dissociation – another cause is Argyll-Robertson pupil)
Vermiform movement may be seen
Once contracted, the pupil is very slow to redilate (tonic)

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21
Q

differentials for a fixed dilated pupil

A

Denervation of postganglionic parasympathetic supply to ciliary muscle and sphincter pupillae
May follow viral illness
May be inherited
Sluggish response to light, but better response to accommodation (light-near dissociation – another cause is Argyll-Robertson pupil)
Vermiform movement may be seen
Once contracted, the pupil is very slow to redilate (tonic)

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22
Q

what are some systemic conditions with iris signs

A

uveal melanoma

Brushfield spots- associated with trisomy 21

coloboma - located in the inferior nasal quadrant

result of failed or incomplete closure of the choroidal fissure during development

kayser - fleshier ring - brown ring around theconeea

due to copper deposition in part of the cornea (descements membrane)

Wilsons disease - abnormal copper handling by the liver resulting in copper accumulation In the body

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23
Q

characteristics of bacterial conj

A

S.epidermidis, S.aureus, S.pneumoniae, H.influenzae, C.trachomatis
Red eye, FB sensation, stuck eyelids, often bilateral, itchy
Purulent discharge
Antibiotics as appropriate

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24
Q

characteristics of viral conj

A

Adenovirus (serovars 3, 4, and 7 – pharyngoconjunctival fever; serovars 8, 19, and 37 – epidemic keratoconjunctivitis), herpes simplex, poxvirus (molluscum)
Red itchy watery eye, often starts with one eye and then both
Watery discharge, oedema
Often conservative, avoid contact, aciclovir if herpes

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25
Q

characteristics of allergic conj

A

Seasonal (summer), perennial (throughout – dust mites…), atopic, vernal (esp in dry hot countries)
Red eye, itchy, may have other symptoms of atopy
Papillae, scarring of conjunctiva in advanced cases
Mast cell stabiliser, antihistamines, identify allergen and avoidance, steroids

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26
Q

what is vernal keratoconjuctivits

A

Recurrent bilateral immune-mediated disease
Affects young boys predominantly
Usually seasonal (worse in spring often)
Usually resolves in teenage years
VKC can be
Palpebral
Limbal
Mixed
May need immunomodulation – e.g. with steroids/ciclosporine

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27
Q

what would you see in limbal viral kertatoconjuctivis

A

horner- truants spots

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28
Q

what is atopic keratconjuctivits

A

Typically presents in adults
Often they have had a long hx of atopy
Some may have had VKC as children
Presents as a much more sever form of VKC
Usually perennial (i.e. year-round)
Corneal involvement can lead to blindness if untreated

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29
Q

what is a pingeglum

A

Actinic damage to conjunctiva
Often present on nasal limbus, but does NOT encroach on limbal/corneal surface
Rarely requires treatment, unless for cosmesis
If inflamed, short course of topical steroids usually sufficient

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30
Q

what is a pterigium

A

Fibrovascular subepithelial growth of degenerative bulbar conjunctival tissue
Cross limbus and encroaches onto cornea
(C.f pinguecula  spares limbus)
No treatment if asymptomatic
If symptomatic  excision

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31
Q

differences between scleritis and episcleritis

A

scleritis - very painful , deep vascular plexus , no blanching with phenelpherine ,

episceleritis - not usually painful, red (superficial vascular plexus) , blanches with phenylephrine

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32
Q

what are the systemic considerations that need to be considered with scleritis and episcleritis

A

Episcleritis often idiopathic, but may be associated with certain systemic inflammatory conditions, e.g. rheumatoid arthritis and Crohn’s disease
Scleritis ALWAYS warrants further investigation and treatment  risk of perforation

33
Q

what is a blue sclera due to

A

Sclera appears blue due to thinning
Blue tinge due to underlying uveal tract
Often seen in connective tissue diseases (e.g. osteogenesis imperfecta and Ehlers-Danlos syndrome)

34
Q

how is a vein occlusion likely to present and what does it loo like

A

looks like a shit ton of red dots

vein occlusion presentation

2nd commonest retinal vascular disease after diabetic retinopathy
Risk factors
Age (main RF)
Cardiovascular disease – hypertension, hyperlipidaemia
Diabetes
Oral contraceptive pill
Haematological disorders (e.g. antiphospholipid syndrome)
Typically presents with sudden painless drop in vision +/- metamorphopsia (distortion)

35
Q

vein occlusion management

A

Assess for cardiovascular risk factors (BP, bloods – ESR, lipids, glucose, ECG)
In some patients (esp. if <50), consider further investigations
CXR – sarcoidosis, TB
Thrombophilia screen
Autoantibodies – rheumatoid factor, ANA
Assess for signs of retinal ischaemia
Neovascularisation (at disc/iris/elsewhere)
Cotton wool spots
Fluorescein angiography is usually diagnostic

36
Q

differences between ischaemic and non ischaemic CRVO

A

.RAPD - non ischaemic - mild or absent RAPD

ischameic CRVO - RAPD is present

visual field defects are rare in non ischameic CRVOS , they are common in ischameic CRVos

prognosis is better for non ischameic CRVO

prognosis is worse for ischameic CRVO

37
Q

what is macular oedema

A

Commonest cause for persistent poor VA in vein occlusion
Treated with anti-VEGF
If poor response, may consider intravitreal dexamethasone implant (Ozurdex)
Occasionally combined with laser

38
Q

neovascualrisation is

A

If present  sign of ischaemic changes
Treated with sector laser or PRP (urgently)
Iris neovascularization can lead to rubeotic glaucoma

39
Q

retinal artery occlusionb

A

Blood supply
Outer retina – ciliary arteries (choriocapillaris)
Inner retina – central retinal artery
Retinal artery occlusion – causes
Atherosclerosis (commonest)
Need to exclude GCA
Other inflammatory conditions – e.g. SLE, GPA, PAN (vasculitides)

40
Q

what assessment needs to be done in retinal artery occlusion

A

Cardiovascular assessment
Treat as a STROKE
Exclude GCA
Carotid ultrasound

41
Q

what is the ocular treatment for retinal artery occlusion

A

Ocular massage
AC paracentesis
Mannitol
However no solid evidence for benefit and not always effective

42
Q

what is the systemic treatment for retinal artery occlusion

A

Treat as a stroke
Start high dose aspirin (300mg)
Oral anticoagulation in certain patients (e.g. warfarin, apixaban)
Carotid endarterectomy if severe stenosis

43
Q

presentation of hypertensive retinopathy

A

yellow circles (large - clearly defined)

Arteriosclerosis leads to arteriovenous nipping at crossing points
As the retinopathy gets more severe, signs of ischaemia are present (e.g. cotton wool spots)
Disc swelling often seen
Macular star may be seen
Vessel tortuosity is a common feature

44
Q

age relate macular degeneration presentation

A

lots of tiny yellow glowing dots

Commonest cause of irreversible visual loss in the developed world
Age is the biggest risk factor
Other risk factors
Smoking
Family history (complement factor H gene)
Hypertension
Poor diet

45
Q

dry vs wet AMD

A

No treatment as such
Smoking cessation!
Antioxidants may help – AREDS2 formula
Vitamin C
Vitamin E
Lutein
Zeaxanthin
Zinc
Copper

46
Q

wet AMD

A

Choroidal neovascularization leads to a sudden decline in VA (often a background of gradually worsening vision due to dry AMD)
Anti-VEGF injections mainstay of treatment

acoutns for 90% of central visual acuity losss

neovascularisation of the maculaa

neovascularisation of the macula

47
Q

thyroid eye disease

A

Orbital disorder secondary to thyroid disease (Grave’s commonly)
Commonest cause of unilateral and bilateral proptosis in adults
F:M = 5:1
Can be sight-threatening if untreated
Optic neuropathy
Keratopathy

autoimmune disease - orbital fibroblasts targeted

Inflammation of EOMs
Fluid retention —> oedema
Increase in orbital fat content
Enlargement of orbital muscles
Fibrosis  limited ocular motility  diplopia

48
Q

diagnostic clues for TED

A

Thyroid abnormalities
Exophthalmos
Optic neuropathy
EOM involvement (e.g. enlargement visible on MRI scan)

inflammatory phase laser for 1-3 year

fibrotic phase follows

49
Q

risk factors for TED

A

smoking

not taking treatment for hyperthyroid

oder age

50
Q

symptons of graves orbitopathy

A

Pain
Gaze-evoked pain
Grittiness
Epiphora
Red eyes
Puffy lids
Photophobia

kosher sign (scared/starttled expression)

lid lag

lid swelling

restrictive myopathy

proptosis

51
Q

evaluation of tED

A

VA
Colour vision
Pupil and RAPD
IOP – in primary gaze and upgaze (often there may be a rise of >4mmHg in upgaze)
Ocular motility and alignment
Proptosis and exophthalmometry
CAS score
Corneal surface
Fundoscopy

52
Q

General and specific management of TED

A

General: Thyroid control
Smoking cessation

mild- lubricants

topical anti - inflammatioories

head elevation

eyelid taping

selenium

moderate /severe (cas more than 3)

systemic steroid therapy

orbital steroid therapy

low dose radiotherapy

combined treatment (steroids, azathioprine _+ rt)

surgery- orbital decompression , strabismuc correction (aim bsv in pp and reading)

lid sx - mullerotomy and LPS recession)

53
Q

uveal tract is

A

choroid

iris

cillary body

54
Q

anterior uveitis

A

Inflammation of the iris and/or ciliary body (pars plicata)
Aka iritis or iridocyclitis
Acute – commonest and usually unilateral
Chronic – usually bilateral and associated with a systemic cause

55
Q

acute anterior uveitis

A

Commonest presentation
Idiopathic
HLA-B27  ankylosing spondylitis and other seronegative spondyloarthropathies (e.g. reactive arthritis, psoriatic arthritis, JIA)
Less common causes include traumatic uveitis and viral infections

56
Q

how does the patient present

A

Pain
Light sensitivity
Red eye
Reduced vision

57
Q

posterior synechaie

A

Adhesions between pupil margin and anterior lens capsule
Usually resolves when inflammation settles
Can be prevented and broken by dilating the pupil – often with cycloplegics (dual benefit as they also prevent ciliary muscle spasm, providing pain relief)
Surgery occasionally required if not settled

58
Q

hypypoyon

A

white blood cells in ac

Most commonly present in HLA-B27-associated disease
Usually immobile due to high fibrin content
If highly mobile with head movements, consider Behçet’s disease (HLA-B51 association)

59
Q

white spots on the corneal endothelium

A

kerattic precipitates

Inflammatory deposits on the corneal endothelium
Granulomatous inflammation (e.g. sarcoidosis, TB) often present with larger KPs (aka mutton-fat KPs)

60
Q

investigations of AAU

A

Often no yield  idiopathic cause
Further investigations needed if:
Bilateral AAU
Recurrent AAU
Severe AAU
Treatment-resistant
Any evidence of intermediate or posterior uveitis
History or evidence of systemic disease

if reccurent tau can be associated with HLA types in recurrent anterior uveitis = HLA -B27

61
Q

initial management of AAU

A

Topical steroids – tapering regime (e.g. hourly for 3 days, then QDS for 5 days) depending on severity
Cycloplegia (often PRN)
Mydriasis – prevention and breaking PS
Regular review – monitor IOP whilst on steroids
Some patients may need systemic steroids or steroid injections
Others may need immunomodulation (e.g. MTX, adalimumab)

62
Q

Different types of glaucoma

A

normal visual fields , high iop, normal cup to disc ration= ocular hypertension

high iop , vf loss normal cup= glaucoma suspect

high iop , enlarged cup, vf loss- glaucoma

63
Q

risk factors for glaucoma

A

Primary angle closure glaucoma
Hypermetropia
Asian ethnicity

Primary open angle glaucoma
Age
Myopia
Black ethnicity
Positive family history

Secondary causes
Trauma
Rubeosis (e.g. vein occlusion, diabetic retinopathy, …)
Steroids
Phacomorphic/lytic glaucoma

Congenital
Primary
Rubella
Aniridia

64
Q

what is phacomoprhic glaucoma

A

Dense cataract causing mechanical obstruction of trabecular meshwork
Presents as angle closure glaucoma and managed as such acutely
Definitive treatment is cataract surgery

65
Q

what is rubeotic/neovascular glaucoma

A

Iris neovascularization may occur in certain ischaemic states, e.g. ischaemic vein occlusion, severe diabetic retinopathy
Neovascular vessels proliferate around the angle, obstructing outflow of aqueous
Treatment of underlying cause essential – laser, anti-VEGF injections

66
Q

what is a risk factor for primary angle closure glaucoma

A

Obstruction of trabecular meshwork by iris, which is pushed forward
A risk factor is (axial) hypermetropia, where the eye is too short and therefore angle is “crowded”

67
Q

risk factor for open angle glaucoma

A

myopia

68
Q

glaucoma and the disc

A

Normal cup disc ratio is around 0.3 – 0.4
As more of the optic nerve gets damages, the cup gets larger

69
Q

what field defects would be seen in glaucoma

A

In primary open angle, visual field loss tends to be gradual and insidious
No one typical pattern, but peripheral fields usually affected first

acute defect

70
Q

what vf defect likely in a right sided optic tract lesion

A

homonymous hemianopia

71
Q

bitemporal hemianopia most likely caused by …

A

B – bitemporal hemianopia (likely chiasmal compressing lesion, e.g. pituitary tumour)

72
Q

a right homonymous superior quandrantopia usually seen in a

A

left temporal optic radiation lesion

73
Q

what drugs can be given for glaucoma

A

beta blockers- timiniol. cartiolil - decrease secretion

prostoglandin anuolouges - pilocarpine - increase outflow, induce miosis ,

sympathomimetics - adrenaline m increase outflow , decrease secretion

alpha antagonist - iodine , apracodli e

carbonic anhydrase inhibitors - acetazolamide m dorzolamide,m brinzolamide, decrease secretion

prostaglandin anolouges - latnaporsrt , travaprosrr , increase outflow

osmotic agents - mannitol, draws water out

74
Q

example of a carbonic anhydrase inhibotor

A

acetazolamide

75
Q

side effects of pilcarpine

A

headache

76
Q

what glaucoma drug should be avoided in patients

A

timolol

77
Q

signs of diabetic retinopathy

A

micranyerums - red dots in the blood vessels

hard exudates - dark yellow spots

intartetial haemhorrgaes

hypoxia - cotton wool spots

neovasuclarsiation

MICROANEURYSM - small deep red dots in the retina (not haemorrhages) but as “out-pouches” from damaged or weakened capillary walls. They may or may not be leaking.
HARD EXUDATE - distinct yellow white deposits of lipids that have leaked from damaged retinal capillaries. They can be seen as small deposits, larger plagues or in distinct circinate pattern around the macular.
HAEMORRHAGES - intraretinal bleeding may be ‘dot’, ‘blot’ or ‘flame’ shaped depending on their depth within the retina.
COTTON WOOL SPOTS - greyish white fluffy patches of discolouration in the nerve fiber layer, linked with focal hypoxia and swelling of nerve fibers.

78
Q
A