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Year 4 Additional Notes > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Features of acute angle closure glaucoma

A

Severe pain, may have headache
Decreased visual acuity
Symptoms worse with pupil dilation (watching tv in a dark room)
Firm, red eye
Haloes around lights
Semi dilated non reacting pupil
Dull or hazy cornea
Systemic upset- nausea and vomiting, abdominal pain

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2
Q

Investigations for acute closure glaucoma

A

Refer to ophthalmology
Check visual fields, acuity, eye movements, cranial nerves
Slit lamp examination (without dilation)
Check intraocular pressure with Goldman Tonometry

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3
Q

Management of acute closure glaucoma

A

Refer to ophthalmology
Combination of eye drops- pilocarpine, beta blocker (timolol), alpha agonist (apraclonidine)
Intravenous acetazolamide
Surgery- laser peripheral iridotomy (do in other eye prophylacticaly)

NB- if in community, lie patient down, give pilocarpine eye drops, antiemetic/analgesic, and oral acetazolamide

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4
Q

Risks for ARMD

A

Advancing age
Smoking
FH
HTN, dyslipidaemia, DM

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5
Q

Dry macular degeneration

A

90% cases
Characterised by drusen

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6
Q

Wet macular degeneration

A

10%
Choroidal neovascularisation
Worst prognosis

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7
Q

Features of ARMD

A

Subacute onset
Reduced visual acuity (near field objects)
Central vision loss
Worse vision at night
Perception of flicking lights
Straight lines become wavy

On exam;
Distorted line perception on Amsler grid
Drusen (dry)
Fluid leak/haemorrhage (wet)
Macula depogmentation (both)

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8
Q

Investigations for ARMD

A

Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp microscopy
Fluorescin angiography
OCT- retinal layers

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9
Q

Treatment of ARMD

A

Refer to ophthalmology, advice on driving

Dry- avoid smoking, control BP, healthy lifestyle, visual aids, social support groups, high dose vitamins and minerals eg. vitamin C, zinc, beta carotene can reduce rate of visual loss

Wet- same stuff, but Anti VEGF injections, then laser therapy 2nd (laser neovascularisation)

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10
Q

Allergic conjunctivitis

A

May be seen alone or in context of hay fever
Bilateral symptoms
Conjunctival erythema and swelling (chemo sis)
Itch
History of atopy

Management- Topical or systemic antihistamines, then mast cell stabilisers eg. Sodium cromoglicate

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11
Q

Features of anterior uveitis

A

Acute onset
Ocular pain (may increase with use)
Pupil may be small and fixed, or abnormally shaped
Intense photophobia
Blurred vision
Red eye
Lacrimation
Ciliary flush (red ring)
Hypopyon (visible fluid level)
Visual acuity normal- gradually gets worse

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12
Q

Conditions associated with anterior uveitis

A

Ankylosing spondylitis
Reactive arthritis
IBD (UC, Crohns)
Beckets disease
Sarcoidosis

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13
Q

Management of anterior uveitis

A

Urgent referral to ophthalmology
Pupil dilation
Steroid eye drops

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14
Q

Argyll Robertson pupil

A

Small, irregular pupils
No response to light, but there is accommodation
Causes- DM, syphyllis

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15
Q

Blepharitis

A

Inflammation of eyelid margin
Due to memobian gland dysfunction, seborrhoeic dermatitis/staph infection

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16
Q

Features of blepharitis

A

Bilateral
Grittiness
Sticky eyes in morning
Red eyelid margins
Styes and chalazions are more common
May get secondary conjunctivitis

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17
Q

Management of blepharitis

A

Hot compress twice a day
Lid hygiene- clear debris away with cotton wool buds dipped in boiling water
Artificial tears

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18
Q

Causes of blurred vision

A

Refractive error (most common)
Cataracts
Retinal detachment
ARMD
Acute angle closure glaucoma
Optic neuritis
Amaurosis fugax

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19
Q

Investigations for blurred vision

A

Visual acuity (logMAR chart- pinhole occluders (if it improves- due to refractive error), fields, cranial nerves, eye movements
Fundoscopy

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20
Q

Causes of cataracts

A

Advancing age
Smoking
Increased alcohol
Trauma
DM
long term corticosteroids
Radiation exposure
Hypocalcaemia

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21
Q

Steroids and intraocular pressure

A

Steroids (whether topical or systemic), can increase intraocular pressure and cause glaucoma
Tell patients who recently start steroids to have an eye test in 3 weeks

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22
Q

Features of cataracts

A

Reduced vision
Faded colour vision (things becoming more brown or yellow), colours not as sharp
Glare- lights appear brighter than usual
Starbursts around lights

Defect in the red reflex

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23
Q

Investigations for cataracts

A

Visual fields, acuity, eye movements, cranial nerves
Ophthalmoscopy (normal)
Slit lamp examination- visible cataract

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24
Q

Management of cataracts

A

Non surgical- stronger glasses, use brighter lights
Surgery- remove cloudy lens and implant an artificial one (referral to surgery depends upon whether visual impairment is present, the impact on quality of life, and patient choice)

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25
Q

Referral to ophthalmology regarding corneal foreign body

A

Penetrating eye injury due to sharp or high velocity object
Significant trauma
Chemical injury (irrigate first)
Organic material foreign body (seeds, twig, soil- infection)
Center of cornea
Red flags- severe pain, irregular dilated or non reactive pupils, reduced visual acuity

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26
Q

Pathophysiology of diabetic retinopathy

A

Hyperglycaemia damages the endothelial cells in retinal vessels
Increased vascular permeability causes leakage from vessels
Blot haemorrhages, hard exudates

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27
Q

Non proliferative diabetic retinopathy

A

Micro aneurysm, blot haemorrhages, hard exudates, Colton wool,spots, venous beading, intra retinal micro vascular abnormalities

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28
Q

Question to always ask in an ophthalmology history

A

DIABETES, well controlled, compliant with meds etc.
ALWAYS CHECK BM during investigations for an eye history

NB- this isn’t a condition that can be easily elucidated from the history

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29
Q

Proliferative diabetic retinopathy

A

Neovascularisation
Vitreous haemorrhage

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30
Q

Diabetic maculopathy

A

Macular oedema
Ischaemic maculopathy

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31
Q

Complications of diabetic retinopathy

A

Retinal detachment
Vitreous haemorrhage
Rebeosis iridis (new blood vessels in iris)
Optic neuropathy
Cataracts

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32
Q

Management of diabetic retinopathy

A

Lifestyle measures (as usual)/ glycaemic control (ask if they need support with this)
Laser photocoagulation
Anti VEGF injections
Vitreoretinal surgery

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33
Q

Features of episcleritis

A

Red eye
Classically not painful (in comparison to scleritis)
Watering and mild photophobia
Injected vessels are mobile when gentle pressure is applied to the sclera (in scleritis, the vessels don’t move)
If phenylepinephrine makes it’s better- confirms epislceritis
50% bilateral

Conservative management
Artificial tears

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34
Q

Herpes simplex keratitis

A

Commonly presents with a dendritic corneal ulcer

Red, painful eye
Photophobia
Watery eye
Decreased visual acuity
Fluorescin staining- ulcer

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35
Q

Management of herpes simplex keratitis

A

Immediate referral to ophthalmologist
Topical aciclovir

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36
Q

Herpes zoster ophthalmicus

A

Reactivation of varicella zoster in the area supplied by the ophthalmic division of the trigeminal nerve

Vesicular rash around eye
Hutchinson’s sign- rash on tip or side of nose (nasociliary involvement)

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37
Q

Management of herpes zoster ophthalmicus

A

Oral aciclovir for 7-10 days, within 3 days
May need topical corticosteroids
Same day ophthalmology referral if Hutchinson’s sign is present (rash on tip of nose)

NB- different to herpes keratitis

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38
Q

Holmes adie pupil

A

Benign
Mostly seen in women
Unilateral
Dilated pupil, when constricted, remains that way for a long time, slowly reacts to accommodation, very poorly to light

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39
Q

Causes of Horner’s syndrome

A

Central lesions
Anhidrosis of the face, arm and trunk
Stroke
Syringomyelia
Sclerosis (Multiple)
SOL
Encephalitis

Pre-ganglionic lesions
Anhidrosis of the face
Tumour (Pancoast)
Thyroidectomy
Trauma
Cervical rib

Post-ganglionic lesions
No anhidrosis
Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

NB- STC

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40
Q

Fundoscopy features of hypertensive retinopathy

A

Silver or copper wiring
Arteriovenous nipping
Cotton wool spots (infarcted retina/damaged nerve fibres)
Hard exudates (lipids leak into retina)
Retinal haemorrhages
Papilloedema (ischameia to optic nerve resulting in optic nerve oedema/swelling)

Keith-Wagener classification
1- silver wires, 2- nipping, 3- cotton wool and haemorrhage, 4- papilloedema

Management- lifetsyle eg. smoking, exercise, diet
Comply with anti BP, control other factors like lipids and DM

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41
Q

Bacterial conjunctivitis

A

Sore eye
Sticky eye (stuck together in morning)
Purulent discharge
Usually unilateral

NB- conjunctivitis does not cause pain, photophobia or reduced visual acuity (vision may be blurry when the eye is covered with discharge)

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42
Q

Viral conjunctivitis

A

Sore, red eye
Serous discharge
Recent URTI
Periauricular lymph nodes
Usually bilateral

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43
Q

Management of infective con

A

Normally self limiting and settles within 1-2 weeks
Don’t wear contacts, eye hygiene (cotton wool), don’t share towels, don’t keep rubbing eye
Chloramphenicol drops (ABX), topical fusidic acid (pregnant women)

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44
Q

Causes of keratitis

A

NB- keratitis is inflammation of the cornea

Bacterial- staph, pseudomonas (contact lens wearers)
Fungal
Amoebic (acanthamoebic keratitis- exposure to soil or contaminated water)
Parasitic- onchocercal keratitis
Viral- herpes simplex
Contact lens acute red eye (CLARE)
Exposure keratitis- inadequate eyelid cover

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45
Q

Clinical features of keratitis

A

Red eye, pain
Photophobia
Gritty sensation
Hypopyon may be seen
Reduced visual acuity
Watery eye

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46
Q

Investigations for keratitis

A

Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp examination
Swabs (bacteria, viruses, chlamydia) and corneal scrapings for PCR (virus) and acanthamoeba

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47
Q

Management of keratitis

A

Refer to ophthalmology
Stop using contacts until symptoms resolve
Topical antibiotics or bacterial (chloramphenicol), oral aciclovir if viral
Pain relief (cyclopentolate (cycloplegic))

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48
Q

Causes of optic neuritis

A

MS
DM
Syphyllis

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49
Q

Features of optic neuritis

A

Unilateral decrease in visual acuity over hours to days
Poor discrimination of colours (red desaturation)
Pain worse on eye movement
RAPD
Central scotoma

NB- fundoscopy may be normal (or may show blurring of the optic disc, if it is involved)

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50
Q

Management of optic neuritis

A

High dose steroids
Recovery usually takes 4-6 weeks

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51
Q

What is orbital cellulitis

A

Infection affecting the fat and muscles posterior to the orbital septum within orbit (but not involving the globe)

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52
Q

Risks factors for orbital cellulitis

A

Childhood
Previous sinus infection
Recent insect bite near eye
Ear of facial infection

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53
Q

Presentation of orbital cellulitis

A

Redness and swelling around the eye
Severe ocular pain
Visual disturbance
Proptosis
Painful eye movements (ophthalmolplegia)l Diplopia
Eyelid oedema and ptosis
Nausea and vomiting
Drowsiness
Fever
Difficulty perceiving colour

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54
Q

Orbital cellulitis vs pre septal (peri orbital) cellulitis

A

Reduced visual acuity, proptosis, ophthalmoplegia not seen in preseptal cellulitis

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55
Q

Investigations for orbital cellulitis

A

Ophthalmology review- visual fields, acuity, eye movements, pupils, cranial nerves, eye swab
Bloods- culture, FBC UE LFT CRP
Head CT with contrast (inflammation of orbital tissue, sinusitis)

NB- admit to hospital for IV ABX (cellulitis near the eyes or nose- co-amoxiclav (amoxicillin and clavulanic acid))

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56
Q

Features of papilloedema on fundoscopy

A

Almost always bilateral
Venous engorgement
Blurring of optic disc margin
Elevation of optic disc
Loss of optic cup
Patons lines

NB- When looking for elevation of the optic disc, look at the way the retinal vessels flow across the disc. Vessels are able to flow straight across a flat surface, whereas they will curve over a raised disc.

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57
Q

Causes of papilloedema

A

SOL- neoplastic, vascular
Malignant hypertension
Idiopathic intracranial hypertension
Hydrocephalus
Hypercapnia
Hyperparathyroidism
Hypocalcaemia
Vitamin A toxicity

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58
Q

Posterior vitreous detachment

A

Separation of vitreous membrane from retina
Common, doesn’t cause pain or loss of vision
But, it can lead to tears and detachment of retina

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59
Q

Risk factors for PVD

A

Older age
Near sighted people

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60
Q

Symptoms of PVD

A

Sudden appearance of floaters
Flashes of light in vision
Blurred vision
Cobwebs across vision
Appearance of dark curtain descending (Also retinal detachment)

Weiss ring on Ophthalmoscopy

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61
Q

Investigations for PVD

A

Refer to ophthalmology
Visual acuity, fields, eye movements, cranial nerves
Fundoscopy
Slit lamp

NB- no treatment if no retinal tears or retinal detachment

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62
Q

Preseptal cellulitis

A

Infection of soft tissue around the eye eg. Eyelids, skin, soft tissue, but not the contents of the orbital cavity

Infection spreads from nearby sites eg. Breaks in skin, sinusitis, URTI (common in children)
Usually staph aureus, staph epidermidis, strep etc.

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63
Q

Symptoms of preseptal cellulitis

A

Red swollen painful eye of acute onset
Fever
Erythema and oedema or eyelids
Partial or complete ptosis

If orbital signs- visual disturbance, restricted eye movements, then it’s orbital cellutlitis

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64
Q

Investigations for preseptal cellulitis

A

Same as orbital cellulitis

65
Q

Management of preseptal cellulitis

A

Refer to ophthalmology
Oral antibiotics (co amoxiclav)
Children may require admission for observation

66
Q

Primary open angle glaucoma

A

Trabecular network offers increased resistance to drainage of aqueous humour (close angle- the iris has moved forward and sealed off the trabecular network)

67
Q

Risk factors for open angle glaucoma

A

Older age
Genetics
Black patients
Myopia
HTN
DM
Corticosteroids

68
Q

Features of open angle glaucoma

A

Peripheral visual field loss (nasal scotomas progressing to tunnel vision)
Decreased visual acuity
Optic disc cupping
Haloes around lights
Headaches, impaired adaption to darkness

Optic disc cupping (cup to disc ratio greater than 0.7, normally 0.4-0.7)
Optic disc pallor (atrophy)
Bayoneting of vessels
Cup notching
Disc haemorrhages

69
Q

Investigations for open angle glaucoma

A

Ophthalmology referral
Visual fields, acuity, eye movements, cranial nerves
Fundosocpy WITHOUT DILATION (don’t dilated pupils with increased IOP)
Slit lamp examination with pupil dilation
Tonometry to measure IOP
Gonioscopy (measure chamber configuration and depth)

70
Q

RAPD/Marcus Gunn Pupil

A

Found by swinging light test
Caused by lesion anterior to chiasm
Caused by retinal detachment and optic neuritis (MS)

71
Q

Risk factors for retinal detachment

A

Age
Previous cataract surgery
Myopia
Ear trauma
FH
Previous history of the condition

72
Q

Retinitis pigmentosa

A

Night blindness
Tunnel vision
Fundiscopy- pigmented peripheral retina

Alport syndrome

73
Q

Ocular manifestations of RA

A

Keratoconjunctivitis Sicca (most common)
Episcleritis (erythema)
Scleritis (erythema and pain)
Corneal ulceration
Keratitis

Iatrogenic;
Steroid induced cataract s
Chloroquinine retinopathy

74
Q

Features of scleritis

A

Red eye
Painful
Watering and photophobia
Gradual decrease in vision

75
Q

Causes of sudden loss of vision

A

Ischaemic/vascular (amaurosis fugax)- thrombosis, embolism, temporal arteritis etc.
vitreous haemorrhage
Retinal detachment
Retinal migraine

76
Q

Posterior vitreous detachment

A

Flashes of light (photopsia) in peripheral field of vision
Floaters (temporal)

77
Q

Retinal detachment

A

Dense shadow that peripherally progresses towards central vision
Veil or curtain over filed of vision
Flashing lights
Spider Webs
Straight lines appear curved
Central vision loss
GREY RETINA ON FUNDOSCOPY

78
Q

Vitreous haemorrhage

A

Large bleeds cause sudden painless visual loss
Numerous dark spots and floaters (days preceding)
Red hue in vision

Signs;
Decreased visual acuity
Visual field defect

NB- predisposed by blood thinning agents, diabetes, and trauma

79
Q

Causes of tunnel vision

A

Paipilloedema
Glaucoma
Retinitis pigmentosa

80
Q

Most common cause of sudden painless loss of vision

A

Vitreous haemorrhage

81
Q

Causes of vitreous haemorrhage

A

Proliferative diabetic retinopathy
Posterior vitreous detachment
Ocular trauma (children and young adults)

82
Q

Investigations for retinal tears, PVD, vitreous haemorrhage

A

Referral to ophthalmology
Visual fields, acuity, eye movements, cranial nerves
Fundoscopy (dilated)
Slit lamp examination (red blood cells in anterior vitreous for haemorrhage)
OCT

NB- below are for vitreous haemorrhage

Fluorescin angiography (neovascularisation)
Obrital CT (if open globe injury)

83
Q

Management of open angle glaucoma

A

Supportive- reading aids, support groups, home adoptions etc.
First line- prostaglandin analogue eye drop
Second line- beta blocker, carbonic anhydrase inhibitor, sympathomimetic eye drops
Surgery- trabeculectomy

NB- if FH, screening from 40

NB- reassessment important to exclude progression and visual field loss, do frequently

84
Q

Strabismus

A

A squint. The eyes are misaligned and this causes double vision

85
Q

Amblyopia

A

A lazy eye
This happens when a squint isn’t corrected in childhood- it’s signals are cut off and it becomes less functional

86
Q

Causes of squint

A

Idiopathic
Hydrocephalus
Cerebral palsy
SOL (retinoblastoma)
Trauma

87
Q

Corneal reflections / Hirschbergs tests

A

When a light is shone at the eyes there should be equal and symmetrical corneal reflections
A squint will show an abnormality in alignment on one side

88
Q

Investigations for a squint

A

Same as usual

89
Q

Management of strabismus

A

Refer to ophthalmology
Occlusive patch over good eye (make weaker eye work)- after referral

90
Q

Funduscopy dry AMD

A

Drusen
Retinal hypopigmentation

91
Q

Fundoscopy Wet ARMD

A

Retinal discolouration
Retinal haemorrhages

92
Q

Intraocular pressure and pupil dilation

A

Don’t dilate pupils if increased IOP eg. Glaucoma

93
Q

Management of open angle glaucoma

A

Refer to ophthalmology, lifestyle stuff, driving
Medical- eye drops
Surgical- trabeculectomy

94
Q

Myopia (near sightedness)

A

Clear near vision, far vision unclear

95
Q

Hyperopia (far sightedness)

A

Far vision clear, near vision unclear eg. Reading

96
Q

Astigmatism

A

Abnormal curvature of cornea
Unclear vision at all distances

97
Q

Risks for acute angle closure glaucoma

A

Increased age, females, FH, south Asian origin, medications eg. Noradrenaline, oxybutinin, TCA eg. Amitriptyline

98
Q

Causes of CRAO

A

Embolism- carotid artery sclerosis, emboli from atria (AF),
Thrombosis of retinal vessels (atherosclerosis)
Vasculitis (GCA)

99
Q

Causes of CRVO

A

HTN, DM
Hypercoaguable (polycythaemia Vera, sickle cell disease, OCP, laukaemia)

100
Q

Features of CRAO

A

Sudden painless loss of vision
RAPD

101
Q

Features of CRVO

A

Sudden painless loss of vision
NO RAPD

102
Q

Fundoscopy CRAO

A

Pale retina
Cherry red spot (fovea- choroid underneath)

103
Q

Fundoscopy CRVO

A

Flame and blot haemorrhages
Optic disc oedema
Macula oedema

104
Q

Investigations for retinal vessels occlusion

A

Bedside- fundoscopy and all other eye tests
Bloods- FBC (leukaemia), exclude diabetes, ESR (inflammatory disorder eg. GCA), autoimmune profile (SLE (vein), vasculitis (artery))
Imaging and specialist tests

CRAO- carotid Doppler, echocardiogram, temporal arteritis tests

105
Q

Management of CRAO

A

Treat reversible risk factors and secondary prevention of CVD

NB- intravenous tissue-type plasminogen activator (tPA) may be an option in some patients

106
Q

Management of CRVO

A

Refer to ophthalmology
Laser photocoagulation
Intravitreal steroids
Anti VEGF injections

107
Q

What is amaurosis fugax

A

Sudden painless loss of vision that lasts seconds to minutes and is followed by spontaneous recovery (transient occlusion caused by microemboli, not permanent, so not a CRAO)

108
Q

Causes of amaurosis fugax

A

Atherosclerosis, carotid artery stenosis, cardiac thrombi
Vasculitides eg. GCA, polyarteritis nodosa

109
Q

Management of amaurosis fugax

A

Same day ophthalmology review
Bedside- visual acuity, fields, fundoscopy, eye movements, cranial nerves
Check temporal Artery for tenderness
Bloods- FBC UE KFT lipids BM glucose ESR CRP
Imaging and specialist- Carotid Doppler ultrasound

110
Q

Posterior vitreous detachment

A

Detachment of the vitreous from the lining of the retina

111
Q

Features of endophthalmitis

A

Severe, deep seated ocular pain
Acute loss of vision
Features of sepsis
Floaters

NB- usually after eye surgery

On examination;

Conjunctival hyperaemia and chemosis
Hazy cornea
Hypopyon
RAPD
Decreased visual acuity

112
Q

Investigations for endophthalmitis

A

Same as for cellulitis

113
Q

Which muscles does CN III innervate

A

Medial rectus
Superior rectus
Inferior rectus
Inferior oblique
LPS

114
Q

Which muscle does CN IV innervate

A

Superior oblique

115
Q

Which muscle does CN VI innervate

A

Lateral rectus

116
Q

CN III palsy at rest

A

Ptosis
Dilated pupil
Down and eye position

117
Q

CN III palsy on examination

A

Inability to adduct eye
Inability to gaze upwards
Inability to gaze downwards

118
Q

CN IV palsy at rest

A

Tilted head
Hypertropia (eye high up)

119
Q

CN IV palsy on examination

A

Limited depression of adduction

120
Q

CN VI palsy at rest

A

Eye turns inwards

121
Q

CN VI palsy on examination

A

Can’t abduct eye

122
Q

Third nerve palsy with sparing of the pupil causes

A

Diabetes
HTN
Ischaemic

123
Q

Third nerve palsy without sparing of the pupil causes

A

Idiopathic
Tumour
Trauma
Cavernous sinus thrombosis
PCAA (pupil dilated, often associated pain)
Raised ICP
MS

124
Q

Investigations for an eye cranial nerve palsy

A

Observations, diabetes check, full ophthalmic examination
HBA1c, CRP, lipids, FBC UE LFT
MRI head may need MRI angiography if pupil is involved

125
Q

Features of orbital floor fracture

A

Unilateral periorbital pain, oedema, echymosis
Enophthalmos
Orbital rim step off
Diplopia
Restricted eye movements
Infraorbital paraesthesia

NB- CT head, but rule out brain or spinal cord injury first (severe impact to head)

126
Q

Features of retinoblastoma

A

Leukocoria
Strabismus
Painful, red eye
Loss of vision
Retinal detachment

127
Q

Management of retinoblastoma

A

Cryotherapy, photocoagulation, brachytherapy if low risk

Chemotherapy

Surgery (enucleation)

128
Q

Features of congenital cataracts

A

Leukocoria
Strabismus
Nystagmus
Delay in motor skills

129
Q

Associations with congenital cataracts

A

Hereditary congenital cataracts
TORCH infections eg. Rubella
Tetany
Trisomy
Alport syndrome

130
Q

Causes of Leukocoria

A

Retinoblastoma until proven otherwise in children

Congenital cataracts
Retinopathy of prematurity
Retinal detachment
Coats disease

131
Q

Management of non urgent diplooia (CN palsy)

A

Refer to optometry
Can have eye patch, or if they wear spectacles a prism can be attached to glasses
Surgery can be preformed as a last resort to realign eyes

132
Q

Steroids and eye disease

A

Steroids can cause cataracts and increase intraocular pressure, causing glaucoma

NB- people on steroids, tell them to go to optician after 3 weeks to have eye pressure measured

133
Q

Non medical support for ARMD

A

Magnification, enlargement of print, contrast enhancement, use of other senses, low vision clinic, support groups, patient education, sensory teams

134
Q

Sudden visual loss in one eye

A

Optic neuritis
CRAO (CRVO)
AACG
Retinal detachment
Wet macular degeneration
Vitreous haemorrhage

135
Q

Side effects of prostaglandin analogues

A

increased eyelash length, iris pigmentation and periocular pigmentation

136
Q

Causes of bitemporal hemianopia

A

Lesion of optic chiasm
Upper quadrant more than lower- pituitary tumour
Lower quadrant more than upper- craniopharyngioma

137
Q

What is optic neuropathy

A

A lesion of the optic nerve

reduced acuity in the affected eye
a scotoma (usually central)
impaired colour vision
an afferent pupillary defect
optic atrophy – pale disc

138
Q

Causes of optic neuropathy

A

Inflammatory (optic neuritis), e.g. demyelination, sarcoidosis, vasculitis
Optic nerve trauma or compression, e.g. glioma, meningioma, aneurysm, bone disorders affecting orbit
Toxic, e.g. tobacco/alcohol, ethambutol, methyl alcohol, quinine, hydroxy chloroquine, radiation
Ischaemic optic neuropathy, e.g. giant cell arteritis
Nutritional deficiency, e.g. vitamins B1 and B12
Infection, e.g. orbital cellulitis, syphilis, tuberculosis
Papilloedema

139
Q

Prostaglandin analogue

A

Latanoprost

Increases uveoscleral outflow

SE- brown iris, increased eyelash length

NB- first line treatment in patients with heart block

140
Q

Beta-blockers

A

Timolol

Reduces aqueous production

SE- avoid in asthma/ heart block

141
Q

Sympathomimetics/Alpha agonists

A

Brimonidine

Reduces aqueous production and increases outflow

SE- hyperaemia, and avoid with TCA’s/MAOI’s

142
Q

Miotics/ Muscarinic receptor agonists

A

Pilocarpine

Increases uveoscleral outflow

SE- constricted pupil, headache, blurred vision

143
Q

Causes of an abnormal pupil shape

A

Anterior uveitis

Acute angle closure glaucoma-vertical oval.

Rubeosis iridis

Coloboma- can cause a hole in the iris

Tadpole pupil- usually temporary and associated with migraines.

144
Q

Causes of mydriasis (dilated pupil)

A

Third nerve palsy
Holmes-Adie syndrome
Raised intracranial pressure
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics

145
Q

Causes of miosis (constricted pupil)

A

Horners syndrome (cocaine eye drops have no effect)
Cluster headaches
Argyll-Robertson pupil (in neurosyphilis)
Opiates
Nicotine
Pilocarpine

146
Q

Difference between Horner syndrome and 3rd nerve palsy

A

Both- ptosis

Horner- anhidrosis, constricted pupil (miosis)

(Surgical) 3rd nerve palsy- strabismus (down and out eye), dilated pupil (mydriasis)

147
Q

Stye

A

A tender red lump along the eyelid that may contain pus (infected glands of Zeis or Moll)

Hot compresses and analgesia. Consider topical antibiotics (i.e. chloramphenicol) if it is associated with conjunctivitis or persistent.

148
Q

Cholazion

A

Infected memobian glands (memobian cyst) It presents with a swelling in the eyelid that is typically not tender. It can be tender and red.

Hot compress and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if acutely inflamed. Rarely, surgical drainage needed.

149
Q

Essential treatment needed for eyelid dysfunction eg. Bell’s palsy, ectropion, entropion etc.

A

Lubricating eye drops (can develop exposure keratitis)- Bell’s palsy: tape eyelid shut

150
Q

Trichiasis

A

Inward growth of the eyelashes (entropion- eyelid moves inwards, not the eyelash growth itself)

151
Q

Corneal abrasion

A

Corneal abrasions are scratches or damage to the cornea. They are a cause of red, painful eye. There are some common causes:

Contact lenses
Foreign bodies
Finger nails
Eyelashes
Entropion (inward turning eyelid)

152
Q

Features of a corneal abrasion

A

History of contact lenses or foreign body
Painful red eye
Foreign body sensation
Watering eye
Blurring vision
Photophobia

A fluorescein stain (not angiography) is used to diagnose corneal abrasions

153
Q

Management of a corneal abrasion

A

Simple analgesia (e.g. paracetamol)
Lubricating eye drops can improve symptoms
Antibiotic eye drops (i.e. chloramphenicol)
Bring the patient back after 1 week to check it has healed
Cyclopentolate eye drops dilate the pupil and improve significant symptoms, particularly photophobia.

154
Q

Subconjunctival haemorrhage

A

When small blood vessels within the conjunctiva rupture and release blood into the space between the sclera and the conjunctiva

They often appear after episodes of strenuous activity such as heavy coughing, weight lifting or straining when constipated (or trauma)

155
Q

Causes of a subconjunctival haemorrhage

A

Idiopathic
Hypertension
Bleeding disorders (e.g thrombocytopenia)
Whooping cough
Medications (warfarin, NOACs, antiplatelets)
Non-accidental injury
Trauma

156
Q

Causes of a subconjunctival haemorrhage

A

Idiopathic
Hypertension
Bleeding disorders (e.g thrombocytopenia)
Whooping cough
Medications (warfarin, NOACs, antiplatelets)
Non-accidental injury

157
Q

Horner’s syndrome features

A

miosis + ptosis + enophthalmos +/- anhydrosis

158
Q

PVD vs retinal detachment

A

Although this can cause flashes and floaters, PVD can be thought of as the preceding events leading to retinal detachment. The retina can be thought of as being tugged on, leading to the flashes and floaters until it eventually detaches, causing progressive visual loss peripherally inwards to the centre. Given that this patient has had this progressive visual loss, retinal detachment has occurred.

159
Q

Quadrantinopias

A

PITS refers to which part of the visual field is affected: parietal-inferior visual field / temporal-superior visual field. However, the optic radiations are ‘opposite’ to the visual fields!

NB- PITS lesions are usually caused by an MCA infarction (however, the branch that supplies the area is opposite too eg. inferior quadrantopias (parietal region) are due to superior branch occlusion etc.))

Year 4 Additional Notes (17 decks)

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