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
Referral to ophthalmology regarding corneal foreign body
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
26
Pathophysiology of diabetic retinopathy
Hyperglycaemia damages the endothelial cells in retinal vessels Increased vascular permeability causes leakage from vessels Blot haemorrhages, hard exudates
27
Non proliferative diabetic retinopathy
Micro aneurysm, blot haemorrhages, hard exudates, Colton wool,spots, venous beading, intra retinal micro vascular abnormalities
28
Question to always ask in an ophthalmology history
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
29
Proliferative diabetic retinopathy
Neovascularisation Vitreous haemorrhage
30
Diabetic maculopathy
Macular oedema Ischaemic maculopathy
31
Complications of diabetic retinopathy
Retinal detachment Vitreous haemorrhage Rebeosis iridis (new blood vessels in iris) Optic neuropathy Cataracts
32
Management of diabetic retinopathy
Lifestyle measures (as usual)/ glycaemic control (ask if they need support with this) Laser photocoagulation Anti VEGF injections Vitreoretinal surgery
33
Features of episcleritis
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
34
Herpes simplex keratitis
Commonly presents with a dendritic corneal ulcer Red, painful eye Photophobia Watery eye Decreased visual acuity Fluorescin staining- ulcer
35
Management of herpes simplex keratitis
Immediate referral to ophthalmologist Topical aciclovir
36
Herpes zoster ophthalmicus
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)
37
Management of herpes zoster ophthalmicus
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
38
Holmes adie pupil
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
39
Causes of Horner’s syndrome
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
40
Fundoscopy features of hypertensive retinopathy
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
41
Bacterial conjunctivitis
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)
42
Viral conjunctivitis
Sore, red eye Serous discharge Recent URTI Periauricular lymph nodes Usually bilateral
43
Management of infective con
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)
44
Causes of keratitis
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
45
Clinical features of keratitis
Red eye, pain Photophobia Gritty sensation Hypopyon may be seen Reduced visual acuity Watery eye
46
Investigations for keratitis
Visual acuity, fields, eye movements, cranial nerves Fundoscopy Slit lamp examination Swabs (bacteria, viruses, chlamydia) and corneal scrapings for PCR (virus) and acanthamoeba
47
Management of keratitis
Refer to ophthalmology Stop using contacts until symptoms resolve Topical antibiotics or bacterial (chloramphenicol), oral aciclovir if viral Pain relief (cyclopentolate (cycloplegic))
48
Causes of optic neuritis
MS DM Syphyllis
49
Features of optic neuritis
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)
50
Management of optic neuritis
High dose steroids Recovery usually takes 4-6 weeks
51
What is orbital cellulitis
Infection affecting the fat and muscles posterior to the orbital septum within orbit (but not involving the globe)
52
Risks factors for orbital cellulitis
Childhood Previous sinus infection Recent insect bite near eye Ear of facial infection
53
Presentation of orbital cellulitis
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
54
Orbital cellulitis vs pre septal (peri orbital) cellulitis
Reduced visual acuity, proptosis, ophthalmoplegia not seen in preseptal cellulitis
55
Investigations for orbital cellulitis
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))
56
Features of papilloedema on fundoscopy
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.
57
Causes of papilloedema
SOL- neoplastic, vascular Malignant hypertension Idiopathic intracranial hypertension Hydrocephalus Hypercapnia Hyperparathyroidism Hypocalcaemia Vitamin A toxicity
58
Posterior vitreous detachment
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
59
Risk factors for PVD
Older age Near sighted people
60
Symptoms of PVD
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
61
Investigations for PVD
Refer to ophthalmology Visual acuity, fields, eye movements, cranial nerves Fundoscopy Slit lamp NB- no treatment if no retinal tears or retinal detachment
62
Preseptal cellulitis
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.
63
Symptoms of preseptal cellulitis
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
64
Investigations for preseptal cellulitis
Same as orbital cellulitis
65
Management of preseptal cellulitis
Refer to ophthalmology Oral antibiotics (co amoxiclav) Children may require admission for observation
66
Primary open angle glaucoma
Trabecular network offers increased resistance to drainage of aqueous humour (close angle- the iris has moved forward and sealed off the trabecular network)
67
Risk factors for open angle glaucoma
Older age Genetics Black patients Myopia HTN DM Corticosteroids
68
Features of open angle glaucoma
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
Investigations for open angle glaucoma
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
RAPD/Marcus Gunn Pupil
Found by swinging light test Caused by lesion anterior to chiasm Caused by retinal detachment and optic neuritis (MS)
71
Risk factors for retinal detachment
Age Previous cataract surgery Myopia Ear trauma FH Previous history of the condition
72
Retinitis pigmentosa
Night blindness Tunnel vision Fundiscopy- pigmented peripheral retina Alport syndrome
73
Ocular manifestations of RA
Keratoconjunctivitis Sicca (most common) Episcleritis (erythema) Scleritis (erythema and pain) Corneal ulceration Keratitis Iatrogenic; Steroid induced cataract s Chloroquinine retinopathy
74
Features of scleritis
Red eye Painful Watering and photophobia Gradual decrease in vision
75
Causes of sudden loss of vision
Ischaemic/vascular (amaurosis fugax)- thrombosis, embolism, temporal arteritis etc. vitreous haemorrhage Retinal detachment Retinal migraine
76
Posterior vitreous detachment
Flashes of light (photopsia) in peripheral field of vision Floaters (temporal)
77
Retinal detachment
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
Vitreous haemorrhage
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
Causes of tunnel vision
Paipilloedema Glaucoma Retinitis pigmentosa
80
Most common cause of sudden painless loss of vision
Vitreous haemorrhage
81
Causes of vitreous haemorrhage
Proliferative diabetic retinopathy Posterior vitreous detachment Ocular trauma (children and young adults)
82
Investigations for retinal tears, PVD, vitreous haemorrhage
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
Management of open angle glaucoma
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
Strabismus
A squint. The eyes are misaligned and this causes double vision
85
Amblyopia
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
Causes of squint
Idiopathic Hydrocephalus Cerebral palsy SOL (retinoblastoma) Trauma
87
Corneal reflections / Hirschbergs tests
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
Investigations for a squint
Same as usual
89
Management of strabismus
Refer to ophthalmology Occlusive patch over good eye (make weaker eye work)- after referral
90
Funduscopy dry AMD
Drusen Retinal hypopigmentation
91
Fundoscopy Wet ARMD
Retinal discolouration Retinal haemorrhages
92
Intraocular pressure and pupil dilation
Don’t dilate pupils if increased IOP eg. Glaucoma
93
Management of open angle glaucoma
Refer to ophthalmology, lifestyle stuff, driving Medical- eye drops Surgical- trabeculectomy
94
Myopia (near sightedness)
Clear near vision, far vision unclear
95
Hyperopia (far sightedness)
Far vision clear, near vision unclear eg. Reading
96
Astigmatism
Abnormal curvature of cornea Unclear vision at all distances
97
Risks for acute angle closure glaucoma
Increased age, females, FH, south Asian origin, medications eg. Noradrenaline, oxybutinin, TCA eg. Amitriptyline
98
Causes of CRAO
Embolism- carotid artery sclerosis, emboli from atria (AF), Thrombosis of retinal vessels (atherosclerosis) Vasculitis (GCA)
99
Causes of CRVO
HTN, DM Hypercoaguable (polycythaemia Vera, sickle cell disease, OCP, laukaemia)
100
Features of CRAO
Sudden painless loss of vision RAPD
101
Features of CRVO
Sudden painless loss of vision NO RAPD
102
Fundoscopy CRAO
Pale retina Cherry red spot (fovea- choroid underneath)
103
Fundoscopy CRVO
Flame and blot haemorrhages Optic disc oedema Macula oedema
104
Investigations for retinal vessels occlusion
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
Management of CRAO
Treat reversible risk factors and secondary prevention of CVD NB- intravenous tissue-type plasminogen activator (tPA) may be an option in some patients
106
Management of CRVO
Refer to ophthalmology Laser photocoagulation Intravitreal steroids Anti VEGF injections
107
What is amaurosis fugax
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
Causes of amaurosis fugax
Atherosclerosis, carotid artery stenosis, cardiac thrombi Vasculitides eg. GCA, polyarteritis nodosa
109
Management of amaurosis fugax
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
Posterior vitreous detachment
Detachment of the vitreous from the lining of the retina
111
Features of endophthalmitis
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
Investigations for endophthalmitis
Same as for cellulitis
113
Which muscles does CN III innervate
Medial rectus Superior rectus Inferior rectus Inferior oblique LPS
114
Which muscle does CN IV innervate
Superior oblique
115
Which muscle does CN VI innervate
Lateral rectus
116
CN III palsy at rest
Ptosis Dilated pupil Down and eye position
117
CN III palsy on examination
Inability to adduct eye Inability to gaze upwards Inability to gaze downwards
118
CN IV palsy at rest
Tilted head Hypertropia (eye high up)
119
CN IV palsy on examination
Limited depression of adduction
120
CN VI palsy at rest
Eye turns inwards
121
CN VI palsy on examination
Can’t abduct eye
122
Third nerve palsy with sparing of the pupil causes
Diabetes HTN Ischaemic
123
Third nerve palsy without sparing of the pupil causes
Idiopathic Tumour Trauma Cavernous sinus thrombosis PCAA (pupil dilated, often associated pain) Raised ICP MS
124
Investigations for an eye cranial nerve palsy
Observations, diabetes check, full ophthalmic examination HBA1c, CRP, lipids, FBC UE LFT MRI head may need MRI angiography if pupil is involved
125
Features of orbital floor fracture
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
Features of retinoblastoma
Leukocoria Strabismus Painful, red eye Loss of vision Retinal detachment
127
Management of retinoblastoma
Cryotherapy, photocoagulation, brachytherapy if low risk Chemotherapy Surgery (enucleation)
128
Features of congenital cataracts
Leukocoria Strabismus Nystagmus Delay in motor skills
129
Associations with congenital cataracts
Hereditary congenital cataracts TORCH infections eg. Rubella Tetany Trisomy Alport syndrome
130
Causes of Leukocoria
Retinoblastoma until proven otherwise in children Congenital cataracts Retinopathy of prematurity Retinal detachment Coats disease
131
Management of non urgent diplooia (CN palsy)
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
Steroids and eye disease
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
Non medical support for ARMD
Magnification, enlargement of print, contrast enhancement, use of other senses, low vision clinic, support groups, patient education, sensory teams
134
Sudden visual loss in one eye
Optic neuritis CRAO (CRVO) AACG Retinal detachment Wet macular degeneration Vitreous haemorrhage
135
Side effects of prostaglandin analogues
increased eyelash length, iris pigmentation and periocular pigmentation
136
Causes of bitemporal hemianopia
Lesion of optic chiasm Upper quadrant more than lower- pituitary tumour Lower quadrant more than upper- craniopharyngioma
137
What is optic neuropathy
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
Causes of optic neuropathy
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
Prostaglandin analogue
Latanoprost Increases uveoscleral outflow SE- brown iris, increased eyelash length NB- first line treatment in patients with heart block
140
Beta-blockers
Timolol Reduces aqueous production SE- avoid in asthma/ heart block
141
Sympathomimetics/Alpha agonists
Brimonidine Reduces aqueous production and increases outflow SE- hyperaemia, and avoid with TCA's/MAOI's
142
Miotics/ Muscarinic receptor agonists
Pilocarpine Increases uveoscleral outflow SE- constricted pupil, headache, blurred vision
143
Causes of an abnormal pupil shape
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
Causes of mydriasis (dilated pupil)
Third nerve palsy Holmes-Adie syndrome Raised intracranial pressure Congenital Trauma Stimulants such as cocaine Anticholinergics
145
Causes of miosis (constricted pupil)
Horners syndrome (cocaine eye drops have no effect) Cluster headaches Argyll-Robertson pupil (in neurosyphilis) Opiates Nicotine Pilocarpine
146
Difference between Horner syndrome and 3rd nerve palsy
Both- ptosis Horner- anhidrosis, constricted pupil (miosis) (Surgical) 3rd nerve palsy- strabismus (down and out eye), dilated pupil (mydriasis)
147
Stye
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
Cholazion
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
Essential treatment needed for eyelid dysfunction eg. Bell's palsy, ectropion, entropion etc.
Lubricating eye drops (can develop exposure keratitis)- Bell's palsy: tape eyelid shut
150
Trichiasis
Inward growth of the eyelashes (entropion- eyelid moves inwards, not the eyelash growth itself)
151
Corneal abrasion
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
Features of a corneal abrasion
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
Management of a corneal abrasion
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
Subconjunctival haemorrhage
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)
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Causes of a subconjunctival haemorrhage
Idiopathic Hypertension Bleeding disorders (e.g thrombocytopenia) Whooping cough Medications (warfarin, NOACs, antiplatelets) Non-accidental injury Trauma
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Causes of a subconjunctival haemorrhage
Idiopathic Hypertension Bleeding disorders (e.g thrombocytopenia) Whooping cough Medications (warfarin, NOACs, antiplatelets) Non-accidental injury
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Horner's syndrome features
miosis + ptosis + enophthalmos +/- anhydrosis
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PVD vs retinal detachment
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.
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Quadrantinopias
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.))