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3B Hospital Specialities > Opthalomology > Flashcards

Opthalomology Flashcards

1
Q

Small depression in centre of macula

A

Fovea

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2
Q

Where is the highest concentration of cones

A

Macula, highest visual acuity area. 3mm temporal from optic disc.
In the centre is the fovea with the highest concentration of cones

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3
Q

What are cones

A

Found in central retina

Colour vision and acuity

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4
Q

What are rods

A

Found in outer retina

Night vision

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5
Q

How can you test visual acuity

A

Snellen chart at 6 metres away.

20/80 = the pt can read at 20 feet what a person can normally read at 80 feet.

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6
Q

Name some risk factors for cataracts and causes

A 
Ageing
High-dose corticosteroids
Smoking
Exposure to UV B light.
FHx
Co-morbidities = Diabetes mellitus, Atopic dermatitis/eczema, Neurofibromatosis type 2.

Causes:
Complication of secondary eye disease - anterior uveitis acute angle-closure glaucoma.
Trauma to eye - electric shock, radiation, blunt or penetrating trauma to eye, from surgical procedures to eye.

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7
Q

What are cataracts

A

Opacity that forms within the eye lens.

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8
Q

Presentation of cataracts

A
  • Gradual, PAINLESS, reduced viral acuity. Pt will find difficulty in reading, watching TV, recognising faces.
  • Visual difficulty in bright light/glare.
  • Radial reduction in colour intensity perception.
  • Monocular diplopia.
  • Poor sight despite glasses/frequent change of lens prescription.

O/E

  • With ophthalmoscope = opacity of lens, reduced red reflex.
  • Slit lamp shows opacity.
  • Reduced acuity with Snellen Chart.
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9
Q

Mx of cataract (including risks and benefits)

A
  • Decision for surgery based on impact not on clinical extent of disease.
  • Phacoemulsification surgery + intraocular lens implant. This involves removing the nucleus of the lens and inserting an implant to prevent the patient having a high refractive error.
  • Benefits = improved visual acuity, colour vision and clarity of vision.
  • Risks = capsular opacification, intraocular infection (endophthalmitis) and some other.
  • Fitness to drive a car = contact DVLA and can’t drive if they can’t read a number plate and must be at least Snellen 6/12.
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10
Q

Presentation of congenital cataract or severe age-related cataract

A

Leukocoria - white pupillary reflex.

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11
Q

Types of age-related macular degeneration

A

Dry

  • Geographic atrophy
  • Drusen = waste products build up in and below retinal pigment epithelium and are seen as yellow spots on retina. Also get pigmentary changes on retina (hypo or hyper).

Wet
- Exudative
- Neovascular age related macular degeneration = new blood vessels in retina which can easily bleed and leak serum causing scarring of retina. More rapid loss of vision.
Can get a change from dry macular degeneration to wet!

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12
Q

Modifiable and non-modifiable risk factors for macular degeneration

A 
Modifiable = smoking, HTN.
Non-modifiable = age, FHx, blue iris.
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13
Q

Mx of age-related macular degeneration

A

Lifestyle advice = increase vitamin A–> eat more dark green leafy veg + oily fish. Weight loss to control BP and stop smoking.
If advanced wet AMD = can use anti-VEGF
Register as blind.

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14
Q

Presentation of macula degenreation

A

Dry - central scotoma, good peripheral vision, straight lines appear wavy. O/E - Drusen can become confluent, geographic atrophy and pigmentary changes

Wet - more rapid vision loss. Central distortion and central scotoma. O/E - Drusen, choroidal neovascularisation and exudate.

Complain of = difficulty reading, need larger prints, straight lines are wavy (metamorphopsia), central grey patch (scotoma), poor adaptation to dark.

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15
Q

Ix for age related macula degeneration and Management

A

Amsler grid = metamorphopsia, scotoma. Advise those with dry AMD who may develop wet AMD to test often.
Fundscopy, Slit-lamp biomicroscopy, ∆ = ocular coherence tomography.

Vitamin supplementation, lifestyle advice, register as visually impaired.
Rx is limited. Wet AMD can be helped with anti-vascular endothelial growth factor e.g. Ranibizumab.

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16
Q

Normal intra-ocular pressure

A

11-21mmHg

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17
Q

What is this angle they speak of in glaucomas and how does it cause the disease?

A
  • Space between posterior surface of cornea and anterior surface of iris. Where trabecular meshwork is to drain aqueous humour.
  • Can get closed or open glaucoma depending on whether there is clogging of meshwork (open) or lens pushed onto iris occluding flow of aqueous humour (closed).
  • Increase in intra-ocular pressure damages optic nerve.
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18
Q

Main drainage aqueous humour

A

Trabecular meshwork. At apex of anterior chamber angle. From trabecular meshwork it drains to Canal of Schlemm and to episceral veins.

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19
Q

Ways to classify glaucoma

A

Open or closed anterior chamber angle
Acute or chronic
Cause - primary or secondary
Age of onset - infantile, adult etc.

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20
Q

Risk factors and secondary causes of open angle glaucoma.

A
  • Open more common than closed + less likely acutely presentation.
  • RFx = older age, black ethnicity, FHx, use of corticosteroids, T2DM, HTN and CVD, MYOPIA
  • 2nd causes = neovascular and ischaemia, angle-recession from trauma.
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21
Q

Risk factors and secondary causes of primary closed angle glaucoma.

A
  • RFx = old age, female, asian ethnicity, FHx.
    LESS COMMON IN MYOPIA.
  • 2nd causes = sublimated lens, chronic anterior uveitis.
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22
Q

Presentation of primary open angle glaucoma

A 
Tunnel vision (arcuate scotoma, join to form ring scotoma) and later total vision loss. Visual acuity is usually alright.
O/E with ophthalmoscopy = cupped optic disc as loss of neurones.
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23
Q

Presentation of primary closed angle glaucoma

A

Acute angle closure = painful, red eye, blurred vision, sees halos around lights, poor visual acuity.
Headache, nausea and vomiting.
Pupil is fixed in a vertically oval shape.

Chronic angle closer glaucoma = tunnel vision, ophthalmoscopy shows cupped optic disc.

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24
Q

Triad for glaucoma

A

Raised IOP >21mmHg
Abnormal optic disc (cupped, haemorrhage)
Visual field defect.

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25
Q

How to measure intra-ocular pressure

A

Tonometer

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26
Q

Mx for acute closed angle glaucoma

A
  1. Lie flat facing upwards (no pillows).
  2. Pilocarpoine eye drops (2% if blue eyed, 4% if brown eyed).
  3. Acetazolamide/Diamox to reduce aqueous humour production.
  4. Laser iridotomy for acute closed angle glaucoma.
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27
Q

Ix and Mx for non-acute glaucoma

A

Ix - visual fields, measure pressure with tonometry, view retina with ophthmoscopy = cup-to-disc ratio over 0.6.
Reduce pressure via
- reduced aqueous humour production with topical beta-blockers (timolol ophthalmic).
- increased outflow of aqueous humour with topical prostaglandin analogue (latanoprost).
- achieve both with topical alpha-2 adrenergic agonist (apraclonidine ophthalmic).
Laser treatment
- Laser trabeculoplasty for open angle glaucoma
- Laser iridotomy for closed angle glaucoma.

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28
Q

3 causes of gradual vision loss

A

Cataract.
Chronic open-angle glaucoma.
Age related macular degeneration.

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29
Q

What genetic condition is associated with cataracts

A

Down’s syndrome

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30
Q

High intra-ocular pressure but normal disc and visual fields

A

Ocular hypertension.

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31
Q

Differentials for sudden loss of vision

A 
- Vascular occlusion including:
Branch/central retinal artery occlusion.
Branch/central retinal vein occlusion.
Anterior ischaemic optic neuropathy.
- Inflammation with optic neuritis.
- Retinal detachment.
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32
Q

Pathology behind a rapid afferent pupillary reflex and some causes

A

Affected eye has pathology with optic nerve so can not process visual information at all. In normal Leith both pupils are the same size.

  • Shine light in affected eye and neither eye react as no information of light is processed.
  • Shine light in unaffected eye and both will constrict as pathway in this eye is intact.
  • Shine light back on affected eye and the pupil will dilate to the normal ‘resting’ size (appear to dilate to light but actually just re-adjusting).

Causes = retinal detachment, central retinal artery occlusion, optic neuritis, anterior ischaemic optic neuropathy, advanced glaucoma.

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33
Q

Retinal vein occlusion presentation

A

Branch occlusion will have less severe loss of vision, more blurriness and visual field defects.
Central retinal vein occlusion = painless, sudden, unilateral vision loss. Less acute onset than artery occlusion.

O/E

  • Relative afferent pupillary defect.
  • Dilated and tortuous retinal veins (neovascularisation), cotton wool spots, retinal and disc oedema, intra-retinal flame haemorrhages. (looks a bit like pizza).
  • Ix = fluorescein angiography
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34
Q

Rfx for retinal vein occlusion

A

Hypertension
Atherosclerosis
Diabetes mellitus
Blood coagulation disorders e.g. Factor V Leiden.

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35
Q

Mx for retinal vein occulsion

A

Must establish retinal perfusion with Fluorescein angiography.

Laser photocoagulation
Intravitreal steroids

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36
Q

Retinal artery occulsion

A
  • Similar Rfx as for stroke/emboli (atherosclerosis, aortic stenosis, Factor V Leiden)
  • Sudden, unilateral, painless vision loss with central artery occlusion. Altitudinal loss with branch occlusion.
  • O/E relative afferent pupillary defect. CHERRY RED SPOT (fovea) + RETINAL OEDEMA (pale). Maybe able to visualise emboli. If a branch is occluded only a sector of the retina will be pale.
  • Ix could include carotid artery doppler USS.
  • Can not cure vision back but can manage risk factors to prevent reoccurence e.g aspirin, clopidogrel.
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37
Q

What is amaurosis fugax

A

Transient monocular visual loss.
‘Curtain coming over vision.’
Complete resolution usually within 30mins.

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38
Q

Anterior iscahemic optic neuropathy

A

Non-arterial = unilateral vision loss on waking up. Vision loss is usually in a horizontal half of eye (altitudinal). Rfx include DM, HTN, high lipids. O/E = relative afferent pupillary defect, opthalmoscope shows disc oedema. Secondary prevention by controlling RFx.

Arterial = less common. Sudden painless vision loss. Can be manifestation of GCA so look for those symptoms, ESR and biopsy of temporal artery. Start prednisolone ASAP.

39
Q

Optic neuritis causes

A 
Multiple sclerosis
Post-viral
Syphilis
HIV
Sarcoidosis.
Neuroretinitis close to optic neuritis = Toxoplasmosis.
40
Q

Types of optic neuritis and how to differentiate

A

Retrobulbar optic neuritis = normal appearance of optic disc on opthalmoscope. more common
Anterior optic neuritis = oedema of optic disc on opthalmoscope.

41
Q

Pathology, presentation, Ix and Mx for optic neuritis

A
  • Inflammation and demyelination of optic nerve.
  • Periocular pain, worse on eye movement. Loss of colour vision, relative afferent pupillary defect, central scotoma vision loss.
  • Uhthoff’s phenomenon (Exercise or heat-induced deterioration of visual symptoms).
  • Ix = opthalmoscope to see if anterior or posterior. MRI (?MS).
  • Mx = Vision will recover spontaneously. IV steroids can quicken recovery times.
42
Q

Retinal detachment presentations and pathology

A

Mostly due to a retinal tear.

  • Floaters from a vitreous haemorrhage.
  • Visual field loss from detached retina. If there is a superior retinal detachment will cause inferior visual field defect.
  • Flashes from retinal traction (photopsia).
43
Q

Mx of retinal detachment

A
  • If tear identified (horseshoe shape) before retina detaches, laser to fix.
  • Ophthalmology urgent referral + surgery.
44
Q

Describe the pathology behind diabetic retinopathy

A
  • Non-proliferative retinopathy = microaneurysm formation, leaky capillaries, macular oedema, cotton-wool spots.
  • Preproliferaive retinopathy = increased as vascular tortuosity and haemorrhages.
  • Proliferative retinopathy = retinal ischaemia, neovascularisation. Can lead to glaucoma, vitreous haemorrhage, retinal detachment and blindness.
45
Q

Presentation and management of diabetic retinopathy

A
  • Often asymptomatic even when proliferative so need annual monitoring by ophthalmologists. Can have blurring of vision, floaters from vitreous haemorrhage,
  • Ix can include fluorescein angiogram or ocular coherence tomography.
  • Mx depends on extent of disease. Photocoagulation laser treatment, topical antiangiogenic biologic drugs (Ranibizumab)
  • CONTROL HbA1c <48mmol/mol, annual review!!!!!
46
Q

Differential for a red eye 👁

A

🚩 Acute closed angle glaucoma

Eyelid pathology = blepharitis, malposition, Herpes simplex/shingles.
Conjunctival pathology = subconjunctival haemorrhage, conjunctivitis.
Cornea pathology = keratitis, trauma, foreign body or abrasions.
Iris pathology = Anterior uveitis
Episclera pathology = episcleritis
Sclera pathology = scleritis.

47
Q

Blepharitis presentation

A
  • Can be due to ingrowing eyelash, granulomas of the meibomian glands (chalazion), seborrhoea.
  • Complain of ‘gritty’, irritable, red eyes with watery discharge.
  • O/E thick, red inflamed eyelids, loss of lashes, poor closure of affected eye, can get plaques of keratinised epithelium.
48
Q

Mx for blepharitis

A

Lubricants.
Lid hygiene = massage eye lid with flannel. Can use baby shampoo or scrubs.
Topical or oral antibiotics.
Hot spoon bathing for meibomian gland

49
Q

Chalazion

A

Chronic glamuloma inflammation of the meibomain gland. Can develop from a stye or occur spontaneously. May need to biopsy to rule out carcinoma.

50
Q

Malposition of the eyelid

A

Entropion - rotate towards cornea.

Ectropion - rotate away from cornea.

51
Q

Subconjunctival haemorrhage

A

Blood accumulates in potential space between conjunctiva and sclera.
Sudden onset, bright red eye.
No Rx necessary

52
Q

Causes of conjunctivitis

A 
Bacterial
Viral
Allergic
Chemical irritants
Mechanical irritation
53
Q

Viral conjuncitivits

A

Commonly adenovirus.

  • Watery, sticky discharge.
  • Follicles (white lesions) on conjunctiva.
  • Pre-auricular lymphadenopathy.
  • Can get simultaneous keratitis.
  • No Rx needed. Safety net with some red flags and advice PHE does not recommend exclusion from school or care.
54
Q

Bacterial conjunctivitis

A

Commonly S.pneumoniae, S.aureus, H.influenzae, Chlamydia (persistent), N.gonorrhoeae.

  • Purulent discharge, red eyes, eyelids stuck together in morning.
  • Conjunctival papillae (not seen in viral).
  • Less frequent lymphadenopathy compared to viral.
  • Rx usually self-limiting, if severe give topical ABx e.g. fusidic acid or chloramphenicol. Safety net with some red flags and advice PHE does not recommend exclusion from school or care.
55
Q

Allergic conjunctivitis

A
  • Acute from a type 1 hypersensitivity reaction = swelling (oedema) of eyelids, itch, onset after exposure to an allergen, will resolve on own, avoid future exposure.
  • Chronic allergic in atopy patients = sticky mucous discharge, ulcerated cornea, Rx with topical steroids.
  • Allergy to eyedrops.
56
Q

Chemical conjunctivitis

A
  • Red, bleeding eye.
  • On healing can get scarring.
  • Rx = irrigate eye until pH is normal.
57
Q

Bacterial Keratitis

A
  • Staph, epidermidis, S.aureus.
  • Infection of cornea.
  • Purulent discharge, soreness, visual opacity/hazziness in cornea.
  • Ix = biopsy/scrapes of cornea for mc+s.
  • Rx = topical ABx.
58
Q

Acute anterior uveitis causes

A

Sero-neg arthropathies e.g. Ank spond, IBD, psoriatic arthritis.

Granulomatous diseases e.g. sarcoidosis, syphilis.

59
Q

What makes up the uvea

A

iris, ciliary body and choroid

60
Q

Presentation of acute anterior uveitis

A
  • Acute, painful, red eye.
  • Usually unilateral.
  • Photophobia
  • do good systemic enquiry*

Slit lamp examination:
Irregular pupil
Posterior synechiae (iris adhered to lens, binding pupil)
Aqueous cells and flare (from protein exudates)
Keratic precipitates (clumps of inflammatory cells)
Hypopyon (yellowish exudate in the lower part),

61
Q

Mx of acute anterior uveitis

A

Steroids.

62
Q

Which is more serious episcleritis or scleritis

A

Scleritis - rarer but more serious and often associated with systemic vasculitis.

63
Q

Presentation of scleritis

A

Painful red eye. Pain is worse at night and on eye movement.

Violet hue.

64
Q

Presentation of episleritis

A

Redness of eye but no pain, no discharge and no treatment needed (NSAIDs can speed up recovery).

65
Q

Red 🚩flags for red eyes

A
  • Severe pain
  • Photophobia
  • Coloured halos (corneal oedema in acute closed angle glaucoma).
  • Reduced acuity
66
Q

Stye

A

Horeolum
Sterile, inflammation of the gland or hair follicle on eyelid.
Rx = lid hygiene with warm compress, massage with flannel.

67
Q

Red reflex

A

Light reflected on the fundus of a patient produces a red reflex on opthalmoscope.

68
Q

Cotton wool spot

A

Ischaemic of the nerve fibres, soft exudates.

69
Q

Innervation to constrict pupil

A

Parasympathetic CN3, acetylcholine neurotransmitter.

Can do it artificially with phenylephrine.

70
Q

Innervation to dilate pupil

A

Sympathetic, noradrenaline neurotransmitter. Can do it artificially with Tropicamide, atropine, cyclopentolate.

71
Q

3 reflex of the pupil

A

Reaction to light = constrict.
Reaction to dark = dilate
Reaction to near-target = mitosis, convergence, accommodation of lens.

72
Q

Horner’s syndrome presentation and causes

A
  • Miosis, ptosis, anhydrosis, normal light and near-large reflex, increased anisocoria in dark.
  • Pancoast’s tumour, neck surgery e.g. thyroidectomy, internal carotid artery aneurysm.
73
Q

3rd nerve palsy

A

Dilated, un-reactive pupil.
Ptosis
Divergent eyes.

Causes = vascular disease, compression (do angiogram for posterior communicating artery aneurysm).

74
Q

Differentials for anisocoria (unequal pupils)

A

Acute anterior uveitis
Acute closed angle glaucoma
Adie’s pupil

75
Q

How to describe the optic disc from opthalmoscope

A
  • Is red reflex present?

- Colour, contour, cup, circulation.

76
Q

Dot and blot haemorrhages

A

Seen in severe diabetic retinopathy. Deep in retina haemorrhages.

77
Q

Flame haemorrhages

A

Seen in hypertensive retinopathy and retinal vein occlusion.

Superficial haemorrhages

78
Q

What can you use to examine the anterior and posterior segments of the eye?

A 
Anterior = slit lamp.
Posterior = dilate pupil and use additional lenses to magnify.
79
Q

New blood vessels on the iris

A

Rubeosis.
Seen in diabetic retinopathy, central retinal vein occlusion, retinal detachment, and ocular ischaemia.
Rx with pan-retinal photocoagulation.

80
Q

Features of hypertensive retinopathy

A

Microinfarcts
Flame haemorrhages
Heightened reflex to artery (silver wiring)
Hard exudate
Arteriovenous crossing change (nipping) - vein disappears under artery as arterial wall is thickened

81
Q

Questions to include in hx of vision loss

A 
Rapid onset?
Pain?
Central, peripheral
Unilateral, bilateral
Loss of colour
Loss of night vision
82
Q

Painful red eye ∆∆

A

Acute closed angle glaucoma

Scleritis

83
Q

Viral keratitis

A

Herpes simplex 1:

  • Fever, vesicles on lid, conjunctivitis, red eye, pre-auricular lymphadenopathy.
  • DENDRITIC ULCER visible in cornea.
  • Rx with topical antivirals eg. acyclovir.

Varicella zoster/Shingles:

  • Reactivation in ophthalmic division of the trigeminal nerve.
  • Systemically unwell, red eye, pain, vesicles in dermatome, lid swelling, cornea inflammation (keratitis).
  • Rx with acyclovir usually oral.
84
Q

Adie’s pupil

A
  • Ciliary ganglionitis, decreasing innervation to the iris and ciliary body.
  • Enlarged pupil, poor/slow reaction to light (tonic), miosis on accommodation.
  • Ix dilute pilocarpine will cause pupil to constrict (hypersensitivity).
85
Q

Pupil which reacts to accommodation but not light. Pt has a history of risky sexual behaviours and genital ulcer like lesions

A

Argyll Robertson pupil secondary to neurosyphilis.

86
Q

O/E of papilloedema

A
  • Large blind spot on visual field testing.

Opthalmoscope:

  • Swollen optic disc with blurred edges.
  • Dilated and prominent superficial capillaries.
  • No spontaneous venous pulsation.
  • if acute or severe then can see flame hemorrhages and cotton wool spots.
87
Q

Opthalmoscope of atherosclerosis of retinal arterial vessels

A
  • Copper and silver wiring.

- Nipping of retinal vein where it crosses an arteriole.

88
Q

Why do you get cherry red spot at fovea in retinal artery occlusion?

A

Very thin retina layer here with no overlying nerve fibres. See dense vasculature when the thin layer dies from ischaemia.

89
Q

Differentials for bilateral miosis

A

Opiates
Topical pilocarpine
Pontine stroke

90
Q

Differentials for bilateral dilated pupils

A

Cocaine
Amphetamine OD
Guillian Barre
Tricyclic antiDx OD

91
Q

Name 3 causes of a retinal haemorrhage

A

Diabetic retinopathy
Hypertensive retinopathy
Subarachnoid haemorrhage

92
Q

Night blindness + tunnel vision

FHx of vision problemos

A

Retinitis pigmentosa.
Hereditary dystrophy of photoreceptors in retina.
CFx start in childhood.
Loss of peripheral vision, poor night vision, short-sighted (myopia), open angle glaucoma.
Fundoscopy = mottling of retina and black pigmentation.

93
Q

Driving and eye sight

A

Need 6/10 on Snellen chart and to be able to read a reg plate from 20meters with glasses if needed.

94
Q

How to assess potential cause of sudden vision loss?

A

HELLP you distinguish from differentials of sudden loss:

  • Headache associated? – do ESR urgently in all >50 for GCA and anterior ischaemic optic neuropathy.
  • Eye movements hurt? – optic neuritis
  • Lights / flashes / 4Fs preceding visual loss? retinal detachment.
  • Like a curtain? – Amaurosis fugax (may precede permanent loss)
  • Poorly controlled DM? – ?Vitreous haemorrhage

3B Hospital Specialities (17 decks)

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