theory

Question 1

afferent and efferent pupillary pathways are

Answer 1

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

Question 2

light reflex what nucleus is involved

Answer 2

pretectal nucleus

Question 3

what are the pupillary light reflexes

Answer 3

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

Question 4

what are the afferent and efferent light reflex pathways

Answer 4

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

Question 5

what is the near reflex

Answer 5

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

Question 6

describe the near reflex

Answer 6

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

Question 7

describe the oculosympathetic pathway

Answer 7

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

Question 8

how to examine the pupils

Answer 8

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

Question 9

how to assess aniosocoria

Answer 9

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

Question 10

components of the parasympathetic pathway

Answer 10

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

Question 11

cranial nerve 3rd palsy characteristics

Answer 11

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)

Question 12

surgical third nerve palsy

Answer 12

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

Question 13

what is a relative afferent pupillary defect

Answer 13

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

Question 14

what is RAPD due to

Answer 14

Asymmetrical retinal or optic nerve pathology

Question 15

causes of an RAPD

Answer 15

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

Question 16

how do media opacities cause RAPD

Answer 16

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

Question 17

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

Answer 17

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

Question 18

causes of horners

Answer 18

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

Question 19

what are the pharmacological tests caused Horners syndrome

Answer 19

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

Question 20

what is adies tonic pupil

Answer 20

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)

Question 21

differentials for a fixed dilated pupil

Answer 21

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)

Question 22

what are some systemic conditions with iris signs

Answer 22

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

Question 23

characteristics of bacterial conj

Answer 23

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

Question 24

characteristics of viral conj

Answer 24

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

Question 25

characteristics of allergic conj

Answer 25

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

Question 26

what is vernal keratoconjuctivits

Answer 26

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

Question 27

what would you see in limbal viral kertatoconjuctivis

Answer 27

horner- truants spots

Question 28

what is atopic keratconjuctivits

Answer 28

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

Question 29

what is a pingeglum

Answer 29

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

Question 30

what is a pterigium

Answer 30

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

Question 31

differences between scleritis and episcleritis

Answer 31

scleritis - very painful , deep vascular plexus , no blanching with phenelpherine , episceleritis - not usually painful, red (superficial vascular plexus) , blanches with phenylephrine

Question 32

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

Answer 32

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

Question 33

what is a blue sclera due to

Answer 33

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)

Question 34

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

Answer 34

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)

Question 35

vein occlusion management

Answer 35

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

Question 36

differences between ischaemic and non ischaemic CRVO

Answer 36

.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

Question 37

what is macular oedema

Answer 37

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

Question 38

neovascualrisation is

Answer 38

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

Question 39

retinal artery occlusionb

Answer 39

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)

Question 40

what assessment needs to be done in retinal artery occlusion

Answer 40

Cardiovascular assessment Treat as a STROKE Exclude GCA Carotid ultrasound

Question 41

what is the ocular treatment for retinal artery occlusion

Answer 41

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

Question 42

what is the systemic treatment for retinal artery occlusion

Answer 42

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

Question 43

presentation of hypertensive retinopathy

Answer 43

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

Question 44

age relate macular degeneration presentation

Answer 44

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

Question 45

dry vs wet AMD

Answer 45

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

Question 46

wet AMD

Answer 46

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

Question 47

thyroid eye disease

Answer 47

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

Question 48

diagnostic clues for TED

Answer 48

Thyroid abnormalities Exophthalmos Optic neuropathy EOM involvement (e.g. enlargement visible on MRI scan) inflammatory phase laser for 1-3 year fibrotic phase follows

Question 49

risk factors for TED

Answer 49

smoking not taking treatment for hyperthyroid oder age

Question 50

symptons of graves orbitopathy

Answer 50

Pain Gaze-evoked pain Grittiness Epiphora Red eyes Puffy lids Photophobia kosher sign (scared/starttled expression) lid lag lid swelling restrictive myopathy proptosis

Question 51

evaluation of tED

Answer 51

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

Question 52

General and specific management of TED

Answer 52

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)

Question 53

uveal tract is

Answer 53

choroid iris cillary body

Question 54

anterior uveitis

Answer 54

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

Question 55

acute anterior uveitis

Answer 55

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

Question 56

how does the patient present

Answer 56

Pain Light sensitivity Red eye Reduced vision

Question 57

posterior synechaie

Answer 57

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

Question 58

hypypoyon

Answer 58

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)

Question 59

white spots on the corneal endothelium

Answer 59

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

Question 60

investigations of AAU

Answer 60

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

Question 61

initial management of AAU

Answer 61

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)

Question 62

Different types of glaucoma

Answer 62

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

Question 63

risk factors for glaucoma

Answer 63

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

Question 64

what is phacomoprhic glaucoma

Answer 64

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

Question 65

what is rubeotic/neovascular glaucoma

Answer 65

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

Question 66

what is a risk factor for primary angle closure glaucoma

Answer 66

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”

Question 67

risk factor for open angle glaucoma

Answer 67

myopia

Question 68

glaucoma and the disc

Answer 68

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

Question 69

what field defects would be seen in glaucoma

Answer 69

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

Question 70

what vf defect likely in a right sided optic tract lesion

Answer 70

homonymous hemianopia

Question 71

bitemporal hemianopia most likely caused by ...

Answer 71

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

Question 72

a right homonymous superior quandrantopia usually seen in a

Answer 72

left temporal optic radiation lesion

Question 73

what drugs can be given for glaucoma

Answer 73

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

Question 74

example of a carbonic anhydrase inhibotor

Answer 74

acetazolamide

Question 75

side effects of pilcarpine

Answer 75

headache

Question 76

what glaucoma drug should be avoided in patients

Answer 76

timolol

Question 77

signs of diabetic retinopathy

Answer 77

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.